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<option value="hydrology"> Hydrology </option>
<option value="hygiene"> Hygiene </option>
<option value="immuno"> Immuno </option>
<option value="idr"> Infectious Disease Reports </option>
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<option value="infrastructures"> Infrastructures </option>
<option value="inorganics"> Inorganics </option>
<option value="insects"> Insects </option>
<option value="instruments"> Instruments </option>
<option value="ijerph"> International Journal of Environmental Research and Public Health (IJERPH) </option>
<option value="ijfs"> International Journal of Financial Studies (IJFS) </option>
<option value="ijms"> International Journal of Molecular Sciences (IJMS) </option>
<option value="IJNS"> International Journal of Neonatal Screening (IJNS) </option>
<option value="ijpb"> International Journal of Plant Biology (IJPB) </option>
<option value="ijtm"> International Journal of Translational Medicine (IJTM) </option>
<option value="ijtpp"> International Journal of Turbomachinery, Propulsion and Power (IJTPP) </option>
<option value="ime"> International Medical Education (IME) </option>
<option value="inventions"> Inventions </option>
<option value="IoT"> IoT </option>
<option value="ijgi"> ISPRS International Journal of Geo-Information (IJGI) </option>
<option value="J"> J </option>
<option value="jal"> Journal of Ageing and Longevity (JAL) </option>
<option value="jcdd"> Journal of Cardiovascular Development and Disease (JCDD) </option>
<option value="jcto"> Journal of Clinical & Translational Ophthalmology (JCTO) </option>
<option value="jcm"> Journal of Clinical Medicine (JCM) </option>
<option value="jcs"> Journal of Composites Science (J. Compos. Sci.) </option>
<option value="jcp"> Journal of Cybersecurity and Privacy (JCP) </option>
<option value="jdb"> Journal of Developmental Biology (JDB) </option>
<option value="jeta"> Journal of Experimental and Theoretical Analyses (JETA) </option>
<option value="jfb"> Journal of Functional Biomaterials (JFB) </option>
<option value="jfmk"> Journal of Functional Morphology and Kinesiology (JFMK) </option>
<option value="jof"> Journal of Fungi (JoF) </option>
<option value="jimaging"> Journal of Imaging (J. Imaging) </option>
<option value="jintelligence"> Journal of Intelligence (J. Intell.) </option>
<option value="jlpea"> Journal of Low Power Electronics and Applications (JLPEA) </option>
<option value="jmmp"> Journal of Manufacturing and Materials Processing (JMMP) </option>
<option value="jmse"> Journal of Marine Science and Engineering (JMSE) </option>
<option value="jmp"> Journal of Molecular Pathology (JMP) </option>
<option value="jnt"> Journal of Nanotheranostics (JNT) </option>
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<option value="ohbm"> Journal of Otorhinolaryngology, Hearing and Balance Medicine (OHBM) </option>
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<option value="jor"> Journal of Respiration (JoR) </option>
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<option value="jvd"> Journal of Vascular Diseases (JVD) </option>
<option value="jox"> Journal of Xenobiotics (JoX) </option>
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<option value="journalmedia"> Journalism and Media </option>
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<option value="marinedrugs"> Marine Drugs </option>
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<option value="medicina"> Medicina </option>
<option value="medicines"> Medicines </option>
<option value="membranes"> Membranes </option>
<option value="merits"> Merits </option>
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<option value="metals"> Metals </option>
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<option value="mps"> Methods and Protocols (MPs) </option>
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<option value="microbiolres"> Microbiology Research </option>
<option value="micromachines"> Micromachines </option>
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<option value="microplastics"> Microplastics </option>
<option value="minerals"> Minerals </option>
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<option value="modelling"> Modelling </option>
<option value="molbank"> Molbank </option>
<option value="molecules"> Molecules </option>
<option value="mti"> Multimodal Technologies and Interaction (MTI) </option>
<option value="muscles"> Muscles </option>
<option value="nanoenergyadv"> Nanoenergy Advances </option>
<option value="nanomanufacturing"> Nanomanufacturing </option>
<option value="nanomaterials"> Nanomaterials </option>
<option value="ndt"> NDT </option>
<option value="network"> Network </option>
<option value="neuroglia"> Neuroglia </option>
<option value="neurolint"> Neurology International </option>
<option value="neurosci"> NeuroSci </option>
<option value="nitrogen"> Nitrogen </option>
<option value="ncrna"> Non-Coding RNA (ncRNA) </option>
<option value="nursrep"> Nursing Reports </option>
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<option value="obesities"> Obesities </option>
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<option value="optics"> Optics </option>
<option value="oral"> Oral </option>
<option value="organics"> Organics </option>
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<option value="osteology"> Osteology </option>
<option value="oxygen"> Oxygen </option>
<option value="parasitologia"> Parasitologia </option>
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<option value="prosthesis"> Prosthesis </option>
<option value="proteomes"> Proteomes </option>
<option value="psych"> Psych </option>
<option value="psychiatryint"> Psychiatry International </option>
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<option value="qubs"> Quantum Beam Science (QuBS) </option>
<option value="quantumrep"> Quantum Reports </option>
<option value="quaternary"> Quaternary </option>
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<option value="reactions"> Reactions </option>
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<option value="reports"> Reports </option>
<option value="reprodmed"> Reproductive Medicine (Reprod. Med.) </option>
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<option value="rheumato"> Rheumato </option>
<option value="risks"> Risks </option>
<option value="robotics"> Robotics </option>
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<option value="scipharm"> Scientia Pharmaceutica (Sci. Pharm.) </option>
<option value="sclerosis"> Sclerosis </option>
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<option value="separations"> Separations </option>
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<option value="signals"> Signals </option>
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<option value="spectroscj"> Spectroscopy Journal </option>
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<option value="surfaces"> Surfaces </option>
<option value="surgeries"> Surgeries </option>
<option value="std"> Surgical Techniques Development </option>
<option value="sustainability"> Sustainability </option>
<option value="suschem"> Sustainable Chemistry </option>
<option value="symmetry"> Symmetry </option>
<option value="synbio"> SynBio </option>
<option value="systems"> Systems </option>
<option value="targets"> Targets </option>
<option value="taxonomy"> Taxonomy </option>
<option value="technologies"> Technologies </option>
<option value="telecom"> Telecom </option>
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<option value="thalassrep"> Thalassemia Reports </option>
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<option value="tourismhosp"> Tourism and Hospitality </option>
<option value="toxics"> Toxics </option>
<option value="toxins"> Toxins </option>
<option value="transplantology"> Transplantology </option>
<option value="traumacare"> Trauma Care </option>
<option value="higheredu"> Trends in Higher Education </option>
<option value="tropicalmed"> Tropical Medicine and Infectious Disease (TropicalMed) </option>
<option value="universe"> Universe </option>
<option value="urbansci"> Urban Science </option>
<option value="uro"> Uro </option>
<option value="vaccines"> Vaccines </option>
<option value="vehicles"> Vehicles </option>
<option value="venereology"> Venereology </option>
<option value="vetsci"> Veterinary Sciences </option>
<option value="vibration"> Vibration </option>
<option value="virtualworlds"> Virtual Worlds </option>
<option value="viruses"> Viruses </option>
<option value="vision"> Vision </option>
<option value="waste"> Waste </option>
<option value="water"> Water </option>
<option value="wind"> Wind </option>
<option value="women"> Women </option>
<option value="world"> World </option>
<option value="wevj"> World Electric Vehicle Journal (WEVJ) </option>
<option value="youth"> Youth </option>
<option value="zoonoticdis"> Zoonotic Diseases </option>
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<option value="64883">Alterations in Cis-Regulatory Elements and Non-Coding RNAs in Human Cancer</option>
<option value="45314">Alternative and Aberrant Splicing in Cancer: How Can We Fix It?</option>
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<option value="69364">Autologous Stem Cell Transplantation or New Cellular Therapies for Neoplasias</option>
<option value="87429">Biological Relevance and Therapeutic Potential of G-Quadruplexes in Cancer</option>
<option value="29866">Blood Coagulation Factors and platelet-derived Mediators in Tumor Cell Biology</option>
<option value="55716">Blood Stem Cells in Pre-leukaemia</option>
<option value="35693">Bone Metastasis: Its Cellular and Molecular Mechanisms</option>
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<option value="61768">Calcium Signaling Remodeling and Functional Role in Cancer Cells</option>
<option value="46876">Cancer Drug Resistance: An Epigenetic Approach</option>
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<option value="43411">Cancer Therapy and the p53-MDM2 Autoregulatory Feedback Loop</option>
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<option value="172366">Circular RNAs: New Insights into the Molecular Biology of Cancer</option>
<option value="61114">Circular RNAs: New Insights into the Molecular Biology of Cancer</option>
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<option value="123145">Combined Hepatocellular-Cholangiocarcinoma: An Update on Epidemiology, Classification, Diagnosis and Management</option>
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<option value="118644">From Chronic Disorders toward Carcinogenesis: Molecular Mechanisms and Potential Therapeutic Approaches</option>
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<option value="51790">Genomic Instability and the DNA Damage Repair Response in Malignant Brain Tumors: Factors Underpinning Cancer Progression, Treatment Resistance, and Inter/Intra-Tumoral Heterogeneity</option>
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<option value="59432">Genomics- and Proteomics-Driven Discoveries on Cancer Metastasis: Impacts on Therapeutics and Diagnostics</option>
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<option value="64443">Harnessing Cancer Vulnerability by Targeting the DNA Damage Response</option>
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<option value="134272">Identification and Clinical Application of Immunological Receptors Targeting Mutated Antigens Expressed by Solid Tumors (Volume II)</option>
<option value="120064">Immune and Genetic Landscape of Lymph Nodes in Cancer</option>
<option value="134570">Immune System Pathways in Inflammatory Tumor Microenvironment and Carcinogenesis</option>
<option value="123209">Immunogenic Cell Death and Associated Antitumor Immunity</option>
<option value="29889">Incorporating DNA Damage Response (DDR) Mechanisms in Cancer Systems</option>
<option value="89179">Influence of Insulins, IGFs, Their Receptors and PI3-Kinase/Akt Pathway Activation on Cancer Development, Progression, and Resistance to Therapy</option>
<option value="22886">Inhibitor of Growth (ING) Genes</option>
<option value="47141">Inside Cancer Genomics: From Structure to Therapy</option>
<option value="61980">Insight into Fatty Acid Metabolism in Colorectal Cancer</option>
<option value="44556">Intra-tumoral Heterogeneity—Experimental Models, Molecular Mechanisms and Clinical Relevance</option>
<option value="98476">Involvement of RNA Polymerases I and III in Cancer Progression</option>
<option value="39954">Involvement of the Substance P/Neurokinin-1 Receptor System in Cancer</option>
<option value="44024">Kidney Cancers</option>
<option value="62054">Large Granular Lymphocytic Leukemia: Genomics and Immunome</option>
<option value="38231">Liquid Biopsy: Latest Advances and Future Challenges</option>
<option value="136105">Liver Cancers Molecular Biomarkers Predicting Outcome</option>
<option value="69445">Lung Adenocarcinoma: Issues and Challenges</option>
<option value="145680">Lung Cancer Proteogenomics: New Era, New Insights</option>
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<option value="98475">MAPK/Akt Signaling Pathways: Function, Regulation, Signaling, and Implications for Cancer Treatment</option>
<option value="50610">Mechanism Underlying Tumor Relapse and Targeted Treatment Strategies</option>
<option value="62644">Mechanisms of Resistance in EGFR-Mutated Non-Small Cell Lung Cancer</option>
<option value="33963">Mechanisms of Resistance in Genito-Urinary Cancers: Innovative Insights in Signaling and Therapeutic Targetings</option>
<option value="42838">Melanoma Signaling Pathways</option>
<option value="158015">Mesenchymal Stem Cells: Key Players in Cancer Progression</option>
<option value="50007">Mesenchymal-Epithelial Transition in Cellular Reprogramming and Cancer</option>
<option value="120512">Metabolic Hallmarks of Malignant Cells</option>
<option value="41091">Metabolic Pathways and Redox Homeostasis in Cancer</option>
<option value="58771">Metabolic Reprogramming as an Exploitable Vulnerability in NSCLC</option>
<option value="94003">Metabolic Rewiring in Cancer</option>
<option value="75235">Metabolism in Ovarian Cancer</option>
<option value="57638">Metastatic Brain Tumors Research</option>
<option value="113228">Metastatic Melanoma: From Gene Profiling to Targeted Therapy</option>
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<option value="70705">miRNAs: New Insights in Tumor Biology</option>
<option value="64965">Mitochondria and Metabolism of Pancreatic Adenocarcinoma Cells</option>
<option value="133362">Mitochondria as Targets for Cancer Therapy</option>
<option value="68633">Models, Mechanisms, and Biomarkers of Prostate Cancer Progression</option>
<option value="63508">Molecular Advances in Diffuse Large B-Cell Lymphoma</option>
<option value="30837">Molecular Alterations in Thyroid Cancer – with Special Focus on Diagnosis, Prognosis and Treatment</option>
<option value="100199">Molecular and Cellular Heterogeneity in an Evolving Tumor Landscape: When Diversity Gives Rise to Aggressive and Drug Resistant Cells</option>
<option value="164025">Molecular and Genetic Diagnosis and Targeted Therapy of Myeloproliferative Neoplasms</option>
<option value="123045">Molecular Biology of Colorectal Cancers</option>
<option value="30924">Molecular Biology of Ovarian Cancer: From Mechanisms of Intraperitoneal Metastasis to Therapeutic Opportunities</option>
<option value="158842">Molecular Biology, Diagnosis and Management of Cervical Cancer</option>
<option value="156826">Molecular Biology, Diagnosis and Management of Endometrial Cancer</option>
<option value="81251">Molecular Characterization of Renal Cell Carcinoma</option>
<option value="97094">Molecular Classification of Cancers</option>
<option value="67739">Molecular Genetics and Treatment of Chronic Myeloid Leukemia</option>
<option value="27464">Molecular Genetics of Breast and Ovary Cancer</option>
<option value="163406">Molecular Landscape in Liver, Pancreas and Gastrointestinal Tumors</option>
<option value="169413">Molecular Mechanism in Wilms Tumor</option>
<option value="63752">Molecular Mechanism of the Interaction Between Cells and Extracellular Matrix in Cancer Progression</option>
<option value="126214">Molecular Mechanisms and Signaling Pathways in Melanoma</option>
<option value="161022">Molecular Mechanisms in Breast Cancer Therapy and Resistance</option>
<option value="166440">Molecular Mechanisms in Prostate Cancer Development</option>
<option value="47066">Molecular Mechanisms of Cancer Drug Resistance: Emerging Biomarkers and Promising Targets to Overcome Tumor Progression</option>
<option value="53377">Molecular Mechanisms of Skin Cancer</option>
<option value="90632">Molecular Mechanisms Underlying Cancer Prevention and Intervention with Bioactive Food Components</option>
<option value="45015">Molecular Mechanisms Underlying Resistance and New Therapeutic Approaches in Pancreatic Cancer</option>
<option value="73054">Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers</option>
<option value="63701">Molecular Pathogenesis and Management of Anaplastic Large Cell Lymphoma</option>
<option value="49793">Molecular Pathways in Cancers</option>
<option value="97008">Molecular Pathways in Cancers</option>
<option value="80369">Molecular Pharmacology of Anti-Cancer Drugs</option>
<option value="127193">Molecular Profiling, Detection, and Therapy of Squamous Cell Carcinomas</option>
<option value="112036">Molecular Signatures in Head and Neck Cancer</option>
<option value="104744">Molecular Targets and Promising Therapeutics of Triple-Negative Breast Cancer</option>
<option value="58814">Molecular Targets for Head and Neck Cancer</option>
<option value="119627">Morphological, Biological, and Molecular Pathways in Cancer and Role of Adjuvant Integrative Medicine</option>
<option value="125888">Mucins and Cancers</option>
<option value="59433">Multi-Omics Approaches in Oncology</option>
<option value="95065">Mutations Driving Human Solid Tumors</option>
<option value="75001">New Insights into Hereditary Cancer Syndromes</option>
<option value="51570">New Insights into the Molecular Mechanism of Epithelial Plasticity in Cancer</option>
<option value="89713">New Insights on Genomics in Thyroid Cancers: Impact on Diagnosis, Prognosis and Therapy</option>
<option value="56138">New Molecular Insights for GC Characterization and Treatment</option>
<option value="86793">New Perspectives of Renal Cell Cancer</option>
<option value="69671">New Solutions for Old Problems. Can Non-Invasive Biomarkers Be the Clue?</option>
<option value="176802">New Treatments for Hepatobiliary Cancer</option>
<option value="30263">Non-canonical Kinases and Substrates in Cancer Progression</option>
<option value="120519">Nonlethal Functions of Caspases in Tumors</option>
<option value="103570">Notch Signaling Pathway in Cancers</option>
<option value="42704">Novel Biomarkers and Molecular Targets in Cancer</option>
<option value="99549">Novel Insights into the Molecular Mechanisms of Treatment Resistance and Predictive Biomarkers in Metastatic Prostate Cancer</option>
<option value="41268">Novel Perspectives on Hypoxia in Cancer</option>
<option value="169191">Novel Transcriptional Factors Regulating Cancer Stemness</option>
<option value="38124">O-GlcNAcylation and Cancer</option>
<option value="54271">Omics in Ovarian Cancer</option>
<option value="100949">Optical Genome Mapping in Hematological Malignancies</option>
<option value="122198">Oxidative Phosphorylation System Dysfunction Role and Mechanisms in Cancer and Its Therapies</option>
<option value="40871">P53 and Hallmarks of Cancer</option>
<option value="58587">p53 and Ralbp1 in Carcinogenesis</option>
<option value="54909">PARPs in Cancer</option>
<option value="67976">Peripheral T-cell Lymphoma: From Biological Research to New Therapies</option>
<option value="94977">Phase Separation, Chromatin Organization and Transcription for Cancers</option>
<option value="56553">Phenotypic Plasticity and the Oncogenic Epithelial-Mesenchymal Transition</option>
<option value="30138">Plasma Proteins and Cancer</option>
<option value="150381">Pleiotropic Pro-tumor Activities Regulated by Overexpressed Yin Yang 1 (YY1) in Human Cancers: Clinical Implications</option>
<option value="150952">Positive and Negative Influences of Senescence on Therapy Response</option>
<option value="102462">Precision Medicine in Thoracic Oncology</option>
<option value="47523" selected="selected">Prostate Cancer—from Molecular Mechanisms to Clinical Care</option>
<option value="40237">Protein Kinase in Leukemia</option>
<option value="120087">Protein Kinases and Pseudokinases in Cancers</option>
<option value="60303">Protein Synthesis in Cancer Cells: Mechanisms and Novel Targeted Therapies</option>
<option value="115399">Proteogenomics Targeting Cervical Cancer</option>
<option value="57206">Proteomics in Cancer</option>
<option value="123359">Rare Gynecological Cancers</option>
<option value="71351">Rare Skin Cancers: Recent Advances in Classification and Management</option>
<option value="89030">Recent Advances in Carcinogenesis Transcription Factors: Biomarkers and Targeted Therapies</option>
<option value="126909">Recent Advances in Diagnosis and Treatment of Pancreatic Cancer</option>
<option value="46807">Recent Advances in Hodgkin’s Lymphoma</option>
<option value="29994">Recent Advances in Tumor Suppressor</option>
<option value="63056">Research in MicroRNA Profiling of Prostate Cancer</option>
<option value="50186">Resistance Mechanisms in Malignant Brain Tumors</option>
<option value="81865">Role of Oxidative Stress in Cancer</option>
<option value="62647">Role of Small GTPase Signaling in Tumorigenesis</option>
<option value="56662">Role of Stromal Cells in Determining Tumor and Cancer Stem Cell Behaviors and Therapeutic Response</option>
<option value="67398">Salivary Gland Adenoid Cystic Carcinoma</option>
<option value="30746">Schwannomas – So-Called Benign Nervous System Tumors</option>
<option value="93997">Signaling by Lysophosphatidic Acid, Sphingosine 1-Phosphate, and Other Lysophospholipids in Cancers</option>
<option value="161989">Signaling Pathway Regulation in Neuroblastoma Oncogenesis</option>
<option value="98870">Signaling Pathways in Breast Cancer</option>
<option value="59056">Signalling Pathways in Metabolic Disease and Cancer</option>
<option value="99849">Signalling Pathways of Cancer Stem Cells</option>
<option value="174401">Significance of KRAS Gene Mutations in Colorectal Cancer</option>
<option value="144872">Single Cell RNA Sequencing in Breast Cancer</option>
<option value="88289">Skull Base Tumours</option>
<option value="48899">Small Molecule Regulators of Cancer-Related Proteins: Where Are We in Precision Medicine?</option>
<option value="44573">Stemness and Differentiation in Cancer</option>
<option value="92630">Stemness and Drug-Persistence in Cancer</option>
<option value="50908">Strategies for Isolation and Phenotypic, Genetic, and Functional Characterization of Circulating Tumor Cells</option>
<option value="63501">Stromal-Epithelial Interactions in Cancer Progression and Therapy Response</option>
<option value="56867">Systems Biology and Intra-tumor Heterogeneity</option>
<option value="48123">Targeted Therapies for the Treatment of Glioblastoma</option>
<option value="95683">Targeted Therapy Based on Cancer Genomics</option>
<option value="40507">Targeting Blood Vessel Components to Treat Cancer</option>
<option value="29890">Targeting Calcium Signaling in Cancer Cells</option>
<option value="44840">Targeting Cyclin-Dependent Kinases in Human Cancers</option>
<option value="43553">Targeting KRAS: Elucidating Mechanisms of Sensitivity and Resistance</option>
<option value="97824">Targeting the (Un)Usual Suspects in Cancer</option>
<option value="103884">Targeting the PI3K–Akt–mTOR Pathway in Cancers: Impact on Tumor Cells and Their Microenvironments</option>
<option value="52597">Targeting Tumor Cell-Intrinsic Checkpoint Molecules: Beyond the Control of Anti-tumor Immunity</option>
<option value="138528">Targeting VEGF Signaling Pathway in Cancer: Angiogenesis and Beyond</option>
<option value="39958">Targeting Wnt Signaling in Cancer: Opportunities Abound If We Can Avoid the Sword of Damocles</option>
<option value="104316">Telomere Biology and Its Role in Cancer Progression: From Basic Science to Application</option>
<option value="93260">Telomeres in Cancer Research</option>
<option value="99990">TGF-β Signaling in Squamous Cell Carcinoma</option>
<option value="122410">The Analysis of Circulating Tumor Cells (CTCs): A New Insights into the Biology of Cancers</option>
<option value="117601">The Biological Mechanism of Cancer Proliferation and Metastasis</option>
<option value="147953">The Biology and Clinical Implementation of Circulating Tumor Cells in Cancer Metastasis</option>
<option value="166883">The Biology of CD44 and Its Role in Cancer Progression: Therapeutic Implications</option>
<option value="43945">The Bright and Dark Sides of Apoptosis and Other Modes of Cell “Death” in Cancer Therapy</option>
<option value="37152">The Emerging Hallmarks of Cancer Metabolism for Precision Oncology Applications</option>
<option value="74400">The Endocrine Basis of Breast Cancer</option>
<option value="119834">The Expressions, Targets, Mechanisms of Action and Functions of RNAs in Brain Tumor</option>
<option value="38196">The Intersection of Cell Death and Metabolism in Cancer</option>
<option value="35138">The Isoforms of the p53 Gene Family and Their Role in Cancer and Aging：Selection Papers from International p53/p63/p73 Isoforms Workshop</option>
<option value="44219">The KEAP1-NRF2 Pathway in Cancer</option>
<option value="42797">The Long Journey into BRCA1/2 Genes Goes On: The Emerging Landscape in BRCA-Mediated Tumors</option>
<option value="157974">The Long Reach of the Retinoblastoma Tumor Suppressor Pathway</option>
<option value="64605">The Migration and Invasion of Oral Squamous Carcinoma Cells: Matrix, Growth Factor and Signaling Involvement</option>
<option value="119606">The Molecular Basis of Thyroid Cancer</option>
<option value="94886">The Pivotal Role of Lipids in Cancer Pathophysiology, Diagnosis and Therapy</option>
<option value="144356">The Response of Prostate Cancers to Androgen Deprivation Therapies</option>
<option value="81249">The Role and Therapeutic Target Potential of RBPs in Cancer</option>
<option value="174083">The Role of Cancer Stem Cells (CSCs) in Cancer Immunotherapy</option>
<option value="33099">The Role of Ceramide Synthases in Cancers</option>
<option value="30526">The Role of Drug Resistance-Associated Proteins in Cancer: from Conventional Anticancer Drugs to Targeting Drugs</option>
<option value="138689">The Role of E3 Ubiquitin Ligases in Cancers</option>
<option value="71195">The Role of Hedgehog Pathway in Cancer</option>
<option value="69809">The Role of Mitochondrial Ion Channels and Transporters in Cancer Development and Progression</option>
<option value="87169">The Role of Natural and Environmental Estrogens in Metabolic Regulation, Inflammation and Advanced Cancer</option>
<option value="54142">The Role of p53 Family in Cancer</option>
<option value="62163">The Role of PGRMC1 and PGRMC2 in Metabolism and Cancer Biology</option>
<option value="101531">The Role of Plasminogen Receptors in Cancers</option>
<option value="136548">The Role of T-cells in Cancer: Circulating Soldiers in Adaptive Immune System</option>
<option value="54484">The Role of the Ubiquitin-Proteasome-System in Human Cancer</option>
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<option value="cleantechnol">Clean Technologies</option>
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<option value="computation">Computation</option>
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<option value="crystals">Crystals</option>
<option value="cimb">Current Issues in Molecular Biology</option>
<option value="curroncol">Current Oncology</option>
<option value="dairy">Dairy</option>
<option value="data">Data</option>
<option value="dentistry">Dentistry Journal</option>
<option value="dermato">Dermato</option>
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<option value="digital">Digital</option>
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<option value="diseases">Diseases</option>
<option value="diversity">Diversity</option>
<option value="dna">DNA</option>
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<option value="ejihpe">European Journal of Investigation in Health, Psychology and Education</option>
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<option value="immuno">Immuno</option>
<option value="idr">Infectious Disease Reports</option>
<option value="informatics">Informatics</option>
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<option value="inorganics">Inorganics</option>
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<option value="instruments">Instruments</option>
<option value="ijerph">International Journal of Environmental Research and Public Health</option>
<option value="ijfs">International Journal of Financial Studies</option>
<option value="ijms">International Journal of Molecular Sciences</option>
<option value="IJNS">International Journal of Neonatal Screening</option>
<option value="ijpb">International Journal of Plant Biology</option>
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<option value="jcto">Journal of Clinical & Translational Ophthalmology</option>
<option value="jcm">Journal of Clinical Medicine</option>
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<option value="jof">Journal of Fungi</option>
<option value="jimaging">Journal of Imaging</option>
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<option value="jmse">Journal of Marine Science and Engineering</option>
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<option value="mps">Methods and Protocols</option>
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<option value="psychiatryint">Psychiatry International</option>
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<option value="reactions">Reactions</option>
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<option value="sclerosis">Sclerosis</option>
<option value="seeds">Seeds</option>
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<option value="signals">Signals</option>
<option value="sinusitis">Sinusitis</option>
<option value="smartcities">Smart Cities</option>
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<option value="solids">Solids</option>
<option value="spectroscj">Spectroscopy Journal</option>
<option value="sports">Sports</option>
<option value="standards">Standards</option>
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<option value="stresses">Stresses</option>
<option value="surfaces">Surfaces</option>
<option value="surgeries">Surgeries</option>
<option value="std">Surgical Techniques Development</option>
<option value="sustainability">Sustainability</option>
<option value="suschem">Sustainable Chemistry</option>
<option value="symmetry">Symmetry</option>
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TOPICAL COLLECTION "PROSTATE CANCER—FROM MOLECULAR MECHANISMS TO CLINICAL CARE"
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A topical collection in Cancers (ISSN 2072-6694). This collection belongs to the
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EDITORS
Dr. Alfonso Urbanucci
E-Mail Website
Collection Editor
Department of Tumor Biology, Institute for Cancer Research, Oslo University
Hospital, 0424 Oslo, Norway
Interests: precision medicine; patients stratification; prostate cancer;
molecular signatures; androgen receptor; MYC; bromodomain; chromatin;
transcriptomics; single cell; gene regulation; radiobiology
Special Issues, Collections and Topics in MDPI journals
Special Issue in BioTech: Biomarkers in the "Omics" Era
Dr. Delila Gasi Tandefelt
E-Mail Website
Collection Editor
Sahlgrenska Cancer Center, Institute of clinical studies, University of
Gothenburg, Gothenburg, Sweden
Interests: prostate cancer; personalized medicine; molecular medicine; liquid
biopsies; cfDNA; cancer biomarkers; cancer genomics
TOPICAL COLLECTION INFORMATION
Dear Colleagues,
Prostate cancer is the second leading cause of cancer-related death in men
worldwide.
The treatment options for men with advanced form of the disease have been
focused on targeting the androgen receptor signaling axes for decades. Recent
technical developments that allow better resolution have increased our
understanding of the molecular mechanisms that are important for prostate cancer
biology and disease evolution.
As new, possibly druggable, targets are discovered and novel treatment options
enter clinical trials, the need to improve the link between molecular
discoveries and clinical management also increases.
This Collection will focus on the current status and challenges in treating
early and progressive prostate cancer, covering topics from basic research and
technical developments to specific new and emerging targets, and the clinical
management of prostate cancer patients.
Dr. Alfonso Urbanucci
Dr. Delila Gasi Tandefelt
Collection Editors
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KEYWORDS
* prostate cancer
* castration resistance
* neuroendocrine prostate cancer
* personalized medicine
* precision medicine
* molecular medicine
* liquid biopsies
* cancer biomarkers
* cancer screening
* PSA
* androgens
* androgen receptor
PUBLISHED PAPERS (31 PAPERS)
Download All Papers
2022
JUMP TO: 2021, 2020
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Open AccessArticle
Multiparametric Magnetic Resonance Imaging Grades the Aggressiveness of Prostate
Cancer
by
Juan Morote
,
Angel Borque-Fernando
,
Marina Triquell
,
Anna Celma
,
Lucas Regis
,
Richard Mast
,
Inés M. de Torres
,
María E. Semidey
,
Anna Santamaría
,
Jacques Planas
,
Luis M. Esteban
and
Enrique Trilla
Cancers 2022, 14(7), 1828; https://doi.org/10.3390/cancers14071828 - 05 Apr 2022
Cited by 3 | Viewed by 1250
Abstract
We sought to find further evidence showing the increase in PCa aggressiveness as
PI-RADS score increases from four surrogates of PCa aggressiveness: i. prostate
biopsy GG (≤3 vs. >3), ii. type of pathology in surgical specimens (favourable
vs. unfavourable), iii. clinical stage (localised [...] Read more.
We sought to find further evidence showing the increase in PCa aggressiveness as
PI-RADS score increases from four surrogates of PCa aggressiveness: i. prostate
biopsy GG (≤3 vs. >3), ii. type of pathology in surgical specimens (favourable
vs. unfavourable), iii. clinical stage (localised vs. advanced), and risk of
recurrence of localised PCa after primary treatment (low-intermediate vs. high).
A group of 692 PCa patients were diagnosed after 3-T multiparametric MRI (mpMRI)
and guided and/or systematic biopsies, showing csPCa (GG ≥ 2) in 547 patients
(79%) and insignificant PCa (iPCa) in 145 (21%). The csPCa rate increased from
32.4% in PI-RADS < 3 to 95.5% in PI-RADS 5 (p < 0.001). GG ≥ 3 was observed in
7.6% of PCa with PI-RADS < 3 and 32.6% in those with PI-RADS > 3 (p < 0.001).
Unfavourable pathology was observed in 38.9% of PCa with PI-RAD < 3 and 68.3% in
those with PI-RADS > 3 (p = 0.030). Advanced disease was not observed in PCa
with PI-RADS ≤ 3, while it existed in 12.7% of those with PI-RADS > 3 (p <
0.001). High-risk recurrence localised PCa was observed in 9.5% of PCa with
PI-RADS < 3 and 35% in those with PI-RADS > 3 (p = 0.001). The PI-RADS score was
an independent predictor of all surrogates of PCa aggressiveness as PSA density.
We confirmed that mpMRI grades PCa aggressiveness. Full article
►▼ Show Figures
Figure 1
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Open AccessReview
Unravelling Prostate Cancer Heterogeneity Using Spatial Approaches to Lipidomics
and Transcriptomics
by
Shadrack M. Mutuku
,
Xander Spotbeen
,
Paul J. Trim
,
Marten F. Snel
,
Lisa M. Butler
and
Johannes V. Swinnen
Cancers 2022, 14(7), 1702; https://doi.org/10.3390/cancers14071702 - 27 Mar 2022
Cited by 3 | Viewed by 2850
Abstract
Due to advances in the detection and management of prostate cancer over the past
20 years, most cases of localised disease are now potentially curable by surgery
or radiotherapy, or amenable to active surveillance without treatment. However,
this has given rise to a [...] Read more.
Due to advances in the detection and management of prostate cancer over the past
20 years, most cases of localised disease are now potentially curable by surgery
or radiotherapy, or amenable to active surveillance without treatment. However,
this has given rise to a new dilemma for disease management; the inability to
distinguish indolent from lethal, aggressive forms of prostate cancer, leading
to substantial overtreatment of some patients and delayed intervention for
others. Driving this uncertainty is the critical deficit of novel targets for
systemic therapy and of validated biomarkers that can inform treatment
decision-making and to select and monitor therapy. In part, this lack of
progress reflects the inherent challenge of undertaking target and biomarker
discovery in clinical prostate tumours, which are cellularly heterogeneous and
multifocal, necessitating the use of spatial analytical approaches. In this
review, the principles of mass spectrometry-based lipid imaging and
complementary gene-based spatial omics technologies, their application to
prostate cancer and recent advancements in these technologies are considered. We
put in perspective studies that describe spatially-resolved lipid maps and
metabolic genes that are associated with prostate tumours compared to benign
tissue and increased risk of disease progression, with the aim of evaluating the
future implementation of spatial lipidomics and complementary transcriptomics
for prognostication, target identification and treatment decision-making for
prostate cancer. Full article
►▼ Show Figures
Figure 1
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Open AccessReview
Crosstalk between Long Non Coding RNAs, microRNAs and DNA Damage Repair in
Prostate Cancer: New Therapeutic Opportunities?
by
Folake Orafidiya
,
Lin Deng
,
Charlotte Lynne Bevan
and
Claire Emily Fletcher
Cancers 2022, 14(3), 755; https://doi.org/10.3390/cancers14030755 - 31 Jan 2022
Cited by 4 | Viewed by 2522
Abstract
It is increasingly appreciated that transcripts derived from non-coding parts of
the human genome, such as long non-coding RNAs (lncRNAs) and microRNAs (miRNAs),
are key regulators of biological processes both in normal physiology and
disease. Their dysregulation during tumourigenesis has attracted significant
interest [...] Read more.
It is increasingly appreciated that transcripts derived from non-coding parts of
the human genome, such as long non-coding RNAs (lncRNAs) and microRNAs (miRNAs),
are key regulators of biological processes both in normal physiology and
disease. Their dysregulation during tumourigenesis has attracted significant
interest in their exploitation as novel cancer therapeutics. Prostate cancer
(PCa), as one of the most diagnosed malignancies and a leading cause of
cancer-related death in men, continues to pose a major public health problem. In
particular, survival of men with metastatic disease is very poor. Defects in DNA
damage response (DDR) pathways culminate in genomic instability in PCa, which is
associated with aggressive disease and poor patient outcome. Treatment options
for metastatic PCa remain limited. Thus, researchers are increasingly targeting
ncRNAs and DDR pathways to develop new biomarkers and therapeutics for PCa.
Increasing evidence points to a widespread and biologically-relevant regulatory
network of interactions between lncRNAs and miRNAs, with implications for major
biological and pathological processes. This review summarises the current state
of knowledge surrounding the roles of the lncRNA:miRNA interactions in PCa DDR,
and their emerging potential as predictive and diagnostic biomarkers. We also
discuss their therapeutic promise for the clinical management of PCa. Full
article
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2021
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Open AccessReview
Proteomic Landscape of Prostate Cancer: The View Provided by Quantitative
Proteomics, Integrative Analyses, and Protein Interactomes
by
Nithin Sadeesh
,
Mauro Scaravilli
and
Leena Latonen
Cancers 2021, 13(19), 4829; https://doi.org/10.3390/cancers13194829 - 27 Sep
2021
Cited by 5 | Viewed by 2939
Abstract
Prostate cancer is the second most frequent cancer of men worldwide. While the
genetic landscapes and heterogeneity of prostate cancer are relatively
well-known already, methodological developments now allow for studying basic and
dynamic proteomes on a large scale and in a quantitative fashion. [...] Read
more.
Prostate cancer is the second most frequent cancer of men worldwide. While the
genetic landscapes and heterogeneity of prostate cancer are relatively
well-known already, methodological developments now allow for studying basic and
dynamic proteomes on a large scale and in a quantitative fashion. This aids in
revealing the functional output of cancer genomes. It has become evident that
not all aberrations at the genetic and transcriptional level are translated to
the proteome. In addition, the proteomic level contains heterogeneity, which
increases as the cancer progresses from primary prostate cancer (PCa) to
metastatic and castration-resistant prostate cancer (CRPC). While multiple
aspects of prostate adenocarcinoma proteomes have been studied, less is known
about proteomes of neuroendocrine prostate cancer (NEPC). In this review, we
summarize recent developments in prostate cancer proteomics, concentrating on
the proteomic landscapes of clinical prostate cancer, cell line and mouse model
proteomes interrogating prostate cancer-relevant signaling and alterations, and
key prostate cancer regulator interactomes, such as those of the androgen
receptor (AR). Compared to genomic and transcriptomic analyses, the view
provided by proteomics brings forward changes in prostate cancer metabolism,
post-transcriptional RNA regulation, and post-translational protein regulatory
pathways, requiring the full attention of studies in the future. Full article
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Open AccessArticle
Androgen Receptor-Mediated Nuclear Transport of NRDP1 in Prostate Cancer Cells
Is Associated with Worse Patient Outcomes
by
Thomas Steele
,
Anhao Sam
,
Shawna Evans
,
Elizabeth Browning
,
Sheryl Krig
,
Katelyn Macias
,
Adarsh Konda
,
Salma Siddiqui
,
Blythe Durbin-Johnson
,
Paramita Ghosh
and
Ruth Vinall
Cancers 2021, 13(17), 4425; https://doi.org/10.3390/cancers13174425 - 02 Sep
2021
Viewed by 1756
Abstract
To our knowledge, our group is the first to demonstrate that NRDP1 is located in
the nucleus as well as the cytoplasm of CaP cells. Subcellular fractionation,
immunohistochemistry, and immunofluorescence analysis combined with confocal
microscopy were used to validate this finding. Subcellular fractionation [...]
Read more.
To our knowledge, our group is the first to demonstrate that NRDP1 is located in
the nucleus as well as the cytoplasm of CaP cells. Subcellular fractionation,
immunohistochemistry, and immunofluorescence analysis combined with confocal
microscopy were used to validate this finding. Subcellular fractionation
followed by western blot analysis revealed a strong association between AR and
NRDP1 localization when AR expression and/or cellular localization was
manipulated via treatment with R1881, AR-specific siRNA, or enzalutamide.
Transfection of LNCaP with various NRDP1 and AR constructs followed by
immunoprecipitation confirmed binding of NRDP1 to AR is possible and determined
that binding requires the hinge region of AR. Co-transfection with NRDP1
constructs and HA-ubiquitin followed by subcellular fractionation confirmed that
nuclear NRDP1 retains its ubiquitin ligase activity. We also show that increased
nuclear NRDP1 is associated with PSA recurrence in CaP patients (n = 162, odds
ratio; 1.238, p = 0.007) and that higher levels of nuclear NRDP1 are found in
castration resistant cell lines (CWR22Rv1 and PC3) compared to androgen
sensitive cell lines (LNCaP and MDA-PCa-3B). The combined data indicate that
NRDP1 plays a role in mediating CaP progression and supports further
investigation of both the mechanism by which nuclear transport occurs and the
identification of specific nuclear targets. Full article
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Open AccessArticle
Identification of Androgen Receptor Metabolic Correlome Reveals the Repression
of Ceramide Kinase by Androgens
by
Laura Camacho
,
Amaia Zabala-Letona
,
Ana R. Cortazar
,
Ianire Astobiza
,
Asier Dominguez-Herrera
,
Amaia Ercilla
,
Jana Crespo
,
Cristina Viera
,
Sonia Fernández-Ruiz
,
Ainara Martinez-Gonzalez
,
Veronica Torrano
,
Natalia Martín-Martín
,
Antonio Gomez-Muñoz
and
Arkaitz Carracedo
Cancers 2021, 13(17), 4307; https://doi.org/10.3390/cancers13174307 - 26 Aug
2021
Cited by 5 | Viewed by 1894
Abstract
Prostate cancer (PCa) is one of the most prevalent cancers in men. Androgen
receptor signaling plays a major role in this disease, and androgen deprivation
therapy is a common therapeutic strategy in recurrent disease. Sphingolipid
metabolism plays a central role in cell death, [...] Read more.
Prostate cancer (PCa) is one of the most prevalent cancers in men. Androgen
receptor signaling plays a major role in this disease, and androgen deprivation
therapy is a common therapeutic strategy in recurrent disease. Sphingolipid
metabolism plays a central role in cell death, survival, and therapy resistance
in cancer. Ceramide kinase (CERK) catalyzes the phosphorylation of ceramide to
ceramide 1-phosphate, which regulates various cellular functions including cell
growth and migration. Here we show that activated androgen receptor (AR) is a
repressor of CERK expression. We undertook a bioinformatics strategy using PCa
transcriptomics datasets to ascertain the metabolic alterations associated with
AR activity. CERK was among the most prominent negatively correlated genes in
our analysis. Interestingly, we demonstrated through various experimental
approaches that activated AR reduces the mRNA expression of CERK: (i) expression
of CERK is predominant in cell lines with low or negative AR activity; (ii) AR
agonist and antagonist repress and induce CERK mRNA expression, respectively;
(iii) orchiectomy in wildtype mice or mice with PCa (harboring prostate-specific
Pten deletion) results in elevated Cerk mRNA levels in prostate tissue.
Mechanistically, we found that AR represses CERK through interaction with its
regulatory elements and that the transcriptional repressor EZH2 contributes to
this process. In summary, we identify a repressive mode of AR that influences
the expression of CERK in PCa. Full article
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Open AccessArticle
Definition of Outcome-Based Prostate-Specific Antigen (PSA) Thresholds for
Advanced Prostate Cancer Risk Prediction
by
Simona Ferraro
,
Marco Bussetti
,
Niccolò Bassani
,
Roberta Simona Rossi
,
Giacomo Piero Incarbone
,
Filippo Bianchi
,
Marco Maggioni
,
Letterio Runza
,
Ferruccio Ceriotti
and
Mauro Panteghini
Cancers 2021, 13(14), 3381; https://doi.org/10.3390/cancers13143381 - 06 Jul
2021
Cited by 23 | Viewed by 2193
Abstract
We defined prostate-specific antigen (PSA) thresholds from a well calibrated
risk prediction model for identifying and excluding advanced prostate cancer
(PCa). We retrieved 902 biopsied patients with a pre-biopsy PSA determination
(Roche assay). A logistic regression model predictive for PCa including the main
[...] Read more.
We defined prostate-specific antigen (PSA) thresholds from a well calibrated
risk prediction model for identifying and excluding advanced prostate cancer
(PCa). We retrieved 902 biopsied patients with a pre-biopsy PSA determination
(Roche assay). A logistic regression model predictive for PCa including the main
effects [i.e., PSA, age, histological evidence of glandular inflammation (GI)]
was built after testing the accuracy by calibration plots and Hosmer-Lemeshow
test for goodness of fit. PSA thresholds were derived by assuming a diagnostic
sensitivity of 95% (rule-out) and 80% (rule-in) for overall and advanced/poorly
differentiated PCa. In patients without GI, serum PSA concentrations ≤ 4.1 (<65
years old) and ≤3.7 μg/L (≥65 years old) excluded an advanced PCa (defined as
Gleason score ≥ 7 at biopsy), with a negative predictive value of 95.1% [95%
confidence interval (CI): 83.0–98.7] and 88.8% (CI: 80.2–93.9), respectively,
while PSA > 5.7 (<65) and >6.1 μg/L (≥65) should address biopsy referral. In
presence of GI, PSA did not provide a valid estimate for risk of advanced cancer
because of its higher variability and the low pre-test probability of PCa. The
proposed PSA thresholds may support biopsy decision except for patients with
asymptomatic prostatitis who cannot be pre-biopsy identified. Full article
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Open AccessReview
Chromatin and Epigenetic Dysregulation of Prostate Cancer Development,
Progression, and Therapeutic Response
by
Konsta Kukkonen
,
Sinja Taavitsainen
,
Laura Huhtala
,
Joonas Uusi-Makela
,
Kirsi J. Granberg
,
Matti Nykter
and
Alfonso Urbanucci
Cancers 2021, 13(13), 3325; https://doi.org/10.3390/cancers13133325 - 02 Jul
2021
Cited by 8 | Viewed by 4579
Abstract
The dysregulation of chromatin and epigenetics has been defined as the
overarching cancer hallmark. By disrupting transcriptional regulation in normal
cells and mediating tumor progression by promoting cancer cell plasticity, this
process has the ability to mediate all defined hallmarks of cancer. In [...]
Read more.
The dysregulation of chromatin and epigenetics has been defined as the
overarching cancer hallmark. By disrupting transcriptional regulation in normal
cells and mediating tumor progression by promoting cancer cell plasticity, this
process has the ability to mediate all defined hallmarks of cancer. In this
review, we collect and assess evidence on the contribution of chromatin and
epigenetic dysregulation in prostate cancer. We highlight important mechanisms
leading to prostate carcinogenesis, the emergence of castration-resistance upon
treatment with androgen deprivation therapy, and resistance to antiandrogens. We
examine in particular the contribution of chromatin structure and epigenetics to
cell lineage commitment, which is dysregulated during tumorigenesis, and cell
plasticity, which is altered during tumor progression. Full article
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Open AccessReview
Response to Androgens and Androgen Receptor Antagonists in the Presence of
Cytokines in Prostate Cancer
by
Zoran Culig
Cancers 2021, 13(12), 2944; https://doi.org/10.3390/cancers13122944 - 12 Jun
2021
Cited by 6 | Viewed by 1917
Abstract
Non-steroidal anti-androgens have a major role in the treatment of non-localized
prostate cancer. Interleukins are involved in the regulation of many cellular
functions in prostate cancer and also modify cellular response to
anti-androgens. A specific role of selected IL is presented in this [...] Read
more.
Non-steroidal anti-androgens have a major role in the treatment of non-localized
prostate cancer. Interleukins are involved in the regulation of many cellular
functions in prostate cancer and also modify cellular response to
anti-androgens. A specific role of selected IL is presented in this review. IL-8
is a cytokine expressed in prostate cancer tissue and microenvironment and
promotes proliferation and androgen receptor-mediated transcription. In
contrast, IL-1 displays negative effects on expression of androgen receptor and
its target genes. A subgroup of prostate cancers show neuroendocrine
differentiation, which may be in part stimulated by androgen ablation. A similar
effect was observed after treatment of cells with IL-10. Another cytokine which
is implicated in regulation of androgenic response is IL-23, secreted by myeloid
cells. Most studies on androgens and IL were carried out with IL-6, which acts
through the signal transducer and activator of the transcription (STAT) factor
pathway. IL-6 is implicated in resistance to enzalutamide. Activation of the
STAT-3 pathway is associated with increased cellular stemness. IL-6 activation
of the androgen receptor in some prostate cancers is associated with increased
growth in vitro and in vivo. Molecules such as galiellalactone or niclosamide
have an inhibitory effect on both androgen receptor and STAT-3 pathways. Full
article
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Open AccessCommentary
Novel Target Opportunities in Non-Metastatic Castrate Resistant Prostate Cancer
by
Stephanie Gleicher
,
Baylee A. Porter
,
Disharee Nath
,
Guanqun Li
,
Rakesh Khanna
,
Hanan Goldberg
,
Marcin Kortylewski
,
Gennady Bratslavsky
and
Leszek Kotula
Cancers 2021, 13(10), 2426; https://doi.org/10.3390/cancers13102426 - 17 May
2021
Cited by 1 | Viewed by 2131
Abstract
Nearly one third of men will incur biochemical recurrence after treatment for
localized prostate cancer. Androgen deprivation therapy (ADT) is the therapeutic
mainstay; however, some patients will transition to a castrate resistant state
(castrate resistant prostate cancer, CRPC). Subjects with CRPC may develop [...]
Read more.
Nearly one third of men will incur biochemical recurrence after treatment for
localized prostate cancer. Androgen deprivation therapy (ADT) is the therapeutic
mainstay; however, some patients will transition to a castrate resistant state
(castrate resistant prostate cancer, CRPC). Subjects with CRPC may develop
symptomatic metastatic disease (mCRPC) and incur mortality several years later.
Prior to metastatic disease, however, men acquire non-metastatic CRPC (nmCRPC)
which lends the unique opportunity for intervention to delay disease progression
and symptoms. This review addresses current therapies for nmCRPC, as well as
novel therapeutics and pathway strategies targeting men with nmCRPC. Full
article
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Open AccessArticle
Gene Regulation Network Analysis on Human Prostate Orthografts Highlights a
Potential Role for the JMJD6 Regulon in Clinical Prostate Cancer
by
Mario Cangiano
,
Magda Grudniewska
,
Mark J. Salji
,
Matti Nykter
,
Guido Jenster
,
Alfonso Urbanucci
,
Zoraide Granchi
,
Bart Janssen
,
Graham Hamilton
,
Hing Y. Leung
and
Inès J. Beumer
Cancers 2021, 13(9), 2094; https://doi.org/10.3390/cancers13092094 - 26 Apr 2021
Cited by 5 | Viewed by 2185
Abstract
Background: Prostate cancer (PCa) is the second most common tumour diagnosed in
men. Tumoral heterogeneity in PCa creates a significant challenge to develop
robust prognostic markers and novel targets for therapy. An analysis of gene
regulatory networks (GRNs) in PCa may provide insight [...] Read more.
Background: Prostate cancer (PCa) is the second most common tumour diagnosed in
men. Tumoral heterogeneity in PCa creates a significant challenge to develop
robust prognostic markers and novel targets for therapy. An analysis of gene
regulatory networks (GRNs) in PCa may provide insight into progressive PCa.
Herein, we exploited a graph-based enrichment score to integrate data from GRNs
identified in preclinical prostate orthografts and differentially expressed
genes in clinical resected PCa. We identified active regulons (transcriptional
regulators and their targeted genes) associated with PCa recurrence following
radical prostatectomy. Methods: The expression of known transcription factors
and co-factors was analysed in a panel of prostate orthografts (n = 18). We
searched for genes (as part of individual GRNs) predicted to be regulated by the
highest number of transcriptional factors. Using differentially expressed gene
analysis (on a per sample basis) coupled with gene graph enrichment analysis, we
identified candidate genes and associated GRNs in PCa within the UTA cohort,
with the most enriched regulon being JMJD6, which was further validated in two
additional cohorts, namely EMC and ICGC cohorts. Cox regression analysis was
performed to evaluate the association of the JMJD6 regulon activity with
disease-free survival time in the three clinical cohorts as well as compared to
three published prognostic gene signatures (TMCC11, BROMO-10 and HYPOXIA-28).
Results: 1308 regulons were correlated to transcriptomic data from the three
clinical prostatectomy cohorts. The JMJD6 regulon was identified as the top
enriched regulon in the UTA cohort and again validated in the EMC cohort as the
top-ranking regulon. In both UTA and EMC cohorts, the JMJD6 regulon was
significantly associated with cancer recurrence. Active JMJD6 regulon also
correlated with disease recurrence in the ICGC cohort. Furthermore, Kaplan–Meier
analysis confirmed shorter time to recurrence in patients with active JMJD6
regulon for all three clinical cohorts (UTA, EMC and ICGC), which was not the
case for three published prognostic gene signatures (TMCC11, BROMO-10 and
HYPOXIA-28). In multivariate analysis, the JMJD6 regulon status significantly
predicted disease recurrence in the UTA and EMC, but not ICGC datasets, while
none of the three published signatures significantly prognosticate for cancer
recurrence. Conclusions: We have characterised gene regulatory networks from
preclinical prostate orthografts and applied transcriptomic data from three
clinical cohorts to evaluate the prognostic potential of the JMJD6 regulon. Full
article
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Open AccessArticle
Increased Pathway Complexity Is a Prognostic Biomarker in Metastatic
Castration-Resistant Prostate Cancer
by
Bram De Laere
,
Alessio Crippa
,
Ashkan Mortezavi
,
Christophe Ghysel
,
Prabhakar Rajan
,
Martin Eklund
,
Alexander Wyatt
,
Luc Dirix
,
Piet Ost
,
Henrik Grönberg
,
Johan Lindberg
and on behalf of the CORE and ProBio Investigators
Cancers 2021, 13(7), 1588; https://doi.org/10.3390/cancers13071588 - 30 Mar 2021
Cited by 1 | Viewed by 2273
Abstract
Metastatic castration-resistant prostate cancer (mCRPC) is a heterogeneous
disease, characterized by common and rare driver gene alterations that provide a
selective growth advantage for progressing tumour cells. We hypothesized that
the number of distinct gene driver alteration-affected pathways or gene classes
was associated [...] Read more.
Metastatic castration-resistant prostate cancer (mCRPC) is a heterogeneous
disease, characterized by common and rare driver gene alterations that provide a
selective growth advantage for progressing tumour cells. We hypothesized that
the number of distinct gene driver alteration-affected pathways or gene classes
was associated with poor prognosis in patients initiating androgen receptor
signalling inhibitors (ARSi). We performed a post hoc analysis of an amalgamated
baseline circulating tumour DNA (ctDNA) mutational landscape dataset of
ARSi-treated men with mCRPC (n = 342). We associated the detected hotspot,
pathogenic, and/or high impact protein function-affecting perturbations in 39
genes into 13 pathways. Progression-free (PFS) and overall survival (OS) were
analysed using Kaplan–Meier curves and multivariate Cox regression models.
Driver gene alterations were detected in 192/342 (56.1%) evaluable patients. An
increased number of affected pathways, coined pathway complexity index (PCI),
resulted in a decremental PFS and OS, and was independently associated with
prognosis once ≥3 pathway or gene classes were affected (PFS HR (95%CI): 1.7
(1.02–2.84), p = 0.04, and OS HR (95%CI): 2.5 (1.06–5.71), p = 0.04).
Additionally, visceral disease and baseline PSA and plasma ctDNA levels were
independently associated with poor prognosis. Elevated PCI is associated with
poor ARSi outcome and supports comprehensive genomic profiling to better infer
mCRPC prognosis. Full article
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Open AccessArticle
STAMP2 Expression Mediated by Cytokines Attenuates Their Growth-Limiting Effects
in Prostate Cancer Cells
by
Nicklas Pihlstrøm
,
Yang Jin
,
Zeynep Nenseth
,
Omer F. Kuzu
and
Fahri Saatcioglu
Cancers 2021, 13(7), 1579; https://doi.org/10.3390/cancers13071579 - 30 Mar 2021
Cited by 6 | Viewed by 1842
Abstract
Inflammatory events and dysregulated cytokine expression are implicated in
prostate cancer (PCa), but the underlying molecular mechanisms are poorly
understood at present. We have previously identified six transmembrane protein
of the prostate 2 (STAMP2, also known as STEAP4) as an androgen-regulated gene,
as [...] Read more.
Inflammatory events and dysregulated cytokine expression are implicated in
prostate cancer (PCa), but the underlying molecular mechanisms are poorly
understood at present. We have previously identified six transmembrane protein
of the prostate 2 (STAMP2, also known as STEAP4) as an androgen-regulated gene,
as well as a key regulator of PCa growth and survival. STAMP2 is also regulated
by, and participates in, inflammatory signaling in other tissues and
pathologies. Here, we show that the proinflammatory cytokines interleukin 6
(IL-6) and Interleukin 1 beta (IL-1β) significantly increase and strongly
synergize in promoting STAMP2 expression in PCa cells. The two cytokines
increase androgen-induced STAMP2 expression, but not expression of other known
androgen target genes, suggesting a unique interplay of androgens and cytokines
in regulating STAMP2 expression. Interestingly, STAMP2 knockdown significantly
increased the ability of IL-6 and IL-1β to inhibit PCa cell growth in vitro.
These results suggest that STAMP2 may represent a unique node through which
inflammatory events mediate their effects on PCa growth and survival. Full
article
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Open AccessReview
Preclinical Models in Prostate Cancer: Resistance to AR Targeting Therapies in
Prostate Cancer
by
Wout Devlies
,
Florian Handle
,
Gaëtan Devos
,
Steven Joniau
and
Frank Claessens
Cancers 2021, 13(4), 915; https://doi.org/10.3390/cancers13040915 - 22 Feb 2021
Cited by 9 | Viewed by 2584
Abstract
Prostate cancer is an androgen-driven tumor. Different prostate cancer therapies
consequently focus on blocking the androgen receptor pathway. Clinical studies
reported tumor resistance mechanisms by reactivating and bypassing the androgen
pathway. Preclinical models allowed the identification, confirmation, and
thorough study of these pathways. [...] Read more.
Prostate cancer is an androgen-driven tumor. Different prostate cancer therapies
consequently focus on blocking the androgen receptor pathway. Clinical studies
reported tumor resistance mechanisms by reactivating and bypassing the androgen
pathway. Preclinical models allowed the identification, confirmation, and
thorough study of these pathways. This review looks into the current and future
role of preclinical models to understand resistance to androgen
receptor-targeted therapies. Increasing knowledge on this resistance will
greatly improve insights into tumor pathophysiology and future treatment
strategies in prostate cancer. Full article
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Open AccessReview
The Value of Real-World Data in Understanding Prostate Cancer Risk and Improving
Clinical Care: Examples from Swedish Registries
by
Kerri Beckmann
,
Hans Garmo
,
Ingela Franck Lissbrant
and
Pär Stattin
Cancers 2021, 13(4), 875; https://doi.org/10.3390/cancers13040875 - 19 Feb 2021
Cited by 4 | Viewed by 3379
Abstract
Real-world data (RWD), that is, data from sources other than controlled clinical
trials, play an increasingly important role in medical research. The development
of quality clinical registers, increasing access to administrative data sources,
growing computing power and data linkage capacities have contributed to [...]
Read more.
Real-world data (RWD), that is, data from sources other than controlled clinical
trials, play an increasingly important role in medical research. The development
of quality clinical registers, increasing access to administrative data sources,
growing computing power and data linkage capacities have contributed to greater
availability of RWD. Evidence derived from RWD increases our understanding of
prostate cancer (PCa) aetiology, natural history and effective management. While
randomised controlled trials offer the best level of evidence for establishing
the efficacy of medical interventions and making causal inferences, studies
using RWD offer complementary evidence about the effectiveness, long-term
outcomes and safety of interventions in real-world settings. RWD provide the
only means of addressing questions about risk factors and exposures that cannot
be “controlled”, or when assessing rare outcomes. This review provides examples
of the value of RWD for generating evidence about PCa, focusing on studies using
data from a quality clinical register, namely the National Prostate Cancer
Register (NPCR) Sweden, with longitudinal data on advanced PCa in
Patient-overview Prostate Cancer (PPC) and data linkages to other sources in
Prostate Cancer data Base Sweden (PCBaSe). Full article
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Open AccessEditor’s ChoiceReview
Preclinical and Clinical Status of PSMA-Targeted Alpha Therapy for Metastatic
Castration-Resistant Prostate Cancer
by
Asta Juzeniene
,
Vilde Yuli Stenberg
,
Øyvind Sverre Bruland
and
Roy Hartvig Larsen
Cancers 2021, 13(4), 779; https://doi.org/10.3390/cancers13040779 - 13 Feb 2021
Cited by 29 | Viewed by 4304
Abstract
Bone, lymph node, and visceral metastases are frequent in castrate-resistant
prostate cancer patients. Since such patients have only a few months’ survival
benefit from standard therapies, there is an urgent need for new personalized
therapies. The prostate-specific membrane antigen (PSMA) is overexpressed in
[...] Read more.
Bone, lymph node, and visceral metastases are frequent in castrate-resistant
prostate cancer patients. Since such patients have only a few months’ survival
benefit from standard therapies, there is an urgent need for new personalized
therapies. The prostate-specific membrane antigen (PSMA) is overexpressed in
prostate cancer and is a molecular target for imaging diagnostics and targeted
radionuclide therapy (theragnostics). PSMA-targeted α therapies (PSMA-TAT) may
deliver potent and local radiation more selectively to cancer cells than
PSMA-targeted β− therapies. In this review, we summarize both the recent
preclinical and clinical advances made in the development of PSMA-TAT, as well
as the availability of therapeutic α-emitting radionuclides, the development of
small molecules and antibodies targeting PSMA. Lastly, we discuss the
potentials, limitations, and future perspectives of PSMA-TAT. Full article
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Open AccessReview
Identification of Germline Genetic Variants that Increase Prostate Cancer Risk
and Influence Development of Aggressive Disease
by
Edward J. Saunders
,
Zsofia Kote-Jarai
and
Rosalind A. Eeles
Cancers 2021, 13(4), 760; https://doi.org/10.3390/cancers13040760 - 12 Feb 2021
Cited by 16 | Viewed by 2661
Abstract
Prostate cancer (PrCa) is a heterogeneous disease, which presents in individual
patients across a diverse phenotypic spectrum ranging from indolent to fatal
forms. No robust biomarkers are currently available to enable routine screening
for PrCa or to distinguish clinically significant forms, therefore late [...]
Read more.
Prostate cancer (PrCa) is a heterogeneous disease, which presents in individual
patients across a diverse phenotypic spectrum ranging from indolent to fatal
forms. No robust biomarkers are currently available to enable routine screening
for PrCa or to distinguish clinically significant forms, therefore late stage
identification of advanced disease and overdiagnosis plus overtreatment of
insignificant disease both remain areas of concern in healthcare provision. PrCa
has a substantial heritable component, and technological advances since the
completion of the Human Genome Project have facilitated improved identification
of inherited genetic factors influencing susceptibility to development of the
disease within families and populations. These genetic markers hold promise to
enable improved understanding of the biological mechanisms underpinning PrCa
development, facilitate genetically informed PrCa screening programmes and guide
appropriate treatment provision. However, insight remains largely lacking
regarding many aspects of their manifestation; especially in relation to genes
associated with aggressive phenotypes, risk factors in non-European populations
and appropriate approaches to enable accurate stratification of higher and lower
risk individuals. This review discusses the methodology used in the elucidation
of genetic loci, genes and individual causal variants responsible for modulating
PrCa susceptibility; the current state of understanding of the allelic spectrum
contributing to PrCa risk; and prospective future translational applications of
these discoveries in the developing eras of genomics and personalised medicine.
Full article
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Open AccessReview
Pharmacoepidemiological Evaluation in Prostate Cancer—Common Pitfalls and How to
Avoid Them
by
Aino Siltari
,
Anssi Auvinen
and
Teemu J. Murtola
Cancers 2021, 13(4), 696; https://doi.org/10.3390/cancers13040696 - 09 Feb 2021
Cited by 4 | Viewed by 2019
Abstract
Pharmacoepidemiologic research provides opportunities to evaluate how commonly
used drug groups, such as cholesterol-lowering or antidiabetic drugs, may affect
the prostate cancer risk or mortality. This type of research is valuable in
estimating real-life drug effects. Nonetheless, pharmacoepidemiological studies
are prone to multiple [...] Read more.
Pharmacoepidemiologic research provides opportunities to evaluate how commonly
used drug groups, such as cholesterol-lowering or antidiabetic drugs, may affect
the prostate cancer risk or mortality. This type of research is valuable in
estimating real-life drug effects. Nonetheless, pharmacoepidemiological studies
are prone to multiple sources of bias that mainly arise from systematic
differences between medication users and non-users. If these are not appreciated
and properly controlled for, there is a risk of obtaining biased results and
reaching erroneous conclusions. Therefore, in order to improve the quality of
future research, we describe common biases in pharmacoepidemiological studies,
particularly in the context of prostate cancer research. We also list common
ways to mitigate these biases and to estimate causality between medication use
and cancer outcomes. Full article
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Open AccessReview
Molecular and Functional Links between Neurodevelopmental Processes and
Treatment-Induced Neuroendocrine Plasticity in Prostate Cancer Progression
by
Roosa Kaarijärvi
,
Heidi Kaljunen
and
Kirsi Ketola
Cancers 2021, 13(4), 692; https://doi.org/10.3390/cancers13040692 - 09 Feb 2021
Cited by 12 | Viewed by 2878
Abstract
Neuroendocrine plasticity and treatment-induced neuroendocrine phenotypes have
recently been proposed as important resistance mechanisms underlying prostate
cancer progression. Treatment-induced neuroendocrine prostate cancer (t-NEPC) is
highly aggressive subtype of castration-resistant prostate cancer which develops
for one fifth of patients under prolonged androgen deprivation. In [...] Read
more.
Neuroendocrine plasticity and treatment-induced neuroendocrine phenotypes have
recently been proposed as important resistance mechanisms underlying prostate
cancer progression. Treatment-induced neuroendocrine prostate cancer (t-NEPC) is
highly aggressive subtype of castration-resistant prostate cancer which develops
for one fifth of patients under prolonged androgen deprivation. In recent years,
understanding of molecular features and phenotypic changes in neuroendocrine
plasticity has been grown. However, there are still fundamental questions to be
answered in this emerging research field, for example, why and how do the
prostate cancer treatment-resistant cells acquire neuron-like phenotype. The
advantages of the phenotypic change and the role of tumor microenvironment in
controlling cellular plasticity and in the emergence of treatment-resistant
aggressive forms of prostate cancer is mostly unknown. Here, we discuss the
molecular and functional links between neurodevelopmental processes and
treatment-induced neuroendocrine plasticity in prostate cancer progression and
treatment resistance. We provide an overview of the emergence of neurite-like
cells in neuroendocrine prostate cancer cells and whether the reported t-NEPC
pathways and proteins relate to neurodevelopmental processes like neurogenesis
and axonogenesis during the development of treatment resistance. We also discuss
emerging novel therapeutic targets modulating neuroendocrine plasticity. Full
article
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Open AccessReview
Grading Evolution and Contemporary Prognostic Biomarkers of Clinically
Significant Prostate Cancer
by
Konrad Sopyllo
,
Andrew M. Erickson
and
Tuomas Mirtti
Cancers 2021, 13(4), 628; https://doi.org/10.3390/cancers13040628 - 05 Feb 2021
Cited by 7 | Viewed by 1984
Abstract
Gleason grading remains the strongest prognostic parameter in localized prostate
adenocarcinoma. We have here outlined the evolution and contemporary practices
in pathological evaluation of prostate tissue samples for Gleason score and
Grade group. The state of more observer-independent grading methods with the aid
[...] Read more.
Gleason grading remains the strongest prognostic parameter in localized prostate
adenocarcinoma. We have here outlined the evolution and contemporary practices
in pathological evaluation of prostate tissue samples for Gleason score and
Grade group. The state of more observer-independent grading methods with the aid
of artificial intelligence is also reviewed. Additionally, we conducted a
systematic review of biomarkers that hold promise in adding independent
prognostic or predictive value on top of clinical parameters, Grade group and
PSA. We especially focused on hard end points during the follow-up, i.e.,
occurrence of metastasis, disease-specific mortality and overall mortality. In
peripheral blood, biopsy-detected prostate cancer or in surgical specimens, we
can conclude that there are more than sixty biomarkers that have been shown to
have independent prognostic significance when adjusted to conventional risk
assessment or grouping. Our search brought up some known putative markers and
panels, as expected. Also, the synthesis in the systematic review indicated
markers that ought to be further studied as part of prospective trials and in
well characterized patient cohorts in order to increase the resolution of the
current clinico-pathological prognostic factors. Full article
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Open AccessReview
Targeting the Hippo Pathway in Prostate Cancer: What’s New?
by
Kelly Coffey
Cancers 2021, 13(4), 611; https://doi.org/10.3390/cancers13040611 - 04 Feb 2021
Cited by 10 | Viewed by 3087
Abstract
Identifying novel therapeutic targets for the treatment of prostate cancer (PC)
remains a key area of research. With the emergence of resistance to androgen
receptor (AR)-targeting therapies, other signalling pathways which crosstalk
with AR signalling are important. Over recent years, evidence has accumulated
[...] Read more.
Identifying novel therapeutic targets for the treatment of prostate cancer (PC)
remains a key area of research. With the emergence of resistance to androgen
receptor (AR)-targeting therapies, other signalling pathways which crosstalk
with AR signalling are important. Over recent years, evidence has accumulated
for targeting the Hippo signalling pathway. Discovered in Drosophila
melanogasta, the Hippo pathway plays a role in the regulation of organ size,
proliferation, migration and invasion. In response to a variety of stimuli,
including cell–cell contact, nutrients and stress, a kinase cascade is
activated, which includes STK4/3 and LATS1/2 to inhibit the effector proteins
YAP and its paralogue TAZ. Transcription by their partner transcription factors
is inhibited by modulation of YAP/TAZ cellular localisation and protein
turnover. Trnascriptional enhanced associate domain (TEAD) transcription factors
are their classical transcriptional partner but other transcription factors,
including the AR, have been shown to be modulated by YAP/TAZ. In PC, this
pathway can be dysregulated by a number of mechanisms, making it attractive for
therapeutic intervention. This review looks at each component of the pathway
with a focus on findings from the last year and discusses what knowledge can be
applied to the field of PC. Full article
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Open AccessReview
Eighty Years of Targeting Androgen Receptor Activity in Prostate Cancer: The
Fight Goes on
by
Eva Estébanez-Perpiñá
,
Charlotte L. Bevan
and
Iain J. McEwan
Cancers 2021, 13(3), 509; https://doi.org/10.3390/cancers13030509 - 29 Jan 2021
Cited by 24 | Viewed by 4117
Abstract
Prostate cancer (PCa) is the most common cancer in men in the West, other than
skin cancer, accounting for over a quarter of cancer diagnoses in US men. In a
seminal paper from 1941, Huggins and Hodges demonstrated that prostate tumours
and metastatic [...] Read more.
Prostate cancer (PCa) is the most common cancer in men in the West, other than
skin cancer, accounting for over a quarter of cancer diagnoses in US men. In a
seminal paper from 1941, Huggins and Hodges demonstrated that prostate tumours
and metastatic disease were sensitive to the presence or absence of androgenic
hormones. The first hormonal therapy for PCa was thus castration. In the
subsequent eighty years, targeting the androgen signalling axis, where possible
using drugs rather than surgery, has been a mainstay in the treatment of
advanced and metastatic disease. Androgens signal via the androgen receptor, a
ligand-activated transcription factor, which is the direct target of many such
drugs. In this review we discuss the role of the androgen receptor in PCa and
how the combination of structural information and functional screenings is
continuing to be used for the discovery of new drug to switch off the receptor
or modify its function in cancer cells. Full article
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Open AccessReview
Derivation and Application of Molecular Signatures to Prostate Cancer:
Opportunities and Challenges
by
Dimitrios Doultsinos
and
Ian G. Mills
Cancers 2021, 13(3), 495; https://doi.org/10.3390/cancers13030495 - 28 Jan 2021
Cited by 9 | Viewed by 2919
Abstract
Prostate cancer is a high-incidence cancer that requires improved patient
stratification to ensure accurate predictions of risk and treatment response.
Due to the significant contributions of transcription factors and epigenetic
regulators to prostate cancer progression, there has been considerable progress
made in developing [...] Read more.
Prostate cancer is a high-incidence cancer that requires improved patient
stratification to ensure accurate predictions of risk and treatment response.
Due to the significant contributions of transcription factors and epigenetic
regulators to prostate cancer progression, there has been considerable progress
made in developing gene signatures that may achieve this. Some of these are
aligned to activities of key drivers such as the androgen receptor, whilst
others are more agnostic. In this review, we present an overview of these
signatures, the strategies for their derivation, and future perspectives on
their continued development and evolution. Full article
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Open AccessFeature PaperReview
Resistance to Antiandrogens in Prostate Cancer: Is It Inevitable, Intrinsic or
Induced?
by
Norman J. Maitland
Cancers 2021, 13(2), 327; https://doi.org/10.3390/cancers13020327 - 17 Jan 2021
Cited by 23 | Viewed by 3340
Abstract
Increasingly sophisticated therapies for chemical castration dominate first-line
treatments for locally advanced prostate cancer. However, androgen deprivation
therapy (ADT) offers little prospect of a cure, as resistant tumors emerge
rather rapidly, normally within 30 months. Cells have multiple mechanisms of
resistance to even [...] Read more.
Increasingly sophisticated therapies for chemical castration dominate first-line
treatments for locally advanced prostate cancer. However, androgen deprivation
therapy (ADT) offers little prospect of a cure, as resistant tumors emerge
rather rapidly, normally within 30 months. Cells have multiple mechanisms of
resistance to even the most sophisticated drug regimes, and both tumor cell
heterogeneity in prostate cancer and the multiple salvage pathways result in
castration-resistant disease related genetically to the original hormone-naive
cancer. The timing and mechanisms of cell death after ADT for prostate cancer
are not well understood, and off-target effects after long-term ADT due to
functional extra-prostatic expression of the androgen receptor protein are now
increasingly being recorded. Our knowledge of how these widely used treatments
fail at a biological level in patients is deficient. In this review, I will
discuss whether there are pre-existing drug-resistant cells in a tumor mass, or
whether resistance is induced/selected by the ADT. Equally, what is the cell of
origin of this resistance, and does it differ from the treatment-naïve tumor
cells by differentiation or dedifferentiation? Conflicting evidence also emerges
from studies in the range of biological systems and species employed to answer
this key question. It is only by improving our understanding of this aspect of
treatment and not simply devising another new means of androgen inhibition that
we can improve patient outcomes. Full article
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2020
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Open AccessArticle
ATM Kinase Inhibition Preferentially Sensitises PTEN-Deficient Prostate Tumour
Cells to Ionising Radiation
by
Conor Hanna
,
Victoria L. Dunne
,
Steven M. Walker
,
Karl T. Butterworth
,
Nuala McCabe
,
David J. J. Waugh
,
Richard D. Kennedy
and
Kevin M. Prise
Cancers 2021, 13(1), 79; https://doi.org/10.3390/cancers13010079 - 30 Dec 2020
Cited by 2 | Viewed by 1968
Abstract
Radical radiotherapy, often in combination with hormone ablation, is a safe and
effective treatment option for localised or locally-advanced prostate cancer.
However, up to 30% of patients with locally advanced PCa will go on to develop
biochemical failure, within 5 years, following initial [...] Read more.
Radical radiotherapy, often in combination with hormone ablation, is a safe and
effective treatment option for localised or locally-advanced prostate cancer.
However, up to 30% of patients with locally advanced PCa will go on to develop
biochemical failure, within 5 years, following initial radiotherapy. Improving
radiotherapy response is clinically important since patients exhibiting
biochemical failure develop castrate-resistant metastatic disease for which
there is no curative therapy and median survival is 8–18 months. The aim of this
research was to determine if loss of PTEN (highly prevalent in advanced prostate
cancer) is a novel therapeutic target in the treatment of advanced prostate
cancer. Previous work has demonstrated PTEN-deficient cells are sensitised to
inhibitors of ATM, a key regulator in the response to DSBs. Here, we have shown
the role of PTEN in cellular response to IR was both complex and
context-dependent. Secondly, we have confirmed ATM inhibition in PTEN-depleted
cell models, enhances ionising radiation-induced cell killing with minimal
toxicity to normal prostate RWPE-1 cells. Furthermore, combined treatment
significantly inhibited PTEN-deficient tumour growth compared to PTEN-expressing
counterparts, with minimal toxicity observed. We have further shown PTEN loss is
accompanied by increased endogenous levels of ROS and DNA damage. Taken
together, these findings provide pre-clinical data for future clinical
evaluation of ATM inhibitors as a neoadjuvant/adjuvant in combination with
radiation therapy in prostate cancer patients harbouring PTEN mutations. Full
article
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Open AccessReview
Commercialized Blood-, Urinary- and Tissue-Based Biomarker Tests for Prostate
Cancer Diagnosis and Prognosis
by
Wieke C. H. Visser
, Hans de Jong, Willem J. G. Melchers, Peter F. A. Mulders and Jack A. Schalken
Cancers 2020, 12(12), 3790; https://doi.org/10.3390/cancers12123790 - 16 Dec
2020
Cited by 13 | Viewed by 2950
Abstract
In the diagnosis and prognosis of prostate cancer (PCa), the serum
prostate-specific antigen test is widely used but is associated with low
specificity. Therefore, blood-, urinary- and tissue-based biomarker tests have
been developed, intended to be used in the diagnostic and prognostic setting
[...] Read more.
In the diagnosis and prognosis of prostate cancer (PCa), the serum
prostate-specific antigen test is widely used but is associated with low
specificity. Therefore, blood-, urinary- and tissue-based biomarker tests have
been developed, intended to be used in the diagnostic and prognostic setting of
PCa. This review provides an overview of commercially available biomarker tests
developed to be used in several clinical stages of PCa management. In the
diagnostic setting, the following tests can help selecting the right patients
for initial and/or repeat biopsy: PHI, 4K, MiPS, SelectMDx, ExoDx, Proclarix,
ConfirmMDx, PCA3 and PCMT. In the prognostic setting, the Prolaris, OncotypeDx
and Decipher test can help in risk-stratification of patients regarding
treatment decisions. Following, an overview is provided of the studies available
comparing the performance of biomarker tests. However, only a small number of
recently published head-to-head comparison studies are available. In contrast,
recent research has focused on the use of biomarker tests in relation to the
(complementary) use of multiparametric magnetic resonance imaging in PCa
diagnosis. Full article
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Ablative Radiotherapy in Prostate Cancer: Stereotactic Body Radiotherapy and
High Dose Rate Brachytherapy
by
Ting Martin Ma
,
Oscar Lilleby
,
Wolfgang A. Lilleby
and
Amar U. Kishan
Cancers 2020, 12(12), 3606; https://doi.org/10.3390/cancers12123606 - 02 Dec
2020
Cited by 6 | Viewed by 1771
Abstract
Prostate cancer (PCa) is the most common noncutaneous solid organ malignancy
among men worldwide. Radiation therapy is a standard of care treatment option
that has historically been delivered in the form of small daily doses of
radiation over the span of multiple weeks. [...] Read more.
Prostate cancer (PCa) is the most common noncutaneous solid organ malignancy
among men worldwide. Radiation therapy is a standard of care treatment option
that has historically been delivered in the form of small daily doses of
radiation over the span of multiple weeks. PCa appears to have a unique
sensitivity to higher doses of radiation per fraction, rendering it susceptible
to abbreviated forms of treatment. Stereotactic body radiation therapy (SBRT)
and high-dose-rate brachytherapy (HDRBT) are both modern radiation modalities
that allow the precise delivery of ablative doses of radiation to the prostate
while maximally sparing sensitive surrounding normal structures. In this review,
we highlight the evidence regarding the radiobiology, oncological outcomes,
toxicity and dose/fractionation schemes of SBRT and HDRBT monotherapy in men
with low-and intermediate-risk PCa. Full article
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Open AccessReview
Inflammation as a Driver of Prostate Cancer Metastasis and Therapeutic
Resistance
by
Maddison Archer
,
Navneet Dogra
and
Natasha Kyprianou
Cancers 2020, 12(10), 2984; https://doi.org/10.3390/cancers12102984 - 15 Oct
2020
Cited by 52 | Viewed by 4740
Abstract
Prostate cancer is the most common malignancy among men, and progression to
metastasis and the emergence of therapeutically resistant disease confers a high
mortality rate. Growing evidence implicates inflammation as a driver of prostate
cancer development and progression, resulting in increased cancer risk [...]
Read more.
Prostate cancer is the most common malignancy among men, and progression to
metastasis and the emergence of therapeutically resistant disease confers a high
mortality rate. Growing evidence implicates inflammation as a driver of prostate
cancer development and progression, resulting in increased cancer risk for
prostate cancer. Population-based studies revealed that the use of
antinflammatory drugs led to a 23% risk reduction prostate cancer occurrence, a
negative association that was stronger in men who specifically used COX-2
inhibitors. Furthermore, patients that were taking aspirin had a 21% reduction
in prostate cancer risk, and further, long-term users of daily low dose aspirin
had a 29% prostate cancer risk reduction as compared to the controls.
Environmental exposure to bacterial and viral infections, exposure to mutagenic
agents, and genetic variations predispose the prostate gland to inflammation,
with a coordinated elevated expression of inflammatory cytokines (IL-6, TGF-β).
It is the dynamics within the tumor microenvironment that empower these
cytokines to promote survival and growth of the primary tumor and facilitate
disease progression by navigating the immunoregulatory network, phenotypic
epithelial-mesenchymal transition (EMT), angiogenesis, anoikis resistance, and
metastasis. In this review, we discuss the sources of inflammation in the
prostate, the functional contribution of the critical inflammatory effectors to
prostate cancer initiation and metastatic progression, and the therapeutic
challenges that they impose on treatment of advanced disease and overcoming
therapeutic resistance. Growing mechanistic evidence supports the significance
of inflammation in localized prostate cancer, and the systemic impact of the
process within the tumor microenvironment on disease progression to advanced
therapeutically-resistant prostate cancer. Rigorous exploitation of the role of
inflammation in prostate cancer progression to metastasis and therapeutic
resistance will empower the development of precise biomarker signatures and
effective targeted therapeutics to reduce the clinical burden and lethal disease
in the future. Full article
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Open AccessArticle
Impact of Vasectomy on the Development and Progression of Prostate Cancer:
Preclinical Evidence
by
Takashi Kawahara
,
Yuki Teramoto
,
Yi Li
,
Hitoshi Ishiguro
,
Jennifer Gordetsky
,
Zhiming Yang
and
Hiroshi Miyamoto
Cancers 2020, 12(8), 2295; https://doi.org/10.3390/cancers12082295 - 15 Aug 2020
Cited by 4 | Viewed by 2460
Abstract
Some observational studies have implied a link between vasectomy and an elevated
risk of prostate cancer. We investigated the impact of vasectomy on prostate
cancer outgrowth, mainly using preclinical models. Neoplastic changes in the
prostate were compared in transgenic TRAMP mice that underwent [...] Read more.
Some observational studies have implied a link between vasectomy and an elevated
risk of prostate cancer. We investigated the impact of vasectomy on prostate
cancer outgrowth, mainly using preclinical models. Neoplastic changes in the
prostate were compared in transgenic TRAMP mice that underwent vasectomy vs.
sham surgery performed at 4 weeks of age. One of the molecules identified by DNA
microarray (i.e., ZKSCAN3) was then assessed in radical prostatectomy specimens
and human prostate cancer lines. At 24 weeks, gross tumor (p = 0.089) and poorly
differentiated adenocarcinoma (p = 0.036) occurred more often in vasectomized
mice. Vasectomy significantly induced ZKSCAN3 expression in prostate tissues
from C57BL/6 mice and prostate cancers from TRAMP mice. Immunohistochemistry
showed increased ZKSCAN3 expression in adenocarcinoma vs. prostatic
intraepithelial neoplasia (PIN), PIN vs. non-neoplastic prostate, Grade Group ≥3
vs. ≤2 tumors, pT3 vs. pT2 tumors, pN1 vs. pN0 tumors, and prostate cancer from
patients with a history of vasectomy. Additionally, strong (2+/3+) ZKSCAN3
expression (p = 0.002), as an independent prognosticator, or vasectomy (p =
0.072) was associated with the risk of tumor recurrence. In prostate cancer
lines, ZKSCAN3 silencing resulted in significant decreases in cell
proliferation/migration/invasion. These findings suggest that there might be an
association between vasectomy and the development and progression of prostate
cancer, with up-regulation of ZKSCAN3 expression as a potential underlying
mechanism. Full article
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Open AccessArticle
Characteristics of PSA Bounce after Radiotherapy for Prostate Cancer: A
Meta-Analysis
by
Narisa Dewi Maulany Darwis
,
Takahiro Oike
,
Nobuteru Kubo
,
Soehartati A Gondhowiardjo
and
Tatsuya Ohno
Cancers 2020, 12(8), 2180; https://doi.org/10.3390/cancers12082180 - 05 Aug 2020
Cited by 7 | Viewed by 3922
Abstract
The rate and characteristics of prostate-specific antigen (PSA) bounce
post-radiotherapy remain unclear. To address this issue, we performed a
meta-analysis. Reports of PSA bounce post-radiotherapy with a cutoff of 0.2
ng/mL were searched by using Medline and Web of Science. The primary endpoint
[...] Read more.
The rate and characteristics of prostate-specific antigen (PSA) bounce
post-radiotherapy remain unclear. To address this issue, we performed a
meta-analysis. Reports of PSA bounce post-radiotherapy with a cutoff of 0.2
ng/mL were searched by using Medline and Web of Science. The primary endpoint
was the occurrence rate, and the secondary endpoints were bounce characteristics
such as amplitude, time to occurrence, nadir value, and time to nadir.
Radiotherapy modality, age, risk classification, androgen deprivation therapy,
and the follow-up period were extracted as clinical variables. Meta-analysis and
univariate meta-regression were performed with random-effect modeling. Among 290
search-positive studies, 50 reports including 26,258 patients were identified.
The rate of bounce was 31%; amplitude was 1.3 ng/mL; time to occurrence was 18
months; nadir value was 0.5 ng/mL; time to nadir was 33 months. Univariate
meta-regression analysis showed that radiotherapy modality (29.7%), age (20.2%),
and risk classification (12.2%) were the major causes of heterogeneity in the
rate of bounce. This is the first meta-analysis of PSA bounce post-radiotherapy.
The results are useful for post-radiotherapy surveillance of prostate cancer
patients. Full article
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Mechanisms of Androgen Receptor Agonist- and Antagonist-Mediated Cellular
Senescence in Prostate Cancer
by
Miriam Kokal
,
Kimia Mirzakhani
,
Thanakorn Pungsrinont
and
Aria Baniahmad
Cancers 2020, 12(7), 1833; https://doi.org/10.3390/cancers12071833 - 08 Jul 2020
Cited by 19 | Viewed by 5230
Abstract
The androgen receptor (AR) plays a leading role in the control of prostate
cancer (PCa) growth. Interestingly, structurally different AR antagonists with
distinct mechanisms of antagonism induce cell senescence, a mechanism that
inhibits cell cycle progression, and thus seems to be a key [...] Read more.
The androgen receptor (AR) plays a leading role in the control of prostate
cancer (PCa) growth. Interestingly, structurally different AR antagonists with
distinct mechanisms of antagonism induce cell senescence, a mechanism that
inhibits cell cycle progression, and thus seems to be a key cellular response
for the treatment of PCa. Surprisingly, while physiological levels of androgens
promote growth, supraphysiological androgen levels (SAL) inhibit PCa growth in
an AR-dependent manner by inducing cell senescence in cancer cells. Thus,
oppositional acting ligands, AR antagonists, and agonists are able to induce
cellular senescence in PCa cells, as shown in cell culture model as well as ex
vivo in patient tumor samples. This suggests a dual AR-signaling dependent on
androgen levels that leads to the paradox of the rational to keep the AR
constantly inactivated in order to treat PCa. These observations however opened
the option to treat PCa patients with AR antagonists and/or with androgens at
supraphysiological levels. The latter is currently used in clinical trials in
so-called bipolar androgen therapy (BAT). Notably, cellular senescence is
induced by AR antagonists or agonist in both androgen-dependent and
castration-resistant PCa (CRPC). Pathway analysis suggests a crosstalk between
AR and the non-receptor tyrosine kinase Src-Akt/PKB and the PI3K-mTOR-autophagy
signaling in mediating AR-induced cellular senescence in PCa. In this review, we
summarize the current knowledge of therapeutic induction and intracellular
pathways of AR-mediated cellular senescence. Full article
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