Targeting apoptosis in prostate cancer.
The understanding of apoptotic pathways provides new insights into cancer therapy. Therapies that modulate these pathways may induce apoptosis or sensitize tumor cells to other agents. Because many of the components of these pathways are altered in tumor cells compared with normal cells, therapies that target these abnormal apoptotic proteins may be more selective than traditional cytotoxic agents. Difficulties include the translation of the knowledge of these pathways into clinical trials and monitoring the predicted biologic effects in patients. The continued study of new targets, agents capable of modulating these targets, and markers of biologic effect in patients should improve clinical results.
DiPaola
R S
RS
Dean and Betty Gallo Prostate Cancer Center, New Brunswick, New Jersey, USA.
Patel
J
J
Rafi
M M
MM
D000230:Adenocarcinoma / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects*; D020169:Caspases / Q000502:physiology; D003546:Cysteine Endopeptidases; D015853:Cysteine Proteinase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D018450:Disease Progression; D015195:Drug Design; D019008:Drug Resistance, Neoplasm / Q000235:genetics; D004791:Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D053222:Fas Ligand Protein; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D019254:Genes, bcl-2; D016158:Genes, p53; D006801:Humans; D007372:Interferons / Q000627:therapeutic use; D008297:Male; D008562:Membrane Glycoproteins / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout; D008928:Mitochondria / Q000502:physiology; D009097:Multienzyme Complexes / Q000037:antagonists & inhibitors; D016328:NF-kappa B / Q000502:physiology; D009363:Neoplasm Proteins / Q000235:genetics / Q000502:physiology; D016376:Oligonucleotides, Antisense / Q000627:therapeutic use; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D000081082:Phosphoinositide-3 Kinase Inhibitors; D010865:Pilot Projects; D011471:Prostatic Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D046988:Proteasome Endopeptidase Complex; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins / Q000037:antagonists & inhibitors / Q000502:physiology; D051057:Proto-Oncogene Proteins c-akt; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000502:physiology; D012176:Retinoids / Q000627:therapeutic use; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
D000970:Antineoplastic Agents; D020169:Caspases; D003546:Cysteine Endopeptidases; D015853:Cysteine Proteinase Inhibitors; D004791:Enzyme Inhibitors; D053222:Fas Ligand Protein; D007372:Interferons; D008562:Membrane Glycoproteins; D009097:Multienzyme Complexes; D016328:NF-kappa B; D009363:Neoplasm Proteins; D016376:Oligonucleotides, Antisense; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D046988:Proteasome Endopeptidase Complex; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins; D051057:Proto-Oncogene Proteins c-akt; D019253:Proto-Oncogene Proteins c-bcl-2; D012176:Retinoids; D016159:Tumor Suppressor Protein p53; C505661:FASLG protein, human; C505658:Fasl protein, mouse