Genetic basis of pituitary adenoma invasiveness: a review.
Compatible with contemporary paradigms of the role of genetic aberrations in the progression of human tumors, the growth of pituitary tumors into a state of invasiveness appears to be due to genetic alterations. Amplification of H-ras and c-myc oncogenes and mutations of p53, nm23 and Rb genes have been identified disproportionately more in aggressive tumors and, in the case of Rb gene, in pituitary carcinomas, providing evidence that amplification of these oncogenes (H-ras and c-myc) and inactivation of tumor suppressor genes (p53, nm23 and Rb) seem to be at least one mechanism by which pituitary tumors progress. The current level of management of invasive pituitary adenomas should become more comprehensive as the advances in our understanding of genetic basis of pituitary adenoma invasiveness becomes translated into development of novel chemotherapy or gene transfer technique.
Suhardja
A
A
Division of Neurosurgery, University of Toronto, Ontario, Canada.
Kovacs
K
K
Rutka
J
J
D000236:Adenoma / Q000188:drug therapy / Q000235:genetics / Q000473:pathology* / Q000628:therapy; D000970:Antineoplastic Agents / Q000627:therapeutic use; D002453:Cell Cycle / Q000235:genetics; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D002877:Chromosomes, Human / Q000235:genetics; D004252:DNA Mutational Analysis; D004273:DNA, Neoplasm / Q000235:genetics; D018450:Disease Progression; D015195:Drug Design; D015972:Gene Expression Regulation, Neoplastic; D016161:Genes, Retinoblastoma; D016147:Genes, Tumor Suppressor; D016259:Genes, myc; D016158:Genes, p53; D011905:Genes, ras; D015316:Genetic Therapy; D006801:Humans; D020559:Monomeric GTP-Binding Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D009154:Mutation; D054778:NM23 Nucleoside Diphosphate Kinases; D009361:Neoplasm Invasiveness / Q000235:genetics*; D009701:Nucleoside-Diphosphate Kinase; D009857:Oncogenes; D010911:Pituitary Neoplasms / Q000188:drug therapy / Q000235:genetics / Q000473:pathology* / Q000628:therapy; D016271:Proto-Oncogene Proteins c-myc / Q000172:deficiency / Q000502:physiology; D016283:Proto-Oncogene Proteins p21(ras) / Q000172:deficiency / Q000502:physiology; D016160:Retinoblastoma Protein / Q000172:deficiency / Q000502:physiology; D014157:Transcription Factors / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000172:deficiency / Q000502:physiology
D000970:Antineoplastic Agents; D004273:DNA, Neoplasm; D054778:NM23 Nucleoside Diphosphate Kinases; D016271:Proto-Oncogene Proteins c-myc; D016160:Retinoblastoma Protein; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53; C517938:NME1 protein, human; D009701:Nucleoside-Diphosphate Kinase; C501009:HRAS protein, human; D020559:Monomeric GTP-Binding Proteins; D016283:Proto-Oncogene Proteins p21(ras)