Kahn A
Institut Cochin de Génétique Moléculaire, Unité 129 de l'INSERM, Paris France.
Pathol Biol (Paris). 1995 Mar;43(3):139-42.
Cancer genes can be ranged in three families: oncogenes, stimulating cell divisions; antioncogenes, blocking cell division; anti-apoptotic genes, blocking programmed cell death. Tumor progression usually results from cooperation between modifications of genes belonging to these different families. The familial predispositions to cancer are most frequently due to mutations of antioncogenes or of repair genes; in this later case, the original mutation results in abnormal DNA repair, then in accumulation of somatic mutations which could involve cancer genes. Recently, genes predisposing to familial forms of breast and colon cancers have been identified. Knowledge of such genes leads to possible presymptomatic prediction of the disease, but the preventive possibilities seem to be limited, today, to a preventive surgical exeresis. In the future, it would be desirable that elucidation of the mechanisms of cancer predisposition leads to less aggressive preventive or curative treatments.
癌基因，刺激细胞分裂；抑癌基因，阻断细胞分裂；抗凋亡基因，阻断程序性细胞死亡。肿瘤进展通常源于属于这些不同家族的基因修饰之间的协同作用。癌症的家族易感性最常见的原因是抑癌基因或修复基因的突变；在后一种情况下，最初的突变导致DNA修复异常，进而导致体细胞突变的积累，而这些突变可能涉及癌症基因。最近，已鉴定出导致家族性乳腺癌和结肠癌的基因。对这些基因的了解使得有可能在症状出现前预测疾病，但目前，预防的可能性似乎仅限于预防性手术切除。未来，希望对癌症易感性机制的阐明能带来侵入性较小的预防或治疗方法。
