CAJ | 학술논문

人类许多肿瘤的发生与P53功能失活有关,其中约有50%具有野生型P53,此种情况下,P53抑癌功能的丧失是由,INK4a、ARF、ASPP等抑癌基因的异常引起,5'CpG岛异常甲基化是INK4a/ARF功能失活的主要途径,也是ASPP失活的方式之一.逆转DNA异常甲基化有望重新激活这些抑癌基因的表达,为肿瘤的治疗提供新途径.
인류허다종류적발생여P53공능실활유관,기중약유50%구유야생형P53,차충정황하,P53억암공능적상실시유,INK4a、ARF、ASPP등억암기인적이상인기,5'CpG도이상갑기화시INK4a/ARF공능실활적주요도경,야시ASPP실활적방식지일.역전DNA이상갑기화유망중신격활저사억암기인적표체,위종류적치료제공신도경.
Many tumorigenesis in human are closely linked to the functional loss of P53. The tumor-suppressive functions of P53 are abrogated by mutations, but in 50% of all tumors it remains wild type. In these cases, loss of P53 tumor-suppressive function mainly results from the abnormal methylation of 5' CpG islands of tumor suppressor genes such as INK4a, ARF and ASPP. Restoring to normal methylation state of these genes might provide a new strategy for tumor therapy.