Fujiwara Toshiyoshi, Tanaka Noriaki
Division of Surgical Oncology, Dept. of Surgery, Okayama University Graduate School of Medicine and Dentistry.
Gan To Kagaku Ryoho. 2003 Apr;30(4):460-7.
Recent advances in molecular biology have fostered remarkable insights into the molecular basis of neoplasms. This new understanding of cancer pathogenesis suggests that restoration of the function of critical gene products could halt or reverse these mechanisms, thus having a therapeutic effect in cancer. The tumor suppressor p53 gene has been implicated in many inherited and sporadic forms of malignancy in humans. A number of preclinical experiments have demonstrated that restoration of the wild-type p53 function in the cancer cell by gene transfer is sufficient to cause antitumor effects such as cell-cycle arrest and induction of apoptosis. This approach has entered initial clinical testing and provided intriguing information about the intratumoral administration of an adenovirus vector expressing the wild-type p53 gene in non-small cell lung cancer patients.
分子生物学的最新进展极大地增进了我们对肿瘤分子基础的认识。对癌症发病机制的这一新认识表明,关键基因产物功能的恢复可能会阻止或逆转这些机制,从而对癌症产生治疗效果。肿瘤抑制基因p53与人类许多遗传性和散发性恶性肿瘤有关。多项临床前实验表明,通过基因转移在癌细胞中恢复野生型p53功能足以产生抗肿瘤作用,如细胞周期阻滞和诱导凋亡。这种方法已进入初步临床试验,并提供了关于在非小细胞肺癌患者中瘤内注射表达野生型p53基因的腺病毒载体的有趣信息。