Burger R, Alvarezsalas L, Wilczynski S, Monk B, Dipaolo J
NCI,BIOL LAB,BETHESDA,MD 20892. CITY HOPE NATL MED CTR,DEPT PATHOL,DUARTE,CA 91010. UNIV CALIF IRVINE,UCI MED CTR,CTR CLIN CANC,DEPT OBSTET & GYNECOL,DIV GYNECOL ONCOL,ORANGE,CA 92717.
Int J Oncol. 1995 Aug;7(2):261-6. doi: 10.3892/ijo.7.2.261.
Polymorphism of the human papillomavirus type 16 (HPV-16) genome has been reported to occur within the noncoding regulatory long control region (LCR) and in the E7 and L1 genes. The current study focuses on the HPV-16 E6 oncogene which interacts with the antioncogenic regulator p53. Seventy-eight HPV-16-positive DNA samples derived from cervical carcinomas were screened for the presence of polymorphism in the HPV-16 E6 gene by polymerase chain reaction (PCR) linked single stranded conformational polymorphism (SSCP) analysis. Nine DNA samples had heterozygous mutations within the same region of the E6 gene 3' terminus; T to C transitions at HPV-16 position 511 (silent) and one of the nine also had a 513 mutation (Met to Thr). These mutations correlated with the clinical aggressiveness of the tumor, suggesting that the presence of these mutations may be due to genomic instability of advanced cervical carcinoma.
据报道，人乳头瘤病毒16型（HPV - 16）基因组的多态性发生在非编码调控长控制区（LCR）以及E7和L1基因中。当前的研究聚焦于与抗癌调节因子p53相互作用的HPV - 16 E6癌基因。通过聚合酶链反应（PCR）连锁单链构象多态性（SSCP）分析，对78份源自宫颈癌的HPV - 16阳性DNA样本进行筛查，以检测HPV - 16 E6基因中多态性的存在情况。9份DNA样本在E6基因3'末端的同一区域存在杂合突变；HPV - 16第511位发生T到C的转换（沉默突变），9份样本中的1份在第513位也有突变（甲硫氨酸突变为苏氨酸）。这些突变与肿瘤的临床侵袭性相关，表明这些突变的存在可能归因于晚期宫颈癌的基因组不稳定性。
