Massenkeil G, Oberhuber H, Hailemariam S, Sulser T, Diener P A, Bannwart F, Schäfer R, Schwarte-Waldhoff I
Division of Cancer Research, University Hospital, Zürich, Switzerland.
Anticancer Res. 1994 Nov-Dec;14(6B):2785-90.
We analysed 39 prostatic carcinomas for loss of heterozygosity on chromosomal arms 8p, 10q, 16q, 17p and 18q and for mutations in the p53 anti-oncogene. Loss of heterozygosity (LOH) on 8p was detected in one out of 5 informative tumors, LOH on 16q in 3 out of 21 tumors, LOH on 17p in 2 out of 18 tumors, and LOH on 18q in 2 out of 17 tumors. No deletions were observed on 10q in 14 informative tumors. p53 alterations occurred in 3 out of 38 examined tumors, comprising two point mutations and a small deletion. Chromosomal deletions and p53 mutations were confined to locally invasive prostatic carcinomas, suggesting that they are associated with the progression of some prostate cancers rather than with tumor initiation.
我们分析了39例前列腺癌,以检测8号染色体短臂、10号染色体长臂、16号染色体长臂、17号染色体短臂和18号染色体长臂上的杂合性缺失以及p53抗癌基因的突变情况。在5例信息充分的肿瘤中,有1例检测到8号染色体短臂杂合性缺失(LOH);在21例肿瘤中,有3例检测到16号染色体长臂LOH;在18例肿瘤中,有2例检测到17号染色体短臂LOH;在17例肿瘤中,有2例检测到18号染色体长臂LOH。在14例信息充分的肿瘤中,未观察到10号染色体长臂的缺失。在38例检测的肿瘤中,有3例发生了p53改变,包括2个点突变和1个小缺失。染色体缺失和p53突变仅限于局部浸润性前列腺癌,这表明它们与某些前列腺癌的进展相关,而非与肿瘤起始相关。