Cuatrecasas M, Erill N, Musulen E, Costa I, Matias-Guiu X, Prat J
Department of Pathology, Hospital de Sant Pau, Autonomous University of Barcelona, Spain.
Cancer. 1998 Mar 15;82(6):1088-95.
To assess the putative prognostic value of K-ras mutations in nonmucinous ovarian tumors, the authors looked for K-ras point mutations at codons 12 and 13 in 144 nonmucinous ovarian tumors.
A series of 144 consecutive, unselected, archival, nonmucinous ovarian tumors (35 benign, 12 borderline, and 97 malignant) were studied. K-ras mutations at codons 12 and 13 were determined by polymerase chain reaction using the restriction fragment length polymorphism method with mismatched nested primers. Extensive clinicopathologic and follow-up data on all patients were evaluated.
The overall prevalence of K-ras mutations at codons 12 and 13 was 30.5% (44/144). In benign tumors, it was 20% (7/35); in borderline tumors, 25% (3/12); and in carcinomas, 35% (34/97). The presence of K-ras point mutations did not correlate with survival. Among the benign tumors, K-ras mutations were detected in three Brenner tumors with a mucinous component.
These results indicate that K-ras mutations are not initial events in the pathogenesis of nonmucinous ovarian tumors and do not appear to be related to survival.
为评估K-ras突变在非黏液性卵巢肿瘤中的假定预后价值,作者对144例非黏液性卵巢肿瘤进行了第12和13密码子的K-ras点突变检测。
研究了一系列连续的、未经选择的、存档的144例非黏液性卵巢肿瘤(35例良性、12例交界性和97例恶性)。采用错配巢式引物的聚合酶链反应-限制性片段长度多态性方法检测第12和13密码子的K-ras突变。评估了所有患者广泛的临床病理和随访数据。
第12和13密码子K-ras突变的总体发生率为30.5%(44/144)。在良性肿瘤中为20%(7/35);在交界性肿瘤中为25%(3/12);在癌中为35%(34/97)。K-ras点突变的存在与生存无关。在良性肿瘤中,在3例有黏液成分的勃勒纳瘤中检测到K-ras突变。
这些结果表明,K-ras突变不是非黏液性卵巢肿瘤发病机制中的初始事件,似乎与生存无关。