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Detection of preferential NRAS mutations in human male germ cell tumors by the polymerase chain reaction
Author(s) -
Ganguly Sabyasachi,
Murty Vundavalli V. V. S.,
Samaniego Felipe,
Reuter Victor E.,
Bosl George J.,
Chaganti R. S. K.
Publication year - 1990
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.2870010307
Subject(s) - neuroblastoma ras viral oncogene homolog , hras , germ cell tumors , kras , biology , embryonal carcinoma , cancer research , mutation , germ cell , gene , teratoma , polymerase chain reaction , genetics , pathology , medicine , chemotherapy , cellular differentiation
We have studied 31 male germ cell tumors (GCTs) for probable mutations in codons 12, 13, and 61 of HRAS, KRAS , and NRAS oncogenes using the polymerase chain reaction. Twenty of the thirty‐one tumors exhibited NRAS gene mutations, 14 in codon 61, and six in codon 12, whereas no mutations were detected in HRAS and KRAS genes. The NRAS mutations were equally prevalent in seminomatous and nonseminomatous GCTs. Thus 13 of 22 seminomas, six of seven embryonal carcinomas, and one of two mixed tumors exhibited mutations. Two non‐seminomatous tumors (an embryonal carcinoma and a yolk sac/teratoma) had mutations in both codons 12 and 61. The high frequency of NRAS mutations observed in the present study suggests that NRAS gene products may play an important role in growth regulatory functions of premalignant and malignant germ cells.