Frequent Occurrence of Activated ras Oncogenes in Seminomas but Not in Nonseminomatous Germ Cell Tumors

Mulder, Marlies; Keijzer, W.; Splinter, T. A. W.; Bos, Johannes L.

doi:10.1007/978-3-642-84485-0_14

Cited by 5 publications

(1 citation statement)

References 11 publications

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“…A study comparing k-ras-2 gene sequences between mediastinal and testicular seminomas showed that 8 % (1 of 13) of mediastinal seminomas had a k-ras mutation in codon 13, while 15 % (2 of 13) of testicular seminomas had k-ras mutations in codon 12 [62]. Other studies confirmed that k-ras mutations in testicular GCT, if identified, are in codon 12 [64,65]. Furthermore, weak p53 immunostaining was identified in 31 % of mediastinal seminomas in contrast to 77-90 % of testicular seminomas and 94 % of testicular nonseminomatous GCT [66].…”

Section: Histogenesismentioning

confidence: 86%

Mediastinal Germ Cell Tumors

Roden

2017

Pathology and Biology of Human Germ Cell Tumors

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Section: Histogenesismentioning

confidence: 86%

Mediastinal Germ Cell Tumors

Roden

2017

Pathology and Biology of Human Germ Cell Tumors

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Detection of RAS mutations in archival testicular germ cell tumors by polymerase chain reaction and oligonucleotide hybridization

Moul

Theune

Chang

1992

Genes Chromosomes & Cancer

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Preliminary studies of RAS mutational activation in human testicular germ cell neoplasms have yielded conflicting results. Whereas two studies of clinical material revealed a significant incidence of N- and KRAS mutations, two studies of a variety of germ cell lines failed to document RAS mutations. To clarify the incidence of RAS mutations in these tumors, we studied archival paraffin-embedded, formalin-fixed orchiectomy specimens from 25 nonseminomas (NSGCT), 18 seminomas (SEM), and one Leydig cell tumor. For 14 of the 44 neoplasms, DNA was also available from nonmalignant testis adjacent to the tumor. Six age-matched patients had testes removed because of nonmalignant disease and were studied as controls. Polymerase chain reaction (PCR) amplified the K-, N-, and HRAS 12, 13, and 61 codons of these specimens, and mutations were detected with mutation-specific oligonucleotide probe hybridization of Southern and slot blots. Four mutations were found in KRAS 12 (4/44;[9.1%]). One seminoma [1/18(5.6%)] contained the mutation GGT(GLY)----CGT(ARG), and three NSGCT [3/25(12%)] were found to have GGT(GLY)----GAT(ASP) mutations. One of the NSGCT mutations was detected in adjacent nonmalignant tissue, but the corresponding tumor did not contain any detectable mutation. No mutations were detected at KRAS 13 or 61, in NRAS or HRAS 12, 13, or 61, or in the control normal testes. PCR, slot blots, and hybridizations were performed twice by two separate investigators for confirmation of results. PCR-generated mutation-specific positive controls were created for all possible RAS mutations, and these along with wild-type DNA controls were integral to interpretation of the oligonucleotide mismatch hybridization assay. By using positive and negative controls, we have detected a relatively low incidence of RAS mutations in archival human testicular germ cell tumors.

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Zebrafish Germ Cell Tumors

Sanchez

Amatruda

2016

Advances in Experimental Medicine and Biology

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Frequent Occurrence of Activated ras Oncogenes in Seminomas but Not in Nonseminomatous Germ Cell Tumors

Cited by 5 publications

References 11 publications

Mediastinal Germ Cell Tumors

Mediastinal Germ Cell Tumors

Detection of RAS mutations in archival testicular germ cell tumors by polymerase chain reaction and oligonucleotide hybridization

Zebrafish Germ Cell Tumors

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