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Ki‐ ras oncogene mutations in non‐HPV‐associated anal carcinoma
Author(s) -
Hiorns Lynne R.,
Scholefield John H.,
Palmer James G.,
Shepherd Neil A.,
Kerr Ian B.
Publication year - 1990
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711610203
Subject(s) - oncogene , polymerase chain reaction , biology , mutation , oncogene proteins , cancer research , dna , in vitro , malignant transformation , oligonucleotide , human papillomavirus , virology , cell , gene , genetics , cell cycle , medicine , regulation of gene expression
Human papillomavirus 16 (HPV 16) DNA is found in a high proportion of anal squamous cell carcinomas in whose genesis it is thought to play an important role. In addition, it can be shown to cooperate in vitro with activated ras oncogenes in cellular transformation. We have therefore screened a series of such tumours for activating mutations of the ras oncogene family using DNA amplified in vitro by the polymerase chain reaction (PCR) and a series of synthetic oligonucleotide probes. Mutations were seen in only two cases (both Ki‐ ras codon 12), neither of which was HPV‐associated. Our results suggest that ras activation is not a common event in the genesis of these tumours and, when it does occur, it does not appear to cooperate with HPV.