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Ki-ras oncogene mutations in non-HPV-associated anal carcinoma
L R Hiorns1, J H Scholefield, J G Palmer
1Academic Unit of Radiotherapy and Oncology, Institute of Cancer Research, Sutton, Surrey, U.K.
The Journal of Pathology
|June 1, 1990
Summary
Activating ras oncogene mutations are uncommon in anal squamous cell carcinomas, suggesting they do not commonly cooperate with human papillomavirus (HPV) in cancer development.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Human papillomavirus 16 (HPV 16) is implicated in the development of anal squamous cell carcinomas.
- HPV 16 is known to cooperate with activated ras oncogenes in cellular transformation in vitro.
Purpose of the Study:
- To investigate the presence and role of ras oncogene family mutations in anal squamous cell carcinomas.
- To determine if ras activation cooperates with HPV in the genesis of these tumors.
Main Methods:
- Screening of anal squamous cell carcinomas for activating ras mutations.
- Utilizing polymerase chain reaction (PCR) for DNA amplification.
- Employing synthetic oligonucleotide probes for mutation detection.
Main Results:
- Activating ras mutations were identified in only two cases (both Ki-ras codon 12).
- Neither of the identified ras mutations were associated with HPV.
- Ras activation appears to be an infrequent event in the genesis of these tumors.
Conclusions:
- Ras activation is not a common event in the development of anal squamous cell carcinomas.
- When ras mutations occur, they do not appear to cooperate with HPV in the genesis of these cancers.