ArticlePathology oncology research : POR2010
Human papillomavirus DNA and oncogene alterations in colorectal tumors.
Article in Pathology oncology research : POR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Human papillomavirus and colorectal cancer.Medical oncology (Northwood, London, England) · 2018Pooled it
- Mendelian randomization analyses support causal relationships between HPV infection and colorectal cancer.Discover oncology · 2024Article
- Association of G12D mutation in the KRAS gene with HPV and EBV in gastrointestinal cancer tissues.The Journal of international medical research · 2024Article
- Human Papillomavirus and Risk of Colorectal Cancer: An Analysis of Nationwide Claims Data.Medicina (Kaunas, Lithuania) · 2022Article
- Review
- Interpretation of P16 expression as a marker of HPV in colorectal cancer.Histology and histopathology · 2022Article
- Human Papillomaviruses and Epstein-Barr Virus Interactions in Colorectal Cancer: A Brief Review.Pathogens (Basel, Switzerland) · 2020Review
- Does human papillomavirus cause human colorectal cancer? Applying Bradford Hill criteria postulates.Ecancermedicalscience · 2020Article
- Article
- Evaluation of HPV DNA positivity in colorectal cancer patients in Kerman, Southeast IranAsian Pacific journal of cancer prevention : APJCP · 2018Article
- Molecular evidence of high-risk human papillomavirus infection in colorectal tumours from Cuban patients.Memorias do Instituto Oswaldo Cruz · 2016Article
- High Prevalence of Human Papillomavirus in Colorectal Cancer in Hispanics: A Case-Control Study.Gastroenterology research and practice · 2016Article
- Opportunistic intestinal infections and risk of colorectal cancer among people with AIDS.AIDS research and human retroviruses · 2012Article
- No evidence for human papillomavirus in the etiology of colorectal polyps.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study is to determine the presence and molecular integrity of high-risk HPV types in colorectal adenocarcinomas and to assess whether viral DNA is related to common proto-oncogene alterations, such as k-ras mutations and c-myc gene amplification, in colorectal cancer. Seventy-five colorectal adenocarcinomas were screened for HPV infection using nested-PCR (MY09/11-GP5+/6+). HPV typing was performed by type-specific PCR for HPV 16 and HPV 18 DNA. Unidentified samples were subsequently sequenced to determine the viral genotype. The physical status of HPV was determined by a nested PCR approach for type-specific E2 sequences. C-myc amplification was assessed by co-amplification with β-globin as control locus, and mutation in k-ras codons 12 and 13 by ARMS-PCR. Overall, HPV was detected in thirty-three colorectal specimens (44%). HPV 16 was the prevalent type (16/75), followed by HPV 18 (15/75), HPV 31 (1/75) and HPV 66 (1/75). E2 disruption was detected in 56.3% of HPV 16 and in 40% of HPV 18 positive tumors. C-myc amplification was detected in 29.4% of cases, while k-ras mutations in 30.7%. There was no significant trend for HPV infection in tumors harboring either k-ras or c-myc alterations. This study demonstrates HPV DNA and viral integration in colorectal tumors, suggesting a potential role of this virus in colorectal carcinogenesis. There was no concurrence, however, of k-ras and c-myc activation with viral infection.
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Registered trials
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