Murat,
as Nadia and Nelson already said it, yes, high risk HPV is seen more frequently in cervical cancers than low risk counterparts.
About the cut-off level of low-risk to high-risk: the main difference between the two types is the presence (low) or not (high) of transcription factor E2, a protein that suppresses E6 and E7 (the main oncoproteins) expression. High-risk HPVs often lose E2 during viral DNA integration into host genome. See attached file for more details.
regards.
Yes. Subtypes HPV 16 and 18 are found in over 70 percent of all cervical cancers.
High-risk (oncogenic or cancer-associated) types
Common types: 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 69, 82
Low-risk (non-oncogenic) types
Common types: 6, 11, 40, 42, 43, 44, 54, 61, 72, 81
http://www.cancer.gov/cancertopics/factsheet/Risk/HPV
Dear Murat,
Yes, the HPV types are classified by their association with cancer into two categories: High risk HPV and Low risk HPV. From a virologic perspective, the definitive proof of carcinogenicity of an HPV type is finding transcriptionally active HPV in a tumour. Further details can be found in the attached article:
Regards
Murat,
as Nadia and Nelson already said it, yes, high risk HPV is seen more frequently in cervical cancers than low risk counterparts.
About the cut-off level of low-risk to high-risk: the main difference between the two types is the presence (low) or not (high) of transcription factor E2, a protein that suppresses E6 and E7 (the main oncoproteins) expression. High-risk HPVs often lose E2 during viral DNA integration into host genome. See attached file for more details.
regards.
Low risk types are no risk HPV for cervical ,vulvar and vaginal cancers
Then is not useful and may be misleading to serch for them
When you decide to use HPV test for screening it means that you search for HPV HR types.It is not so important to identify the subtypes because mangement is not influenced by genotyping.
I have been convinced that high risk HPV types more frequently observed in patients with cervical cancer than low risk HPV types. But causal relationship seems has not been confirmed yet. When neoplastic process started it might also independently induce the silent viral DNA to replicate and therefore viral DNA could be more frequently expressed in patients with cancer than normal population. HPV high risk subtypes might be coincidentally found more often than HPV low risk subtypes in cancer patients. What is your comment?
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