I would like to add another dimension to the question: HPV-positive oral cancer represents a very well defined group. They occur in the Waldeyer's ring, are relatively undifferentiated and have very consistent molecular features (p16 positive, often p53 wild-type, cyclin D1 low, RB negative or low etc) and etiological features (often non-smokers and non-alcoholics). These sets of features does not seem to apply to cervical cancer and I have no idea why. My impression is that there is a subset of cervical cancer that fits the molecular data of HPV-positive oral cancer but why not all? Isn't the majority of cervical cancer driven by the same types of HPVs?
This has always confused me: oral HPV cancer is a relatively uniform group while HPV-positive cervical cancer is not.
Is my view off? Do is misinterpret cervical cancer? I am talking about cervical SCC...
The etiological factors leading to oral HPV+ oral cancer appear obvious but has it been shown that it is a sexually transmitted disease? Didn't one of the more famous oral cancer victims- no not Sigmund Freud- Michael Douglas make comments in this line of thought? Not that Michael Douglas is an expert in oral cancer epidemiology but he made it sound like that this is the current dogma on how you get oncogenic HPV into the keratinocytes associated with the Waldeyer's ring.
It is still an interesting topic once you go beyond the fact that half of the tumors of this region are HPV-oncogene driven. But what are the common features with other SCCs from other squamous epithelia that are or may be also driven by the same oncogenes?
ahuja hospital faridabad indian
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