The molecular features, I think there’s many molecular features and the two that are promising. The two subtypes are really distinct molecularly in many, many, many different ways. Interestingly, the subtype that is low risk with better survival tends to have all of the markers that have been identified before for good prognosis in HPV-associated cancer. They tend to have lower smoking...
The molecular features, I think there’s many molecular features and the two that are promising. The two subtypes are really distinct molecularly in many, many, many different ways. Interestingly, the subtype that is low risk with better survival tends to have all of the markers that have been identified before for good prognosis in HPV-associated cancer. They tend to have lower smoking. They tend not to have HPV gene genome integration into the somatic genome. They tend not to have PIK3CA mutations, which those mutations have been associated with poor prognosis. And they have a higher immune infiltration, which has been associated with good prognosis. So all of the markers that have been identified for good prognosis tend to segregate based on subtypes. And I think it’s because they’re driven by different carcinogenesis mechanisms. And therefore, that is defining not only the tumor status, the cancer cell status, but also the tumor microenvironment. So it’s all very interesting. And one point that we’re working on pretty aggressively now is we can activate NF-kappa B in the high-risk subtype and basically sensitize that to radiation therapy. So the hope is that we can make the high-risk subtype sensitive to radiation so that now it can also be treated with a lower dose of radiation with fewer side effects.
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