Signed, a guy who spent most of his PhD studying cancer.
Signed, a guy who spent most of his PhD studying cancer.
Simultaneously, one of the largest criticisms of osimertinib in resectable NSCLC has been that some oncologists got overexcited about the DFS results and patients have been unfortunately not receiving the traditional standard of care adjuvant therapy (old school platinum based drugs) which have a proven overall survival benefit (until today osimertinib did not, it now possibly does).
Targeted gene-directed therapy is cool but conventional chemotherapy is still really important.
ICIs are magic when they work.
And thanks for trying to question my expertise. Please look up the no true Scotsman fallacy and see if that may apply here.
They share the same DNA in the sense that every cell in that body does. But the different types of cancers have different mutations per cell type and the increasingly precise identification of those is the basis of the recent new treatment options. Histological classifications become less and less relevant, instead mutations and subtypes of mutations give directions for treatment paths. So I think that statement is a bit confusing.
What do you mean by "histological classification" because every interpretation I can think of is very incorrect.
If you mean diagnosing the type of cancer (e.g. clear cell renal cell carcinoma) we've already been using molecular markers for over a decade now.
Since you mention "describing the look": mitotic rate and local staging (depth of invasion, lymphovascular invasion, perineurial invasion) matter far more than any DNA/type of cancer and this isn't changing at all nor will it ever change.
Do you mean this literally or figuratively? Isn't one of the serious problems with tumors that the mutation rate inside them goes through the roof? (And then they eventually figure out how to be metastatic?)