Thursday, June 19, 2014

Opinion on Melanoma treatment

*Having listen to the treatment on Melanoma
it appears to me the V600 or BRAF positive patient
have a short lived progression free because of a rapid development of secondary amplifications of gene that will force a resistance ...
and it may be that there is a secondary activation of lymphocyte during this treatment.   This secondary amplification of activation, prep the disease to use of anti-CTL4 or anti-PD1 or PDL1 (or a combination there of since this combination has greater efficacy)

Meaning in BRAF positive, the anti-BRAF could be used as an induction to have higher response rate but instead of waiting for a more likely recurrence rate, give within 2-3 months a combination of Ipilimumab and Nivolumab to obtain for sure long term progression free survival.  The only objection to this strategy right now is money....what insurance will cover this expensive strategy...But clearly it makes the logical sense!

what worry a local oncologist is of course the episode of Hypotension that may result for the combination of Ipilimumab to Nivolumab or anti-PD-1

My fear is because of expense, what makes sense will not be completed for a decade!
trial should start now please!

fort those with KIT, Sutent could serve as induction therapy prior to combination Ipilimumab-Nivolumab.

Now I wonder if this combination would be appropriate for my patient with NF1 + GIST which failed Gleevec....wonder if she can sign a consent for this!

will check this out
BRAF resistance 
due to reactivation of MAPK pathways through MEK amplification (is there a secondary overexpression of mesodermal expression?) should we measuring COT overexpression, or amplification of c-MET, IGF1R, or PDGFR, can use of ASPIRIN help, can Nexavar prolong the effect of Dabrafenib...? oh hell all thins thinking just drive you crazy....but that one should do in research!

few dosages to check!

Dabrafenib 150 mg PO BID
Nivolumab 1 mg/kg
Ipilimumab 3 mg/Kg
Trametinib 2mg PO QD
Vemurafenib 960mg in 4 tab Q12 h

===============================why the Kerato-Acantoma in anti-BRAF inhibitor, is the receptor in the same membrane fold?
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