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How melanomas develop resistance to the B-RAF kinase inhibitor PLX4032

Forums General Melanoma Community How melanomas develop resistance to the B-RAF kinase inhibitor PLX4032

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      Tim–MRF
      Guest

        This is a great article.  MRF is currently funding Roger Lo, the last author on the publication, and I had the chance to visit with him in early February.  I asked if his work might lay the groundwork for being able to determine in advance who will respond to the BRAF inhibitor.  We know that about 60% of people with mutated BRAF respond to PLX 4032.  Why don't the other 40% respond? 

        Roger's work shows that melanoma cells develop resistance to the BRAF inhibitor by activating alternate pathways.  Think of trying to get into New York City via the Lincoln Tunnel.  If that tunnel is shut down, you can go south to the Holland Tunnel or north to the George Washington Bridge to get into the city.  That is what these cells are doing.

        It may be that people who do not respond to the BRAF inhibitor have cells that have already pre-activated these alternate pathways.  If that is the case, researchers could test tumor tissue for this activation.  If the other pathways are activated, they would know that the BRAF inhibitor alone is unlikely to work, and would look for alternate therapies.

        Tim–MRF

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          FormerCaregiver
          Participant

            Thanks for your valuable feedback. It is great to hear that MRF is funding Roger Lo. He is certainly involved in some groundbreaking research!

            Frank

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            FormerCaregiver
            Participant

              Thanks for your valuable feedback. It is great to hear that MRF is funding Roger Lo. He is certainly involved in some groundbreaking research!

              Frank

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            Tim–MRF
            Guest

              This is a great article.  MRF is currently funding Roger Lo, the last author on the publication, and I had the chance to visit with him in early February.  I asked if his work might lay the groundwork for being able to determine in advance who will respond to the BRAF inhibitor.  We know that about 60% of people with mutated BRAF respond to PLX 4032.  Why don't the other 40% respond? 

              Roger's work shows that melanoma cells develop resistance to the BRAF inhibitor by activating alternate pathways.  Think of trying to get into New York City via the Lincoln Tunnel.  If that tunnel is shut down, you can go south to the Holland Tunnel or north to the George Washington Bridge to get into the city.  That is what these cells are doing.

              It may be that people who do not respond to the BRAF inhibitor have cells that have already pre-activated these alternate pathways.  If that is the case, researchers could test tumor tissue for this activation.  If the other pathways are activated, they would know that the BRAF inhibitor alone is unlikely to work, and would look for alternate therapies.

              Tim–MRF

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              Looks very interesting — 2 research articles and a News and Views review in the same issue of Nature.  Haven't read them yet, but if anyone wants them, email me at [email protected]. I will be happy to send them to you.

              ellen

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              Looks very interesting — 2 research articles and a News and Views review in the same issue of Nature.  Haven't read them yet, but if anyone wants them, email me at [email protected]. I will be happy to send them to you.

              ellen

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