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potidaean

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      potidaean
      Participant

        I excitedly went to read the actual paper and am sorry to say the news article was misleading. First, the 70% of responsive melanomas was done with cells in a flask, not in a mouse. Second, the cells were not "eradicated completely", only closely so. Finally, when they did try it in mice, they only reported that the tumors were successfully infected, and did not report what effect was seen on the tumor.

         

        Not trying to be a wet blanket – I hope it works out in the long run! Just be careful of these kinds of reports.

        potidaean
        Participant

          I excitedly went to read the actual paper and am sorry to say the news article was misleading. First, the 70% of responsive melanomas was done with cells in a flask, not in a mouse. Second, the cells were not "eradicated completely", only closely so. Finally, when they did try it in mice, they only reported that the tumors were successfully infected, and did not report what effect was seen on the tumor.

           

          Not trying to be a wet blanket – I hope it works out in the long run! Just be careful of these kinds of reports.

          potidaean
          Participant

            I excitedly went to read the actual paper and am sorry to say the news article was misleading. First, the 70% of responsive melanomas was done with cells in a flask, not in a mouse. Second, the cells were not "eradicated completely", only closely so. Finally, when they did try it in mice, they only reported that the tumors were successfully infected, and did not report what effect was seen on the tumor.

             

            Not trying to be a wet blanket – I hope it works out in the long run! Just be careful of these kinds of reports.

            potidaean
            Participant

              Hi Lucy, do you know your Braf/Nras status? There are two two different trials:

              http://clinicaltrials.gov/show/NCT01781572 for Nras melanoma, which is MEK + LEE

              http://clinicaltrials.gov/show/NCT01543698 for Braf melanoma, which is MEK + LEE + Tafinlar

              potidaean
              Participant

                Hi Lucy, do you know your Braf/Nras status? There are two two different trials:

                http://clinicaltrials.gov/show/NCT01781572 for Nras melanoma, which is MEK + LEE

                http://clinicaltrials.gov/show/NCT01543698 for Braf melanoma, which is MEK + LEE + Tafinlar

                potidaean
                Participant

                  Hi Lucy, do you know your Braf/Nras status? There are two two different trials:

                  http://clinicaltrials.gov/show/NCT01781572 for Nras melanoma, which is MEK + LEE

                  http://clinicaltrials.gov/show/NCT01543698 for Braf melanoma, which is MEK + LEE + Tafinlar

                  potidaean
                  Participant

                    Congratulations on the great news!

                    Scientists have found that in some cases, the tumor becomes "addicted" to the BRAF inhibitor. I know, it's very weird, but it happens – and sounds like your husband was one of the lucky ones. Basically, the drug keeps the BRAF activity down (let's say it cuts it down from a 10 to a 2), but over the years, the BRAF activity rises within the tumor (let's say a total level of 18, but because the drug stops 8 of it, the net balance is 10), causing it to regrow. What happens is that once you go off drug, it releases the whole bunch of BRAF activity at once (total level of 18) which actually turns out to be too toxic for the tumor, so it starts shrinking .

                    One idea that's out there is that, if the tumor ever starts re-growing yet again, it might still be responsive to BRAF inhibitor, because the "level 18" cells have died and it leaves behind some "level 10" cells which now re-grow in the absense of drug, and which should still be sensitive to it. This is why there are clinical trials out there with 2-weeks-on, 2-weeks-off regimens, trying to make use of this idea. You might want to discuss with your oncologist the possibility of trying dabrafenib again, should the tumor ever regrow (hopefully not, of course!).

                    potidaean
                    Participant

                      Congratulations on the great news!

                      Scientists have found that in some cases, the tumor becomes "addicted" to the BRAF inhibitor. I know, it's very weird, but it happens – and sounds like your husband was one of the lucky ones. Basically, the drug keeps the BRAF activity down (let's say it cuts it down from a 10 to a 2), but over the years, the BRAF activity rises within the tumor (let's say a total level of 18, but because the drug stops 8 of it, the net balance is 10), causing it to regrow. What happens is that once you go off drug, it releases the whole bunch of BRAF activity at once (total level of 18) which actually turns out to be too toxic for the tumor, so it starts shrinking .

                      One idea that's out there is that, if the tumor ever starts re-growing yet again, it might still be responsive to BRAF inhibitor, because the "level 18" cells have died and it leaves behind some "level 10" cells which now re-grow in the absense of drug, and which should still be sensitive to it. This is why there are clinical trials out there with 2-weeks-on, 2-weeks-off regimens, trying to make use of this idea. You might want to discuss with your oncologist the possibility of trying dabrafenib again, should the tumor ever regrow (hopefully not, of course!).

                      potidaean
                      Participant

                        Congratulations on the great news!

                        Scientists have found that in some cases, the tumor becomes "addicted" to the BRAF inhibitor. I know, it's very weird, but it happens – and sounds like your husband was one of the lucky ones. Basically, the drug keeps the BRAF activity down (let's say it cuts it down from a 10 to a 2), but over the years, the BRAF activity rises within the tumor (let's say a total level of 18, but because the drug stops 8 of it, the net balance is 10), causing it to regrow. What happens is that once you go off drug, it releases the whole bunch of BRAF activity at once (total level of 18) which actually turns out to be too toxic for the tumor, so it starts shrinking .

                        One idea that's out there is that, if the tumor ever starts re-growing yet again, it might still be responsive to BRAF inhibitor, because the "level 18" cells have died and it leaves behind some "level 10" cells which now re-grow in the absense of drug, and which should still be sensitive to it. This is why there are clinical trials out there with 2-weeks-on, 2-weeks-off regimens, trying to make use of this idea. You might want to discuss with your oncologist the possibility of trying dabrafenib again, should the tumor ever regrow (hopefully not, of course!).

                        potidaean
                        Participant

                          Hello. Mekinist works on non-BRAF as well, but it is only FDA-approved for BRAF. So if you want to try Mekinist on a non-BRAF tumor, you will have to find a trial.

                          potidaean
                          Participant

                            Hello. Mekinist works on non-BRAF as well, but it is only FDA-approved for BRAF. So if you want to try Mekinist on a non-BRAF tumor, you will have to find a trial.

                            potidaean
                            Participant

                              Hello. Mekinist works on non-BRAF as well, but it is only FDA-approved for BRAF. So if you want to try Mekinist on a non-BRAF tumor, you will have to find a trial.

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