NRAS postive, BRAF Negative

These are the newer treatment drugs and the first 3 do not relate to BRAF status.

Ipilimumab (trade name Yervoy, formerly known as MDX-010[1] and MDX-101), is a monoclonal antibody that works to activate the immune system by targeting CTLA-4, a protein receptor that downregulates the immune system.

Nivolumab (nye vol' ue mab; ONO-4538, BMS-936558, or MDX1106), marketed as Opdivo, is a human IgG4 anti-PD-1 monoclonal antibody developed by Ono Pharmaceutical and Medarex (later acquired by Bristol-Myers Squibb) for the treatment of cancer. Nivolumab acts as an immunomodulator by blocking ligand activation of the programmed cell death 1 (PD-1) receptor on activated T cells.

Pembrolizumab (formerly MK-3475 and lambrolizumab, trade name Keytruda) is a humanized antibody used in cancer immunotherapy. It targets the programmed cell death 1 (PD-1) receptor. The drug was initially used in treating metastatic melanoma.

Vemurafenib (INN, marketed as Zelboraf) is a B-Raf enzyme inhibitor developed by Plexxikon (now part of Daiichi-Sankyo) and Genetech for the treatment of late-stage melanoma. The name "vemurafenib" comes from V600E mutated BRAF inhibition.

Dabrafenib (trade name Tafinlar) is a drug for the treatment of cancers associated with a mutated version of the gene BRAF. Dabrafenib acts as an inhibitor of the associated enzyme B-Raf, which plays a role in the regulation of cell growth. Dabrafenib has clinical activity with a manageable safety profile in clinical trials of phase 1 and 2 in patients with BRAF(V600)-mutated metastatic melanoma.

Trametinib (trade name Mekinist) is a cancer drug. It is a MEK inhibitor drug with anti-cancer activity. It inhibits MEK1 and MEK2.  Trametinib had good results for metastatic melanoma carrying the BRAF V600E mutation in a phase III clinical trial. In this mutation, the amino acid valine (V) at position 600 within the BRAF gene has become replaced by glutamic acid (E) making the mutant BRAF gene constituitively active.  In May 2013, trametinib was approved as a single-agent by the FDA for the treatment of patients with V600E mutated metastatic melanoma. Clinical trial data demonstrated that resistance to single-agent trametinib often occurs within 6 to 7 months. To overcome this, trametinib was combined with the BRAF inhibitor dabrafenib. As a result of this research, on January 8, 2014, the FDA approved the combination of dabrafenib and trametinib for the treatment of patients with BRAF V600E/K-mutant metastatic melanoma.

These are the newer treatment drugs and the first 3 do not relate to BRAF status.

Ipilimumab (trade name Yervoy, formerly known as MDX-010[1] and MDX-101), is a monoclonal antibody that works to activate the immune system by targeting CTLA-4, a protein receptor that downregulates the immune system.

Nivolumab (nye vol' ue mab; ONO-4538, BMS-936558, or MDX1106), marketed as Opdivo, is a human IgG4 anti-PD-1 monoclonal antibody developed by Ono Pharmaceutical and Medarex (later acquired by Bristol-Myers Squibb) for the treatment of cancer. Nivolumab acts as an immunomodulator by blocking ligand activation of the programmed cell death 1 (PD-1) receptor on activated T cells.

Pembrolizumab (formerly MK-3475 and lambrolizumab, trade name Keytruda) is a humanized antibody used in cancer immunotherapy. It targets the programmed cell death 1 (PD-1) receptor. The drug was initially used in treating metastatic melanoma.

Vemurafenib (INN, marketed as Zelboraf) is a B-Raf enzyme inhibitor developed by Plexxikon (now part of Daiichi-Sankyo) and Genetech for the treatment of late-stage melanoma. The name "vemurafenib" comes from V600E mutated BRAF inhibition.

Dabrafenib (trade name Tafinlar) is a drug for the treatment of cancers associated with a mutated version of the gene BRAF. Dabrafenib acts as an inhibitor of the associated enzyme B-Raf, which plays a role in the regulation of cell growth. Dabrafenib has clinical activity with a manageable safety profile in clinical trials of phase 1 and 2 in patients with BRAF(V600)-mutated metastatic melanoma.

Trametinib (trade name Mekinist) is a cancer drug. It is a MEK inhibitor drug with anti-cancer activity. It inhibits MEK1 and MEK2.  Trametinib had good results for metastatic melanoma carrying the BRAF V600E mutation in a phase III clinical trial. In this mutation, the amino acid valine (V) at position 600 within the BRAF gene has become replaced by glutamic acid (E) making the mutant BRAF gene constituitively active.  In May 2013, trametinib was approved as a single-agent by the FDA for the treatment of patients with V600E mutated metastatic melanoma. Clinical trial data demonstrated that resistance to single-agent trametinib often occurs within 6 to 7 months. To overcome this, trametinib was combined with the BRAF inhibitor dabrafenib. As a result of this research, on January 8, 2014, the FDA approved the combination of dabrafenib and trametinib for the treatment of patients with BRAF V600E/K-mutant metastatic melanoma.

These are the newer treatment drugs and the first 3 do not relate to BRAF status.

Ipilimumab (trade name Yervoy, formerly known as MDX-010[1] and MDX-101), is a monoclonal antibody that works to activate the immune system by targeting CTLA-4, a protein receptor that downregulates the immune system.

Nivolumab (nye vol' ue mab; ONO-4538, BMS-936558, or MDX1106), marketed as Opdivo, is a human IgG4 anti-PD-1 monoclonal antibody developed by Ono Pharmaceutical and Medarex (later acquired by Bristol-Myers Squibb) for the treatment of cancer. Nivolumab acts as an immunomodulator by blocking ligand activation of the programmed cell death 1 (PD-1) receptor on activated T cells.

Pembrolizumab (formerly MK-3475 and lambrolizumab, trade name Keytruda) is a humanized antibody used in cancer immunotherapy. It targets the programmed cell death 1 (PD-1) receptor. The drug was initially used in treating metastatic melanoma.

Vemurafenib (INN, marketed as Zelboraf) is a B-Raf enzyme inhibitor developed by Plexxikon (now part of Daiichi-Sankyo) and Genetech for the treatment of late-stage melanoma. The name "vemurafenib" comes from V600E mutated BRAF inhibition.

Dabrafenib (trade name Tafinlar) is a drug for the treatment of cancers associated with a mutated version of the gene BRAF. Dabrafenib acts as an inhibitor of the associated enzyme B-Raf, which plays a role in the regulation of cell growth. Dabrafenib has clinical activity with a manageable safety profile in clinical trials of phase 1 and 2 in patients with BRAF(V600)-mutated metastatic melanoma.

Trametinib (trade name Mekinist) is a cancer drug. It is a MEK inhibitor drug with anti-cancer activity. It inhibits MEK1 and MEK2.  Trametinib had good results for metastatic melanoma carrying the BRAF V600E mutation in a phase III clinical trial. In this mutation, the amino acid valine (V) at position 600 within the BRAF gene has become replaced by glutamic acid (E) making the mutant BRAF gene constituitively active.  In May 2013, trametinib was approved as a single-agent by the FDA for the treatment of patients with V600E mutated metastatic melanoma. Clinical trial data demonstrated that resistance to single-agent trametinib often occurs within 6 to 7 months. To overcome this, trametinib was combined with the BRAF inhibitor dabrafenib. As a result of this research, on January 8, 2014, the FDA approved the combination of dabrafenib and trametinib for the treatment of patients with BRAF V600E/K-mutant metastatic melanoma.

Yes, it's special to connect with others who have the mucosal variety, as it's rare and can be more aggressive so there's not a whole lot of time to make decisions. Is your mom seeing a melanoma specialist, or has she traveled to one of the major melanoma centers for a second opinion (Dana Farber, John Hopkins, MD Anderson, Yale/Smilow, Sloan)? I'm not sure why she was given a chemo combo rather than an immunotherapy combo…this concerns me.

My side effects have been rough, but under control because my oncologist is watching me like a hawk. I'm under good care which I'm very grateful for. Communication is key because the side effects could get very serious if they are not addressed at the first sign of trouble…but everyone's different. I don't mind the side effects knowing that the immunotherapy combo is my best shot at sticking around as long as I can….

Yes, it's special to connect with others who have the mucosal variety, as it's rare and can be more aggressive so there's not a whole lot of time to make decisions. Is your mom seeing a melanoma specialist, or has she traveled to one of the major melanoma centers for a second opinion (Dana Farber, John Hopkins, MD Anderson, Yale/Smilow, Sloan)? I'm not sure why she was given a chemo combo rather than an immunotherapy combo…this concerns me.

My side effects have been rough, but under control because my oncologist is watching me like a hawk. I'm under good care which I'm very grateful for. Communication is key because the side effects could get very serious if they are not addressed at the first sign of trouble…but everyone's different. I don't mind the side effects knowing that the immunotherapy combo is my best shot at sticking around as long as I can….

My blood draws have been mostly normal, only once was it off when they found an inflammation in my liver (caused by the immunotherapy, not the cancer).

Thank you for sharing more about the cisplatin/temodar route…I'm in Stage IV with mets already to the brain, so at a different stage than your mom. I have been told the ipi/nivo combo has been effective with mucosal, though the stats are a bit lower (~10% lower) than cutenous…

My blood draws have been mostly normal, only once was it off when they found an inflammation in my liver (caused by the immunotherapy, not the cancer).

Thank you for sharing more about the cisplatin/temodar route…I'm in Stage IV with mets already to the brain, so at a different stage than your mom. I have been told the ipi/nivo combo has been effective with mucosal, though the stats are a bit lower (~10% lower) than cutenous…

My blood draws have been mostly normal, only once was it off when they found an inflammation in my liver (caused by the immunotherapy, not the cancer).

Thank you for sharing more about the cisplatin/temodar route…I'm in Stage IV with mets already to the brain, so at a different stage than your mom. I have been told the ipi/nivo combo has been effective with mucosal, though the stats are a bit lower (~10% lower) than cutenous…

Yes, it's special to connect with others who have the mucosal variety, as it's rare and can be more aggressive so there's not a whole lot of time to make decisions. Is your mom seeing a melanoma specialist, or has she traveled to one of the major melanoma centers for a second opinion (Dana Farber, John Hopkins, MD Anderson, Yale/Smilow, Sloan)? I'm not sure why she was given a chemo combo rather than an immunotherapy combo…this concerns me.

My side effects have been rough, but under control because my oncologist is watching me like a hawk. I'm under good care which I'm very grateful for. Communication is key because the side effects could get very serious if they are not addressed at the first sign of trouble…but everyone's different. I don't mind the side effects knowing that the immunotherapy combo is my best shot at sticking around as long as I can….