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Rare cancer: ovarian clear cell carcinoma

Gynecologic Cancers | Last Active: 1 day ago | Replies (170)
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@jchantler

Thank you so very much for the clarification. I want to get on Herceptin/trastuzumab because my HER 2 score is 3+ , the worst. Insurance wouldn't approve it and won't until other treatments have proved useless. Right now I have "mixed results." My oncologist tried hard to get it for me, and also appealed to the drug company for compassionate freebie, but no luck. The justification for denial is that it isn't yet approved for uterine cancer - just breast cancer. I have Untited Health Medicare. Would love to hear from others if you got approved for Herceptin/trastuzumab with your insurance, and what insurance you have. Maybe I could use that to make an appeal. "All these other companies approve it, so join the club." I haven't seen PD-1 on my lab report. I'll look again. There is a study on using Ivermectin against PD one at Cedar Sinai in LA . Not sure how it worked out. Any know anything about Ivermectin use? It doesn't cost much so there isn't any incentive for drug companies to spend a lot of dollars to study it. No return on investment. If I'm pMMR how does that connect with PD -1, if at all?

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Replies to "Thank you so very much for the clarification. I want to get on Herceptin/trastuzumab because my..."
birdergirl | @birdergirl | 3 days ago

ive got basic medicare w aarp medigap g. love it. basically if medicare approves it, medigap pays the copay. basic medicare has no maximum out of pocket which is VERY bad but the additional medigap does. have to get your own drug policy tho

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val64 | @val64 | 2 days ago

Here's an explanation of how anti-PD-1 drugs work. It's probably TMI.

PD-1 is a protein found on the surface of immune cells (not cancer cells). When the immune cell is in position to kill a target cell, PD-1 can bind to a protein on the surface of the target cell called PD-L1 and this prevents the killing. So expressing PD-L1 is one way that cancer cells escape killing by the immune system. Keytruda, Jemperli, and several similar drugs prevent the PD-1 to PD-L1 interaction and restore killing of cancer cells by immune cells.

But there's something else needed for the immune system to want to kill the cancer cells in the first place. It has to recognize the cancer cells as abnormal. The main way this happens is because the cancer has mutations, some of which cause it to make abnormal proteins. The immune system can detect these abnormal proteins.

Some cancers have thousands of mutations and so make thousands of abnormal proteins that can generate an immune response. Other cancers only have a few mutations. So using Keytruda etc. to unleash the immune system works much, much better on cancers with lots of mutations. Cancers that are defective in the DNA repair process called mismatch repair (MMR) have lots of mutations. So do cancers with mutations in the gene POLE, as well as melanomas (which have uv-induced mutations) and lung cancers, particularly in smokers. So Keytruda etc can have dramatic effects on these cancers.

Endometrial cancers that are proficient in MMR (pMMR) tend not to have many mutations, so there's not a high likelihood of a major response to Keytruda or Jemperli. They do give them to people anyway, since there is a modest improvement in prognosis with them.

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