Are you currently (or have you been) in a Clinical Trial?
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@cure-ious Thank you.
@snow-drop I’m hoping that Orserdu kicks in for your next scan. I’m waiting until the six-month mark to scan. I can’t believe I’m already starting my fourth bottle.
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Kbl I’m sorry about the trial. I hope the Orserdu works for a long time as well.
I am hoping and praying for more combination trials as well. It seems the more lines I go through the more trials I disqualify myself from.
I wanted to update on my trial. I’m on the ARV-471 with Afinitor trial at UCLA. I have been on it since the end of September and in December I had a bad reaction to Afinitor and wound up with pneumonitis in the hospital on O2. They had taken me off the Afinitor in mid December around the 12th when I had a bad cough and a CT showed ground glass opacities in my lungs. But even off the Afinitor my lungs kept getting worse over the next few weeks and I wound up in the hospital on 02 and steroids after Christmas. I don’t exactly understand the drug mechanism and why I continued to get worse after I was off the drug? Anyway, the steroids really helped and I’m off the O2 now and the trial allowed me to continue with ARV as a monotherapy. At my labs last week my regular oncologist drew my tumor markers and they had all more than doubled so we started talking about my next line which she suggested would be truqap and fulvestrant. I went in for my 2nd 8 week CT scans at UCLA last Friday and I got my results which said my cancer is still stable no new lesions?!!!! I am thrilled. So it appears the ARV is working solo at this point. My regular oncologist did not have confidence it would but my trial oncologist said she has had people on it that have been on it as a monotherapy for a couple years. The scans showed ground glass still on my lungs and some nodules which they said are most likely related to the pneumonitis so I am seeing a pulmonologist Monday. I am not sure why my tumor markers were so elevated? Possibly all of the lung inflammation or steroids? But regardless I’m thrilled there is no progression at this point. It’s the only treatment I have had so far that has given me a stable scan. This is my second one. I’m a little nervous because I have nothing going after the Pik3ca mTor pathway now but I’m sure not going back on Afinitor. My trial doc wouldn’t let me anyway. So I’ll just be happy with the stable scan and keep praying the ARV keeps things at bay. :)
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MommaCJ, Fantastic news, it never gets old to hear "stable"!!! It is possible that TMs could increase further, I saw a video of Hope Rugo explaining why she never switches meds based on TMs alone, she says even increasing it can be 10+ months before anything shows on a scan…
You could add Celebrex (if you didn't already) and I forget, what mutations (Pi3KCA, ESR1, etc) came up on the genomics report?
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Stanford has been looking carefully at why there are fewer deaths each year in 2019 compared to 1975:
"The four models came up with remarkably similar estimates for the impact of each intervention: screening mammography, treatment of early-stage (stages 1, 2 or 3) breast cancer and treatment of metastatic breast
cancer. The models reproduced the decline in mortality in breast cancer known from SEER data, from 48 per 100,000 women dying of breast cancer each year in 1975 to 27 per 100,000 in 2019 — a decrease of about 44%. The models arrived at a larger estimated reduction in mortality of about 58% because the incidence of breast cancer has risen during the same period and more women would have died had screening and treatments not improved.The models concluded that about 47% of this reduction in mortality is the result of improved treatments for early-stage breast cancer, and about 25% is attributed to screening mammography. The remainder, or
about 29%, is due to improvements in treating metastatic disease.“Designing the new model, which had to account for individuals with non-metastatic cancer who underwent treatment but later progressed to metastatic cancer, and who may have been treated with multiple drugs
over the course of their disease, was extremely complex,” Plevritis said. “It took about four years. But it was really satisfying when we were able to validate the model’s behavior and see that all four models from different institutions, which used the new model inputs in different ways, delivered consistent findings. The models not only make sense, but also produce meaningful insights.”The impact of treating metastatic disease is exemplified by the increases in median survival time after metastasis: Patients diagnosed in 2000 with metastatic disease lived an average of 1.9 years versus an
average of 3.2 years for those diagnosed in 2019. Survival time varies by subgroup status, however. Patients with what are known as estrogen receptor-positive and HER2 positive cancers saw an average increase in
survival time of 2.5 years. Those with estrogen receptor-positive and HER2-negative cancers lived an average of 1.6 years longer, but those with cancers that are estrogen receptor-negative and HER2-negative lived
about 0.5 years longer in 2019 than in 2000."2 -
Now the finding that ER-positive Her2-negative MBC patients live 1.6 years longer in 2019 than in 1975 is progress, but we need to get better, faster, longer, etc
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Thank you cure-ious! It sure doesn’t get old to hear stable. Especially since this is my 3rd line and the first treatment I’ve ever had to actually hear stable. I do have the Pi3Ca mutation and PTen. Interestingly I don’t have the ESR1 mutation according to my last Caris report but I’m kind of wondering because ARV-471 has shown greater efficacy in people with the ESR1 mutation. It’s interesting my oncologist doesn’t have a lot of faith in the drug as a monotherapy since I’m off the Afinitor but my trial doctor still has initial trial patients on it and she seems more positive. I’m just glad I finally got a few months out of something. :)
I was taking celebrex occasionally for pain but I had some reflux but now that I’m off Afinitor I’m going to try it again.
That’s interesting about progress in overall survival. I agree we need better faster. And I wish the patient centered dosing approach would be implemented more.
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@mommacj Thank you.
I was diagnosed de novo in 2019, but a missed diagnosis for six years before that with no treatment. I have now had known cancer in my stomach for over five years. To say I’m appreciative of how slow my cancer has grown is an understatement. Man, I hope Orserdu works for a really long time.
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MommaCJ, AlabamaDee was on an early 2020 trial for ARV-471, when it was only offered as monotherapy, and she got 11 months on that, w/ liver lesions. She said she'd recommend it to anyone with strong ER expression, SEs could be readily managed, etc
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A global phase 3 trial for 532 patients is about to open (will be a roll out of sites, starting w/China and then moving to US, Europe and beyond) for a new ADC that targets Her2-low MBC. Results from phase 1/2 looked very promising, with 38.5% ORR (tumors shrinking) and 85% making stable or better at 6 months, the PFS was a year. This trial is for those progressing from hormone therapy but who have not had chemo in the metastatic setting. The control group will be getting Xeloda or another standard chemo.
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Thank you for sharing, @cure-ious!
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Thank you cure-ious! I hope I have as good a response to the ARV as Alabama Dee. Without the Afinitor it really is not bad to tolerate at all. Just some fatigue and mild nausea. But the fatigue may be more from the pneumonitis and recovery.
That trial sounds promising. The more I learn the more bummed I am I did Enhertu as my second line… is it considered targeted therapy or chemo? I think it’s chemo so that will disqualify me from some future trials But hopefully I’ll be on this one for awhile. :)
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Thank you @cure-ious these 2 trials look very interesting. I have been hoping that the guys at BioNTech would come up with something exciting - I used to live in Hong Kong so maybe I could get us a place on a trial in China 🤣. Hope all good with you.
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Enhertu is a targeted therapy that is also a chemotherapy, @mommacj. It's made up of 3 parts:
- fam-trastuzumab: an anti-HER2 medicine that has the same basic structure as Herceptin (chemical name: trastuzumab)
- a topoisomerase I inhibitor chemotherapy called DXd: topoisomerase I inhibitors work by interfering with a cancer cell’s ability to replicate
- a compound that links the fam-trastuzumab molecule to the topoisomerase I inhibitor chemotherapy molecule.
Also I feel like I've probably shared this in group on Tuesdays, but the website changed the URL. It used to be Trialjectory, but now it's https://leal.health. You could take a look at that just to see what's out there, @mommacj! But yes, hoping that your current treatment works for a long time. ❤️
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Thank you mods! That is very helpful. :) I will check out the website too.
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What to try after Faslodex-Verzenio fails?
So, last summer I had two successive bone scans indicated minor but worsening progression (CT scans were stable). In addition, my TMs went above normal for the first time. We did genomic testing, which showed new ESR1 (Y537S) and PI3KCA (H1047R) mutations. These are each very common mutations that arise as a way for the cancer to resist endocrine therapy.
I tried to get into the LOXO-783 trial, but the one arm that would hit each of these mutations (LOXO-783 plus the oral SERD Imlunestrant) was not yet available.
So we decided to stay on Faslodex-Verzenio, but try adding in supplements.
First, I added Celebrex, which is a potent inhibitor of PI3KCA, and also pitavastatin, because statins can synergize with Celebrex/NSAIDs to help block mutant PI3KCA. The TMs dropped back to normal range and subsequent scans in October were stable!
However, the TMs then started to creep back up in Oct-Nov. This wasn't so surprising because the Celebrex and statin would not work to inhibit the mutant ESR1, and the mutation I had (Y537S) is fairly resistant to Fulvestrant. So in December I added enobosarm, the androgen booster that is currently in phase 3 clinical trials for secondline MBC. Boosting androgen receptors inhibits ER activity, including mutant ESR1 activity. The drug can be bought online at bodybuilding sites (Chemyo) and I took the dose used in the clinical trials, which is 9mg daily. In Jan the TMs started to go back down, and by Feb they were back in normal range. I had new scans just last week, which remain stable! So obviously I am hoping to be able to stay on Faslodex-Verzenio, with these three new additions, for a longer period of time, and we are now at 6 months after the treatment was starting to fail…
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Chico, If these add-ons just start failing again, I'm joining you in Hong Kong!!!
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@cure-ious I think what you’ve done to get 6 more months is amazing. You and your MO make one heck of a good team. Wishing you continued success!
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Cure-ious - thank you so much for this info . I have endless admiration for you and your knowledge about all of this ! I added Celebrex a year ago after reading a post of yours (and I have joint pain ). I'll be looking in to enobosarm although I don't know if I have the ESR1mutation (yet). I've been on fulvestrant for 4 years and 4 months .
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Great work Cure-ious! Thanks for sharing. I have a bottle of Celebrex now but haven't started taking it yet.
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Thanks, y'all, you're the best!!!
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and I want to send a big shout-out to, Luce,too, for pushing me to try enobosarm…
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ARV-471 was approved for "Fast Track" by the FDA- the link below gives the updated stats from the various ARV-471 trials, and the numbers look really good. MommaCJ adding to those numbers now
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@cure-ious Thank you for this info. After testing positive for ESR1, I could have gone into a clinical trial for this drug but chose the Orserdu route. I’m almost to the end of bottle number 4, and I think it’s working. 😬
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kbl,good to hear from you! Enhertu is on my list too, that's the one they gave a standing ovation for,hope you get a long run…
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@cure-ious Did you mean Orserdu? I think Enhurtu is next in my list, and I’d like to keep Orserdu for a long time.
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oops, yes, my bad!! Its the Elascestrant v Enhertu keeps mixing me up! Elascestrant has this short PFS (3.2 months) but then some people go a long time, and now that more oral SERD stats have come in, it seems to look better than it did initially.. Are you allowed to take it in combination with anything?
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@cure-ious I’ve been on it almost a full four months, and my tumor markers have been consistently trending down. Yay. There is a clinical trial with a CDK7, but I was already on Orserdu before I saw it, so they said I didn’t qualify. Other than that, it’s a monotherapy.
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A really exciting new paper is just out in Nature (thanks Luce for the link!)- Its a big improvement on CAR-T cells, discovered by engineering T cells to express various proteins that are normally found in cancerous T cells and seem to make them much stronger and last longer- the idea is that putting these proteins into normal cells this might improve the ability of the CAR-T cells to infiltrate solid tumors and persist longer fighting the cancer. Out of 71 proteins tested, they identified one that was a home-run, tumors melted away using just 20,000 T cells, compared to the million-plus CAR-T cells that are normally used in trials. This newly-identified gene expresses a fusion protein that massively improves normal CAR-T effectiveness, and, importantly for safety concerns, did not render the CAR-T cells cancerous… A company has been set up with the plan to get this into clinical trials in 2-3 years time…
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the backstory of this new finding is really interesting:, it was a grad student who was sure that this one gene would be a superstar! And the approach is being targeted for metastatic cancers…
And now he's saying maybe it will get into clinical trials in 1-2 years, saying this really goes fast..
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Dear Cureious and others, really, thanks for the link. I do not comment here often but this one seems a very interesting one:) Time to harvest our immune systems to fight cancer, as conventional medicines (all of them that use chemicals and not living organisms) are so advanced that probably they already are reaching their limits (even ADCs) and balance on the edge of toxicity, effectiveness of drug delivery, and what's most important - the synthesis to create them is completely becoming computer based, i.e. territory where it gets too complicated for human brain to comprehend. So, it is logical that if it is possible, with the knowledge we already have, to take what is already in us, modify a bit, and re-inject to fight. Most probably TILs and T-Cells is the future, and it is happening now. Let's hope this research will not get tangled in corporate disputes and papers like many promising drugs have!
Saulius
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