Are you currently (or have you been) in a Clinical Trial?
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Here is a recent update of their results, looking at 13 mo PFS, OS benefit, and works on brain mets too. I think some of the activity is coming from the Her2 antibodies their vaccine generates, since they get tumor shrinkage much higher in Her2-positive patients, but they do see PFS benefits for Her2-low and ER-positive as well, and most studies were in later lines.
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They do accept requests for compassionate use of their vaccine, but this is for patients not eligible for their clinical trials
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Here is a link to their trial, but they only list US locations, so I'm not sure why I thought it was in Canada, they are actively setting up other sites so maybe your MO can check. they have an office in Canada… OTOH, they are hoping to announce results in first half of next year, so maybe will go to FDA while you are still on Enhertu…
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Here is an update from last month:
BriaCell is pleased to announce that its ongoing pivotal Phase 3 clinical study (listed on ClinicalTrials.gov as NCT06072612) has consented over 100 and has enrolled over 75 patients. BriaCell anticipates completing patient enrollment in late 2025 or early 2026, and may report top line data as early as H1-2026. BriaCell’s pivotal Phase 3 clinical study is evaluating BriaCell’s lead clinical candidate, Bria-IMT, plus immune check point inhibitor versus physician’s choice in advanced metastatic breast cancer (Bria-ABC).
“We are pleased at the expanding patient enrollment in our Phase 3 study, and expect this to continue to grow,” stated Dr. William V. Williams, BriaCell’s President & CEO. “We believe our novel therapeutic approach has the potential to transform cancer care for metastatic breast cancer patients, and are determined to bring our novel immunotherapy to market to help these patients.”
Fifty-four clinical sites in the US are actively enrolling patients in BriaCell’s pivotal Phase 3 study in metastatic breast cancer. Additional sites are in various stages of start-up.
Interim data will be analyzed once 144 patient events (deaths) occur, comparing the overall survival (OS) in patients treated with the Bria-IMT combination regimen versus those treated with physician’s choice as the primary endpoint. Positive results of the pivotal Phase 3 study could result in full approval and marketing authorization for Bria-IMT in MBC patients. BriaCell recently announced positive Phase 2 survival data in a similar MBC patient population treated with the same Bria-IMT combination regimen. The Bria-IMT combination regimen has received FDA Fast Track designation.
For additional information on BriaCell’s pivotal Phase 3 study of Bria-IMT and an immune check point inhibitor in metastatic breast cancer, please visit ClinicalTrials.gov NCT06072612.
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Thanks for the extra information cure-ious. It looks like the stocks trade in Canada but no trials yet. I'll keep watching.
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Another paper showing immunotherapy can work in ER-positive MBC was just published in Nature Com
This report is from Sara Tolaney (see attached) on a phase II trial (NIMBUS) that looked at the response of high tumor mutation burden metastatic Her2-negative cancers to immunotherapy. A previous trial had indicated that response depends on a high tumor mutation burden (TMB).
Some of the highlights:
- Immunotherapy on cancers with tumor mutation burden (TMB) over 9 mut/MB gave an ORR (overall response rate; ie, those whose tumors shrank 30% or more) of 20%.
- Looking at those with even higher TMB (equal or over 14 mut/MB), the response rate jumped to 60%, compared to 12% for those cancers with TMB lower than 14.
- "Overall, the median TMB was 10.9 mut/Mb (range:9–110); 25 patients (83.3%) had TMB ≥ 9–<14 mut/Mb, two patients (6.7%) had TMB ≥ 14–<20 mut/Mb, and three patients (10%) had TMB ≥ 20 mut/Mb".
- Of the 6 patients who had TMB over 14, "The median PFS was 9.5 months (95% CI: 4.6–Not Reached), compared to 1.4 months (95% CI: 1.3–2.6) among patients with TMB < 14 mut/Mb. The median OS was not reached (95% CI: 18.6–Not Reached) in patients with TMB ≥ 14 mut/Mb compared to 8.2 months (95% CI:5.1–Not Reached) in patients with TMB < 14 mut/Mb. Among the 6 responders, the median time to response was 1.9 months and the median duration of response was 10.2 months.
Importantly, two patients of the six very high TMB patients in the trial have remained progression-free for more than two years since starting immunotherapy
They conclude that very high tumor mutation burden MBC patients may respond well to immunotherapy, especially for those with cancers with of 14 TMB- where TMB comes not just from the blood biopsy (eg Guardant) but also the TMB numbers reported in tissue biopsy.
They see no difference between ER-positive or Triple-negative cancers, but note that TMB numbers tend to be higher in lobular cancers.
PS In my experience, the TMB can increase a lot over time on therapy, so its good to keep an eye on it from time to time…
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I got into the Briacell study. I started last week (Providence, Santa Monica, California).
Fingers crossed. Toes crossed. Super hoping.
This will be my forth clinical trial.
I am 9+ years MBC.4 -
Hi MikainSB!!!
Great to hear from you, Congrats on NINE FREAKING YEARS!!!
And Congrats to qualify for the BriaCell Trial!!! If you read up, CBL saw a jump up in tumor mutation burden (TMB) from 5 to 15, and if you read above, that would be sufficient to be among those much more likely to respond to immunotherapy….
Please keep posting on this trial, its on my shortlist too
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CBL,
How are you doing, did the Orserdu rash die down finally?
Also you were saying due to promoter methylation you now have a BRCA-like phenotype and can be sensitive to PARP inhibitors (yet a new line!)
I wanted to point out that a trial at MDA is testing BRCA-deficient tumors by combining PARP inhibitor with immunotherapy and are getting a very very high response to that!!!
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Ooh, very very high response sounds awesome! Do you have a study number? I'd need to beat this damn cancer back a bit before I try another trial, but that sounds promising!
The Orserdu rash is gone on the lower dose. We'll see next week what my tumor markers are doing. Apparently, Orserdu is known for spiking TMs.
I had TMs taken 3/4/25 and they were 810. On 4/29/25 they were 3810. Not a typo!
The problem is I had been on a reduced dose for only 4 days, so I doubt that would cause a 3K point spike. So this Friday, we'll do tumor markers again and hopefully they've dropped. I don't know when my next scan will be.
Last year at 1250, I was in the hospital with a liver that was 65% tumor. But at 3810, I feel perfectly fine. I did have some liver pain this past week, but that is also apparently (according to my FB group) a sign the Orserdu is working and healing.
All this to say I really don't have a clue what is happening in my body, haha.
Thanks for checking in and hope you are well!
CBL
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It has been a while since I last updated on my Kat6 trial NCT04606446. Tumor markers have been bouncing around since Jan so I wasn't sure where things were going. Last scans showed liver progression so looking for my next line. I have been in the trial since 12/23!! Long run for sure! SEs have been very tolerable. I understand they are opening a phase 3 PF-07248144 combined with vepdegestrant if I remember correctly from what my MO said.
I am considering larotrectinib (Vitrakvi) for NTRK fusion–positive solid tumors. It was just FDA approved in April/25. I understand NTRK is not a common mutation but one I have.
Also wondering about an immunotherapy trial. My MO has one opening soon she says for those that it is effective, it can be durable. I definitely like that thought!! My tumor burden is 4.7, ER dropped to 10%positive,.PR- and hR2 dropped to 1. No ESR1, PIK3 nor BRACA
MO also talked about a trial opening soon of an ADC with something that makes it more targeted to the tumor.
She will have more specifics.for.me at our next meeting in 2 weeks.
There are so many drugs making progress my head is spinning!
Any other ideas for me that you guys have at the top of your list?
Thank you so much for everyone's love, support and generous sharing of research!!
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@cblaurenceauthor I got a terrible rash on Orserdu, reduced dose. But here is the thing, I was able to return to full dose if instead I took it twice a day, meaning 2x86mg pills in the morning and 2x86mg pills in the evening. If it is effective for you, see if you can try to challenge back up to full dose, but split the timing.
I had to stop Orserdu. Absolutely every tumor I had on prior scans was responding to Orserdu, but a popcorn explosion of little new tumors (more than 15) showed up in my liver. I kept saying, I feel like I have a pearl in my liver. I knew something was not right, but it also wasn't obvious.
We all hope for the forever drug, the drug with low side-effects that just works for a long time. I hope this for you CBL.0 -
@mikainsb Oh wow! I hate to hear that about the liver tumors. Sometimes our instincts are exactly right. I hope you're on a great treatment now as well.
Interesting about the split dose. I will absolutely bring it up with my doctor when I see him again. I'd really love if this was the magic bullet no matter how I have to take it.
Thanks for the info and wishing you good health!
CBL
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CBL: Here is the write-up I saw, the trial is called KEYLYNK-007 and is for various solid tumors with DNA repair mutations
According to the results of a molecularly matched, tumor-agnostic phase II trial, the combination of the PARP inhibitor olaparib and the PD-1 inhibitor pembrolizumab demonstrated antitumor activity with no new safety signals, particularly in patients with BRCA1/2 mutations. Data from this KEYLYNK-007 trial were presented by Timothy Yap, MBBS, PhD, Professor of Investigational Cancer Therapeutics and Vice President and Head of Clinical Development in the Therapeutics Discovery Division of The University of Texas MD Anderson Cancer Center, at the 2025 American Association for Cancer Research (AACR) Annual Meeting (Abstract CT004).
332 patients with 30 different cancer types, according to three different genetic alteration groups defined in advance: patients with BRCA1/2 mutations (n =132), those with non-BRCA1/2 homologous recombination repair (HRR) mutations (n = 104), and those with homologous recombination deficiency (HRD; n = 96).
A total of 18 patients had a complete response to this treatment as determined by radiologic imaging, with 11 of them in the BRCA1/2 mutation subgroup. Responses were seen in multiple tumor types for which these therapies are not currently approved. The median duration of response was highest in the BRCA1/2 mutation subgroup, at 19.1 months (95% confidence interval = 10.7 months to not reached). The disease control rate was more than 60% in all three subgroups. The safety profile was consistent with the known safety profiles of both therapies.
“It’s notable that this trial represents the largest data set of molecularly matched patients for this combination therapy,” Dr. Yap said. “We hope further analysis of these data can help identify new predictive biomarkers to better identify patients likely to have exceptional responses to this combination.”
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Perky, A year and half on Kat6 inhibitor? Wow!!! How is that trial done, ie was it some combination with fulvestrant? I think PFS was pretty good in the first trial, like 7-8 months. What were the side effects you noticed? I hope this one can move through trials to the clinic quickly…
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Cure- yes, the Kat6 was combined with a CDK4 inhibitor and Falsodex. SEs: dry eyes, fatigue, very low white cell count we had to use granix to keep them up high enough to stay on the trial, loss of taste. Quite tolerable! Even though at times I was taking long naps daily, other times I was hiking 8 miles with elevation gain!
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I need the wise evidence-based people. I have been on Kisqali since March of last year. After about three months, my dose was reduced from 600 to 400 because of neutropenia. That seemed ok, though my neutrophils were on the low end. Today, even on the 400 dose, my neutrophils were .9, and my team is considering a further reduction to 200. The PA said that 200 was still effective. True? Is there any evidence (ie. trials) that the 200mg dose is nearly or as effective? Thanks!
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Hey there TOC,
First thing is low neutrophils on CDK4,6i are truly nothing to get concerned about- unlike chemo, which kills off those cells, CDK4,6i just pause their growth and maturation. They will rebound much more quickly on pausing these drugs than pausing chemo, and you are not immune suppressed in the way you are on chemo. I was way lower than you on my 9 years on CDKis, and at most just paused, tho I eventually reduced dose of Ibrance because of fatigue, but low neutrophils were a constant. Also, as I recall they have a funny cycle where the lowest point is like a couple weeks after you stop the drug, so it may take awhile for them to rebound fully.
I don't know about Kisquali per se, but if the team thinks 200 is fine it probably is, however you could offer to try a temporary reduction, like 5 days on-2days off, and see if you can do better. However, my MO wouldn't blink an eye at 0.9… Supposedly neutrophil levels will be higher if you go up and down the stairs a few times right before the bloodwork, you can get a temporary boost with some burst of exercise
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Much appreciated, @cure-ious . This gives me some key points to discuss as I move forward. I thought many MOs were using .8 as a cut-off. The Kisqali site seems to point to no reductions in efficacy even at 200mg. I'm really healthy. I've never even gotten Covid. The flu has passed me by for years. I'll try the stair trick. Anyway, you are such a great help to many.
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@tougholdcrow Some of us on the Ibrance thread noted that our ANC levels were higher if we had our labs in the afternoon rather than in the morning. Definitely the case for me. My MO only gets concerned if my ANC is below .7.
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@tougholdcrow I agree with Chicagoan, my anc is always higher later in the afternoon. Once I switched the time of my blood draw to the afternoon vs early am , my anc was usually 1.0 or 1.2 vs .80.
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Hi y'all,
I have continued to track PCSK9 and all of the various different things it does to promote metastasis, I wish there were a review of the big picture. As a reminder, there are monoclonal antibody injections that inhibit PCSK9, and these are primarily used to control cholesterol when one cannot tolerate statins due to muscle and joint pain (which is me!). It has huge effects lowering the bad cholesterol and triglycerides and raising the good cholesterol, but what about its anti-metastatic-cancer activities?!
A new paper just out in Nature shows that PCSK9 is "necessary and sufficient" to direct mets to specific organs. Using a mouse model for pancreatic cancer, they showed that mets with low PCSK9 levels migrate into the liver, where they use the cholesterol to grow via the PIK3CA/Akt/mTOR pathway. Mets with high PCSK9 are able to withstand the environment in the lungs, so they end up there. Amazingly, when they engineered the low-PCSK9 liver mets to make more PCSK9, those cells migrated up to lungs, and when they reduced PCSK9 in the high-expressing lung mets, those cells migrated down to liver. So the level of PCSK9 in the mets determines which tissue the cancer will invade.
Then, to recap, a paper in Cell last Jan showed that a common mutation in PCSK9 (found in 70% of white females, and a big population in east Asia and west Africa) gives very high PCSK9 activity that promotes the start of metastasis. Analysis of a cohort of breast cancer patients showed that those with the mutation had a 22% of developing mets within 15 years, whereas those with the normal protein only had a 2% risk. This argues strongly that the med that inhibits PCSK9 should really be tested for prevention of mets in those with high-risk early stage cancers. Moreover, they found the drug has a small but real effect of shrinking existing MBC mets for all subtypes.
And then in 2020 a paper in Nature showed that PCSK9 plays a big role in creating an immune-suppressed environment for breast cancer mets, and that the monoclonal antibodies that inhibit PCSK9 strongly boost the effect of immunotherapy drugs.
All of this and the drug fixes your cholesterol as well?, sounds amazing~ will be keeping an eye out for any clinical trials of PCSK9 inhibitors, they are on my short list to try at some point in future…
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More good news! UCLA researchers have a paper out in Cell showing that antidepressants (specifically seratonin reuptake inhibitors, called SSRIs, including drugs like Prozac and Celexa ) have a big effect activating T cells and synergize with immunotherapy for breast and many other cancer types:
The researchers tested SSRIs in mouse and human tumor models representing melanoma, breast, prostate, colon and bladder cancer. They found that SSRI treatment reduced average tumor size by over 50% and made the cancer-fighting T cells, known as killer T cells, more effective at killing cancer cells.
“SSRIs made the killer T cells happier in the otherwise oppressive tumor environment by increasing their access to serotonin signals, reinvigorating them to fight and kill cancer cells,”
They tested a combination of an SSRI and anti-PD-1 antibody — a common immune checkpoint blockade, or ICB, therapy — in mouse models of melanoma and colon cancer. ICB therapies work by blocking immune checkpoint molecules that normally suppress immune cell activity, allowing T cells to attack tumors more effectively.
The results were striking: the combination significantly reduced tumor size in all treated mice and even achieved complete remission in some cases.
“Immune checkpoint blockades are effective in fewer than 25% of patients,” said James Elsten-Brown, a graduate student in the Yang lab and co-author of the study. “If a safe, widely available drug like an SSRI could make these therapies more effective, it would be hugely impactful.”
So many people take these drugs, they will now dive into previous trials to see whether people on SSRIs had a better response to checkpoint inhibitors and/or other cancer therapies, and hope to move this to clnical trials.
https://newsroom.ucla.edu/stories/antidepressants-could-help-immune-system-fight-cancer-ucla-study-finds
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So, considering the many reasons one might not respond to immunotherapy shows why this approach is still not ready for prime time:
- Not having high tumor mutation burden. Not sure we have a workaround for this as yet.
- Having inherited the PCSK9 variant, which dials down the ability of immune cells to detect the tumor. PCSK9 inhibitors available for this
- Having high estrogen signaling and/or ESR1 mutation- estrogen signaling is inhibitory to immune system fighting off the tumor. Need to wait till cancer is strongly estrogen resistant or include endocrine therapy with the immunotherapy
- Need to add SSRI anti-depressant, these make T-cells really "happy"
- And there are other blocks people have found. Immunotherapy is still early, esp for ER-positive MBC.
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Always interesting.
So i just finished 6 months of chemo with Keytruda for TNBC. I also take Paxil an SSRI. I had a positive response of about 90%. So glad. Keytruda continues about 7 more months.
Doctor did not think i needed to add Xeloda because the study that suggests I use it did not include patients that also used Carboplatin and Keytruda like me. He said the tumor board all thought i should take it. Any opinions?
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Wonderful, GailMary, Maybe taking that Paxil is helping!!! Why would you need to add chemo when its working so well? The studies they are looking at probably didn't have an anti-depressant in the mix..
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Dr considers me cured of early stage TNBC SINCE SURGERY.
The chemo combo in the study done in SE asia did not include Carboplatin and Keytruda! Not available there. Back to AI anastrazole for ER+ stage 4.
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The New York Times has an article on blood tests to detect ESR1 in breast cancer progression (ER+), and also mentions camizestrant, an estrogen receptor degrader, given after the tests showed progression. This is a pretty splashy, front-age announcement, so I am assuming this will be standard of care. Here's the New England Journal of Medicine article on the study.
https://www.nejm.org/doi/full/10.1056/NEJMoa2502929
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Thanks so much for the positive news report and journal article. I read both, and was particularly cheered by the reactions of the MOs, although confused as to whether this breakthrough would apply to patients like me.
I already take a SERD (faslodex) with Kisqali, although this new drug is an improvement as it would not require the painful monthly injections.
Is there a hope here, even for those of us already on a SERD?
Thanks as always,
Eleanora
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My understanding of this potential new medication is that it is akin to Oserdu in the sense that it's an oral SERD, not an injection, and only helpful when the ESR1 mutation is detected. I believe Oserdu was found to be as effective in those without the ESR1 mutation as it was for those with it, but for whatever reason, the FDA only approved Oserdu for those with the mutation. So, whether it will be of any use to you, will likely depend on whether the ESR1 mutation is detected. The good news is that apparently a great number of those with ER/PR positive breast cancers who progress on either AIs or SERDs will develop the ESR1 mutation; which tends to be what drives progession.
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