Ibrance (Palbociclib)
Comments
-
Jaycee49, I’m thinking of you. I’m so sorry for what you’re going through.
I’m sorry for anyone having trouble.
I’m reposting from my de novo thread:
I have received my medical marijuana approval. Now I just need to go to a dispensary. I want my daughter to go with me for support. I may have to wait a bit as she's very busy. I'm really not in a huge rush. Lol. My sister gave me Tylenol Arthritis. I took it yesterday. I slept from 9:30-4:30 this morning and then fell back to sleep until 7. Is it pain keeping me up at night? Who knows. I'll come back after I try the MM and say what my experience is. I feel like such a newbie. I'm nervous and want to make sure I get the right thing. I know it will be trial and error.
0 -
Hello to all the women on this thread! I am popping in to say I read that news about Jaycee which makes me sad. I am not sure if it is a brain lesion she's dealing with or a brain tumor, but either way, it is something more for her to deal with and I know she was having trouble after getting the Covid vaccine. I think she also deals with MS. It is so much for the human body to take! And seems so incredibly unfair. I've sent her a PM to let her know I'm thinking of her. Please let us know, Snowdrop, when there are updates for her.
Also, candy, I am sorry to hear about JSCLibrarian. I've gotten to know her a bit on another thread but I hadn't heard the news. I feel very badly. I will also send her a PM. I realize the two women have a lot to deal with and don't expect any reply but am sending the pm's in case they're well enough to visit the forum.
Other than that, things presently seem to be reasonably good with me. I pop in and read the Ibrance thread here and there and glad to know it's still working well for many of you.
0 -
Oh no! Jaycee you're in my thoughts and prayers.
0 -
KBL, I'm glad you got your medical marijuana card...I find it very helpful. I have bought the gummies - nice & easy the dosage is static. They do take about 45 min to take effect. Smoking is the quick way to get relief - my favorite is one called Skywalker ( not sure if every place labels these the same ). There is a high but It's very mellow, great for insomnia - I only take 1-2 hits of it. There are tintures too, to put under your tongue, but I haven't tried that. I've found the store employees to be pretty knowledgeable & helpful.
Jaycee, you're in my prayers...
0 -
I just got off the phone with my MO. I wanted to post while it is fresh in my mind and to get my own thoughts straight. This is so confusing.
So the liver tumor they biopsied (I have 4 tumors and they biopsied 1) showed ER- PR+ HER2-. But with heterogeneity, another tumor could show ER+ still if they checked it. She said less is known about ER- PR+. Said hesitant about continuing to use hormone therapy, but then went to say may continue to use the AI in case the other tumors are still driven by hormones. With my CDKN1B mutation we may circle back to a CDK 4/6 inhibitor later-- maybe Verzenio next time-- if insurance would agree. She did mention antibody drug conjugates--- I forgot what those are and Googled that after the call. Those are used in triple negative cancer. So maybe in my future??? But not now.
******So the plan is rescan in June (3 month scan, no date yet for scan) and see amount of growth then. And maybe move to a PARP, with or without an AI. I mentioned fulvestrant. She said insurance will not approve a PARP and Fulvestrant due to both being expensive. That I could do the AI out of pocket if needed as it is a cheap drug. She said cannot do a PARP and a CDK together as both hit the blood counts hard and that would be too much on my body-- I was thinking about continuing the CDK with the mutation shown on the biopsy.
I think that is it.
0 -
Candy, it does sound very confusing. I hope whatever path you take calms your liver mets down.
Amanda, thank you. I’m totally new to this. I am definitely going to start low and slow, as they say. My two things are to ease the pain and to sleep at night. I know I’m probably going to have to try a few different things to see which one I’m comfortable with.
0 -
KBL- This is confusing. I know cancer is confusing and tumors can be different from each other. And it is good to think I may have different options going forward. But it seems reading on here that a person has progression and they move to ____. Cut and dry. Mine, not so much. "we may do this, or we may do this". Sometimes too much for me to take in. Does my MO have a true plan? When we do change treatments going forward will my MO say "we are doing this next" or will she be undecided? I don't know enough to make the final decision on what should be next.
0 -
Candy, what I understood from your post your MO does have some plans and she is evaluating all factors plus has good knowledge about insurance things as well. It is good she does not jump to conclusion. I understand it is not easy to wait for next scan in 3 months, my best wishes for stable scans.
0 -
Candy, I’m really sorry. I find myself always looking on the Internet to try to understand. It’s a never-ending battle to get a grasp on how this stuff works.
0 -
Candy, I understand your frustration with still not knowing your next treatment. I would want to know what’s next too. To me it sounds like she’s expecting your next scan to be the decision maker. Maybe I’m reading too much into her indecisiveness. Sorry I’m not much help. Luckily June isn’t too far away.
0 -
Candy, You asked very good questions for a situation that is unclear. I would be hesitant to give up on endocrine therapy based just on biopsy of one tumor. What I hate is when they consider the options based predominantly on what they think insurance will approve.
Is the PARP recommended due to BRCA1/2 or PALB2 mutation? I was reading of a phase 2 trial of Olaparib monotherapy in MBC patients with either germline or somatic mutations was presented at the 2020 ASCO meeting. Patients with germline PALB2 mutations had a strong objective response rate of 82%, and 100% had stable disease for at least 18 weeks: 100%, with the median PFS of 13.3 months (90% CI: 12 months- not yet reached) and those with somatic BRCA1/2 mutations had ORR of 50%, CBR at 18 weeks of 67%, and mPFS: 6.3 months (90% CI: 4.4 months to not reached). Similarly, the phase 3 EMBARCA trial showed Talazoparib had a PFS of 9.4 months as monotherapy on patients with germline BRCA1/2. So a PARPi sounds really promising if you are in one of those categories
If they don't allow hormone therapy, maybe you can try immunotherapy? That can work well on those tumors that converted from ER-positive to ER-negative...
0 -
Cross posted from another Thread, but I know several on this Thread are scientific minded----
Ok guys, I am going to put something out there that could affect all of us. I may be all wrong in my reasoning as I am not a doctor and all this is confusing.
So most of us with MBC are ER+ PR+ and hormones are feeding our cancers. We go on hormonal therapy to block the hormones and, say, a CDK inhibitor. We progress. We are taken off those meds and moved to the next treatment-- a PARP, or Piqray or immunotherapy or IV chemo, etc etc. But our cancers are not black and white. With heterogeneity (diversity), say in my case with 4 liver lesions, 1 lesion may be driven by ___ and another lesion by ___. Same with all of us.
So my thought is, why not keep the hormonal therapy for the other lines of treatment and change the CDK, PARP, Piqray, etc. If by stopping the hormonals the cancer says "hey they opened the food lines again" and then the cancer grows.
Am I crazy in my thoughts???? Someone with a more scientific mind and more understanding please explain why the hormonals are not continued.
Cure-ious---- Yes, the PARP is based on the biopsy results. BRCA 2 mutation was seen both on the 2017 liver biopsy and the recent one. So we think that a PARP would be a good option for me. But I think I still want to treat the possible hormone driver with my PR still being positive and because the ER- was just from a biopsy of 1 of the 4 lesions. I cannot do immunotherapy. We discussed that. I have 2 autoimmune disorders so immunotherapy is out. I wish the insurance was not the deciding factor. If I/ we want to try a PARP + say Fulvestrant it should be me and my docs decision, not insurance.
0 -
Candy, You are right, its why most of the targeted therapies are combinations that include an estrogen-inhibiting component; the goal is to inhibit other pathways and get the endocrine-resistant cancer to revert back to estrogen-dependence. I think how they deal with tumor heterogeneity is very confusing, for example, when you have progression there are still a lot of tumors that did not progress and the hormone therapy is continuing to work on them, right?
0 -
Cure-ious--- So why do we/ the docs then stop the hormonals and go to something else totally 2nd line, 3rd line, etc?????? And why can I not continue the hormonal therapy AND do the PARP? Why it is considered "out there" thinking, and a PARP or Piqray is used as monotherapy??
Does anyone have any idea or have asked their MO about continuing hormonal therapy as 2nd or 3rd line?
Cure-ious--- Just to clarify, I may not be looking at all of this correctly or I misread your statement. You said we want the cancer to change pathways and feed off the estrogen again??? Don't we give the anti-hormonals, the AI's and the ovarian suppression, because the cancer is feeding off the hormones and we want to starve them--- inhibit the hormones? So, do you mean we go to the other lines WITHOUT the anti-hormonals to push the cancer towards the hormones again? Then can go back to the anti-hormonals at a later time? Just to clarify.
0 -
Hi Candy- It's a simple question, do anti-estrogens help response to PARPi in MBC, but most reports I've seen are about trying PARPi with other DNA-damage agents like chemo, to improve cell killing. I guess the strategy is different here, right, its not that the BRCA2 mutation is giving you resistance to endocrine therapy. Something else has done that. In other words, you are not trying to reverse the resistance to I-F here, you are now going to start trying to kill cancer cells by inhibiting DNA repair. You could have decided to take the PARPi drugs from the start, right, nothing has changed about that as a result of resistance to I-F.
There is an abstract in ASCO 2021 that discusses the EMBRACA1 trial of talazoparib monotherapy. Average PFS was 8.6 months, but when they looked at top ten percent of responders (average 2 years) and bottom ten percent short-responders (progression or death within 3 months) the former group had ER+ disease and no prior chemo, whereas the latter had TNBC and greater than two chemos. That's not surprising but encouraging that there can be some long responses to monotherapy, if taken prior to chemo. Perhaps this is the best outcome then, to take it without endocrine therapy, and then may be able to move back onto a SERD or ARV-471 with CDK4,6 inhibitor upon progression? Give the cancer time to reset to estrogen-dependence then hit it again, delay the time to chemo?
0 -
Cure-ious--- The way I understand it, Yes I could have started with a PARP, due to the BRCA2 mutation being seen since the start. But, I guess, the standard is an AI and CDK 4/6 inhibitor for first line. And I did get 3 1/2 years from that treatment plan. I can see the thought of "resetting the estrogen-dependence and then hit it again". If it will reset.
0 -
Hi Candy, I am new to this and this is all a bit over my head but I did get three opinions before I started my first line treatment. I am at MSK but received my second opinion from Dana Farber. DF is too far for me to travel to regularly, but I liked the MO I met with and she told me I could, and should, go to her for a second opinion if/when I need to switch treatments. Is getting a second opinion for your next line of treatment an option for you? It may give you more confidence in determiningyour next steps.
0 -
Hi Sunshine. I do not really have somewhere to go for a 2nd opinion. I do like 2nd opinions and think that they are good. But I switched from my local onc (rural area) to this onc and so I do not have anywhere close to go next. And my current MO is with a large cancer center so I think she is smart and has the most up to date information at hand. I think my question about continuing hormone therapy after 2nd line is more of a big picture question--- like standard of care question with all MO's.
0 -
Candy, I think that part of the strategy to consider is that when you are taking I-F, you are actively suppressing the growth of the estrogen-dependent cancer cells. Under those conditions, any cancer cell that mutates in a way that lets it to grow via another pathway (mTOR, PI3K, ESR1) will eventually take over, even if they are relatively slower growing cells, because the drug is providing what is called "active selection" allowing those mutant cells to grow. When you remove the I-F, then that selective pressure goes away. The cancer cells may then find their way back to estrogen-dependence, especially if its the most efficient/fastest way to grow in that environment. That's the reason to take endocrine drug "holidays" from time to time, to mix it up and confuse the cancer, and then hopefully it allows you can come back in again and hit them with endocrine therapy, in this case using the newer stronger SERDs, maybe with Verzenio, and hopefully get another long run on that. To me, the main point is that fortunately you have the BRCA2 that makes PARPi a good option, these are powerful drugs from a completely different class, and ideally you would want to take them sometime before chemo.
Terri C- You got amazing seven years on anti-estrogens, and have not yet even had the SERDs or Verzenio. If necessary to take chemo, the ADCs like Enhertu are targeted so SEs are less and effectiveness is higher than regular chemo, people go a long time on those. It seems you have still many options, being seven years out and just needing to move to some other type of drug for a bit of a break before trying endocrine therapy again. It would be helpful to know if the progression you have is due to an ESR1 mutation (can find out with a liquid biopsy) because then the ideal would be to move to Lasofoxifene (tamoxifen derivative, very gentle) or a SERD or the ARV-471 PROTAC, which Dee is on..
0 -
Candy - you raise a question that I did not really get an answer for when asked: why not stay on the hormonal drugs when moving to a new treatment. Liquid biopsy showed PDL-1, and DR said that meant I would be eligible for immunotherapy, Pembrolizumab (Keytruda), and that I would cease Exemestane, hormonal drug. If cancer is feeding on Estrogen, why not continue to "starve" it? The info sheet she gave me has all the reasons I should not take the new drug, potential very nasty SEs, does not say why I should take it or if there is any conflict with hormonal drugs.
0 -
There ya go BlueGirlRedState. That is what I mean. Why not still starve the cancer of estrogen when going to another treatment? Why stop the hormonals?
Though Cure-ious I can see your point of taking a drug "holiday" and confusing the cancer. But I turned from ER+ to ER- per the biopsy. And another poster on another Thread said that it is rare to gain those receptors back after lost. For example, usually doesn't see a triple negative change to HR+ later. So will I flip back to ER+ after "confusing" the cancer by using another drug pathway-a PARP- for a bit?
0 -
Gosh, Candy, you are great at asking all these questions I know nothing about! I saw a report saying the ER-pos status changes to ER-neg about 5% of the time, whereas loss of PR expression is more common (24%), and gain of ER expression from triple negative cancers happens less than 1% of the time. This report said all ER-PR+ primary tumors they saw changed to ER-PR− in the metastatic tumors, whereas primary ER-PR− tumors rarely turned positive at the metastatic sites, and never became positive for both ER and PR. Those tumors who lost ER expression usually were not so high to begin with (35%) and almost all were luminal B cancers. The loss of ER expression was more commonly found in liver mets, compared to skin, bone or brain. They did not mention any losing ER and keeping PR, so you are an outlier there. Interestingly, the paper said that conversion was associated with worse outcome UNLESS it was picked up in biopsy so that the treatment could be changed accordingly, and in those cases there was no statistical difference in overall survival, so its why biopsy after progression is so important.
I think Lynne here had skin mets that on biopsy had changed to ER-neg, but a later biopsy showed that mets at other location(s) remained ER-pos? So that comes back to your question about heterogeneity..I guess this is where the FES-PET scan could be so helpful, to show what fraction of the tumors have active uptake of estrogen, and what fraction are really endocrine-insensitive. This type of imaging was FDA approved more than a year ago but still not many places offer it.
It is common for progression to cause increase in HER2, not to high gene-amplified levels but still to a higher activity than in normal cells, due to a HER2 mutation or increased activity of the HER2 gene promoter. That is a change seen as a result of treatment so you would want to check about that after every progression, to see if Enhertu or other HER2 drugs might be good options.
0 -
Cure-ious--- Your last post was chock full of valuable information. The ER+ changing to ER- 5% of the time. And "those tumors who lost ER expression usually were not so high to begin with", mine was strong Intensity ER positive and Allred Score of 8 on my first liver biopsy in 2017 so that does not reflect my situation. And me being an outlier because I still have PR+ (Allred score 2/5 and Intensity of 2/3 now). Also "worse outcome unless picked up in biopsy so that treatment could change accordingly"--- is my treatment changing accordingly going to a PARP? Should I do another type of treatment--- for Triple Negative for example?
Yes, heterogeneity. Should we still treat with endocrine therapy in case another site is still ER+??
I do not know if my cancer center has the FES-PET, but I can ask. My MO did say the regular PET is not good for liver images, due to liver highly vascular and the glucose is taken up so much that the images are cloudy. She prefers MRI to PET for liver mets.
My HER2 was equivocal this time and had to verify still negative with FISH so not an increase in HER2 with this progression. Is that what you mean?
I am definitely taking notes from this conversation.
0 -
I am taking notes too. My original cancer was strongly ER+ and PR+ and HER2- (IHC). My bone mets were strongly ER+, PR-, HER2- (IHC). Ovarian mets on 4/7/21 were completely ER-, moderately PR+ (61 - 70%), and HER2 equivocal (negative by FISH). My ovaries, tubes and uterus were removed. The pelvic washings were positive for cancer cells as well so that remains. After consulting with colleagues it was recommended that I start Xeloda.
I was bone mets only but now is in my abdomen. I was told hormone blockers target estrogen. Candy seems to have some ER+ and ER- mets in her liver so a bit different scenario.
0 -
Sorry to interrupt here, but a question for any de novo still with breasts - has anyone experienced ongoing discharge when on Ibrance weeks? Because of the nipple retraction it gets rather sticky and crusty (but clear) in there and I have to keep things clean. This doesn't happen on the weeks off, so it's not sweat. I'll bring it up Monday at onc chat, but this has happened every month since the start.
This nipple is so retracted at this point you could sew over it and I would have a normal, but blank, breast.
0 -
Sorry Sondra I cannot help you as I had a mastectomy. Hope someone chimes in to help with your question. Good that you have an appointment Monday to ask.
dutchiris- I am wondering about Xeloda versus the PARP as my next treatment. So many seems to have went to Xeloda. Mine too was completely ER- (0%) PR+ moderately and HER2 equivocal and negative per FISH-- same as yours. I do not know if I have ER+ left in the liver as we biopsied 1 of the 4 lesions. I am going to ask MO about Xeloda versus PARP.
0 -
Candy, The PARPi will be targeting both ER-positive and ER-negative cancer cells, so I think the endocrine therapy can wait for a future treatment, like a SERD-Verzenio...
0 -
Cure-ious...you are very knowledgeable. I have one question. Actually two. My MO did a liquid biopsy and found I have the PIQ3 mutation. Is Piqray the best or only way to go at this point. I am in the process of getting Piqray approved through insurance so I haven't started it yet. Also, I have been off Ibrance/Faslodex (still getting Xgeva) since April 5th and my platelets have risen slightly over normal. Is that normal or do I have to worry it's in my bone marrow or something now? Thanks for any input.
0 -
Jack5ie, Altho Piqray is a pain in the butt and you have to take anti-histamine to avoid rash and avoid sugar, it is the only thing we have right now for PI3KCA mutations and the data from the trials were impressive, other drugs targeting PI3K/mTOR are in trials so more options may show up that you can take in the future. My platelet levels dropped below normal awhile back but then bounced back, so no idea about that- they can even be affected by vaccines or infections, so if your MO is not worried, let it ride...
0 -
Cure-ious, thank you for sharing your knowledge with us! I've been reading along and learning. You are awesome. And thanks to everyone for the whole dang thread, I learn so much here!
0
