All about Xeloda
Comments
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I lurk more than post here, but I wrote this yesterday and posted it on the "Inspire" Advanced Breast Cancer site...so ignore this if you read it there....
The short message about how I am doing both on Xeloda and in general is "I have no idea..."
The longer report is that I am just starting month 6 on 7/7 Xeloda (3000mg/day.) Despite feeling well-- I have more energy than I did on Ibrance, and other than very tender, burning and occasionally cracking and peeling feet, I like being on this med-- BUT we don't think it's being particularly effective for me. When I switched to this last Sept. it was because my CA27-29 had risen steadily over the summer from the low 40's to the mid-high 50's and was climbing a bit more each month...that, coupled with the findings last May that I have colon mets (multiple small scattered mets were found on colonoscopy, although a CT scan done at the same time didn't see them...not surprising since most were in the 2-4 mm range and the largest was 6mm) made us conclude that it was probably time to switch to a new regimen. I chose Xeloda in order to take the pressure off the ER and hopefully forestall new resistance mutations that were not evident on the genomic analysis of the colon mets, and to preserve fulvestrant for future use (hopefully in some promising trial, and s[ecifically in hopes that a ROLO-like trial would get started in the U.S.)
On the day I started Xeloda my CA27-29 was 59, and my CTC count was 2; monthly CA 27-29 values after that were 57, 67, 69, 62, 64; my CTC done every 1-2 months were: 2 again in mid Oct., then 3 in Dec. and 4 at the end of January. Unfortunately the CTC and the CA27-29 don't really match each other and we haven't been doing them long enough to get a real sense if one rises before another, or falls sooner than the other. It will take more months of testing to see a pattern, if there is one.
I am getting scans in about month to see if for once something other than the extensive bone mets show up, and to take a good look at my bones because I have tender places on the base and side of my skull, my left shoulder and one rib, although NO numbness, tingling or pain on my face/chin/lips. If anything evaluable or measurable shows up there are a few clinical trials I would try to get into. If something targetable by radiation shows up we will do that for those bone lesions.
If nothing shows up (which is what I am expecting, not because I think there is no cancer activity outside of the bone mets, but because as so many of you with lobular disease know, scans don't often detect our small scattered lesions in soft tissue) then it depends on the next round of labs what I will do.If CA27-29 stays below 70 and CTC stays at 4 or fewer (multiple studies have linked CTC>4 with significantly worse overall survival), then I will stay on Xeloda a few more cycles....stable or slowly progressing disease is tolerable for me. I know that in reality there aren't that many treatment options, and I want to stretch out time on treatment as long as is reasonably possible. For me, that means until there is evidence of obvious progression or new symptoms appear.
My onc knows about my interest in the crizotinib trials in Europe (the ROLO trials, for lobular MBC, that uses this ROS-1 inhibitor--it is FDA approved for lung cancer here in the U.S.). She is prescribing it for me off-label, with the full expectation that my insurance will deny it for my MBC. But once insurance denies it, I MIGHT be eligible for the Pfizer Patient Assistance program for it. I am filling out the application this weekend so it will be ready for my onc to complete and submit once we go through the insurance request and appeal process...if that comes together, then I will use it with fulvestrant and see if it works to reverse the rise in tumor markers. The appeal of this approach for me is that I don't need measurable disease to get into a trial, if one ever opens ip here in the US.
If I can't get Pfizer assistance for crizotinib (it costs around $14,000-15,000/month), then I'm not sure what I will do next. My de novo lobular MBC was very responsive to anti-estrogen treatment with Ibrance and letrozole (I had 42 cycles--39 months-- before minor progression was suspected last summer....) so I'm thinking about using exemestane (Aromasin), a steroidal AI, alone or possibly with everolimus (Afinitor.) I don't currently have a PI3K mutation, and everolimus is not quite as effective for those of us with wild type PI3K than it is with mutated PI3K. Plus there is a much better (more effective, less severe side effects) drug called Alpelisib likely coming to market this summer, but only for PI3K mutated MBC. In the event that I develop that mutation (it frequently occurs as one of the resistance mechanisms after AI's/fulvestrant) I don't want to preclude use of that med should it be approved only for patients without prior mTOR exposure.
I think way too much about the treatment options, future medication possibilities and/or the trials I would be interested in....there are so many things outside our control (RECIST-measurable disease being my most confounding obstacle) that it seems absurd to make treatment decisions with all these possibilities and considerations in mind, but that is the way I work...my onc is very supportive of my questions, musings and requests for atypical tests and treatment approaches, but thinks (rightfully so) that I over-think a lot of this. It makes me feel just a bit more in charge of my destiny (deluded thinking, I am quite willing to acknowledge) and so I devote many hours to reading and learning. I should have a degree in cell biology by now...
I am grateful that I generally feel well; I reliably have a bit more (some days far more) energy than I did on Ibrance so I'm happy for the ability to do a bit more in the evenings and weekends. But I have lost a great deal of muscle strength. It's a combination of less activity than in the past, the effects of the anti-estrogen meds, and the consequences of my paraneoplastic neuromuscular disease that is causing actual muscle death, especially in my thighs, calves and some muscles in my hands. I just started working with a physical therapist for strengthening and re-conditioning and will start with an occupational therapist in 2 weeks to deal with the hand muscle issues in order to preserve and possibly improve their functioning.
My daughter is in the middle of her sophomore year in high school. I am so thankful that we have a very good relationship. We truly like and enjoy each other....She is very bright, and active in social justice and women's leadership issues in her school as well as in the city of Portland, and is one of the city's representatives on a council that is coordinating a state-wide young woman's leadership conference later this spring. I so want to see the path she takes in her life. I think she has the potential to make some sort of meaningful contribution to our world. She's getting lots of literature and some invitations for visits from colleges and she is starting to think about her choices. She is considering a few universities in Europe, which is very appealing to her, but said she doesn't want to be so far from me in case I get seriously sick (she didn't say "dying" but I know that must be on her mind...). I HATE that those thoughts and fears have to pass through her mind. I desperately want to live for at least three and a half more years (get her through HS and her first year at college, wherever that is.) Of course I'd really like to live to see her graduate, but that would mean I would have lived with MBC for over 10 years by then. I know how very very small that possibility is, although I do hold onto hope for that. The many women on this site that have survived for 10+ years is inspiring!
So that's the news in my cancer world. We have plans to again join my dear friend on the boat (yacht, really, it has 7 guest cabins and a crew of 20) in Indonesia this summer; my daughter and I are planning to spend 5 days in Singapore and the surrounding little islands for 5 days before we head on to Bali and then Laumbajo to get on to the boat for 14 days. I am so blessed to have the chance to do this every summer. We are treated like royalty and the chance to just rest, read, snorkel, kayak, walk on the beaches of deserted islands and in general be totally pampered is divine. I am fed 4 meals a day that I don't have to plan, prepare or clean up after. Our cabin is tended to and even my laundry gets done daily. It's surreal. My friend invites us and the others to be his guest for those 2 weeks. Dear friends we have made on these summer trips from Amsterdam will be there again, and a new couple will be joining our core group as well (a chemist and a biologist, so good conversation for me!)
I hope you all have something exciting or soul-nourishing to look forward to--I believe that it helps me feel "normal" and gives me something other than cancer to think about.
I hope that you all have a treatment that brings you a good, durable response with tolerable side effects.
I hope that each of you finds that 2019 surpasses 2018 in terms of health and happiness.
I hope that you all find a moment of joy in each and every day.
Peace,
Elizabeth0 -
I do!!!
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Elizabeth, I surely identify with you. I, too, read voraciously, but your understanding clearly far exceeds my own. Currently I am poring over the FoundationOne genomic report I just received on Friday.
In the appendix, under Genes Assayed in FoundationOne CDx, there is no reference I can find specifically to PI3K. My own strongest mutation is in ERBB2 S310F, but that is HER2, and I am supposedly HER2 negative.
These genes are noted as assayed:
PIK3C2B PIK3C2G PIK3CA PIK3CB PIK3RI
Thoughts?
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Joyner-- PI3K is another way to notate PIK3CA...so that is the particular mutation that I am referring to. You evidently don't have a mutation in the PI3K/AKT/mTOR pathway at this point in time....but mutations can evolve as your cancer cells develop ways to evade treatment; PI3K mutations frequently appear after exposure to anti-estrogen meds, so don't discount that mutation in the future...There is a very promising med for PI3K mutant MBC called Alpelisib that is undergoing FDA review at this point in time and should be approved and on the market this summer...it has been remarkably effective for PI3K-mutant but not wild-type (non-PI3K mutant) tumors. I don't have a PI3K mutation (yet???) but am noting that drug as an option should I develop one in the future...
With regards to your HER2 (ERBB2) mutation-- there is a difference between a gene mutation (where base pairs are altered/swapped/out of sequence/or added or deleted in the gene) and a gene amplification. HER2+ refers to an amplification of the amount of HER2 protein being produced in a cell, which means either that you have more copies of the HER2 gene than is typical (which results in more than usual HER2 protein being created by the greater number of normal HER2 genes) or your normal number of HER2 genes create more protein than is normal. In both of these instances, the HER2 gene is not mutated (if you sequence the base pairs on that gene, they are normal), it just is amplified in its creation of HER2 protein, likely due to other metabolic processes in the cells.
There is lost of speculation (and some convincing evidence) that many HER2 mutated genes will respond to anti-HER2 meds (Herceptin, etc) that previously were reserved for only HER2 amplified tumors. I would definitely discuss with your doc the possibility of adding Herceptin to your regimen. I hope s/he is knowledgable about this and is open to prescribing it for you.
I always appreciate your comments on this site-- I am happy to have this chance to "talk" with you more directly.
Be well....
Elizabeth
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Good explanation, Elizabeth. I’d like to add to the discussion of Her2/ERBB mutations. It has been shown that some that do not respond to herceptin DO respond to some other Her2 treatments such as neratinib. Joyner, did your F1 report comment on the particular mutation? Some are “activating” mutations that drive the cancer and some presumably not. Be careful—my Guardant report suggested mine was and could respond to neratinib, but my onc did not recognize it as an activating one,so I called Guardant and they called my onc and now she says that drug is in my future. I will try to post research links when I am home.
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Neratinib Shows Promise in Her2-mutated Cancers
https://www.onclive.com/conference-coverage/aacr-2...
Her2 mutated breast cancer responds to treatment with single agent neratinib, a second generation Her2/EGFR tyrosine kinase inhibitor
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC47014...
Just a couple hits above. Search "neratinib Her2 mutated". There is at least one ongoing trial, and I see it used with Xeloda and with Faslodex.
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I started X on Thursday. I sometimes feel "out of it" for part of the day. Sometimes dizzy.
Wondering if these symptoms will lessen as my body adjusts to this drug?
Chats
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Shetland and Elizabeth, endless thanks. I'm going to attach below more than you are likely to want or need to see, but I'm not sure what is not relevant to the answers to your questions. These appear to me to be among the most important findings in the FoundationOne report, in order as presented in the report. The first two clippings are from page 1 of 1. The second two are from the immediately following page 1 of 16. The rest are in order,each from different pages which I cherry-picked.
From what I have read related to "explanations" included either within the report or online regarding how to read this report:
Microsatellite status "Stable" (my status) is less likely to respond to immunotherapy than MSI-H (instability high).
MMR (mismatch repair) is labeled "proficient".
Tumor Mutational Burden is intermediate at 10 (between 9-20)
There is a page near the end with possible clinical trials, but to my ignorant eye, none appears likely. My onc runs the trials in their practice, and he says that he wouldn't typically consider me a good candidate, as my cancer is not measurable. He did say, however, that my BC is behaving very unusually and that someone should want to study it...perhaps MSK.
My onc, whom I love, is about to retire, and he just gave me the report. I have asked if the practice has anyone on staff who assists a patient in understanding these reports. To be determined. I am being taken over by another practice onc who comes very highly recommended and who has been following my "case".
At my current onc's suggestion, I am going to send this report to the doc at MSK and ask her thoughts and if I should come back to NYC to meet with her again. Since I saw her on Dec 26th, a BC met has appeared on my forehead, and its receptor status was rated as triple negative. I have always been 40-50% ER positive and PR/HR2 negative. I am having a biopsy this AM (have to get dressed!!) on a new lesion on my cheek, so see if it is also a met. Will wait for that report to approach MSK doc.
Headed to jump into my clothes for the trip to Richmond...
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Lynn, I would definitely take advantage of the opportunity to get an opinion at MSK, and I would start arranging it now. Maybe that onc will pick one of the suggested Her2 drugs for you. There are some trials with them, or you may be able to get one without a trial. What do you mean by “not measurable”? If it is a question of a biopsy, some trials are now allowing or using liquid biopsies that use a blood test when you can't get a tumor sample. CDH1 loss is the hallmark of ILC. I don't know if your mutation qualifies as loss, but I would ask about the possibility of an occult ILC tumor; Her2 (ERBB2) mutations are more common in ILC, too. I'm sorry I don't know much about the other mutations. Yes, without microsatellite instability, I do not believe your onc would be looking at immunotherapy like Keytruda right now.
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Shetland, I'm so impressed with your and Elizabeth's depth of understanding of these tests. You must each have scientific backgrounds.
My onc does have someone through the HCA system who assists in interpreting these tests. On his voice mail to me yesterday (he sounds young), he also mentioned something about additional tests. I wonder what that's about and if he is some sort of a system or testing salesman. I hope not.
I am awaiting a second biopsy on the skin met (the first of which indicated triple negative, which would be a change in 6 weeks) and then will send all to MSK and hope for a response from the doc there. I assume that my local onc means unmeasurable because I do not have any organ involvement and thus no tumor to measure for growth/shrinkage and watch for response. All so far is in the bones, except for the single skin met, which appears to have diminished during my first two cycles of Xeloda (7 on/7 off). I should hear from this second biopsy by Friday and will put all into .pdf format and send to MSK.
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Hi!
I started Xeloda on Sunday. 3000 mg twice a day one week on and one week off. When should I expect most of the side effects? Thank you Ilene0 -
Ilene, as you know through PMing, I am just ahead of you. I will start my third 7-day "on" cycle on Friday. So far, I have had no side effects to speak of, except for some fatigue during the last two days of the first week's cycle. I understand and expect the SE to be cumulative, so I'm not counting my chickens. Good luck! Hoping for positive results and no SE for you with X!
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You ladies are way above my head today. Joyner I didn't know about the cheek met. Your cancer is getting crazy weird, right? But you have bone marrow cancer that is not measurable, correct? I'm excited that you might get to take a HER+ med. That is exciting.
I officially join this club on Monday, if X gets approved and mailed by then. That's another call I need to make today and form I need to fill out. UGH. I have too much to do in one day. I have to be ready by tomorrow, I m spends the night with my son. He lives real close to the airport and will take me. I haven't even altered my gown yet..YIKES. it will be easy. In two days I'll be in NYC. Can hard hardly wait!!
My X is approved for 0 co pay and will be here tomorrow before I leave. Scratch one thing off the list. Okay on to gown alterations.
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Joyner---
With respect to your F1 report, I am out intrigued by your ARID1A mutation-- do you know from their notes if this is an inactivating mutation? If so, there is some evidence that this might confer responsiveness to PD1/PDL1 immunotherapies. The fact that is is subclonal (occurring in only some cells, and farther down the line in the mutation process) may make the immunotherapy treatment less responsive, but that's not bee addressed in any of the research I can find. If it is an activating mutation/amplification then immunotherapy would not be indicated.
In general CCN mutations (cyclin D3, in your case, but there are others in this cyclin family--CCND1, CCND2, and to a lesser extent CCNE1) are often associated with FGFR alterations. Also, the ARID1A mutation (if it causes amplification more than inactivation) is frequently associated with FGFR...It is interesting to see that you don't have that identified (yet...), especially with your history of taking Ibrance (a cyclin-family inhibitor.) It might be useful to follow that in the future.There are a few FGFR-acting meds in trials, although they do seem to have some serious side effects. Perhaps a second generation med will come to trial soon that will have a better side effect profile.
Not to freak you out, but while there is NOT a strong correlation with a CCN mutation and shorter survival (YAY!), there does seem to be a slightly greater tendency for these CCN mutations (especially CCND1, which is NOT the one you have) to be associated with liver mets. This information comes from looking at CCN mutations in a variety of cancers, and it is not broken out for breast cancer in particular, so I can't really give you any info about how relevant this correlation is specifically in breast cancer. But if you have any suspicion that you have liver involvement, I would suggest an MRI rather than a PET or CT to detect liver mets....it seems to be the most sensitive test for the liver.
It will be very interesting to see what alterations appear in your new triple negative skin met...it's uncommon but not unheard of that a clone will lose the estrogen receptor after having that pathway suppressed....it's as if the cell thinks "Well, you aren't of any use to me because the pathway you are in charge of is blocked by the medication, so i'm just not going to keep you in my cellular make-up." The rest of the cells that derive from this cell will also have lost their ER.
I'm similar t0 you in not having measurable disease (Look up RECIST 1.1 for the most current description of the very specific requirements to define measurability, and evaluation of response/lack of response to a drug on trial....) or even the less stringent "evaluable" disease, since many trials include "RECIST measurable" or "evaluable" disease as part of the inclusion criteria... It totally sucks.
I hope that you have a very fruitful discussion with your MSK consult...please let us know what you learn and what you decide to do.
Elizabeth
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Elizabeth, thank you. I'll re-read and study all in your response. However, here is the material in the F1 report related to ARID1a:
I am meeting with some sort of genetic counselor at a local HCA facility tomorrow. Are there any particular questions I should ask this young man (he sounds 12 years old)? I have also requested another appointment with my MSK onc (as of this AM through their website) and have sent the F1 report, the most recent PET scan, and the pathology report on the skin met.
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Joyner-- it is not crystal clear from the F1 notes whether the ARID1A mutation is inactivating, but it seems that it is by the discussion in the first paragraph...that is one thing I would ask the geneticist to confirm (inactivating mutation vs an activating/amplification)....because if so, then I would ask the onc if you could get compassionate use or off-label use of the PD1/PDL1 drug(s). Even if the reply is that you don't qualify for a trial (although if you request compassionate use I don't think you have to meet enrollment criteria...ask the onc about that) so you would have to try off-label use (since compassionate use is for meds in trials, not yet approved) where you and you request coverage from your insurance company, then when denied ask for it from the drug company through their Patient Assistance Programs, DO THAT. The income allowance for their assistance for off-label use is different from their typical patient assistance fund, so you likely will not be excluded based on too much income.
The other thing to ask your onc about is if the skin met meets measurability criteria-- I believe that there isa section in RECIST that discusses visualizable tumors--i.e., skin mets. It may have to be 1cm in size, however, to meet criteria.
It's freaky to meet with the oh-so-young-looking/sounding practitioners, but they can be very up-to-date and not yet jaded, so I find them usually very interested in thinking outside the box...hopefully that is the case with this kid.
Let us know how it goes..
Elizabeth
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Thank you, Elizabeth! I will prepare myself with questions both for this young genetic counselor and for my MSK oncologist!
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Ev-11 - your post resonates with me also. I am trying to learn as much as I can now that I have had a progression on Palbociclib/Fulvestrant after 19 cycles which was after 4.5 years on Arimidex. I don’t want to go down a path that prevents me from a promising drug that is right around the corner. I still have bone and bone marrow only Mets, so am ILC with “no measurable disease”. I was told that liquid biopsy was a research tool and that foundation 1 on bones was technically difficult. Dr O’Shaugnessy seems to address ILC a bit more than many other researchers and says many of the hormonals are inferior in ILC. I am going to get a second opinion at UCSF ( although it has been rescheduled twice so far) but, probably wouldn’t be eligible for apelisib since no measurable disease. I guess I am “assuming “ I have a PIK 3 mutation- and that is why I progressed on palbociclib/ fulvestrant but, may never know. Faced with taking everolimus with a hormonal or Xeloda. Sounds like you chose Xeloda over everolimus-
Hoping the European studies on ILC help and heard that Cleveland clinic is starting a registry for ILC.
Your trip sounds wonderful!
Joyner- thanks for all the info re your foundation1 report. I’m glad that you are doing well for now on Xeloda
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NKB-- Foundation One and Guardant 360 are both blood (liquid) biopsies-- you don't need tissue for either of them; they have evolved over the years and some oncs are not aware of that. Check out their websites...Either of those tests would be able to tell you if you have a PI3K mutation or not...if you do, then alpelisib would be worth waiting for a few months for sit to come to market (should be sometime this summer) so long as you don't have severe symptoms or significant progression going on right now...I would suggest F1 only because they sequence the entire CDH1 gene, and if perchance you want to use % of CDH1 cfDNA as a marker of treatment response/failure it is a nice number to have. G360 only sequences particular regions of that gene, and unfortunately it doesn't cover the region that my (very common in ILC) mutation is in (a Q23 deletion sequence, identified on multiple tissue biopsies over the course of three years) so wile we wanted to use it as a tumor marker to help measure tumor burden and treatment response I don't have that info from it...the genomic information was otherwise useful, though. I'm trying to figure out when I want to do an F1 test...
I'm shockingly surprised that I haven't developed an ESR1 or PI3K mutation yet, since those are common in lobular MBC...but I read just this weekend that while Lobular MBC does have around a 50% incidence of harboring a PI3K mutation after AI/fulvestrant treatment, Luminal B cancers have about half of the incidence... I have Luminal B lobular MBC (PR-, HER2 equivocal and Ki 67 19%) so I thought that I would get a good response from Xeloda--but so far we are underwhelmed with it's activity... I keep hoping that giving it "one more month" will start to show a stronger response (measured by CA27-29 and CTC.) But at least by symptoms and energy level (and unfortunately weight gain!) I'm doing better than I was on Ibrance.
I'm not sure that the research I have read supports Dr. O'Shaugnessy's claim that anti-hormonal are inferior in ILC-- other than there being a higher incidence of both de novo and acquired Tamoxifen resistance in ILC, it is usually exquisitely sensitive to anti-hormonal treatment...which is why chemo is usually deferred in lobular disease....I'd check that assertion with your second-opinion doc at UCSF. I'd also get one of your docs to order a liquid biopsy for you. Both F1 and G360 have policies (at least until recently they have) where they will check with your insurance to confirm coverage--and almost always if (non-Medicare/Medicaid) insurance denies coverage both companies will cover the cost of the test for you...it's definitely worth looking into.
Let us know when you get an appointment at UCSF-- I'm curious to hear what s/he says...
Also, can you tell me a bit more about the Cleveland Clinic's ILC registry?? Do you know how they are enrolling patients in it?? Are they cooperating with the MBC Project and their focus on lobular MBC?? What other info do you have about it??
Thanks, and be well...
Elizabeth
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Ev-11- Here is what John Smith posted and I saw two news releases. it sounds like the Cleveland clinic is going to gather data from 1990 to present and have about 4000-5000 cases and present data at the next San Antonio conference.
“The new patient registry is a win for ILC researchers and should ultimately improve patient outcome. More to follow...
https://consultqd.clevelandclinic.org/new-lobular-breast-cancer-registry-will-shed-light-on-rare-disease/
Here's an excerpt to the story:
"Lobular breast cancer is the second most common type of breast cancer from a histological (tissue type) perspective, but it only represents about 10 to 15 percent of breast cancer cases. Because of its rareness, oncologists have tended to view it and treat it in the same way as the more common ductal breast cancer.
But as more research is performed on lobular cancers, investigators are starting to recognize that it has some distinct features apart from ductal cancer, especially with respect to how it metastasizes and its decreased sensitivity to chemotherapy.
With this in mind, scientists from Cleveland Clinic, University of Pittsburgh Medical Center (UPMC), Ohio State University and University Hospitals Cleveland Medical Center are creating a lobular breast cancer registry that will include cases from 1990 to the present.
"Many of us in the community feel like these cancers need some special attention," says Megan Kruse, MD, Hematology and Medical Oncology, Cleveland Clinic. "That maybe it's not best that we treat lobular breast cancer the same as ductal breast cancer. But the challenge in doing so is that lobular breast cancer cases are pretty rare, and so in order to really get a comprehensive look at its characteristics and treatment patterns, you really have to do it across multiple institutions."Very interesting to know that the foundation 1 is a liquid biopsy- I thought that people seem to be submitting liver, lung, breast or lymph node tissue. I will definitely check out the website. Thanks! Appt has been rescheduled to March 1.
Nanci
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F1 has both tissue (biopsy) and liquid (blood test) tests.
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My F1 was a bone marrow biopsy slide.
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Nkb, what is happening with your treatment plan, I think I might have missed something but did you decide what to do next?
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hi Cure-ious- my appt at UCSF got rescheduled again- it is now March 1. My MO said no hurry to start the next treatment and I have been off meds ( except Zometa) for about a month. I was leaning toward afinitor, but, with apelisib possibly soon to be approved I don’t know if that is a good idea. I listened to a podcast by Joyce O’Shaughnessy who talked a little about ILC and hormonals being inferior in ILC- so lots of questions forming. I will also try to persue Foundation 1 with blood I guess.
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Nanci, I just wanted to make sure you know about this resource:
Lobular Breast Cancer Alliance (LBCA)
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I quit AA 10 days ago. I was really suffering from gastritis and colitis, and felt like my insides were on fire. I'll see my mo on Thursday and then on to Xeloda. Has anyone gotten gastritis from Xeloda? I'm also wondering if I need a longer washout period. It's been a rough 10 days getting off AA, but today I feel pretty good. I have a little appetite so managed to put together a little dinner in the crockpot. Thinking of you all and hoping for mild side effects and a good outcome for all. Nanc
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Hi All,
I just had my first PET/CT scan since starting Xeloda 12 weeks ago. Most of my bone/lung/lymph node mets have resolved or decreased in SUV! I have one stubborn left axillary node which has never responded to any treatment. It's already been treated with proton radiation therapy. I'm very relieved that Xeloda is working overall!
EV11 - My tumor markers have been reliable for 3 years in tracking my cancer. However, my CEA-15 and CA27.29 markers increased slightly since I've been on Xeloda (12 weeks). Thus, I was not expecting the good PET/CT results. Dead, sloughed off tumor cells may have increased my markers. I hope the same is true for you!!
My Xeloda dose is 3000mg/day (3 pills morning and 3 pills night). The UCSF oncologist I meet with to follow my eligibility for trials at UCSF when I change treatment suggested a dose reduction due to my hand/foot syndrome and the feeling that my dosage is high. I'm 5'9" 132 lbs. My Stanford oncologist also thought that a dose reduction was reasonable. I asked about a 7day on/7 day off schedule, but both Stanford and UCSF prefer a 14 day on/7 day off schedule. It seems that there are many dosages and schedules that can be effective for Xeloda...
If anyone has thoughts on a dose reduction, I'd love some input. My original dose was 3500mg/day, so I've already dose reduced once after the first cycle.
Hoping and praying that we all have a long and tolerable run on Xeloda!
Theresa
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Theresa
Theresa, That’s such good news. I am going to ask my mo for a lower dose because of my advanced age. Do you have good quality of life? I’m hoping I can stay in the treatment while still being able to take of just the day to day stuff. Hope you have a good long run on Xeloda. Best wishes , Nanc
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Nancylm , I was diagnosed with ulcer when I was on Ibrance/faslodex combo. I don't know if it was due to Ibrance or the pain medications (NSAID) but I had severe gastritis and pain. The GI doctor suggested PPI (Dexalant) and the pain specialist switched me to milder NSAIDs. I also stopped Ibrance at the same time due to progression in bone mets. A combination of all these helped my stomach heal. I am on Xeloda since 3 weeks now and so far, no stomach issues. My primary care doctor suggested that I take probiotics as a preventive measure. I am on Xeloda 2000 mg/day- one week on and one week off. The MSK onco suggested this regimen since they have data to show that this schedule works for most people (I am sure there are exceptions).
Theresa45, great news that your tumors are resolving ! This is such an inspiration to all of us who are on the same drug. As I mentioned to Nancylm, I have started on a lower dose of Xeloda (2000 mg/day - 2 tabs in the morning and 2 at night).Since I am new on this, I don't know if this is working or not. Will find out after I get an MRI for my bone mets in April. I haven't come across anyone else on this forum with such a low dose of Xeloda. The onco suggested to start on a low dose and based on my tolerance, she will gradually increase.
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Shetland- thanks for that link- I did not know about it. Looks like they are doing at least 2 studies with check point inhibitors in ILC - UK and Norway- hoping they find something good.
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