node negative stage I breast cancer question
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DearLife, I am on my 20th pill this morning of 20 mg Tamoxifen but very concerned about the uterine cancer connection as Tamoxifen sends more estrogen to the uterus (an undesired effect drug companies are unable to control). I had a lumpectomy early this year and finished 20 sessions of radiation 2 weeks ago. I figured that I will take the wait and see approach with meds and change as needed and hope for the best. Other than that, peanuts or peanut butter everyday and ground fiber, at least one teaspoon per day (both prevent breast cancer). I am 52 and it is exactly one year since my last menses, so finally, here I am postmenopausal, but I am very small boned so the side effect of AIs of joint pain and fractures would not be a good thing for me.
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Good luck Swimjames. My friend stopped Tamox because of mood side effects. First she had oncotype test which said low chance of recurrence (though I think this test assumes tamox so I am confused...)
Great news about peanut butter, which I love! I have been afraid to eat so many things - flax seed in my favourite cereal, soy, meat, cheese, wine waaaah.
I do appreciate all your research.
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I have been post menopausal since 2005, still have extremely dense tissue.
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meow: my mom who's in her 70s still has dense tissue too.
Swimljames:
You asked:
Is there a study for lymph node negativepostmenopausal women who have estrogen/progesterone receptive stage 1 grade 1 breast cancer for various time periods who used Tamoxifen for 5 years?
My answer: probably not. I tried to find studies on node neg/stage 1/ low grade breast cancer. Doesn't seem like there are many studies on women like me. Even tried to find studies to join. Not much out there.
I am all of the above but I'm not post menopausal yet. Going through the crazy peri menopausal stage. Grrr.
When I was trying to decide about whether I'd have radiation or go on tamoxifen I asked my surgeon what my recurrence rate would be with low grade low stage small tumor. He has been practicing for 30 yrs at least. Probably more.
The recurrence rate without those things really didn't change a whole lot for me. So I chose to not do them.
My onco' request/requirement was that I go see him often. So I'm seeing him every 6 mo. And we are doing diagnostics every 6 mo. And I'm ok with that.
Just thought I'd share my experience. I'm sure lots of people would think I'm crazy for making that choice but it's the choice I made.
He said if it were to come back more than likely it would be very low grade again...
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Swimjames--Like dtad and several others, I rejected anti-hormonal therapy from the very beginning, and was supported by my surgeon, rad onc, and the med. onc. whom I saw one time only.Since I was 71 with a grade 1 and stage 1 tumor with clean margins and no nodal involvement, they agreed that the risks of the meds would outweigh the benefits (if any). And this January I passed the 5-year mark since lx with no recurrence!
Given the absence of studies about those of us who reject the meds, this kind of experiential support can be of use to you. Don't expect to see research about folks like us--the pharmaceutical industry certainly has no incentive to support research that would show that their concoctions aren't necessarily needed in all cases and that would lower their inordinately huge profit margins!
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That is really strange that there is no research about women with negative lymph nodes, low grade, stage 1 breast cancer, but if you think about it, not so strange. The probability is very high that they do have the numbers but there is no money incentive to release them to the public. When there is that much money involved (radiation is thousands of dollars and I don't know the generic Tamoxifen costs), you can never rely on human decency and you have to do your research. The older you are, the less aggressive they are in treating the cancer if it's small and low grade, so suburban Philadelphia, I am not surprised your cancer did not return and that you chose the path you did. If you get cancer in your 40's and you still have about 40 years to live, the probability is higher for cancer cells to reappear because the hormone levels are much higher and there is more time left. A lot more can happen to you in a 40 year time span than lets say a 10-20 year time-span. I think even as far as family history goes, if you notice, they always ask at what age your mother/sister/grandmother received the breast cancer. That is a very important element. Jons girl, what was the recurrence rate that you were told? Also, much luck to you with continued health and I don't think you are crazy in your choice, you are entitled to it and the risks are high with meds/radiation too. The meds and radiation both can cause cancer!!!
PS I was 52 and 5 months when my breast biopsy came back positive for invasive ductile carcinoma and so I was right on the borderline in terms of timing in the midst of my lifespan. Medicine is not a black and white science like mathematics, but very grey and lots of shade of gray, so no decision is right or wrong, but somewhere in the spectrum. That's what makes decision making so tough.
http://scienceblog.cancerresearchuk.org/2018/04/06...
https://medicalxpress.com/news/2018-04-paper-filte...
https://www.ctsu.ox.ac.uk/research/ebctcg
https://www.cancer.gov/news-events/cancer-currents...
http://ascopubs.org/doi/abs/10.1200/JCO.2017.73.32...
Transitioning Endoxifen to Clinical Trials
Our next step was to develop endoxifen into a drug that could be administered to humans. But because its chemical structure was already public knowledge, there was limited interest in its drug development by pharmaceutical companies.
NCI, however, was in a position to step in again. As a part of its broad mission to bolster cancer research, NCI is uniquely qualified to develop promising new treatments or drugs that have limited potential for commercialization.
With promising results from these preclinical studies, NCI filed an Investigational New Drug application for endoxifen with the Food and Drug Administration (FDA) so that clinical trials could begin.
Through NCI's Cancer Therapy Evaluation Program and clinical trials program, Mayo Clinic and NCI launched the first phase I trials of endoxifen in 2011 in women with metastatic breast cancer whose tumors had progressed following treatment with aromatase inhibitors and tamoxifen.
In 2015, we initiated a randomized phase II trial comparing how well endoxifen and tamoxifen work in women with breast cancer, with results expected in early 2018. The trial is sponsored by NCI's Cancer Therapy Evaluation Program and is conducted by the Alliance for Clinical Trials in Oncology, an NCI-funded clinical trials group.
It's not yet clear how this endoxifen story will end. Drug development is costly and time consuming, and there's no way to know if a drug will benefit patients until it is rigorously tested in multiple clinical trials.
What is clear, however, is that without the commitment and collaborative spirit of the Mayo team—including James Ingle, M.D., Matthew Ames, Ph.D., Joel Reid, Ph.D., Thomas Spelsberg, Ph.D., and John Hawse, Ph.D.—and NCI's continuous support, this potentially promising therapy might never have been developed. I'm thankful to have come this far with our story, and am hopeful that our efforts will ultimately lead to beneficial results for patients.
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hi swimjames,
As I recall he told me my recurrence rate was 10% or below. It was low. And tamoxifen and radiation didnt make a huge change. If my cancer had been more aggressive, my decision probably would have been different.
When you talk about genetics connections to cancer, that's a big curiosity for me.
My maternal grandmother had br cancer twice. Died of it. (2nd time she had been cancer free and begged her gyn to give her hormone pill ex so she could feel better after going off tamoxifen after 7 yrs. cancer came back and killed her) so I think the 2nd round of cancer was brought on by her taking those hormones again.
My maternal aunt got br ca dx two wks or so prior to mine.
My mother has had breast biopsies no cancer tho.
(We have other extended family on maternal side with cancer in their past too).
Idid the gene testing. I was negative which was great! But then my surgeon said well that means if you do have a genetic connection to breast cancer it's a gene we just don't know about yet. Hummm I thought that wasn't really a comforting comment. Lol.
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There is a lot they don't know yet, otherwise there would have been a cure. All you can do is use whatever they have which has not proven to help 100% of time. Most people don't know this, but Tamoxifen is not broken down properly by the liver of 33% of women who take it, so it is ineffective with 33% of women on Tamoxifen. That's a lot! I don't know if they can tell by the level of Tamoxifen in the blood or otherwise, but can you imagine taking on the risks of uterine cancer and blood clots and not doing anything to prevent your cancer? How horrible is that..
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swimjames, do you have a reference for that 33% of women don't metabolize properly stat?
Because I've read it's much lower. "Approximately 5 to 7 percent of European and North American populations are considered poor metabolizers of tamoxifen." https://www.sciencedaily.com/releases/2012/12/1212...It appears to do with CYP2D6 enzyme, which is something we can test for with a blood test.
I also think we need to consider that in those women who metabolize poorly, it's possible that it would have no effect on clotting or uterine cancer risk because of its lack of metabolic pathways. It's possible it just does nothing; but I haven't delved deeply in the pharmacokinetics of tamoxifen and which of its metabolites carries which risks. -
Moth, your article is dated 2012, mine are from 2017 & 2018, much more current, see both links below for references:
Tamoxifen is known world-wide as a blockbuster chemotherapeutic drugfor the treatment of breast cancer, but it is not always effective. Before it can exert its healing effect, the patient's body must first convert it into the active component Z-endoxifen. Unfortunately, the conversion depends on the patient's genes, which can lead to a variable therapeutic response in patients. https://medicalxpress.com/news/2018-04-paper-filte...
Learning from Tamoxifen
Tamoxifen blocks breast cancer cell growth by preventing estrogen from binding to estrogen receptors (ERs). Many women with ER-positive breast cancer are treated with tamoxifen, and it's estimated that the treatment has saved the lives of half a million women around the world.
But the efficacy of tamoxifen treatment varies and the drug does not work at all for about one-third of women with ER-positive breast cancer.https://www.cancer.gov/news-events/cancer-currents...
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Thanks much to everyone who has posted information here -- good fodder for discussion with our doctors on Tamoxifen vs an aromotase inhibitor. I'm on Tamoxifen now and will ask my MO about all this when I see her next.
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A blood test can determine whether a woman has alterations in CYP2D6 and predict how efficiently her body will convert tamoxifen to endoxifen. Approximately 5 to 7 percent of European and North American populations are considered poor metabolizers of tamoxifen.
https://www.sciencedaily.com/releases/2012/12/121226153030.htm
The study showed that women who were born with genetic alterations of CYP2D6 that abolish the enzyme's critical metabolizing activity and who took tamoxifen for five years had recurrence of breast cancer, or died at a rate 2.5 times higher than women with normal CYP2D6 enzyme activity. Women with intermediate levels of the CYP2D6 enzyme had rates of recurrence or death 1.7 times higher than women with normal CYP2D6 activity.
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https://clinicaltrials.gov/ct2/show/NCT03317405?te...
https://www.ncbi.nlm.nih.gov/pubmed/29385237
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC45805...
But because tamoxifen is metabolized in the liver, it is the germline genome that is relevant for considering its metabolism. Using tumor genome data to classify individuals with respect to their ability to metabolize tamoxifen is scientifically, medically, and practically inappropriate when an unacceptably high proportion of individuals will be misclassified with respect to their ability to metabolize tamoxifen. Does HWE matter? Assuredly, yes, from any rational point of view.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4580553/
CONTEXT:
The growth inhibitory effect of tamoxifen, which is used for the treatment of hormone receptor-positive breast cancer, is mediated by its metabolites, 4-hydroxytamoxifen and endoxifen. The formation of active metabolites is catalyzed by the polymorphic cytochrome P450 2D6 (CYP2D6) enzyme.
OBJECTIVE:
To determine whether CYP2D6 variation is associated with clinical outcomes in women receiving adjuvant tamoxifen.
https://www.ncbi.nlm.nih.gov/pubmed/19809024/
Women were classified as having an extensive (n=609), heterozygous extensive/intermediate (n=637), or poor (n=79) CYP2D6 metabolism.
RESULTS:
Median follow-up was 6.3 years. At 9 years of follow-up, the recurrence rates were 14.9% for extensive metabolizers, 20.9% for heterozygous extensive/intermediate metabolizers, and 29.0% for poor metabolizers, and all-cause mortality rates were 16.7%, 18.0%, and 22.8%, respectively. Compared with extensive metabolizers, there was a significantly increased risk of recurrence for heterozygous extensive/intermediate metabolizers (time to recurrence adjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.04-1.90) and for poor metabolizers (time to recurrence HR, 1.90; 95% CI, 1.10-3.28). Compared with extensive metabolizers, those with decreased CYP2D6 activity (heterozygous extensive/intermediate and poor metabolism) had worse event-free survival (HR, 1.33; 95% CI, 1.06-1.68) and disease-free survival (HR, 1.29; 95% CI, 1.03-1.61), but there was no significant difference in overall survival (HR, 1.15; 95% CI, 0.88-1.51).
CONCLUSION:
Among women with breast cancer treated with tamoxifen, there was an association between CYP2D6 variation and clinical outcomes, such that the presence of 2 functional CYP2D6 alleles was associated with better clinical outcomes and the presence of nonfunctional or reduced-function alleles with worse outcomes.
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Swimjames:
You're right they don't have a cure yet, there is too much they don't know yet IMHO. I don't understand why it is taking them so long to find a cure. Sometimes, I wonder if they are trying hard enough to find a cure. I remember walking in the race for the cure after my gma died in 99' thinking at the time wow there are so many people affected by this disease, why haven't they found a cure? And I am still wondering that about 19 years later! I know they have made strides in the right direction....but I just wonder sometimes about all that.
Moth: Thank you for your post about the CYP2D6 gene. That got me to thinking and I went and pulled out some testing I had done a few years ago. I am not sure if they tested me at the time for the CYP2D6 gene. But I WAS tested for the CYP2C19 gene...which I was considered heterozygeously positive for. I don't really understand all the studies on this gene and tamoxifen. I did a search for info on whether it might also have some connection to breast cancer or it's recurrence. I am not finding anything that is conclusive yet. It appears they are researching that though. So I wonder if that is one connection my family may have to breast cancer.
Gene testing and connections to cancer is very interesting to me. I am sure there are quite a few other genes they haven't found conclusively yet are connected to breast cancer but maybe in the future they will have that evidence??
Anyway, thank you for bringing up the CYP2D6 gene....it got me to pull out my test results!
What is interesting too I looked to see which genes they test you for when they tested me for cancer gene testing and I didn't see those genes on the testing. It was on another test I had done that that CYP2C19 test results had been given. I wonder when they will add these type of genes to breast cancer genetic testing in the future?
Swimjames:
I have another question I probably should know this but thought you'd probably know. When does a patient's breast cancer become grade 2? Like what percentage of proliferation is it graded as grade 2? Is grade 1 up to like 10%? And then grade to would go from 11-%? Curious about that.
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jons girl ~ I don't know how to differentiate the grades. I do know with onco testing they do change the guidelines of when some chemo is in order every year or so based on new information. Cancer has been around a long long long long time, I am sure if they could have come up with a preventive pill (with little side effects), they would have given it to almost every 'dense breast/suspicious' girl of a certain age by now. Autoimmune diseases which are similar to cancer are being managed not cured. We, as breast cancer women, are managed. The cure, if there is one, is very very complicated and no one knows the cause for the cancer in each specific woman. Just like we can't figure out why our cells age and how to slow down the progress. Every 'body' is different and has different rates of all kinds of damage affecting it in some way or another and we don't know why, part of nature I guess.
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Jons_girl - grading is explained here. http://pathology.jhu.edu/breast/grade.php
there's even a picture of a slide comparing Grade 1 and Grade 3. If you hover over it there's a small pop up box explaining the features to look for.
It's actually a score of 3 different criteria, each assigned a score of 1-3 so the possible total score falls between 3-9.
3-5 are Grade 1
6-7 are Grade 2
8-9 are Grade 3
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Jon's girl- on the genetic testing, some of the genes they test for today may not have been identified yet when you were tested. Additionally there are several different panels a doc can choose from: just BRCA, just genes associated with breast cancer in general, ovarian panel, standard 16 gene panel, expanded 39 gene panels and variants of uncertain significance (VUS) panels where they find gene mutations but aren't sure if there is any cancer significance to them.
Personally I cringe every time I see someone post they were tested for BRCA and it was negative. Well what about the other 7 breast cancer related genes? You don't know what you don't know and we rely on our docs who are sometimes navigating blindly with genetic testing but will never admit to it. Just another reason to become your own best advocate by researching on your own.
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Really good info Moth! I've wondered about this too but was too chicken to search it. How's that for hugging tight to ignorant bliss lol!!
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This is regarding the 33% of women who cannot metabolize tamoxifen well enough for it to be effective, very important, and very current, as of yesterday:
https://advancingthescience.mayo.edu/2018/04/10/6689/
https://ascpt.onlinelibrary.wiley.com/doi/full/10.1002/cpt.1007
New international practice guidelines for using tamoxifen to treat breast cancer
By Colette Gallagher
An international group of clinicians and scientists representing the Clinical Pharmacogenetics Implementation Consortium (CPIC) published the first-ever clinical practice guideline for using CYP2D6 genotype to guide tamoxifen therapy in Clinical Pharmacology and Therapeutics.Tamoxifen is a hormonal agent used for the prevention and treatment of premenopausal and postmenopausal breast cancer that is estrogen receptor positive. CYP2D6 genotype is an inherited factor that alters the metabolism of tamoxifen.
"The goal of the CPIC Guideline for CYP2D6 and tamoxifen therapy is to provide clinicians information that will allow the interpretation of clinical CYP2D6 genotype tests so that the results can be used to guide prescribing of tamoxifen when genotype information is available," says Matthew Goetz, M.D., a Mayo Clinic medical oncologist, who is the lead author. "The consensus of the consortium tamoxifen group was that there was sufficient evidence to use CYP2D6 genotype to assist with clinical recommendations for women who are being considered for tamoxifen for early stage estrogen receptor positive breast cancer."
Matthew Goetz, M.D.
Tamoxifen is converted through the process of liver metabolism into forms that result in greater anti-estrogenic potency and anti-tumor activity than the parent drug. Antiestrogens are a class of drugs which prevent estrogens from mediating their biological effects in the body.
"The work of the consortium is an example of Mayo's commitment to taking a comprehensive, collaborative team science approach to deliver advanced genomic medicine to our patients. We work with other academic medical centers, hospitals, and clinics to bring the latest discoveries to improve the practice of medicine." - Matthew Goetz, M.D.
"The work of the consortium is an example of Mayo's commitment to taking a comprehensive, collaborative team science approach to deliver advanced genomic medicine to our patients. We work with other academic medical centers, hospitals, and clinics to bring the latest discoveries to improve the practice of medicine," says Dr. Goetz.
Tags: breast cancer, Center for Individualized Medicine, clinical guidelines, Clinical Pharmacogenetics Implementation Consortium, CYP2D6 geneotype, DNA sequencing, Dr. Matthew Goetz, estrogen receptor positive breast cancer, Findings, Genetic testing, Mayo Clinic, medical research, People, Precision Medicine, tamoxifen, targeted therapies
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very interesting swimjames, thanks for sharing!
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I had this test and I am an intermediate metabolizer with one normal allele and one completely non-functional allele. I was close enough to menopause that I opted for a dose adjustment of tamoxifen, rather than AI + OS. This raised my endoxifen level into the therapeutic range. I am switching to an AI alone soon since I am now confirmed to be postmenopausal.
I had to get this test on my own and insist on the dose adjustment two years ago because my MO was NOT into it at all. I was thinking better safe than sorry, and he was thinking "I'll just let this patient fall through the cracks until there is more solid evidence." Now there are guidelines, and I'm thinking about his patients who never got the test, or were told it wasn't clinically relevant when they asked. I wonder how many have had a recurrence because he couldn't be bothered to think more cautiously based on preliminary evidence.
Moral to this story: Be the squeaky wheel! -
I am in the same boat. Because of my family history and seeing what my aunt went through while they took her breasts lump by lump and having radiation and chemo (which obviously didn't do the trick), I opted to have bilateral mastectomy and no radiation, no anti-hormone therapy. I had very large breasts and wanted a reduction anyway, so now I have less of a recurrence problem because of almost zero breast tissue.
My initial MO was rude, said I had decided to over treat my cancer and I should've kept my breasts and just been happy with radiation and tamoxifin. This is when I decided to fire him and find someone who will not degrade me but work with me. Before I left and fired him, he told me that I WAS going to take tamoxifin, even though I have a history of blood clots, and he sent in a prescription.
Needless to say, I have an appointment in one week with my new, and friend-recommended, MO!
What we decide is a personal choice. I was told tamoxifin would make a 1% difference in my recurrence rate. No thanks!
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A1shif, I think you should really consider the source of your info on the 1% improvement in non-recurrence rate of BC with use of Tamoxifen, and look for other reliable sources as well. It's easy to jump to a conclusion based on a small sample of information or information that's not really relevant or comparable to your situation. As far as your decision to have a bilateral mastectomy, my breast surgeon told me that one would get the exact same benefit with a lumpectomy and radiation as they would with a mastectomy and I trusted her. One has to make a personal choice of having very invasive major surgery of a breast removal or exposing oneself to radiation, not a great menu of stuff, but up to person to decide. My breast surgeon recommended the lumpectomy followed with radiation for me and I followed her advice. With regards to Tamoxifen, I've heard rumors from women that as soon as one discontinues the meds, the cancer returns, and I have met women who are successfully on year 11 of Tamoxifen, but my oncologist does not recommend being on Tamoxifen longer than 5 years. The Tamoxifen treatment and dosage is the same for all women who are ER positive regardless of what stage they were and whether there was lymph node proliferation, but it seems from my reading that the earlier detection and treatment of breast cancer leads to smaller recurrence rates than if your cancer was discovered at a later stage. I am no doctor but it seems that here there is no one hard fast rule but many permutations and combinations of things and one has to find what is best for them and be ready to change treatment if the situation changes.
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I've been part of a high-risk breast cancer clinic for about 15 years (since my mom and two aunts all had bc), and get an MRI every year (and a mammogram at the 6-month mark in-between). It was on a MRI that my cancer showed up--nothing visible on the mammogram I had had six months earlier. I've just had surgery, so not quite at the post-everything check-up stage, but I plan to continue this pattern of yearly MRIs. I doubt I would be Stage 1 without it, and grateful my insurance actually covered it.
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Dear sfmred72.. Are you aware your response was deleted? See your original entry below as I'm hoping it will help others..
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Topic:
node negative stage I breast cancer question by swimjames
Post by sfmred72:
I've been part of a high-risk breast cancer clinic for about 15 years (since my mom and two aunts all had bc), and get an MRI every year (and a mammogram at the 6-month mark in-between). It was on a MRI that my cancer showed up--nothing visible on the mammogram I had had six months earlier. I've just had surgery, so not quite at the post-everything check-up stage, but I plan to continue this pattern of yearly MRIs. I doubt I would be Stage 1 without it, and grateful my insurance actually covered it.
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