Stage 1, grade 1 and pre-menopausal
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Hi all, I started this thread and although it is nice to see I am not alone, sorry you are all here with this disease!
Indolent does not meant he same as curable. The problem with BC is that it produces the famous micro metastases that can stay dormant for a long time especially with low grade and ER positive tumours. Whilst the stats are in our favor with stage 1, the ' belt and braces' approach prevents it appearing again in 5 or 10 or 15 years time as a distant metastases. Tamoxifen has the best track record for preventing this. Stage 1 grade 1 in old ladies is considered less 'serious' because if you get stage 1 grade 1 at say 70 years you will probably succumb to something else before the BC gets you.
I want to aggressive with my treatment because I am 42 and have young kids. I am on lupron and tamoxifen but have had an equivocal CYP2D6 test so I am considering ooph but as others have commented the ooph is v definitive and has its drawbacks! If anyone has the answers to these unanswerables please share them with us???
hugs
Annice0 -
Sherryc I am also doing zometa
Annice0 -
I am 39 - and could not take tamax ... i had a systemic reaction to it -- thus, I am on Lupron and femera ---- the side effects are quite difficult to adjust to .....
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I'm 52 and, I believe, pre-menopausal. (I had a uterine ablation 2 yrs ago so no periods, but still seem to have PMS. I see the MO on Wed to get the results of hormone tests.)
I'm not sure I should take Tamox as I have high tryglericides. Plus I already deal with some of the side effects common with these meds such as insomnia, fatigue, constipation, so I want to avoid too many meds. Since I'm 90% ER+, I want to get the ovaries removed. Hopefully, I can take an AI without too many SE's.
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Wow Voracious Reader I always learn so much from your posts. Regarding an old lady's disease- wow. Maybe it explains how I feel sometimes. My ca was a 20 point diamond size which is really pretty small.
Since I do have my ovaries and I am pre- menopausal maybe its time to find a new MO (it was really hard having mine leave). I did not know about zometa- phone calls tomorrow.
thanks!
chocolate
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For what it's worth, I've been post-menopausal for almost 30 years (hysterectomy with both ovaries gone) and have had virtually no HRT except a small amount in my first year after the hysterectomy.
About a week before I was diagnosed, my doctor ordered a blood test to check on my estrogen levels (prior to a bone density scan) and they were unmeasurably low.
The kicker is that my tumor tested ER+ at 100% and PR+ at 97%! Asked my BS about that remarkable irony and she just noted that the breast tissue itself makes hormones. D'oh! Oh, and she told me I'd be taking AI inhibitors for at least 5 years, regardless of my BMX.
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Wow. So many of us with very similar situation. BC found end of Aug, 2011. Stage 1a, Grade 1, less than 1cm in size, highly ER/PR+, Her2-, Onco 12. Age 47. No chemo, UMX/recon, on my third month on Tamoxifen. (Very few SE so of course I worry it isn't working properly
I had one ovary removed in 2009 due to dermoid but had also started the pill again at around 40 and then last year had a Murena IUD, which was immediately removed a week before I started Tamoxifen. So I'm wondering about the birth control hormone issue too. I have my follow up appt with my MO in Feb. I will ask him about the other ovary and if I should be removing or suppressing it.
Very interesting discussion. Thank you all for sharing.
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Hello,
I never post on the boards, rather go to chat, but saw your post and wanted to reply.
Was dx in 2006 at age 49, with same. Stage 1, grade 1 IDLC and 100%Er/Pr+. I have liver dis. so could not take tamox. Rather I had lumpectomy, radiation, and a total hysterectomy. I tried AI therapy, but that caused problems as well. Here I am over 5 yrs out, and just had my MRI a few mo. ago, everything was fine. I was told by very good oncologist that our stage and grade has very good prognosis, and that I've done all I could have done. I pray it never comes back, but at least ER+ women have that choice of estrogen blockade, where as the triple neg. gals only get chemo. ugh. If you are on tamox and its working well, just try (I know its hard) to have faith in knowing your doing all you can do as well. Yes, recurrences and metasteses do happen to stage 1 girls. Cancer doesnt play by the rules, but try to rest easy..
PS-my sister in law was diagnosed 1988 with DCIS. Mastectomy, and tamox. She had metasteses (obviously not only DCIS was present in 88' or they didnt find subsequent breast tumor soon enuff), to her spine in 2000. She has been living with mets since then, which has spread to many other distant sites, bone, lungs, etc. She's traveling the globe and chemo has held her in remission. The grade 1 has to do with that. Anything can happen. It is what it is..
Prayers,
Peachy
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I have often wondered if the pill was the cause or major contributor to my cancer. In the lists of risk factors thats the only one (other than not having babies before 35) that I really have. I have always had a sensitivity to birth control and had a hard time finding one that did not make me sick.
I still have to remind myself every morning that I have had BC. I wake up ready to start the day and I say "oh yeah..I had cancer, damn". Its still hard to believe. Thank you all of you for sharing your issues and concern. I am sorry we have to be members of this sorority.
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http://www.onclive.com/publications/obtn/2011/march-2011/the-final-word-on-cyp2d6-testing-and-tamoxifen
"The Final Word on CYP2D6 Testing and Tamoxifen?
Author: Jason M.
BroderickCYP2D6 phenotype status does not predict tamoxifen efficacy in patients with
early-stage breast cancer, according to a retrospective analysis of data from
the Breast International Group (BIG) 1-98 trial1 presented at SABCS.
Freya R. Schnabel, MD, professor of surgery, NYU School of Medicine, discussed
the findings at the JTCC's SABCS review. Based on the negative results, Schnabel
believes there is no current justification for CYP2D6 pharmacogenetic testing
prior to administering tamoxifen.CYP2D6 is involved in the formation of endoxifen, a metabolite linked to
tamoxifen's efficacy. Previous research, including Schroth et al2,
had suggested an association between lower CYP2D6 activity and worse clinical
outcomes with tamoxifen treatment. Schnabel admitted the data had been
convincing. "I was very sold on the idea that CYP2D6 profiling would be
important in the consideration of women who were going to take tamoxifen for
chemoprevention," she told conference attendees. However, subsequent research,
including the BIG 1-98 retrospective analysis, altered Schnabel's opinion.The BIG 1-98 trial examined tamoxifen and letrozole1 administered
alone and sequentially as adjuvant treatment in 8010 postmenopausal women with
early-stage, endocrine-responsive breast cancer. At SABCS, Brian Leyland-Jones,
MD, PhD, professor of medicine at Emory University, in Atlanta, presented data
from a subanalysis of 2675 BIG 1-98 patients who had received monotherapy with
either tamoxifen or letrozole.1 The patients were genotyped for
CYP2D6 and categorized as poor, intermediate, or extensive metabolizers. The
primary endpoint was breast cancer-free survival.The researchers discovered no association between CYP2D6 status and breast
cancer-free survival. Defying expectations, clinical outcomes were not worse in
poor and intermediate metabolizers than in extensive metabolizers. Previous
chemotherapy treatment was also not a factor. The results suggest CYP2D6
genotyping will provide no indication of tamoxifen's potential
effectiveness.The study also investigated whether CYP2D6 phenotypes associated with reduced
enzyme activity produced fewer hot flashes, a common side effect of tamoxifen.
It has been theorized that lower enzyme activity would reduce tamoxifen's
activity, and thus lower the incidence of its side effects, including hot
flashes. However, the BIG 1-98 subanalysis results showed no association between
hot flash occurrence and metabolizer status. Hot flashes occurred in poor,
intermediate, and extensive metabolizers at rates of 48%, 49%, and 42%,
respectively. Based on these statistically insignificant differences, the study
concluded that hot flash incidence should not be a marker of tamoxifen
efficacy.The negative results of Leyland- Jones et al's study, along with the similar
outcome of Rae et al's3 retrospective analyses presented at SABCS,
have established a convincing argument against CYP2D6 genotyping prior to
tamoxifen administration. The CYP2D6 controversy will likely continue, however,
until the completion of prospective analyses such as the Eastern Cooperative
Oncology Group's ongoing E3108 study (http://bit.ly/ i39SJc).For her part, Schnabel has doubts that the prospective trials will shift the
pendulum back toward testing. "Prospective trials are critical, but the data
presented by Dr Rae and Dr Leyland- Jones were compelling. I will await the
results of these trials with interest, but I am now a bit skeptical, and the
proof will have to be very strong to influence practice in favor of
testing.""References
- Leyland-Jones B, Regan MM, Bouzk M, et al. Outcome according to CYP2D6
genotype among postmenopausal women with endocrineresponsive early invasive
breast cancer randomized in the BIG 1-98 trial. Presented at: 33rd Annual San
Antonio Breast Cancer Symposium; December 9-12, 2010; San Antonio, TX. - Schroth W, Goetz MP, Hamann U, et al. Association between CYP2D6
polymorphisms and outcomes among women with early stage breast cancer treated
with tamoxifen. JAMA. 2009;302(13):1429-1436. - Rae JM, Drury S, Hayes DF, et al. Lack of correlation between gene variants
in tamoxifen metabolizing enzymes with primary endpoints in the ATAC trial.
Presented at: 33rd Annual San Antonio Breast Cancer Symposium; December 9-12,
2010; San Antonio, TX.
0 - Leyland-Jones B, Regan MM, Bouzk M, et al. Outcome according to CYP2D6
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Just wanted to mention that I'm also doing the Zometa based on the Gnant study for premenopausal ER+ Early Stage BC. Recall, his latest finding at 84 months, post treatment, with 2 infusions a year for three years of Zometa, women over 40, who are combining ovarian suppression are doing well. For women under 40, there is no statistical evidence that it is beneficial:
SAN ANTONIO (MedPage Today) -- All but the youngest patients with hormone-sensitive breast cancer had significant improvement in disease-free survival (DFS) when they received zoledronic acid (Zometa) in addition to endocrine therapy, results of two large trials showed.
The two trials -- known as ZO-FAST and ABCSG-12 -- both showed about a 30% reduction in the relative risk of progression in women treated with zoledronic acid, which also improved overall survival (a secondary endpoint) in the ZO-FAST trial. A comparison of immediate versus delayed initiation of the intravenous bisphosphonate demonstrated a significant advantage for starting the drug at the same time as endocrine therapy.
Subgroup analyses showed that only patients younger than 40 did not have improved DFS when treated with zoledronic acid, as reported here at the San Antonio Breast Cancer Symposium.
"The anticancer effects of adjuvant zoledronic acid are now well established in endocrine-responsive patients," said Michael Gnant, MD, of the Medical University of Vienna in Austria, referring to positive results from ZO-FAST, ABCSG-12, and a third trial -- AZURE -- that has been previously reported.
"Bone-targeted treatments may modify the bone microenvironment and may affect cancer stem cells," he added. "Adjuvant zoledronic acid is a successful treatment approach in early breast cancer and should be considered in patients who fit these trials' inclusion criteria."
Long-term results from the ZO-FAST trial showed a 34% improvement in DFS (a secondary endpoint) in postmenopausal breast cancer patients who received zoledronic acid at the same time as the aromatase inhibitor letrozole, compared with women whose treatment with the bone-targeted drug did not start until occurrence of a prespecified clinical event.
Gnant reported findings from ABCSG-12, an Austrian study, after 84 months of follow-up. The presentation updated and affirmed results Gnant and colleagues reported earlier this year.
ABCSG-12 involved 1,800 with early-stage premenopausal breast cancer patients treated with endocrine therapy but no chemotherapy. Following surgery, all patients received goserelin and were randomized to tamoxifen or anastrozole with or without zoledronic acid, continued for three years.
The primary endpoint was DFS.
The patients had a median age of 45, and 22% of the study population was 40 or younger. Additionally, 78% of the patients had T1 disease, 67% had no nodal involvement, 80% had histologic grade 1 or 2, and fewer than 4% were estrogen-receptor (ER) negative.
In the overall analysis, the data reflected a 28% reduction in the DFS hazard for patients treated with zoledronic acid (P=0.01). Gnant said the 84-month results mirrored those of previous analyses: a 26% reduction in the hazard after 48 months of follow-up (P=0.01), 32% after 62 months (P=0.008), and 27% after 76 months (P=0.02).
Subgroup analysis showed a consistent trend in favor of treatment with the bisphosphonate, as results were similar regardless of nodal status, endocrine agent, ER expression level, grade, or stage.
The only exception was the subgroup of patients who were 40 or younger (HR 0.87, P=0.527). Older patients had a statistically significant 34% improvement in DFS (P=0.013).
Gnant said the results are consistent with those of the AZURE and ZO-FAST trials, both of which involved postmenopausal patients.
ABCSG-12 also demonstrated the effectiveness of first-line endocrine therapy for early breast cancer without the use of chemotherapy, he added, as the study population had a seven-year overall survival exceeding 95%.
Zoledronic acid given concurrently with endocrine therapy was associated with a 34% improvement in DFS compared with delayed initiation of the bisphosphonate, according to an exploratory analysis of the ZO-FAST study, said Richard de Boer, MD, of the Royal Melbourne Hospital in Australia.
ZO-FAST involved 1,065 women with early-stage, hormone receptor-positive breast cancer. All the patients were either postmenopausal or amenorrheic due to chemotherapy.
All patients received the aromatase inhibitor letrozole (Femara) and were randomized to start zoledronic acid immediately or to delay therapy until a decline in bone density T-score to less than -2, clinical fracture, or asymptomatic fracture at 36 months.
The patients had a median age of about 57, tumor stage of 0 or 1 in 58% of cases, and involvement of one to three lymph nodes in about 58% of patients. The primary endpoint was change in lumbar spine BMD at 12 months. Secondary outcomes included BMD at 36 and 60 months, disease recurrence, fractures, and safety.
Patients assigned to immediate zoledronic acid had an increase in BMD compared with a decline in the delayed-therapy group, resulting in a difference of 5.9% after 12 months. The pattern persisted during follow-up to 60 months, when the between-group difference reached 10.0%.
The unplanned analysis of DFS showed a advantage for immediate therapy only in the overall population. De Boer said the study's 888 "truly menopausal patients" had a 29% improvement in DFS, and the "recently menopausal" subgroup of 177 patients had a 66% improvement, but neither difference achieved statistical significance.
An analysis of 670 women who were older than 60 or were more than five years postmenopausal showed a 37% improvement in DFS, which also did not reach statistical significance (P=0.052).
An exploratory analysis of overall survival showed a nonsignificant 31% reduction in the hazard in women who received immediate zoledronic acid. The overall result included a 35% improvement (P=0.1035) in truly menopausal patients and a 41% increase in the hazard among the recently postmenopausal subgroup (P=0.7046).
Acknowledging the exploratory nature of the analysis, de Boer said the DFS benefit observed in ZO-FAST is consistent with the improvement observed in AZURE and ABCSG-12.
"The data support the hypothesis that the anticancer potential of zoledronic acid might be best realized in a low-estrogen environment," said de Boer.
ABCSG-12 was supported by Novartis and AstraZeneca.
ZO-FAST was supported by Novartis.
Gnant disclosed relationships with AstraZeneca, Novartis, Pfizer, sanofi-aventis, Roche, Schering, and Amgen. Other investigators disclosed relationships with AstraZeneca, Novartis, Roche, sanofi-aventis, Amgen, Cephalon, and GlaxoSmithKline.
DeBoer disclosed a relationship with Novartis. Other investigators disclosed relationships with Novartis and Amgen. Investigators included employees of Novartis.
Primary source: San Antonio Breast Cancer Symposium Source reference: Gnant M, et al "Long-term follow-up in the ABCSG-12: significantly improved overall survival with adjuvant zoledronic acid in premenopausal patients with endocrine receptor-positive early breast cancer" SABCS 2011; Abstract S1-2
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I laugh at the term of Stage 1 grade 1 being an old lady disease. One of the first things I noticed when I went to the oncologist office if everyone was alot older than me. I was the youngest one in the waiting room. I told my husband cancer is for old people not me.
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For those of us with "mucinous" breast cancers, that are "young," here are the statistics:
Mucinous tumors are diagnosed in about 2% of all breast cancer patients, but they are more common in older women. This subtype is found in about 8% to 10% of women 70 or years or older, but in fewer than 0.5% of those 35 years or younger.
On our Mucinous Breast Cancer thread...we always have premenopausal women finding their way to our thread, scratching their heads and asking, "How could I get THIS 'old lady's disease?'"
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tunkylala Thanks for the Biotin info. About birth control pills - I took them for over 15 years and thought that it helped to prevent BC. Not sure why I thought that, as I read differently about them now. Although I guess the pill would be considered to be similar to HRT, in altering hormones.
voracious reader From the CYP2D6 article that you posted above, the take away for me on this study is that the metabolism test doesn't show much of anything, and it is not really of benefit to give it. I had this test, and was wondering about the results. Tamoxifen SE's for me have been relatively mild - but I've only been taking it for 12 days. I was thinking that it wasn't effective for me, as I don't feel the SE's - this study seems to indicate otherwise. I won't bother getting the results and trying to figure it out.. Thanks for posting.
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Voracious reader thanks for the CYP2D6 info you are awesome!
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Annice...Actually, I haven't seen anyone coming on this board lately asking about the CYP2D6 test...so I am assuming it isn't regularly done anymore......
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Voracious reader yes it seems to be out of favor for now. I am in UK and paid for the test because I was not getting any side effects from tamoxifen and my BS and first oncologist said they thought I was being too aggressive using lupron based on my stats. Although I am probably not going to change my treatment based on my CYP2D6 intermediate metaboliser status, it makes me sure I have done the right thing with lupron, just to be sure, as I am only 42
Joy I thought the birth control pills were safe too although now I am sure they caused my cancer as I have no other risk factors and loads of protective factors that would convincingly suggest that I should not have got BC at all! Just my luck!0 -
Annice...I didn't get side effects from Tamoxifen either...and subsequently found out that I was an ultra metabolizer.....Go figure.....
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Ysa I don't understand why you got ER positive BC, it really doesnt follow the rules does it! Did you take birth control pills before your hysterectomy??
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Peachy thanks for posting, and congratulations on your clear scan 5 years out!
I think the current data suggest that bilateral oophyrectomy which you had is equally as good as tamoxifen to prevent recurrecne for Er+. The SOFT study will clarify whether or not adding oophyrectomy or lupron to tamoxifen provides additional benefit but I don't think it will be published for a few years!0 -
Hi-
I just posted on the IDC forum, so forgive my repetitive question: Did/Do any of you consume a high quantity of aspartame? I'm racking my brain trying to figure out how I got this because I lived a veyr healthy life....the only thing is that I was addicted to diet sodas, consuming scary ammounts on a daily basis because I was so addicted. Anyway, just wondering...BTW: I am waiting for BRAC testing and CDKN2A: might be genetic which would answer my question and help me feel less guilty for allowing myself to become addicted to something which might be harmful.
Thanks for all the posts. You guys (girls) ROCK!
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Thankfully the SOFT trial met its quota of patients... Now we just sit and wait to find out the results...Furthermore, it would be interesting to see if 10 years of hormonal therapy... 5 Tamoxifen and 5 of an AI will eventually make it's way into the NCCN guidelines... To be continued...
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I had lot's of SE from Tamoxifen and my MO ran the CYP2D6 and I am a high metabolizer so MO said that explains why I got just about every SE there is.
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Voracious reader- I knew you would know where the SOFT trial was up to! I couldn't find anything except recruitment info from 2004. Glad to hear results are closer than I thought, it will be a v important study for us.
Lucky48, I don't know anything about aspartame, maybe voracious reader might have some info. Do you have a family history of BC, if so its prob more likely that than the soda, but as our oncs always say one in 10 it's family history, the other 9 is anyone's guess!0 -
Lucky48 I avoided aspartame - all artificial sweeteners and soda altogether - so I don't know if that is a link.
I have a feeling that soy might have something to do with my BC, if not the timing of it. I consumed a lot of soy while living in the States, but abruptly stopped last summer after moving to Budapest as it wasn't as readily available here in Europe. My first 2 periods after moving were extremely heavy - to the point where I thought that I would need medical attention. After the first two, things settled down and everything was okay. I had a mammogram the month before moving, and nothing was detected. I may have already had BC then, maybe it just grew faster with no soy?
Has anyone had the BRAT test?
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Not sure if the above link works...The SOFT trial closed on January 31, 2011 and accrued its 3000 participants.....
SherryC...IMHO, what your doctor told you is not based on fact. Unfortunately there's a lot that we still don't know WHY some women get side effects while others don't.
I never eat or drink anything with artificial sweetners. I hate the taste of anything artificial. I recall when I was diagnosed, the breast surgeon gave me a list of do's and don'ts. Only problem was that I was already doing all the do's and STILL got breast cancer....He told me to toss the list!!
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voraciousreader - the same thing happened to me. I tossed my list as well.
I have the same stats as most of you. My Oncotype DX was 14. No Chemo. Got 3 opinions and all 3 said no. I will finish radiation on 3/5. Then I start tamoxifen. There is a ton of great info in here. Thank you!
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voraciousreader-My MO was kinda joking when he told me that. At the time he did my test was also the time when they came out with the study that they were not sure if the test was really significant in how our bodies deal with the tamoxifen. I am just barely ER+ so I have always had my doubts about how much good the tamoxifen is really doing for me.
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@ Annicemd: You could have knocked me over with a feather when I found out how highly hormone positive my BC was considering my history. I had an oopherectomy followed a year later by the second ovary and my uterus being removed when I was about 24 (I am now 55). I did take birth control pills for a couple of years around 19/20, got pregnant within a month of going off of them at 21 but miscarried. That's about when they started investigating issues with highly cystic ovaries. I did have some HRT for a couple of months right after my hysterectomy but hated the side effects so went off of it. Coincidentally, and leading me to resist taking any other HRT, my mom was diagnosed with BC a few years later (about 20 years ago) but we have no idea of her hormone status (or anything else for that matter). She has since had colon cancer (7 years ago), and now it appears that she may have lung cancer. When tested in mid-December (just a few weeks before I was diagnosed with BC), my Estradiol was <1.4 pg/mL, which is the lowest end of the untreated, post-menopausal range.
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Hawk... Good luck with your active treatment.
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