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Relapse HISTORY for her2+S
I see that many are interested in the relapse history for her2+s. If you look at the 2006 ASCO, there is a virtual presentation, I believe by Winer, that charts some of the relapse natural history to date. From that data it is clear that her2+ bc can and do relapse after the 18-24 peak, albeit less frequently. I would ONLY presume that the relapse time MAY be delayed in cases of hormonal positive and in very early stage disease where it takes longer to seed and spread cancer.
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Hello Robin,
Could you direct me as to how I could find the ASCO information that your referenced ? Many thanks !!! |
Susan, if you scroll to the bottom of this page, you'll find the "forum jump", which contains the ASCO 2006 forum where you should be able to find the link Robin mentions.
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I looked under forum jump on Asco highlights, but can't find the subject on relapse. Would appreciate it if you would be a little more specific, like pointing out the article in the number sequencing. Thanks.
Ann |
I can't find it, hoping Robin posts with some help.
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YOu wrote<<<<From that data it is clear that her2+ bc can and do relapse after the 18-24 peak, albeit less frequently.<<<<
I have been freaked ever since I read this, this morning. Now I just have to go and find the article you mentioned. |
This also freaked me out!!!! I want to read this article and then talk to my oncologist soon!
Susan |
Don't let this freak you out. There is a natural relapse period for all breast cancer. All pathologies. For Her2+ and triple negative, the highest period of recurrence occurs within the first two years. This is also true for "run of the mill" bc that is only hormone positive. However, the "only hormone" positive bc also has a "blip" in relapse in the 7-9 year period (but this blip is smaller than in the first 2 years from diagnosis.
Now the article chronicals relapse after the first year of Herceptin. It is natural that this period would be the same period that is the most common for recurrences for Her2+ cancer. Who relapses? Well - the women who would - what I mean by this is that Herceptin does not work for everyone (about half) so half of those who would relapse do. But remember, even without Herceptin, not everybody relapses. More DO NOT relapse. So, is it logical that if you received Herceptin through this vulnerable period that it would prevent relapse? The only way to start to really evaluate this question is when the Hera trial is completed so one can see if 2 years of Herceptin is better than one year (because 2 years will cover this "relapse" period). Preliminary evidence is pointing to the fact that more does not improve the odds (it may "save" 1-3 women per thousand more - not statistically significant). As good as Herceptin as an adjuvant is, it will not prevent the relapse for some. This will be more relevent and reliable when better tumor testing is available AND when clinical oncologists separate out these pathologies to analyze where the failure rates occur and address them with newer and better drugs (ie: do Her2+ and ER+ (and/or PR+) recur less when on Herceptin and an antihormonal or do ER/PR negatives do better on Herceptin. Do the failures come from women who are also Her1+ or some other tumor marker we don't even know anything about?) So, I would not freak out over this. This vulnerable period exists regardless of drug therapy (be it Herceptin, Tamoxifen, AIs etc). It is a period that every woman with breast cancer has to live through and live beyond. With these drug therapies available and new technologies on the horizon, we have a very bright future in which to go out and live our lives fully. Have a nice weekend Kindest regards Becky |
Becky,
Thank you. I feel much better after reading your message. After being off of Herceptin for three months now I feel as if I lost my security blanket. Susan |
This is a guess on my part, because I went searching for the article RobinP cited also. Go to http://www.asco.org/portal/site/ASCO...y&abstractID=3 and click on "slides" under Associated Presentations 1. Pre-operative therapy for women with Her2 positive breast cancer. Based on RobinP's description of what she read, this was as close as I could find.
Hopeful |
Boy, I didn't mean to stir the pot. I thought everyone knew that her2 bc could relapse after the peak period, again less frequently. My point of posting was to inform, rather than frighten as I notice lately some questions about late her2 reoccurences. Specifically, I wanted to let others know that there is a growing natural history for her2+ bc that is accumulating via the NCI and HERA trials concerning her2+ relapse. Part of that history was presented in the virtual 2006 ASCO presentation. It's been a while, I viewed this last spring, but I believe it was by Dr. Winer on HERA's data.
PS The above abstract is not what I was referring to. It is actually a line graph with observation and study group relapse mapped out from 0-36 months. |
interestingly
They have found (when looking at all breast cancers, not just her2neu+ breast cancers) that the peak of recurrence occurs x number of months (around 24 for her2+ and triple negative as Becky said,with another later "blip" peak of recurrence for those ER+her2-) after surgery NOT x number of months after the lump was discovered. In those who delayed after finding their lump or who were unable to get access to health care right away (this is a global disease) they found the peak occurred x number of months after the surgery even if the tumor had been there quite a long time before.
The thinking is that the surgery starts an inflammatory process and that the gene signature of breast cancer looks a lot like the gene signature of inflammation and that some of those growth factors etc let loose or stimulated by the act of surgery "start the clock ticking" This is one reason why they are moving toward needle and core biopsies, hoping to mimimize the inflammatory reaction by minimizing the surgery. It is another reason why increased usage of preop MRIs to better define the extent of disease and minimize repeat operations to obtain better margins may improve cancer care in the future. Noone it seems has studied whether the 1-5 day course of various types of accelerated partial breast irradiation produce more or less inflammatory cytokines but if/when the long term results of APBI come out, if they are better than conventional radiation this should be one avenue of research as to why. It may be that breast cancer is indeed a stem cell disease and that the "tumors in waiting" are those slowly dividing cells in the bone marrow which get activated by inflammatory cytokines etc just like the mold in bathroom grout gets activated by moisture no matter how much you use Tilex or other bleach-containing compounds. The group in Germany that has been advocating getting preop and post treatment bone marrow biopsies is starting a clinical trial to see how this would influence treatment and the course of disease. They need to test the bone marrow cells not only for cytokeratin but also double stain them for her2 neu as those with her2neu positive isolated tumor cells in the bone marrow have been shown to be associated with a much higher rate of recurrence than those in the graphs Robin P has pointed out. If this, or a more specific and accurate way of isolating circulating tumor cells can become more widespread and found indicative of residual disease there will be a way in those treated adjuvantly rather than neoadjuvantly ie, when there is no longer a tumor present to judge whether there is or is not a response to therapy, to assess whether the best treatment is being utilized. Sorry to be so serious on a Saturday...Have a great weekend! |
Amen Lani, let's ALL lighten up, RELAX and enjoy the weekend. Take care everyone.
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A copy from another post of mine applies here too as a positive note:
These are quotes from the esteemed E. Perez, MD: ''Unlike ER-positive breast cancer, in which events are strung out over the course of 10 to 15 years, in HER2-positive breast cancer most of the events occur in the first five years and a lot of them occur in the first couple of years. That is part of the reason why, in each of these studies, we saw a dramatic benefit early on, even in the first year (Perez 2005b; Piccart-Gebhart 2005; Romond 2005)" I guess Perez is basing her comments on retrospective studies which go back after the event and analyze data. According to Perez, survival after five years for her2+, er-, pr- is a milestone, not a guaranteed cure, but a certainly a positive milestone. Of course, we'll get the full story , and perhaps a more accurate picture, of natural history from prospective studies like the HERA where data is analyzed as it is made. __________________ |
I don't mean to scare others, but my recurrence came 6 years later. I was having headaches for awhile and waited way too long to have them checked out. The mets were everywhere except the bones. After I started Herceptin in July, 04 my tumor markers were normal by the second or third treatment. My pet scan in March indicated no cancer except in the bones. I've been on Navelbine. I had at PET-CT scan yesterday. If all is well I will drop the Navelbine. If not, I will have to consider other options. I really wonder if my outcome would have been different had I been able to have Herceptin early on.
After six years I was feeling too safe, and the lesson for others is that we must question issues in our body that do not feel right and not wait to have them checked out. Best wishes, Barbara H. |
Barbara H.
Hi Barbara,
I have been on xeloda for the last 2 months with very little side effects. It has been by far the easiest treatment I have been on. It is supposed to work well with herceptin and the new trial, tykerb. I havn't been on herceptin since Dec. 05. I had a 5 1/2 month break from all but zometa for the bone mets. I started xeloda in August. I was on 4000mg dailly for 2 weeks, then 1 week off. Doc dropped me back to 3000mg daily, as my feet were swelling. I'm also on lasix. If I don't qualify for the tykerb, I might ask Doc if I can go back on herceptin with xeloda. Blessings from Lu Ann |
Robin,
Is this the link that you're looking for? Vicki posted it above as well. http://content.nejm.org/cgi/data/353/16/1673/DC1/1 I was under the impression that the data was from 'time of radomization' which I take to mean the time for first chemo. In my particular case, I read the data as saying that after three years, I can breathe more easily. Jen |
Yes, that is the link, funny I couldn't cut and paste it when I tried months ago, perhaps the NEJM has publically released it now. I concurr with you about time to randomization Saleboat, thanks for the clarification, it helped. Also, congratulations the graphs look good for your particulars, being three years out stage 3.
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Jen
I think you are right - about time to randomization except for one thing. I do personally know 2 women who participated in the Herceptin trial at my cancer center (I opted not to and can tell you why if interested). These ladies were randomized after the 4 AC treatments. When they showed up for their first weekly taxol that's when they found out if it was taxol alone or taxol with Herceptin (both were randomized to the arm without Herceptin). I met these gals while getting Herceptin and found out everything about the trial and being in the trial because I was on my 3rd weekly Herceptin (started asap after ASCO 2005 when I was 4 1/2 months from my last chemo) but they were both on their 9th weekly. After asking how can this be - I jumped so fast to start as soon as I heard - they commented that since they were on the trial, they were given the option to start Herceptin (if they wanted it) sometime around April 20, 2005 when Genentech made a public announcement. Both ladies were about 7-8 months from their last chemo (but for this group of women, being 6 months or less from the last chemo did not matter). So, randomization started 12 weeks after the beginning of AC (remember the trial used AC every 3 weeks and not the dense dose regime used now). Best regards Becky |
Looks like Chinese to me
Boy, I have a hard time interpreting those graphs etc... Thanks to those of you with the ability that help us understand.
I remember that in a nutshell the other two US trials for early stage herceptin use indicated that after five years 15% of women had recurrence. That is simply stated. What I would like to know is 1) How many of the women who relapsed were ER+/ER- and 2) were their recurrences local or distant. Anyone know? Thanks! |
I can't answer that question fully, Cheryl. But I will say that IN GENERAL (meaning all bc) the statistics say that 80% of recurrences are local. This is not broken out to Her2+ vs hormone only positive vs triple negative etc.
Kind regards Becky |
Thanks Becky,
You are a wealth of knowledge. I love reading your posts. So then if I understand correctly, of this 15%, 3%, statistically speaking, would have had a distant episode, right? That's encouraging to us all, especially if we also have the benefit of hormone therapy such as AI or tamoxifen. We can always use that dose of encouragment. Wonder what HERA will end up showing us about 2 years of Herceptin vs. one. Anyone remember when that is due out? |
Cheryl
My onc is thinking there may be something presented in December on two year use at San Antonio. Joe, any indications of this that you know of?
________ FlirtyCat cam |
Sassy
It is well documented that the absolute earliest results of 2 yrs of Herceptin therapy vs one year will be the end of April 2007 but indications are that there will not be a release of data until 2008. About 6 weeks ago, Eric Winer (of Dana Farber) visited our cancer center. My onc called me beforehand to make sure all the right questions were asked in regard to 2 yrs of therapy vs one year. Preliminary data suggest that 2 yrs gives absolutely no better results than one year. Statistically it is not better and may impact heart function down the road (this is the big fear - what happens to us 10 years down the road. This question is not addressed in the metastatic condition because most women might not survive with mets 10-15 years out and those that do, there is no statistical data). However, there will be data in the long term on if 2 years of Herceptin delay or eliminate possible mets long term. For example, in the initial Tamoxifen studies, there were lots of trials to determine that 5 years of use gave the best benefit. And this was tested using 1 yr of use, 2 yrs, 5 yrs and 10 yrs (of which 10 yrs actually gave a worse outcome). In the future, new members to this board will look at us and say "you used adjuvant Herceptin for a year. OMG!!" because I think they will find that less (let's say 3-6 months) works just as well as a year. Unfortunately, it is difficult to get the funding to do these studies because everyone is awaiting the 2 yrs of Herceptin data. It is rationalized as "what if more is better then why test 3 months vs 6 months vs one year? But I personally think less will be the same as a year and probably have less long and short term side effects. Kind regards Becky |
General Relapse Not Specific For Her2:
http://www.what-is-cancer.com/papers...recurrence.htm
THE ABOVE LINK IS ANNUAL RISK OF RECURRENCE FOR VARIOUS GROUPS, NOT SPECIFICALLY ADDRESSING HER2 GROUPS. HOWEVER, STILL THIS GRAPH IS HELPFUL IN TERMS OF REFLECTING GENERAL HORMONAL POSITIVE AND NEGATIVE RELAPSE. |
You all have me very confused. Let me see if I understand: statistically are you saying that HER2+ER-PR- relapses long term less than HER2+ER+PR- breast cancers? Or is it the other way around?
After reading posts for the last week or so, I started to worry about lower back pain I have been experiencing for the last few months. Have not had blood work since last November so have no indication if tumor marker is up. My oncologist is scheduling me for a bone scan asap. This is not the way I wanted to get Herceptin (not eligible before). Hope it's just old age catching up with me. Keep fingers crossed. Stephanie |
Thanks Becky,
My onc and I have discussed the possibility of long term heart impact, and the fact that statistical data is not available because previously long term use had not been expected due to underestimated effect of Herceptin. Could you share where I might find the documentation of 2 year info being available in April 2007, with release not scheduled until 2008? You are a wealth of information and I appreciate all your help and support!
________ SweetBlackAss3010 |
ER+ and HER2+
I've been on Herceptin 18 months. There's something about being ER+ and HER2+ that needs balancing or it up ticks the other, so it seems you need to take an AI with Herceptin? So I'm on Herceptin and Femara. Really not sure how well researched this is.
sarah |
sarahdalton, here is a link to an article that explores the issue of her2/endocrine therapy: http://erc.endocrinology-journals.or.../full/11/4/623. I will be doing Femara + Herceptin, also; currently doing Rx + Herceptin.
Hopeful |
Hopeful--great article although tough to read
since writing that article Dr. Nicholson has written 24 more. If there are any die-hards who really want to know all the latest before making up their minds (and these are only his articles and there are scores writing on it, but he and Dr. Dowsett seem to be the most interested in this, I supply the following list of references--due to technical problems (my computer ignorance). I will list about 4 and then about another 20 in a second post):
21: Vicent MJ, Greco F, Nicholson RI, Paul A, Griffiths PC, Duncan R. Related Articles, Links Polymer therapeutics designed for a combination therapy of hormone-dependent cancer. Angew Chem Int Ed Engl. 2005 Jun 27;44(26):4061-6. No abstract available. PMID: 15912547 [PubMed - in process] 22: Nicholson RI, Hutcheson IR, Britton D, Knowlden JM, Jones HE, Harper ME, Hiscox SE, Barrow D, Gee JM. Related Articles, Links Growth factor signalling networks in breast cancer and resistance to endocrine agents: new therapeutic strategies. J Steroid Biochem Mol Biol. 2005 Feb;93(2-5):257-62. Epub 2005 Feb 8. Review. PMID: 15860268 [PubMed - indexed for MEDLINE] 23: Taylor KM, Morgan HE, Johnson A, Nicholson RI. Related Articles, Links Structure-function analysis of a novel member of the LIV-1 subfamily of zinc transporters, ZIP14. FEBS Lett. 2005 Jan 17;579(2):427-32. PMID: 15642354 [PubMed - indexed for MEDLINE] 24: Jones HE, Goddard L, Gee JM, Hiscox S, Rubini M, Barrow D, Knowlden JM, Williams S, Wakeling AE, Nicholson RI. Related Articles, Links Insulin-like growth factor-I receptor signalling and acquired resistance to gefitinib (ZD1839; Iressa) in human breast and prostate cancer cells. Endocr Relat Cancer. 2004 Dec;11(4):793-814. PMID: 15613453 [PubMed - indexed for MEDLINE] |
you can infer from the titles which are specific and which are reviews
1: Sarwar N, Kim JS, Jiang J, Peston D, Sinnett HD, Madden P, Gee JM, Nicholson RI, Lykkesfeldt AE, Shousha S, Coombes RC, Ali S. Related Articles, Links
Phosphorylation of ER{alpha} at serine 118 in primary breast cancer and in tamoxifen-resistant tumours is indicative of a complex role for ER{alpha} phosphorylation in breast cancer progression. Endocr Relat Cancer. 2006 Sep;13(3):851-61. PMID: 16954434 [PubMed - in process] 2: Jones HE, Gee JM, Barrow D, Tonge D, Holloway B, Nicholson RI. Related Articles, Links Inhibition of insulin receptor isoform-A signalling restores sensitivity to gefitinib in previously de novo resistant colon cancer cells. Br J Cancer. 2006 Jul 17;95(2):172-80. Epub 2006 Jul 4. PMID: 16819546 [PubMed - in process] 3: Cui Y, Parra I, Zhang M, Hilsenbeck SG, Tsimelzon A, Furukawa T, Horii A, Zhang ZY, Nicholson RI, Fuqua SA. Related Articles, Links Elevated expression of mitogen-activated protein kinase phosphatase 3 in breast tumors: a mechanism of tamoxifen resistance. Cancer Res. 2006 Jun 1;66(11):5950-9. PMID: 16740736 [PubMed - indexed for MEDLINE] 4: De Martino G, Edler MC, La Regina G, Coluccia A, Barbera MC, Barrow D, Nicholson RI, Chiosis G, Brancale A, Hamel E, Artico M, Silvestri R. Related Articles, Links New arylthioindoles: potent inhibitors of tubulin polymerization. 2. Structure-activity relationships and molecular modeling studies. J Med Chem. 2006 Feb 9;49(3):947-54. PMID: 16451061 [PubMed - indexed for MEDLINE] 5: Hiscox S, Morgan L, Green TP, Barrow D, Gee J, Nicholson RI. Related Articles, Links Elevated Src activity promotes cellular invasion and motility in tamoxifen resistant breast cancer cells. Breast Cancer Res Treat. 2006 Jun;97(3):263-74. Epub 2005 Dec 7. PMID: 16333527 [PubMed - in process] 6: Greco F, Vicent MJ, Penning NA, Nicholson RI, Duncan R. Related Articles, Links HPMA copolymer-aminoglutethimide conjugates inhibit aromatase in MCF-7 cell lines. J Drug Target. 2005 Sep-Nov;13(8-9):459-70. PMID: 16332571 [PubMed - indexed for MEDLINE] 7: Yee SW, Jarno L, Gomaa MS, Elford C, Ooi LL, Coogan MP, McClelland R, Nicholson RI, Evans BA, Brancale A, Simons C. Related Articles, Links Novel tetralone-derived retinoic acid metabolism blocking agents: synthesis and in vitro evaluation with liver microsomal and MCF-7 CYP26A1 cell assays. J Med Chem. 2005 Nov 17;48(23):7123-31. PMID: 16279770 [PubMed - indexed for MEDLINE] 8: Britton DJ, Hutcheson IR, Knowlden JM, Barrow D, Giles M, McClelland RA, Gee JM, Nicholson RI. Related Articles, Links Bidirectional cross talk between ERalpha and EGFR signalling pathways regulates tamoxifen-resistant growth. Breast Cancer Res Treat. 2006 Mar;96(2):131-46. Epub 2005 Oct 27. PMID: 16261397 [PubMed - in process] 9: Dowsett M, Nicholson RI, Pietras RJ. Related Articles, Links Biological characteristics of the pure antiestrogen fulvestrant: overcoming endocrine resistance. Breast Cancer Res Treat. 2005;93 Suppl 1:S11-8. Review. PMID: 16247595 [PubMed - indexed for MEDLINE] 10: Nicholson RI, Johnston SR. Related Articles, Links Endocrine therapy--current benefits and limitations. Breast Cancer Res Treat. 2005;93 Suppl 1:S3-10. Review. PMID: 16247594 [PubMed - indexed for MEDLINE] 11: Rampaul RS, Pinder SE, Nicholson RI, Gullick WJ, Robertson JF, Ellis IO. Related Articles, Links Clinical value of epidermal growth factor receptor expression in primary breast cancer. Adv Anat Pathol. 2005 Sep;12(5):271-3. Review. PMID: 16210923 [PubMed - indexed for MEDLINE] 12: Gee JM, Robertson JF, Gutteridge E, Ellis IO, Pinder SE, Rubini M, Nicholson RI. Related Articles, Links Epidermal growth factor receptor/HER2/insulin-like growth factor receptor signalling and oestrogen receptor activity in clinical breast cancer. Endocr Relat Cancer. 2005 Jul;12 Suppl 1:S99-S111. Review. PMID: 16113104 [PubMed - indexed for MEDLINE] 13: Staka CM, Nicholson RI, Gee JM. Related Articles, Links Acquired resistance to oestrogen deprivation: role for growth factor signalling kinases/oestrogen receptor cross-talk revealed in new MCF-7X model. Endocr Relat Cancer. 2005 Jul;12 Suppl 1:S85-97. PMID: 16113102 [PubMed - indexed for MEDLINE] 14: Nicholson RI, Hutcheson IR, Hiscox SE, Knowlden JM, Giles M, Barrow D, Gee JM. Related Articles, Links Growth factor signalling and resistance to selective oestrogen receptor modulators and pure anti-oestrogens: the use of anti-growth factor therapies to treat or delay endocrine resistance in breast cancer. Endocr Relat Cancer. 2005 Jul;12 Suppl 1:S29-36. Review. PMID: 16113097 [PubMed - indexed for MEDLINE] 15: Duncan R, Vicent MJ, Greco F, Nicholson RI. Related Articles, Links Polymer-drug conjugates: towards a novel approach for the treatment of endrocine-related cancer. Endocr Relat Cancer. 2005 Jul;12 Suppl 1:S189-99. Review. PMID: 16113096 [PubMed - indexed for MEDLINE] 16: Jones HE, Gee JM, Taylor KM, Barrow D, Williams HD, Rubini M, Nicholson RI. Related Articles, Links Development of strategies for the use of anti-growth factor treatments. Endocr Relat Cancer. 2005 Jul;12 Suppl 1:S173-82. Review. PMID: 16113094 [PubMed - indexed for MEDLINE] 17: Agrawal A, Gutteridge E, Gee JM, Nicholson RI, Robertson JF. Related Articles, Links Overview of tyrosine kinase inhibitors in clinical breast cancer. Endocr Relat Cancer. 2005 Jul;12 Suppl 1:S135-44. Review. PMID: 16113090 [PubMed - indexed for MEDLINE] 18: Gee JM, Howell A, Gullick WJ, Benz CC, Sutherland RL, Santen RJ, Martin LA, Ciardiello F, Miller WR, Dowsett M, Barrett-Lee P, Robertson JF, Johnston SR, Jones HE, Wakeling AE, Duncan R, Nicholson RI. Related Articles, Links Consensus statement. Workshop on therapeutic resistance in breast cancer: impact of growth factor signalling pathways and implications for future treatment. Endocr Relat Cancer. 2005 Jul;12 Suppl 1:S1-7. Review. PMID: 16113086 [PubMed - indexed for MEDLINE] 19: Hiscox S, Jiang WG, Obermeier K, Taylor K, Morgan L, Burmi R, Barrow D, Nicholson RI. Related Articles, Links Tamoxifen resistance in MCF7 cells promotes EMT-like behaviour and involves modulation of beta-catenin phosphorylation. Int J Cancer. 2006 Jan 15;118(2):290-301. PMID: 16080193 [PubMed - indexed for MEDLINE] 20: Knowlden JM, Hutcheson IR, Barrow D, Gee JM, Nicholson RI. Related Articles, Links Insulin-like growth factor-I receptor signaling in tamoxifen-resistant breast cancer: a supporting role to the epidermal growth factor receptor. Endocrinology. 2005 Nov;146(11):4609-18. Epub 2005 Jul 21. PMID: 16037379 [PubMed - indexed for MEDLINE] Items 1 - 20 of 211 Hope this helps! |
Hi Steph,
You said above that , "You all have me very confused. Let me see if I understand: statistically are you saying that HER2+ER-PR- relapses long term less than HER2+ER+PR- breast cancers? Or is it the other way around?" I will try to clarify your question for you. We do not have long term data on her2 relapse beyond five years from any prospective studies yet. However, we do know the relapse history bc relapse based on hormonal status. From this data, we know that hormonal negatives usually relapse more in the first five years or relapse less after five years than hormonal positives. Hope this helps. Also, hope your back pain is nothing serious. Take care. |
However, I would like to add...
Her2+ women who are also hormone positive relapse less (overall) than those who are hormone negative. The natural progression of the two diseases could be slightly different (with perhaps a blip after hormone therapy is completed) but we just don't really know for sure because Her2s weren't separated out of that hormone positive data. However, it would make sense that the blip is stronger for those who are only hormone positive (but not Her2) because they tend to be very, very strongly positive for ER and PR whereas Her2s who are also hormone positive tend to not be as hormone positive. It is ALWAYS good to be hormone positive. Kind regards Becky |
Just to clarify for others, Becky, in the HERA trial and adjuvant Herceptin NCI trials, the hormonal receptors were separated out. It was found that Her2+ women who are also hormone positive relapse less in the first few years compared to hormonal negatives. However, it was not clear, because the data is not available yet, if these women will acutally relapse later than sooner. It is too soon to fully comment on the hormonal positive, her2 combination long term relapse history, beyond five years, unitl the long term data from the HERA trial is revealed.
http://content.nejm.org/cgi/data/353/16/1673/DC1/1 Just to add, from the above link, the relapse data for hormonal negatives and postives that are her2+ also are grapphed out in the lower last panels for five years out. |
ok I am confused
Although the hormonal status and DFS is mapped out it does not say if these patients were node positive or negative in the context of hormonal status. IE both graphs could be a conglomeration of node + and - patients.
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penelope,
I questioned that too. If you notice panel A only goes out 2 years. I believe that's because node negative women were included only recently in the trials, so there is no data beyond 2 years for them. Hence the panels that show DFS for hormone Positive/negative women probably are based on node positive women. - Anna |
Oh, no you guys still don't see it? Okay,please try again. Click on the website I provided above. Then scroll down below panel A and B and look at fig. 3, for panel E and F which sites hormonal negative and positive data.Got it? I hope so.
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PS. To further help you:
Panel E and F are labeled HR negative and HR positive, the HR stands for hormonal receptor. The data does go out to five years.Once again, here is the link: http://content.nejm.org/cgi/data/353/16/1673/DC1/1 |
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