Anyone on HERCEPTIN+AROMATASE INHIBITORS?
 

One reply (from Taffy) to an other posting revealed a fast & exceptional response to Herceptin+ Arimidex (+ fish oil supplements) after failing on chemo for recurrent disease.

Are there others being treated with at least Herceptin plus one of the aromatase inhibitors such as :
Letrozole (=Femara),
Anastrozole(Arimidex),
Aromasin (Exemestane),
Fulvestrant(Faslodex), etc...?

Did you get unexpected good & fast results for mets &/or primary tumours?

More responders to the regimen than one single woman would increase the probability it may be usefull to a larger population of patients.

Note:
A small clinical trial of Herceptin+ Arimidex is underway in Europe.
For those who are interested in the scientific background you may look at the articles listed in the following post
http://www.her2support.org/vbulletin...ad.php?t=23945

I am on Herceptin, Arimidex and fish oil but I do not have advanced/metastatic disease. I am Stage 2. I have been on Herceptin since mid June, 2005 and Arimidex since Sept 05. I will be on the combination until the end of September, 2006. I have taken fish oil before bc but only one 1g capsule a day. When diagnosed, I upped it to 3 per day and now I am on 5 per day (plus one flaxseed oil capsule as well).


Therefore, I am hoping this combination will reduce my chance of recurrence. After September, I will continue with the Arimidex for 4 additional years. At my next visit, my onco is going to run my estradiol levels to see how well (or if) the Arimidex is working. I will post that on this board. More importantly, if it is not working, I will post what my doc will be doing next (he is the best) so that will be important info. I got my ovaries removed in order to use the Arimidex.

Kind regards

Becky

I am on Herceptin-every 3 weeks, for a year, and Arimidex-for 5 years...began both in Oct. 05. Also early stage...Am taking fish oil supplements, COQ10, calcium/d, magnesuim, glucosamine-chondriotin as well

Fish Oil?
 

I have finished w/chemo; Will have Herceptin-only treatment thru Feb '06;
Just starting radiation; Will start taking Arimidex after radiation.
This is news to me about fish oil being taken to help deter a recurrence.
I am only taking calcium & a multivitamin right now.
Should I be taking fish oil? Anything else?
I heard virgin olive oil is good to take, so I was going to start that.
Would that be a replacement for fish oil?
What about flaxseed oil?
I am also taking coQ10 50mg/day.
Should I take more now that I'm done with chemo?
My dr doesn't recommend anything to me.
She will respond to any questions I have, tho.
But I don't know what questions to ask when it comes to diet or supplemental vitamins etc

I am on 1 year of Herceptin, and monthy injections of Faslodex. I was Stage 1, no lymph node involvement, I had 4 A/C DD, radiation too. Everything is going good. Had my one year mammogram, and blood work up and everthing checked out good. I'll finish Herceptin in Dec 06. Faslodex for 5 years/

I had left mast, DD A/C, Taxol, and have been on Herceptin since June 05 and Arimidex following rads in November 05. Have also added Multi oils, COq-10, B6, glucosomin, Calcium with D, and multi. Not metistatic, no recurrence as yet--so far so good.


DX 2/05
triple positive
5/14 nodes positive
Stage II, grade 2

Sassy
________
LITTLESWEETY

I guess that leaves me to report on metastases. I had skin and lymph node involvement as well as a pleural effusion. Went onto Arimidex and Herceptin and it worked straight away. Next scan was NED, and has been this last 18 months since then. Good luck, my dear. We all have our own unique history and our own story. What happens to one doesn't mean a great deal to another's profile. But what it does do is give us all HOPE,---that we will be one of the ones to beat the odds, and that is what we must do--HOPE.

Interesting post


Sassy - If the omega three six issue is in your thoughts the keys are DHA/EPA intake and balancing the omega threes and sixes.

In most diet six is already high. Multi oils include six. If the multi is your only source it would depend on the composition of the multi oil. If you are also getting six from other sources fish oil is preferable. Fish oils has lots of different fats in it including omega 9 a little six MCTs etc.

You might like to check out omega three and six throught the search engine above.

DHA is important. Women have a higher need and conversion rate than men assuming you metabolism is working well. The safest option has to be to help the body out and take it in the form of fish or similar.

Please talk to your advisor about any dietary changes.

DHA Oestrogen -

DHA/fats and oestrogen are definately linked - eg high exercising low body fat women losing reproductive cycles. I am off to look at annorexia etc to see if there is any information on the mechanisms.

RB

I'm on Herceptin only for Stage 1. My onc does not give AI until Herceptin is completed, but has plans to for me to start when I'm through.

acute and chronic inflammatory conditions, low tissue concentrations of omega-3 fatty
 

More on fats and brains.

This time from the perspective of a search on anorexia.

Key phrase " In patents with acute and chronic inflammatory conditions, low tissue concentrations of omega-3 fatty acids and high concentrations of proinflammatory cytokines are found".

BC is considered by some at least in part to connect to the COX2s inflamatory pathways etc.

RB





1: Curr Opin Clin Nutr Metab Care. 2005 Jul;8(4):403-7. Related Articles, Links
Click here to read
Omega-3 fatty acids and anorexia.

Goncalves CG, Ramos EJ, Suzuki S, Meguid MM.

Surgical Metabolism and Nutrition Laboratory, Department of Surgery, SUNY Upstate Medical University, Syracuse, New York 13210, USA.

PURPOSE OF REVIEW: To review the mechanisms of action of omega-3 fatty acids and their role in the brain, as well as their therapeutic implications in anorexia. RECENT FINDINGS: Recent studies have demonstrated that omega-3 fatty acids modulate changes in the concentrations and actions of several orexigenic and anorexigenic neuropeptides in the brain, including neuropeptide Y, alpha-melanocyte stimulating hormone and the neurotransmitters serotonin and dopamine. In patients with acute and chronic inflammatory conditions, low tissue concentrations of omega-3 fatty acids and high concentrations of proinflammatory cytokines are found, in association with anorexia and decreased food intake. The data suggest that omega-3 fatty acid supplementation suppresses proinflammatory cytokine production and improves food intake by normalizing hypothalamic orexigenic peptides and neurotransmitters. SUMMARY: Based on current data, omega-3 fatty acid supplementation has a role in the treatment of anorexia by stimulating the production and release of orexigenic neurotransmitters in food intake regulatory nuclei in the hypothalamus.

Publication Types:

* Review


PMID: 15930965 [PubMed - indexed for MEDLINE]

Re impacts of fat phobic diets
 

I am NOT suggesting that anybody who has referred to being lean and fit as annorexic.

The point I am trying to illustrate is that some very fit people are very fat intake quantity but not type concious, which could give rise to huge omega three six imbalances, and MAY help explain why it is not just absolute weight that is a factor in BC.

I have postulated the scenario before but this is rather more authoritative and too the point.

RB



1: Prostaglandins Leukot Essent Fatty Acids. 2004 Oct;71(4):205-9. Related Articles, Links
Click here to read
A pilot open case series of ethyl-EPA supplementation in the treatment of anorexia nervosa.

Ayton AK, Azaz A, Horrobin DF.

Hull and East Riding Hospitals Trust, UK.

Anorexia nervosa (AN) carries the highest risk of morbidity and mortality amongst psychiatric disorders. The efficacy of current treatment approaches is limited. Despite the fat-phobic nature of the disease, poly-unsaturated fatty acids (PUFAs) have not received much research attention. Patients who consume western diet, which is rich in n-6 PUFAs and trans-fatty acids, are likely to develop severe n-3 PUFA deficiency during self-induced starvation. Re-feeding programmes do not take into consideration n-3 EFA intake, possibly leading to further n-3 PUFA deficiency during weight restoration, and this might contribute to the maintenance of the disorder. To test this hypothesis, we carried out a systematic case series of E-EPA supplementation in the treatment of AN. Seven young patients received 1g/day E-EPA in addition to standard treatment, and were followed up for 3 months. Three of them recovered and four improved. Randomised controlled trials are warranted to examine the effectiveness of E-EPA in AN further.

Publication Types:

* Clinical Trial


PMID: 15301789 [PubMed - indexed for MEDLINE]

"FAS-dependent endogenous fatty acid metabolism, once considered a minor anabolic-energy-storage pathway in normal cells, has become a jack-of-all-trades in cancer cells".


More evidence as to the importance of fat mechanisms and cancer.

For me DHA EPA are the most likely areas to look at as they are essential to reproduction, have to be made in the body if not eaten, and we are eating less of them and our modern diet may be blocking the pathways to make them. Both are found in fish oil. Hereceptin, and tamoxifen both interact in this pathway and synergies suggest some chemos may too.

I wish they would do some large scale trials looking at outcomes based on fats content in tissues.

RB

ABSTRACT



1: Arch Immunol Ther Exp (Warsz). 2004 Nov-Dec;52(6):414-26. Related Articles, Links

Fatty acid synthase-catalyzed de novo fatty acid biosynthesis: from anabolic-energy-storage pathway in normal tissues to jack-of-all-trades in cancer cells.

Menendez JA, Lupu R.

Department of Medicine, Evanston Northwestern Healthcare Research Institute, Evanston, IL 60201, USA.

In 1994, Kuhajda and colleagues unambiguously identified the oncogenic antigen-519, a prognostic molecule found in breast cancer patients with markedly worsened prognosis, as fatty acid synthase (FAS),the key enzyme for the de novo fatty acid biosynthesis. It now appears that human carcinomas and their pre-neoplastic lesions constitutively over express FAS and undergo significant endogenous fatty acid biosynthesis. Moreover, FAS blockade specifically induces apoptotic cancer cell death and prolongs survival of cancer xenograft hosts. Therefore, FAS signaling seems to play a central role in the maintenance of the malignant phenotype by enhancing cancer cell survival and proliferation. This review documents the rapidly changing perspectives on the function of FAS in cancer biology. First, we describe molecular mechanism by which aberrant transduction cascades driven by oncogenic changes subvert the down-regulatory effects of dietary fatty acids, resulting in tumor-associated FAS insensitivity to nutritional signals. Second, we speculate von the putative function that hypoxia can play as the epigenetic factor that triggers and maintains FAS overexpression in cancer cells by inducing changes in gene expression and in metabolism for survival. Third, we explore the role that FAS exhibits in cancer evolution by specifically regulating cancer-related proteins such as Her-2/neu oncogene and estrogen receptor. Finally, we reveal previously unrecognized functions of FAS on the response of cancer cells to chemo-,endocrine-,and immuno therapies. These findings, all together, should ultimately enhance our understanding of how FAS-dependent endogenous fatty acid metabolism, once considered a minor anabolic-energy-storage pathway in normal cells, has become a jack-of-all-trades in cancer cells.

Publication Types:

* Review


PMID: 15577743 [PubMed - indexed for MEDLINE]

"FAS-dependent endogenous fatty acid metabolism, once considered a minor anabolic-energy-storage pathway in normal cells, has become a jack-of-all-trades in cancer cells".


More evidence as to the importance of fat mechanisms and cancer.

For me DHA EPA are the most likely areas to look at as they are essential to reproduction, have to be made in the body if not eaten, and we are eating less of them and our modern diet may be blocking the pathways to make them. Both are found in fish oil. Hereceptin, and tamoxifen both interact in this pathway and synergies suggest some chemos may too.

I wish they would do some large scale trials looking at outcomes based on fats content in tissues.

RB

ABSTRACT



1: Arch Immunol Ther Exp (Warsz). 2004 Nov-Dec;52(6):414-26. Related Articles, Links

Fatty acid synthase-catalyzed de novo fatty acid biosynthesis: from anabolic-energy-storage pathway in normal tissues to jack-of-all-trades in cancer cells.

Menendez JA, Lupu R.

Department of Medicine, Evanston Northwestern Healthcare Research Institute, Evanston, IL 60201, USA.

In 1994, Kuhajda and colleagues unambiguously identified the oncogenic antigen-519, a prognostic molecule found in breast cancer patients with markedly worsened prognosis, as fatty acid synthase (FAS),the key enzyme for the de novo fatty acid biosynthesis. It now appears that human carcinomas and their pre-neoplastic lesions constitutively over express FAS and undergo significant endogenous fatty acid biosynthesis. Moreover, FAS blockade specifically induces apoptotic cancer cell death and prolongs survival of cancer xenograft hosts. Therefore, FAS signaling seems to play a central role in the maintenance of the malignant phenotype by enhancing cancer cell survival and proliferation. This review documents the rapidly changing perspectives on the function of FAS in cancer biology. First, we describe molecular mechanism by which aberrant transduction cascades driven by oncogenic changes subvert the down-regulatory effects of dietary fatty acids, resulting in tumor-associated FAS insensitivity to nutritional signals. Second, we speculate von the putative function that hypoxia can play as the epigenetic factor that triggers and maintains FAS overexpression in cancer cells by inducing changes in gene expression and in metabolism for survival. Third, we explore the role that FAS exhibits in cancer evolution by specifically regulating cancer-related proteins such as Her-2/neu oncogene and estrogen receptor. Finally, we reveal previously unrecognized functions of FAS on the response of cancer cells to chemo-,endocrine-,and immuno therapies. These findings, all together, should ultimately enhance our understanding of how FAS-dependent endogenous fatty acid metabolism, once considered a minor anabolic-energy-storage pathway in normal cells, has become a jack-of-all-trades in cancer cells.

Publication Types:

* Review


PMID: 15577743 [PubMed - indexed for MEDLINE]

herceptain and arimidex
 

I am a strong triple positive (er, pr her2) started herceptain November 05 - while on tomaxifen - off tomaxifen in Dec. 05 began lupron shots and arimidex - nasty joint aches espceially when I wake up in the morning - fingers elbows, knees, hips and soles of my feet - it sucks - but what is the alternative ? Hoping it will get better when doen with herceptain in November - was recently put down to 1 every three weeks - symptoms a little better but.... only supplments are citri cal, multi, cq10 and folic acid and E.
I was told to be very careful of the supplments such as flaxseed oil b/c stringly er positive

Susanne

Re flax seed.

Please use the seach facility above and check out the posts on flax seed.

Here is one, and there are others. Try flax seed and one word flaxseed in the search engine above - click on search.


http://www.her2support.org/vbulletin...ight=flax+seed


And here is one on fats. The potentially eostrogenic components of flaxseed should not be confused with the compontents of oils DHA EPA etc. They are not the same.

Flaxseed is high in omega three, and I understand the oil contains no phyto - oestrogens.

There does seem to be confusion on the role of flax seed and flax oil.

You may wish to print out the trials and show them to your onc or discuss them with whoever talked to you about flaxseed.

If you can provide any definative answers please do come back.

RB

My initial diagnosis was Stage IV - mets to spine and liver - I take Femara and get avery 3 week infusions of Herceptin (I also get Zometa to protect my bones)

I was NED after 2 treatments

SADIE

Re fats - use the search facility on the bar above right and check out the posts on omega three six.

Flax oil is high in omega three.

There are not many substitutes for fish oil. There are some supplements made from algae. A google search using algae DHA and EPA should produce some suppliers.

RB

Saw this earlier - http://www.nelm.nhs.uk/Record%20View...aspx?id=565643 Link is a little short in detail, but more to be revealed at the appropriate conference.

Was on a combiation of herceptin and arimidex - herceptin year has now finished so its arimidex alone (didn't want Tamoxifen from what I read about it in HER2 disease, so had oophorectomy). Currently NED

I have had 12 Heceptins and this is my third day on Arimidex. When I think about it, I'm amazed that I am taking a daily pill to prevent cancer. No side effects from Arimidex yet. MJo

Thanks to all for the answers.
I am quite please by this short survey (hope more replies to come).
Even if this is not a double blind clinical trial statistical results, one can be optimistic since of 7 women taking Herceptin & one aromatase inhibitor (5 on Arimidex,one on Faslodex,one on Femara) none has reported resistance & 2 (ROZ & Lisa) said they had fast & very good response to this combo.(one with Arimidex the other with Femara). These two cases of quick & strong response must be added to that of Taffy who was the trigger to this survey.
Also impressive is the variety of stages in which the combo works: both early non metastatic & later metastatic settings.
Those who are taking supplements such as fish oil seem to be OK

Mjo is not include in these figures as she just started on Arimidex

The other good news is the phenominally opportune scoop by snoopy in finding today's press release on the results of the clinical trial in Europe of the combo.
http://www.nelm.nhs.uk/Record%20View...aspx?id=565643
Roche announces results claiming trastuzumab combination with anastrozole increases progression-free survival for patients with advanced breast cancer. (Extract)
The TAnDEM study, conducted by Roche is a randomised, Phase III trial, which evaluated trastuzumab in combination with anastozole versus anastrozole alone as first-line therapy (or second line hormonal therapy) in 208 postmenopausal women with advanced (metastatic), HER2-positive and hormone receptor-positive (ER-positive and/or PR-positive) breast cancer. Patients received anastrozole at a dose of 1 mg daily until progression. Trastuzumab was administered in 2 mg/kg weekly doses (after an initial loading dose of 4 mg/kg) until disease progression.

This is not comparing Herceptin+Arimidex to Herceptin alone but it at least demonstrates that there is no antagonism between Herceptin & Arimidex ( which may be the case between Herceptin & Tamoxifen).

The press release has no details. Full reporting awaits the sept 29-oct3 2006 ESMO conference in Turkey.

Herceptin + Arimidex
 

I was diagnosed in 4/2002 at the age of 42. Large ER+, PR-, HER2+++ tumor w/mets to skin of affected (L) breast.

3 rounds neo-adjuvant A/C
mets continued to grow

Immediate left modified radical mastectomy -
13/13 positive nodes
6 months of Taxotere with i.v. Decadron to inhibit extreme allergic response
5,000 rads of radiation
Oopherectomy in February of 2003
Begin taking Arimidex immediately thereafter

Diagnosed in 4/2005 with two small brain mets, otherwise NED
Gamma knife 5/2005
Began taking weekly Herceptin
Discussed with Oncologist the possibility of staying on Arimidex. He stated that one could argue the Arimidex had failed, due to the presence of two small brain mets. However, I could also argue that since Arimidex may not cross the blood brain barrier, it had been extremely effective in my body but only "failed" in the part of the body it could not adequately infiltrate. Oncologist suggested that studies had been conducted which had not specifically demonstrated increased effectiveness with the combination of Herceptin & Arimidex. Theoretically, one could hypothesise that Herceptin would block the HER2 pathways, and the A/I would block the estrogen pathway and would be a very powerful one-two punch. In small studies, however, there was only a small advantage to the combination.

I like any advantage, however small, and seized it. I have been on Arimidex + Herceptin since metastatic diagnosis and remain NED. Only one lesion is visible on MRI and continues to shrink with each and every MRI. Most likely is necrotic.

I am still trying to get into the U of W vaccine trial and continually seek any promising treatment I can find.

Mary-

You ask, what is our aim? I can answer in one word: It is victory, victory at all costs, victory in spite of all terror, victory, however long and hard the road may be; for without victory, there is no survival.

Winston Churchill

adding one more to the thread
 

I have been on Herceptin for almost 5 years weekly, It was given with Tamaxophin and then in my third year we added Lupron, until I had my ovaries removed a bit over a year ago. Now I take Aromasin along with my weekly Herceptin. Remain NED : )
Also take fish oil, flax seed oil, and coq10 vit e bcomplex calcium and vit c.
It is really interesting and exciting to see we seem to be on the same path even if we are from all over the world.
Hugs
Marily
Stage IV her2, er pr +++ mets to lymph, liver. lung , bone
r mast, 13 lymph AC/Tax Hercep
tamox-aromasin
ps seem to be getting back to Herceptin ok after my allergic response to it. Remain on weekly dose double diluted and given over 2 1/2 hours with benedry.. no adverse side effects and gradually decreasing benedryl by 1/2 than next week will have only 1/4. or 12.5mgm. Some cramping so restarted the quinine.

This article gives an idea how complex the whole oestrogen issue is.

It further underlines it is not just a question of oestrogen produced in the ovaries,

BUT as important of even more important the oestrogen produced with the cancer cells and their supporting surrounds.

I have only skimmed bits of it. It will take a while to get to even begin to get to grips with but immediately rasied questions as to the balance of impacts of treatment protocols and whether it would be sufficent to halt local production whilst leaving wider body production alone (Implications for ovarian removal etc. for those to who longer term fertility is important etc) In this case I simply raise the questions as I have not looked sufficiently at the subject subject to do more than have questions.


RB



Sex steroid-producing enzymes in human breast cancer

http://erc.endocrinology-journals.or.../full/12/4/701

ABSTRACT

Biologically active hormones are produced and secreted from the endocrine organs, transported through the circulation, and act on their target tissues where their specific receptors are expressed (Fig. 1AGo). This system is known as the endocrine system, and biological features of hormone-dependent target tissues are generally considered to be influenced by the plasma concentration of the biologically active hormones. In addition, hormones can also act in the same cell (autocrine) (Fig. 1BGo) or neighboring cells (paracrine) (Fig. 1CGo) without release into the circulation. A large proportion of androgens in men (approximately 50%) and estrogens in women (approximately 75% before the menopause, and close to 100% after the menopause) are synthesized in peripheral hormone-target tissues from abundantly present circulating precursor steroids (Labrie et al. 2003), where the enzymes involved in the formation of androgens and estrogens are expressed (Fig. 1DGo). These locally produced bioactive androgens and/or estrogens exert their action in the cells where synthesis occurs without release into the extracellular space. This phenomenon is different from the autocrine, paracrine and classical endocrine action, and is called ‘intracrine’. In classical endocrine systems, only a small amount of hormone is generally utilized in the target tissues, and thereafter the great majority is metabolized or converted to inactive forms. On the other hand, an intracrine system requires minimal amounts of biologically active hormones to exert their maximum effects. Therefore, intracrine is an efficient mode of hormone action and plays important roles especially in the development of hormone-dependent neoplasms. It is also important to note that, in an intracrine system, serum concentrations of hormones do not necessarily reflect the local hormonal activity in the target tissues.



View larger version (42K):
[in this window]
[in a new window]
Figure 1 Summary of endocrine (A), autocrine (B), paracrine (C), and intracrine (D) actions. {701fig1}, inactive hormone; {701fig2}, bioactive hormone; {701fig3}, receptor; {701fig4}, promoter region of the target gene.


Sex steroids, such as estrogens and androgens, play important roles in various target tissues including reproductive organs. A majority of breast carcinoma tissues express estrogen (ER) and androgen (AR) receptors, and estrogens greatly contribute to the growth of breast cancers. Breast carcinoma tissues have been demonstrated to process intracrine activity. Locally produced biologically active estrogens act in breast carcinoma tissues. This mechanism has been considered to play a pivotal role in the proliferation of breast carcinoma cells. The blockade of this pathway potentially reduces cell proliferation of breast tumors, and it is very important to obtain a better understanding of sex steroid-related enzymes in breast carcinoma as potential therapeutic targets of endocrine therapy. Therefore, in this review we summarize the results of recent studies on the expression and regulation of the enzymes related to intratumoral production of sex steroids in human breast carcinoma tissues, and discuss the potential biological and/or clinical significance of intratumoral production of sex steroids in these carcinomas.

PTEN as a factor of fast response to Herceptin
 

Robin has posted a very interesting article at http://www.her2support.org/vbulletin/showthread.php?t=24319

In it the researchers describe,among other things, two of the modes of action of Herceptin.
The attaching of Herceptin to the HER protein on the surface of cancer cells & the destruction of this protein is a relatively slow process while the activation of the PTEN (which control cell division) starts within 10 minutes. PTEN also appears necessary for Herceptin to be effective in any case.
So if a patient starts with a high level of PTEN it no only predicts that she likely will respond to Herceptin but also that she may respond very quickly.
This adds an other possible factor which may explain the fast response of some posters in this thread.

Hi,

I finished Herceptin this past Tuesday. I had been on it for one year, weekly infusions. I started Herceptin and Arimidex at the same time. I have recently changed to Femara hoping it will help my joint pain. I will post to report if I am feeling better after the Herceptin soon. It may be the Arimidex/Femara causing all the side effects. We will see.

Susan

Sadie,

In any case, you shouldn't be on antioxidants during rads. You would be aiding and abetting the enemy cancer cells. After rads, hit the old search key here. Search for Gina Popp's posts as her supplement advice seems reasonable. Good Luck, BB

Bev,
Thanks for THAT info. I had no idea!
I have 4 more rad days to go!

Thanks R.B. for your info too. I'll be checking it out so I can start as soon as I finish with my rad tx
Sadie

add to the list
 

Also take Arimidex....started Jan. 05 and now Herceptin q 3 weeks ...started Feb. 06.
Do have joint pain when I first get up but after a few minutes it is fine. Had the joint soreness when on Arimidex along and did not notice any difference when I started the Herceptin a year later.

Have added omega and CQ 10 to the supplements after reading all the info gathered here.
Hugs, Bonnie

Herceptin and aromatase inhibitors
 

Not on the Herceptin, but taking Arimidex. Am taking a break from it though to see if it is responsible for my moodiness. Am estrogen+ and Her2+ and my onc has decided to treat the estrogen + because I am node negative, but will not treat the Her2+ because I am node negative. Go figure! I am amplified 7.2 on Fish. I am getting a second opinion tomorrow. Why would you treat one and not the other?
Ruth

I am not sure but it may not have been approved for those who are not yet stage II who don't have any positive nodes?

kat in the delta
 

Why fish oil ??? doesnt it make you gain wt ??kat in the delta

kat in the delta
 

I go to my Onc. tomorrow to see the results of my hormone levels---which I am sure I will be post menop. I had my uterus removed 6 yrs ago, but kept my ovaries. He mentioned either Arimidex or Femara, which my sister took and it make her jts/ ache/ Her Onc changed her to Aromasin and she says it is better altho she liked tamoxifen the best---but was on it for 5 yrs. She was not her2. like me. kat
Is there anything I need to know or ask him about before my visit ???? I just finished my only year on herceptin, but see another study of 2 yrs. What is the difference between the Bayer Serum test and the serum blood test/?, elissa(sp?) blood test etc,,,,,,kat

kat in the delta
 

1 thing my surgeon said last week was that: now they are looking at only giving HERCEPTIN to her2+ people, and not any other chemo. my 2cents, kat in the delta

fcrcm
 

Well, sorry to be on the negative side. I have been on Herceptin, Zeloda and Arimadex since Nov. 2005 for bone, lymph and liver mets. My June scans showed a new bone mets in hip. I'm trying to figure out what to do next, or if this is to be expected.

Would love to hear from any others with experiences like mine.

fcrcm

Kaye & Ruthie & Kat,
Yes they do give Herceptin to those with neg nodes.
I am node negative and I was given Adriamyacin x4, then Taxol w/Herceptin x 12, then started Herceptin alone to go thru Feb 07. Also had 30 days rads. Then started Arimidex for next 5 years.
I heard about the Herceptin-only treatment also. (read it on-line at either ACS or John Hopkins site).
I also heard that they are considering giving Herceptin for only 9 weeks instead of 1 yr.
I've read on this site, that many women took Herceptin for 2 years. I don't know what the dr uses as a deciding factor for how long to give it to you.
Sadie

kat in the delta
 

Sadie et al...,
I have been thru A/C,rad,masc,1yr of herceptin. Now, since my cancer has not spread beyond the Positive lymph nodes, my Onc, wants to give me Arimidex.--[I was slightly er+],[pr-]
HOW HAS ARIMIDEX affected YOU ???
My ONC. wants to also give me a dose of Zometa-as my bone density was not so good.
I know it was the first for postmenapausal women,which I am. (52 &was checked)
There is also Femara, which made my sister's bones & jts. ache, so her Onc. changed her to Aromasin.(She was NOT her2++,luckily).
ANYONE ELSE ON ARIMIDEX ??? HOW HAS IT AFFECTED YOU???

Kat,
I have been on Arimidex for about 20 days now. I've noticed in the past 2 weeks, I have been a little crabby. But that could also be from the heat wave we had last week, plus I have been much busier every weekend this month (fun things,tho) and there is alittle more stress at work right now (end of fiscal year).
So it's hard to say whether or not the moodiness comes from the Arimidex or circumstances. Not to forget, my 1 yr anniv is coming up for when I had my physical & mammogram.
I just noticed today, that I have some peach fuzz on the cheeks (the whole area in front of the ears). I am assuming that is from the Arimidex because it is a hormone blocker, but I can't say for sure. Other than that, I don't think I am having any side effects from it. If my onc asks, I would stay on it. I am also 52 post menopause.

kat in the delta
 

kat in the delta,
I am 52, also and did bloodwork that showed I was postmenapausal.
Does anyone know if Arimidex makes you gain weight ??

My sister gained weight on Tamoxifen and is now on Aromasin as Femara made her ache.
kat in the delta

kat in the delta
 

Sorry to hear of your new site. Zometa is given for bone cancer and also for osteoporosis to stop bone loss.
I am almost osteoporisis and my Onc gave my One 15min IV of Zometa while on Taxol and herceptin.
Now I will be on Arimidex, which causes more bone loss.so my Onc. is going to infuse me with Zometa again soon.
So sorry you have it in your hip--I know that is painful.
Be careful, too, don't fall....I might even get a walker if I were you.........keep me informed......my cousin has it in his vertebrae, hip, legs, lungs.......he is cont..rad and chemo. He first had surgery to put in a plate to support his leg to keep it from breaking on its own. He is a fighter.......was on a walker but finally has gotten a wheelchair, thank God--I worry about him-------he tries to do TOO MUCH--
You need to rest daily.......kat

Herceptin and Femara
 

I am stage 4. Diagnosed May 2000. Stage 3b. Her2+++. Single brain mets three times. Now on Herceptin and Femara and have been NED for 2 years.