DESPERATELY need advice

[mom22girlz]

Went to the oncologist tonight. I am more confused than ever. Since I am
stage 1, he leans toward only tamoxofen. He believes the side effects of chemo are greater than the benefit gained by a stage 1 person. But, he would give me chemo if I wanted. Said herceptin is only given in conjuction with chemo so I would not need that even tho I am her+. Asked about the oncotype test and he didn't feel the information was anymore than what we already know. Said if I got a second opinion he feels it would be 99% in favor of chemo, but he has been around a long time (will retire in August) and he knows it isn't always the best choice. I don't know what to think. I feel worse rather than better. will call for a second opinion tomorrow, but...... Please offer any advice. I need it so. I am 47 years old, premenopausal, pr+ er+ her+++ stage 1. thanks. susan

[AlaskaAngel]

Susan,

It takes a while to work your way through some of this stuff because it IS complicated, but see if you can get through the guidelines for breast cancer care. Come back here if you have trouble and ask any questions. It was very hard for me to decide to do chemo and I wish someone would have told me about the guidelines when I was trying to decide. Let me know if this doesn't work.

http://www.nccn.org/patients/patient_gls/_english/_breast/3_work-up.asp

AlaskaAngel

P.S. look under the "decision tree" for stage I, II, III.

[Sherryg683]

I would definatley get a second opinion. Her2+ is a more agressive cancer and from everything I've read, it should be treated more agressively. You are still young and have a long time to live, I wouldn't take a chance on it...sherryg683

[Bev]

Hi, I'm stage 2, triple pos, node neg and 47 and finishing rads. I did chemo, and am not an expert. From your stage and tumor size, no chemo may be appropriate. I did get the impression from the onc, radiologist and surgeon that being relatively young and premenopausal would be a reason to treat the bc more aggressively as it is more likely to come back at you or have more years for it to do so. I guess they also figure your risk for side effects will be lower at your age. Who knows? Your path report should also have a grade, (one scale is 1 to 9)to tell you how the cells look. So in any case get the 2nd opinion and perhaps the oncotype test. You have to make the decisions with the facts you have today and go with it. I'm sorry you're in the gray zone as the mental stress must be much higher than those of us whose path made the decision easier. BB

[karenann]

Susan,

What is the size and grade of your tumor? I am a stage 1, node negative, grade 3, er/pr+, 1.3cm tumor and Her2+++. I did dose dense, AC & T chemo, rads, one year of Herceptin and Aromasin. I would get a 2nd opinion.

Karen

[jsattaw]

Hi Susan --

I agree with the others but at some point you must be in charge and confident in your medical team. As someone mentioned on another thread, our physicians "work" for us and we pay their salary. Once you feel confident in how aggressive you want to be with your treatment, you just need to find a doctor who will support your opinion and reaffirm your decision.

I did a lot of research and wanted to be the most aggressive in my treatment for a recurrence after 7 years -- I did a mast with reconstruction, 4 treatments of Taxol, a complete hysterectomy, Herceptin for 1-year, and am also on Arimedex. After my initial diagnosis for Stage 1 - IDC, I did a lumpectomy with radiation (1998) but didn't know I was Her2+.

Try to ask yourself what course of treatment will provide you with the highest level of peace of mind and enable you to move beyond treatment with less concern about recurrence. Unfortunately, this is an inexact science and doctors like us, have their own opinions as to what works. Also, each of us are individuals and our bodies and cancers are different. So...no one has a crystal ball.

Good luck with your decision -- thanks for allowing us to provide our opinions.

Jill

[Unregistered]

I have NOT been following your posts and am not a sufferer, but have done quite a lot of very amateur reading on the general subject, and these are things that have struck me.

I must emphasise that every one is different and this disease appears to be more and more a disease that is subtly different in every patient.

The following have struck me in my wanders;

1. Cancers take up to ten years to develop, which suggests on the AVERAGE you do not need to panic, and have a sensible time frame in which to make treatment decisions without compomising you position to any significant extent.

2. Resistance CAN develop to chemo treatments which has two implications - the cell has mutated to avoid the impact of the treatment - and that is one more treatment off the protection list.

3. If you can afford them/ have access to them diagnostic tools are improving MRI CAT etc.

4. Various tumour markers are available to try and give you an idea what is happening in your body.

5. Chemo can have implications the immune system etc.

6. Chemo has been shown to have very positive results.

7. Local and bilateral recorrence can be treated. Spread to the rest of the body is the real problem. Cancer that has spread may not be the same as the original.

8. Statisitics are hard to find an pin down, but it is important to kep an eye on survival, as several treatments help with local spread but have not been shown to make a huge difference to survival.

9. It is reported that we all have potentially cancerous cells in our body - it is a question of the bodies ability to deal with them.

10 Check out the "life extension" site where they have some interesting thoughts on steps to take as part of a decision process.

11. Life style factors can influence risk. My personal crusade is to get people to balance their omega threes and sixes, and take some fish oil for the DHA EPA as the body is not very good at it. Women may need it more than men. If nothing else it is established and accepted that it will help with cardiovascular health, which is pretty fundamantal, and because so much of the bodies mechano appears to be similar bits used in different ways.

The decision must be yours. It must be hugely difficult. As an outsider it seems to me that you need to inform yourself as much as you can before taking the decsions you take to try and minimise the what if's and if only's afterwards.

There is lots of information on this site. Talk to your adviser on the impact of a short delay to allow you time to sort things out. Try checking out soms books in the library.

Re tamoxifen there is suggestion that it may be contraindicative for those that express high Cyclin D1. There are posts on this site you may want to check out and show to your adviser referring to trials. (use search engine)

It does take a little while and quite a lot of reading to begin to get a wider perspective on which a decision might be based.

I would reiterate that these are only general observations that have particularly struck me and no more.

So difficult for you


RB

[tousled1]

You must take charge of your treatment by being well informed and you couldn't have come to a better place. My personal opinion on your situation is that I would seek a second opinion. You stated that your oncologist is retiring in August so I assume that he is older. There have been and still are many strides being made in treating breast cancer. I would want a younger oncologist who is well educated on current treatments and fully aware of any clinical trails that are taking place. Good luck to you.

[Unregistered]

Susan,

My understanding is that Herceptin is now recommended for Stage 1 women. I am taking it and my diagnosis is similar to yours, though I'm not er/pr +.
I'm Stage 1, multifocal (1.05 cm), Grade 3, her2+, no vascular invasion, no lymph nodes, premenopausal.

I did 4 doses of AC, but not the Taxol. My onc. said the Taxol was one thing I could skip since I was early stage.

I would definitely get a 2nd opinion.

take care, Anna

[Unregistered]

The whole idea behind adjuvant treatment is to prevent a relapse and cancer from returning with a vengence. That's right should your cancer return it will be harder to treat and less responsive to Herceptin and chemotherapy than if you treated now early stage. If you don't believe me do a little research yourself. I would definately get a second opinoin from an aggressive cancer center such as the Mayo Clinic Rochester in MN or even Memorial Sloan Kettering in NY. Personally, I find older doctors much less aggressive. Perhaps that's because they lost their zest or they just know they won't be around long enough to face their mistakes, undertreatment failures etc.

[Lani]

and encourage him to read the FULL article -- which states that there is even one study showing that tamoxifen alone may ENCOURAGE growth of her2+ tumors rather than inhibit their growth or just be ineffective! Here is the abstract:

1: Ann Oncol. 2006 Feb 23; [Epub ahead of print] Related Articles, Links

Benefit from adjuvant tamoxifen therapy in primary breast cancer patients according oestrogen receptor, progesterone receptor, EGF receptor and HER2 status.

Dowsett M, Houghton J, Iden C, Salter J, Farndon J, A'hern R, Sainsbury R, Baum M.

Academic Department of Biochemistry, The Royal Marsden NHS Trust, London, UK.

BACKGROUND: Most women with oestrogen receptor (ER) positive primary breast cancer receive adjuvant tamoxifen after surgery. The measurement of tumour biomarkers should allow better selection of patients for such treatment or for therapies such as aromatase inhibitors. PATIENTS AND METHODS: Histopathological blocks of primary breast cancer patients who had been randomized to receive 2-years tamoxifen or no adjuvant therapy in two mature randomised clinical trials were retrieved. Immunohistochemical staining for ER, progesterone receptor (PgR), HER2 and epidermal growth factor receptor (EGFR) was undertaken. The primary endpoint was relapse free survival. RESULTS: 813 patients were included in the study. Benefit from tamoxifen was seen in ER-positive patients [Relative risk (rr) 0.77, ci 0.63 - 0.93]. ER-negative patients also showed a strong trend to benefit from tamoxifen (rr 0.73, ci 0.52-1.02) which was largely confined to the PgR-positive group. Amongst the ER-positive group, PgR-positive and PgR-negative patients showed similar benefit (rr 0.81; ci 0.65-1.02 and 0.70; ci 0.49-0.99, respectively). Patients positive for HER2 did not benefit significantly (rr 1.14; ci 0.75-1.73) but this group was small. CONCLUSIONS: Measurement of PgR status in ER-negative patients defines a group of patients that benefit from tamoxifen but would be excluded from tamoxifen therapy on the basis of ER status alone. The data are consistent with HER2 positive tumours being resistant to tamoxifen.

PMID: 16497822 [PubMed - as supplied by publisher]



Noone knows if Herceptin REALLY negates the resistance to tamoxifen therapy
or even if herceptin negates the resistance to aromatase inhibitor therapy (I have a fresh off-the-press article on her2neu resistance to ai treatment as well) Neither does anyone know if fulvestrant is the answer (its effect seems to depend on the ambient estradiol concentration)

Clinical trials to answer these questions have just begun and no results are available as yet.

There are papers out of Yale (I posted them earlier) on adding Herceptin to tamoxifen (preclinical studies done in a petri dish and/or mice, not in people) and an early study by Matthew Ellis on letrozole with Herceptin, I believe.

I believe the doctor you were consulting used the old ADJUVANT online computer program to estimate improvement of odds based on OLD PROGRAM which does not include her2 status. Those who are her2+ have a much higher rate of recurrence. They are relatively chemo- and hormonal-therapy resistant.

But the hormonally positive her2neu tumors are the ones they understand the least about as the 2 her2neu cell lines they study in most research labs are both hormonal receptor negative.

The oncoDx test gives very little additional information according to Dr. Dennis Slamon than ER, PR, her2 by FISH, and Ki67( a measurement of proliferation) If your insurance pays for it, you may consider it, of course

If you have a high Ki67 your tumor is multiplying rapidly and chemo MAY be more likely to help. At the San Antonio Breast Cancer Conference, the feeling was that all her2 positive invasive breast cancer (ie, not DCIS) should be treated with herceptin but Dr. Slamon suggested that to decrease cardiotoxicity the tumor's level of topoII should be tested, as only topoII positive tumors should require an anthracycline and other tumors could be spared the increased cardiotoxicity of an anthracycline. This is still cutting-edge and not generally readily available. His recommendation going forward was that
If someone offers you chemo and herceptin,
to see if it is worth risking your cardiac function by combining an anthracyline (like doxyrubicin) with herceptin have Topo II--which is available from Targeted Molecular Diagnostics (see Robin P's postings)

There is to date no foolproof way to determine if chemo is necessary for
your tumor or for anyone's individual tumor. Hopefully with time microgene arrays will be able to determine not only if chemo will be helpful, but WHICH chemo will be helpful.

Size used to be considered one of the most important prognosticators with respect to breast cancer. The tumor's molecular makeup is superceding that. There are several people posting at this site who started with microinvasion with DCIS only and then developed distant metastases--so I do not know if there is any "size" of her2neu that needs only surgery and radiation.

I gleaned the following not too nice statistics from a talk by Dr. Dennis Slamon:
Her2 positive tumors which receive no systemic treatment are more than twice as likely to recur than her2negative tumors and, once they recur, usually kill patients within one year vs within two years for her2negative

The good news is that those statistics have been superceded by the utilization of Herceptin which has cut the rate of recurrence in half (WHEN utilized WITH chemo) and there are a host of members of this board who can attest to 6,7, and 8 years survivals beyond metastasis!!

Does your oncologist treat more than breast cancer? It is hard to keep up with all the new findings, even for those who specialize in it. Having attended the San Antonio meeting and four other breast cancer meetings this year I saw few old faces (except some illustrious lecturers and they were not near retirement age) among the audience. Cutting-edge knowledge is discussed at these meetings.

Perhaps if you say where you live, members of the board could suggest oncologists for a second opinion or being presented at a tumor board (at specialized institutions oncologists, surgeons, radiation therapists, radiologists, nuclear medicine specialists and pathologists ALL GET TOGETHER and discuss a patient's case especially if the treatment is controversial. As noone knows the best way to treat hormone receptor positive her2neu + early breast cancer perhaps your case might interest them.

Inform yourself! Ask questions! Only you can DO THE HOMEWORK(noone cares about it as much as you do) and only you can decide how to weight the risks and benefits of different treatment options in YOUR particular case

Good luck!

[Cathya]

Strange, unusual things can happen with Her2+ cancers. I had negative nodes but because my tumor was large (3 cm) I was originally staged as 2a. My doctor originally recommended radiation only to follow my lumpectomy as, according to the statistics, there was very limited benefit to me with chemotheraphy. Later, during the same visit upon physical exam he found a tumor in my supraclavicular node which everyone else had missed. This "presentation" is very unusual but it does happen. Her2 likes to travel. A second opinion can't hurt.

All the best,

Cathya

[Lani]

unfortunately this is a clinical trial and it is out of Belgian, but the discussion of the trial should provide food for thought for your oncologist regarding what MAY BECOME state-of-the art--again it is a risk vs benefit analysis:

Related Links


Learning About Clinical Trials

Clinical Trials: Questions and Answers

Questions to Ask Your Doctor

Drug Information from MedlinePlus



The Trial of Principle (TOP Trial)
Basic Trial Information
Trial Description
Summary
Further Trial Information
Eligibility Criteria
Trial Contact Information

Basic Trial Information

Phase
Type
Status
Age
Sponsor
Protocol IDs



Phase II


Treatment


Active


18 to 70


Other


TOP Trial
NCT00162812




Trial Description


Summary

PROSPECTIVE EVALUATION OF TOPOISOMERASE II ALPHA GENE AMPLIFICATION AND PROTEIN OVEREXPRESSION AS MARKERS PREDICTING THE EFFICACY OF EPIRUBICIN IN THE PRIMARY TREATMENT OF BREAST CANCER PATIENTS.

Further Study Information

Clinical evaluation of topo II a as a predictive marker: Preliminary results from a clinical study suggest that complete remission after treatment with anthracyclines for advanced breast cancer is observed only in case of topo II a gene amplification (7 complete remissions, all in patients with topo II a gene amplified tumors, no complete remissions in patients with a normal or deleted topo II a gene).

Moreover, our group has analyzed the predictive value of topo II a in a population of node-positive breast cancer patients randomly treated either with anthracyclines or with CMF (Belgian cooperative trial). In a first study, topo II a was evaluated by immunohistochemistry, which allows the detection of topo II a protein expression. The results of this study suggested that patients deriving the highest benefit from anthracyclines were those in which topo II a protein is immunostained in more than 10% of tumor cells. The main findings of this study should be seen as hypothesis-generating because of the limited number of patients evaluated (about fifty in each study arm) and because topo II a protein levels depend on gene amplification as well as on tumor proliferation rate. Therefore, topo II a protein expression does not necessarily reflect topo II a gene status.

The second study run by our group was based on the same series of patients evaluated in the first study, but, this time, both HER-2 and topo II a genes were evaluated by fluorescence in-situ hybridization (FISH), which allows the detection of gene aberrations. The main findings of the second study were quite consistent with the pre-clinical data suggesting that only HER-2 amplified/topo II a amplified tumours show great sensitivity to anthracyclines while the efficacy of these same agents in HER-2 amplified/topo II a non-amplified tumors is comparable to the efficacy of other drugs or regimens like CMF.

Nevertheless, although the results reported in this study bring some additional support to the hypothesis of topo II a as a marker predicting the efficacy of anthracyclines, no definitive conclusions can be drawn because of the fairly limited number of patients evaluated, and the retrospective nature of the analyses.

The present study protocol: Supported by "in-vitro" and preliminary "in-vivo" data, briefly summarized above, this study is designed to test prospectively the value of topo II alpha gene amplification and protein overexpression in predicting the efficacy of anthracyclines. To our knowledge this is the only prospective trial worldwide which is attempting to prospectively clarify the predictive value of this interesting biological marker. This study could have important practical implications in the daily clinical management of early breast cancer patients because, if the trial confirms that topo II a gene amplification and/or protein overexpression are associated with high efficacy of anthracyclines, while topo II a normal/deleted gene and low protein content are associated with modest efficacy, an important step forward in the direction of anthracycline "tailoring" would be accomplished.

The practical advantage of this approach would be to use anthracyclines primarily in patients who are supposed to derive the largest benefit, thus sparing the long-term anthracycline-related toxicity (i.e. secondary acute myeloid leukemia, cardiac dysfunction, and amenorrhea/sterility in case of fertile women) to those patients for whom no significant gain in antitumor activity is anticipated.

To reach this ambitious aim, early breast cancer patients with tumors of at least 2 cm (defined by breast ultrasound) will be evaluated for topo II a gene and protein expression. For this purpose, a pre-treatment biopsy (tru-cut) will be performed and topo II a gene will be evaluated on fixed samples by FISH. The use of a triple probe will allow the concomitant evaluation of the HER-2 gene status. Topo II a protein will be evaluated by immunohistochemistry (IHC). Afterwards, all patients, independently of the topo II a gene and protein status, will be treated with single-agent epirubicin Eligibility criteria will allow the participation of patients for whom the use of an anthracycline-based adjuvant therapy would have been most probably proposed after breast cancer surgery, mainly because of estrogen receptor (ER) negativity. Therefore, no overtreatment with anthracyclines will occur in this group of patients. Pathological complete response (pCR) to epirubicin will be correlated with the topo II a gene and protein status. The study has two biological hypotheses, one for the subgroup of patients with ER negative/HER-2 amplified tumors, the other one for the subgroup of patients with ER negative/HER-2 non amplified tumors.

1 st hypothesis: Patients with ER negative/HER-2 amplified tumors: In this subgroup of patients, topo II a gene will be amplified in about 40% of cases. We hypothesize that in topo II a amplified tumors a three-fold increase in pCR rate will be observed, as opposed to the pCR rate in tumors with topo II a normal or deleted gene.

2 nd hypothesis : Patients with ER negative/HER-2 non amplified tumors: In this subset of patients, almost no topo II a gene aberrations will be found based on previous data discussed above. However, recent data reported by C. Sotiriou et al using cDNA microarrays, suggest that in this subset of ER-negative HER-2 negative tumors, also defined as the basal-like subset, two distinct subgroups can be identified (i.e. basal-like 1 and 2). While basal-like 1 tumors show a high proliferation rate and high levels of topo II a RNA, basal-like 2 tumors have a moderate-low proliferation rate and normal levels of topo II a RNA. We hypothesize that the topo II a RNA overexpression in basal-like 1 tumors is not related to topo II a gene amplification because no concomitant HER-2 gene amplification is reported in this subset of tumors. The second study hypothesis is that in ER negative/HER-2 non amplified tumors with topo II a protein overexpression, a 2.5 fold increase in pCR rate will be observed, as opposed to the pCR rate in tumors with low topo II a protein content.

A tumor sample drawn at the time of pre-treatment biopsy will be frozen and used to perform oligonucleotide based microarrays (Affymetrix). This technique allows the evaluation of thousands of genes and ultimately provides us with the tumor genetic profile. Homogeneous genetic profiles (genetic clusters) that might be identified, will be correlated with the efficacy of single-agent epirubicin. This correlation will allow us to address the secondary end-point of this study, which is the identification of other genes or eventually a genetic profile playing a role in the determination of sensitivity to anthracyclines. Among the genes that could interfere with sensitivity to anthracyclines, p-53 seems to deserve special attention. Indeed, "in-vitro" data suggest that at least some p-53 mutated tumors are poorly sensitive to anthracyclines, primarily because anthracycline-induced apoptosis is prevented. Interestingly, p-53 mutated tumors display frequently HER-2 gene amplification and therefore topo II a gene amplification (23). Accordingly, p-53 mutations could hamper response to anthracyclines even in tumors carrying topo II a gene amplification. This hypothesis will also be explored in the present study, because p-53 mutations will be evaluated by DNA sequencing, and the efficacy of epirubicin in topo II a amplified and non-amplified tumors will be correlated with p-53 status.

[Unregistered]

Informative and considered posts again Lani. Have a gold star.

RB

[Roz]

It is very hard trying to decide about treatment. however, i would like you to consider the options of chemo-non-chemo overall in the process of your life. chemo will lay you down for a period, and you will recover. You will be able to put this all behind you (all things being equal) and as you progress through your recovery and from time to time panic about a recurrence, you will be able to say to youself -- I DID THE BEST I COULD POSSIBLY DO TO SURVIVE- no more, no less.

[LANI]

an article referring to Dr Slamon's talk at San Antonio regarding the her2neu
TopoIIa group of patients as the one's Dr. Slamon would like in the future to select out to give anthracyclines too (he thinks he can spare the rest, avoiding cardiotoxicity associated with combining Herceptin with anthracyclines)

Anthracyclines are drugs such as epirubicin, doxyrubicin, etc.

HERE IT IS:
Survival Benefit in Early Stage Breast Cancer of Herceptin Plus a Chemotherapy Regimen Lacking Adriamycin

View Article Vol: 5 | Issue: 1 | January 2006 | News

News:


Study is the Fourth to Show a Significantly Reduced Risk of Disease Recurrence

Pairing the targeted therapy Herceptin with chemotherapy in patients with early stage breast cancer significantly increases disease-free survival time in women who test positive for a genetic mutation that results in a particularly aggressive form of the disease, according to a large, international study.

The study also tested Herceptin with a chemotherapy combination that eliminated Adriamycin, an anthracycline commonly used to treat breast cancer but a drug that, when used with Herceptin, can result in heart damage. That regimen also significantly improves survival.

Conducted by the Breast Cancer International Research Group (BCIRG), this study is the fourth large clinical trial to show that Herceptin plus chemotherapy significantly reduces risk of disease recurrence in early breast cancer. Results were presented Thursday at the San Antonio Breast Cancer Symposium by Dr. Dennis Slamon, co-chairman of BCIRG, director of Clinical/Translational Research at UCLA's Jonsson Cancer Center and the scientist whose laboratory and clinical research laid the groundwork for the development of Herceptin.

"The chemotherapy combinations we tested with Herceptin proved to be superior to the best available standard therapy for early breast cancer," said Slamon, principal investigator for the BCIRG study. "This further illustrates the promise of targeted therapies and moves us closer to our goal of minimizing the toxicity of therapy while maximizing efficacy."

Herceptin is effective in women with HER-2 positive breast cancer, about one in four diagnosed with the disease every year. HER-2 positive breast cancer patients have a particularly aggressive form of the disease, a poorer prognosis and shorter survival times, said Slamon, who discovered the link between HER-2 positivity and aggressive breast cancer in 1987.

The study enrolled 3,222 women from all over the world with early stage HER-2 positive breast cancer between March 2001 and February 2004. Patients received one of three regimens:

The standard therapy of Adriamycin and Carboplatin followed by Taxotere (ACT).

An experimental regimen of Adriamycin and Carboplatin followed by Taxotere and one year of Herceptin (ACTH).

An experimental regimen of Taxotere and Carboplatin with one year of Herceptin (TCH).

Reduction in risk of disease recurrence, the study's primary endpoint, was 51 percent in the ACTH study arm and 39 percent in the TCH arm.

"This is very promising news for the 250,000 women worldwide, including 50,000 in the United States, who will be diagnosed every year with this aggressive breast cancer," Slamon said.

The BCIRG study also resulted in two other important findings. Researchers knew that giving Herceptin with Adriamycin resulted in heart damage in some patients, the most severe of which was congestive heart failure. It was theorized, however, that this damage was not long lasting. But the BCIRG study showed the cardiac toxicity was significant and still persisted for more than 18 months at the date of the last follow up, Slamon said. This is vital information for doctors and patients to have when deciding which treatment regimen to use.

Of the 3,222 patients in the study, 306 experienced a greater than 10 percent loss of heart function. Of those, 91 patients (9 percent) were enrolled in the ACT study arm; 82 patients (8 percent) were in the TCH arm; and 180 patients (17.3 percent) were in the ACTH arm, which paired Adriamycin with Herceptin.

"We've always known that the major safety problem with Herceptin has been cardiac toxicity when it is used with Adriamycin," Slamon said. "When breast cancer patients lose their hair, it grows back. When we suppress their bone marrow, that comes back, too. Heart failure, however, is a much larger problem, especially if it does not improve over time."

The good news, Slamon said, is that Herceptin given with the chemotherapy combination that eliminates Adriamycin is still significantly superior to the best available chemotherapy alone, reducing risk of relapse by 39 percent. That gives physicians and patients worried about heart damage an additional option.

The study's other important finding is that a subset of HER-2 positive patients - about 35 percent - also have amplification of a gene called topo II, which makes them more likely to respond to Adriamycin. As Herceptin targets HER-2, Adriamycin targets topo II. Patients who test positive for amplification of both HER-2 and topo II might opt for the drug regimen with Adriamycin, risking heart damage in exchange for a better response to therapy.

Slamon said a test that indicates both HER-2 and topo II amplification is being developed so doctors will better be able to tell which patients should be on which drug regimen.

"Women will have the information they need to decide if the risk is worth the benefit," Slamon said.

At UCLA's Jonsson Cancer Center, doctors are testing Herceptin in combination with other targeted therapies such as the angiogenesis inhibitor Avastin. That, Slamon said, may be the future of breast cancer therapy - the elimination of chemotherapy.

"In the future, we're likely to come up with therapies that are very much improved over what we have now and offer maximum efficacy with little or no toxicity," Slamon said.

UCLA's Jonsson Comprehensive Cancer Center comprises more than 240 researchers and clinicians engaged in research, prevention, detection, control, treatment and education. One of the nation's largest comprehensive cancer centers, the Jonsson center is dedicated to promoting research and translating the results into leading-edge clinical studies. In July 2005, the Jonsson Cancer Center was named the best cancer center in the western United States by U.S. News & World Report, a ranking it has held for six consecutive years.

For more information on the Jonsson Cancer Center, visit our web site at www.cancer.mednet.ucla.edu

Kim Irwin

Director, Media Relations

UCLA's Jonsson Cancer Center

(310) 206-2805








Good luck!

[Unregistered]

Nice research presented Lani...ask for the TOPOII test to determine if AC therapy would be indicated. Should you test negative for TOPOII, perhaps you may consider the less toxic chemotherapy,CMF which may be indicated with your relatively low risk of relapse. And let me just say, CMF has proven to decrease her2 bc relapse, albeit somewhat less than AC. See for yourself, google the research paper from Edith Perez for confirmation of this if you like.

Additionally, perhaps you would consider the 9 week regimen of Herceptin which had no cardiac risks in three year follow-up. I know that a clinic in FL is offering this option for very early stage her2+ bc and for late adjuvant Herceptin. Nine weeks may be adequate for those in the gray zone where the relative benefits of herceptin adjuvant therapy is unknown and the side effects of therapy less. By the way, I had very early stage her2+ breast cancer too and took CMF and tried the late adjuvant 9 week Herceptin Regimen.

[Brian]

Dear Susan:

My wife, Lisa, has been battling this disease for 14 years now. We attacked the disease when she was first diagnosed with as much vigor as we could. She was cancer free for 10 years when she had a recurrance, and we have been fighting it on and off ever since.

My advice would be to take as much treatment now as you can. If there is any question about taking chemo, take it and herceptin and everything else your can. This disease is very difficult to defeat and will lie dormant for years. The adjuvant stage is the point at which you have your best chance to cure yourself. You do not want to look back 3 years from now after a recurrance and say to yourself "Gee if I had only..."

Good Luck and God Bless.

Lisa and Brian

[Unregistered]

This links also relates to this topic - I post in case anybody reading this has missed it.

RB


http://www.her2support.org/vbulletin/showthread.php?t=23087