Triple Negs ..

To keep information about Triple Negative Breast Cancer together and easier to access.
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Postby yowyow » Fri Jun 27, 2008 4:04 pm

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Postby Ruth » Fri Jun 27, 2008 2:46 pm

I am currently doing a review of the new version of 'A Guide for Women with Early Breast Cancer' (the orange book which comes in the My Journey Kit) and note there is no mention in it of Triple Negative Breast Cancer. I have mentioned this in my review notes. Nav, I have your words ringing in my ears!
Ruth :kiwi:

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Postby yowyow » Fri Jun 27, 2008 1:41 pm

sorry, shouldn't say better because I don't want to upset anyone, I should say its very effective

Debs, its hard when we put ourselves in the hands of our oncologists.
You know, I didn't even know the name of the chemo I was having until
I had already had a few rounds when I finally asked the Onc nurse what it was :ouch:

I think your having a kick cancers butt treatment (I have to as I had it too :wink: )
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Postby Debs » Fri Jun 27, 2008 1:31 pm

Thanks Nav, That does sound good news. I will also ask the Onc. about the chemo in the study as I am on FEC x 6. It seems unclear how they choose each chemo for each individual however I hope I am on the best one for my cancer.

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Postby yowyow » Fri Jun 27, 2008 1:22 pm

Debs, I may have posted this here somewhere before but most studies show chemo
is very effective for triple negs

Oh, this from my post below is what I like to hear (although its an opinion)
Five years from now it’s not going to be as simple as ER and HER-2. We’re going to have every pathway mapped out using genomic science so that you’re going to have 10 targets in your tumor as opposed to one. I honestly believe that will be here within the next five to10 years.

of Chemotherapy in Breast Cancer Depends on Estrogen-Receptor Status
M. D. Anderson News Release 04/11/06

When it comes to chemotherapy treatment for women whose breast cancer has spread to their lymph nodes, the estrogen status of their tumors matters, says a team of researchers in the April 12 issue of the Journal of the American Medical Association.

Analyzing data from three clinical trials with a total of 6,644 patients, they determined that chemotherapy works much better in breast cancer that is estrogen receptor-negative (ER-) than many people think, and conversely, doesn't work as well in estrogen receptor-positive (ER+) cancer as believed, says the study's lead author Donald Berry, Ph.D., chair of the Department of Biostatistics and Applied Mathematics at The University of Texas M. D. Anderson Cancer Center.

This conclusion will come as a surprise to many oncologists, Berry says. Women with "node-positive" breast cancer routinely are given chemotherapy, regardless of their tumor type. Women who have ER+ tumors are also given tamoxifen, a drug which inhibits estrogen use by the cancer cells.

"Our analysis shows that tamoxifen works very well for a number of years and taken as a group, there is little or no benefit of even the cumulative effects of modern improvements in chemotherapy for women with ER+ tumors," he says.

"All in all, this is good news because it shows that the benefit of chemotherapy for ER- tumors is surprisingly dramatic in the same way that tamoxifen's effect is substantial for ER+ tumors," Berry says.

The research team, which includes investigators from top cancer centers nationwide, studied outcomes from three large randomized clinical trials which tested the optimal use of chemotherapy in node-positive breast cancer. But none of these trials, all of which were conducted by the Cancer and Leukemia Group B and the U.S. Breast Intergroup, considered estrogen status or whether women had received tamoxifen, largely because the diagnostic importance of estrogen status for chemotherapy was not recognized at the time the trials were designed, Berry says.

Accumulated evidence indicates, however, that improvements in chemotherapy disproportionately benefit women with ER- tumors, Berry says; so the research team decided to statistically model the relative contribution of chemotherapy treatment given estrogen receptor status.

They found the absolute benefits due to chemotherapy were greater for patients with ER- tumors compared to those with ER+ tumors. Specifically, 22.8 percent more ER- patients were disease-free after five years if they received chemotherapy versus 7 percent of ER+ patients. The corresponding improvements for overall survival were 16.7 percent versus 4 percent.

The researchers also compared the different chemotherapy regimens tested in the trials, and found the latest chemotherapy combination studied - biweekly doxorubicin/cyclophosphamide plus paclitaxel - lowered the rate of recurrence and death in ER- patients by more than 50 percent, compared to the low-dose regimen used in the first study.

"This tells us that breast oncology has made enormous strides in treating patients with ER- tumors, a finding which contradicts the prevailing wisdom that with the development of tamoxifen and newer selective estrogen receptor modulator drugs, the benefits of medical science have been primarily focused on ER+ tumors," Berry says.

"It is true that tamoxifen changed the landscape for ER+ tumors, but the playing field has now been leveled somewhat given the fact that ER- tumors respond well to modern improvements in chemotherapy regimens," he says.

The study was funded by the National Cancer Institute through its support of the national cooperative oncology groups: the Cancer and Leukemia Group B, the Southwest Oncology Group, the Eastern Cooperative Oncology Group, and the North Central Cancer Treatment Group.

Co-authors include Constantine Cirrincione with the Cancer and Leukemia Group B Statistical Center; I. Craig Henderson, M.D., from the University of California at San Francisco; Marc Citron, M.D., from Albert Einstein College of Medicine; Daniel Budman, M.D., North Shore University Hospital; Lori Goldstein, M.D., from Fox Chase Cancer Center; Silvana Martino, D.O., from the Los Angeles Clinic and Research Institute; Edith Perez, M.D., from the Mayo Clinic and Mayo Foundation; Hyman Muss, M.D., from the Vermont Cancer Center; Larry Norton, M.D. and Clifford Hudis, M.D., from Memorial Sloan-Kettering Cancer Center; and Eric Winer, from the Dana-Farber Cancer Institute.
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Postby Debs » Fri Jun 27, 2008 1:16 pm

Thanks Nav again for posting this information. I just. hope there is a breakthrough soon for us triple-negs it just real scary knowing we can only be treated with chemo and my Onc says chemo is only effective in 8 out of 20 people! Its hard to digest when your newly diagnosed that this is only option.

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Postby yowyow » Thu Jun 26, 2008 11:59 pm

LBBC Publications
Excerpt from "Medical Advances for Young Women Affected by Breast Cancer"
Triple Negative Tumors
Speaker: Kimberly L. Blackwell, MD

.

[
QUESTION: Are you fully satisfied with the research that there is truly no benefit for tamoxifen or Herceptin or any of those kinds of drugs for those of us who are hormone negative and even HER-2-neu negative?

DR. BLACKWELL: This [refers to the] entity, for which the buzzword is "triple-negative tumors," tumors that are estrogen-receptor-negative, progesterone-receptor negative and HER-2 negative. Although that’s a nice buzzword, we’ve known for 20 years that those are tumors that aren’t eligible for many of the therapies. Therefore, they tend to recur at a higher rate than those tumors that are eligible for the therapies.

I would never be satisfied with any of the research. There are continuing questions that need to be answered about how we treat estrogen-receptor-negative tumors. We need to continue to say, "Gosh, is there a chance that maybe the newer hormonal therapies might offer benefit?"

I’m pretty convinced, though. I wouldn’t say satisfied. One of the things that I didn’t have time to talk about is estrogen-receptor staining. I’m not saying this necessarily applies to you or to any of your colleagues that have this, [but estrogen-receptor staining] is horrifically bad.

I would want my estrogen-receptor staining to be done in a lab that really knows how to do it. In particular, [I would want my] progesterone-receptor staining [done in a lab that really knows how to do it], because those are interlinked. If you have any amount of progesterone receptor, then you have some estrogen receptor. You don’t get progesterone receptor expression without having some ER signaling. So where does that help? There are several new technologies that are being developed to help us do a better job of detecting estrogen receptor. That’s where I think we’ve had some trouble with the previous studies.

Make absolutely certain you’re not eligible for hormonal therapy. I saw a woman just last week who had a low-grade cancer that was read as estrogen-receptor negative. That doesn’t make sense, because typically low histologic grade tumors are ER positive. We restained it and, in fact, she was ER positive. If there is something funny, maybe you had a low-grade tumor and you’re being told that you had estrogen-receptor negativity, it’s worth restaining. When people come to big cancer centers and get a second opinion, many times we will offer the restaining just to be absolutely certain.

Now, if you were 90 years old, and I have nothing [against] 90-year-olds, and you had heart problems and kidney problems and liver problems, would I advocate restaining you so that I could put you on a drug that probably isn’t going to help you very much? No. But when you’re 38 or 40, it’s worth double-checking.

What do we need to do about research? There are several studies. There is one study that I’m involved in. There is another study that someone else is involved in that is primarily related to metastatic breast cancer. There is very little in the early-stage setting, and that’s because these studies are very difficult to design and have large numbers of patients. In the triple-negative setting, the Avastin studies are the ones that I would encourage my triple-negative patients to go on. We are trying to address some of these issues in ongoing trials.

Five years from now it’s not going to be as simple as ER and HER-2. We’re going to have every pathway mapped out using genomic science so that you’re going to have 10 targets in your tumor as opposed to one. I honestly believe that will be here within the next five to10 years.

I will say one other thing. Those triple-negative tumors typically have high levels of EGFR, which is another marker. We have a drug called Tarceva and one called Iressa, even though it didn’t work so well in non-small-cell lung cancer. We routinely stain for epidermal growth factor receptor, EGFR, in those triple-negative tumors, to see if there is another therapeutic option or at least a trial that might benefit those patients. That is one marker that you could talk to your physician about.

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Postby cas145 » Thu Jun 26, 2008 9:24 pm

Thanks Nav very interesting :hugs: Cas

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Postby Debs » Wed Jun 25, 2008 9:49 pm

Thanks Yow Yow for this interesting information. Being newly diagnosed triple negative I am trying to find out as much information as possible. Most of the information I have found has been negative and my Onc has said to me that prognosis is not so good in ER- group compared to ER+. Therefore good to read smeone out there is doing some research and lets hope for good results.

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Postby yowyow » Wed Jun 25, 2008 9:21 pm

Q: What is the breakthrough discovery?
A: We identified a short form of BRCA1 protein named BRCA1a, which is expressed at reduced levels or undetectable in high-grade breast and ovarian cancers. We have shown that inhibition of expression of this protein in normal cells results in cancer and high-level expression results in cell death and growth inhibition. We have a patent for this protein. Our work - published online in the March 26, 2007 issue of Oncogene - has demonstrated for the first time using a gene therapy strategy that introducing BRCA1a gene into triple-negative breast cancers, ovarian and prostate cancers stops tumor development. This major discovery will provide new avenues in the future for the treatment of one of the biggest needs in breast cancer research.
Q: Are Asian or Hispanic women also at risk?
A: Good question. Triple-negative breast cancers are higher among younger African-American women and Hispanic women; Asians show low levels of breast cancers.

Q: How many patients have these triple-negative breast cancers?
A: In a University of North Carolina study reported in the February 2007 issue of SCIENCE, of the 97 pre-menopausal African-American women, 39 percent had triple-negative breast tumors. Among postmenopausal African Americans, the number was 14 percent, whereas among Caucasians, regardless of age, it was 16 percent. Even though breast cancers are more common in whites they are deadlier in blacks.

Q: Those are scary statistics. What has your work shown?
A: For the first time, we have demonstrated [in mice] using a gene therapy strategy that introducing BRCA1a into triple-negative breast cancers and ovarian cancers and prostate cancers stops tumor development. This research is part of our MSM mission to reduce cancer health disparities among minorities.

Q: So you believe that you can increase survival rates with this gene therapy?
A: Yes, if not now, at least in the future. This is just the beginning. We plan to develop novel non-viral vectors expressing BRCAla for in vivo gene therapy into ER-negative and triple-negative breast cancer cells and look for suppression of the tumorgenic phenotype both in vitro and in xenograft mouse models. If successful, these nano-BRCAla vectors can be used in the future for effective and safe treatment for patients with triple-negative breast cancers. In fact, recently a team of British doctors carried out the world's first eye operation using gene therapy to cure a sight disorder.

Q: And that's where the money comes in, right?
A: Yes, that's where the need for money comes in. I have written several federal and private grants and am eagerly waiting to hear from them so that I can start working right away. How fast it all happens depends on the flow of money. We are talking a minimum of $250,000 to $500,000 annually for five years. It's my passion to do cancer research. I really enjoy my work.

Q: That is very promising. Has MSM done this breakthrough work alone?
A: Some of this work was done when I was at Drexel Medical School. Those participating in the research include Shyam P. Reddy, Ph.D., professor and co-director of MSM's Cancer Biology Program. Participating in the research from Morehouse School of Medicine were Yuli Chai, M.D., and Joel Okoli, M.D.; from Drexel University, Ningsheng Shao, Ph.D.; from Emory University, Gabriela Oprea, M.D; from the University of Alabama, Edward Partridge, M.D.; and from the National Cancer Institute, Leo Lee, Ph.D.
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Postby yowyow » Fri Mar 28, 2008 8:37 am

Now this is a GOOD read for hormone negs :clap: :clap: :clap:
mixed message for hormone pos though, sorta says how important hormone therapy is.

Benefit of Chemotherapy in Breast Cancer Depends on Estrogen-Receptor Status
M. D. Anderson News Release 04/11/06

When it comes to chemotherapy treatment for women whose breast cancer has spread to their lymph nodes, the estrogen status of their tumors matters, says a team of researchers in the April 12 issue of the Journal of the American Medical Association.

Analyzing data from three clinical trials with a total of 6,644 patients, they determined that chemotherapy works much better in breast cancer that is estrogen receptor-negative (ER-) than many people think, and conversely, doesn't work as well in estrogen receptor-positive (ER+) cancer as believed, says the study's lead author Donald Berry, Ph.D., chair of the Department of Biostatistics and Applied Mathematics at The University of Texas M. D. Anderson Cancer Center.

This conclusion will come as a surprise to many oncologists, Berry says. Women with "node-positive" breast cancer routinely are given chemotherapy, regardless of their tumor type. Women who have ER+ tumors are also given tamoxifen, a drug which inhibits estrogen use by the cancer cells.

"Our analysis shows that tamoxifen works very well for a number of years and taken as a group, there is little or no benefit of even the cumulative effects of modern improvements in chemotherapy for women with ER+ tumors," he says.

"All in all, this is good news because it shows that the benefit of chemotherapy for ER- tumors is surprisingly dramatic in the same way that tamoxifen's effect is substantial for ER+ tumors," Berry says.

The research team, which includes investigators from top cancer centers nationwide, studied outcomes from three large randomized clinical trials which tested the optimal use of chemotherapy in node-positive breast cancer. But none of these trials, all of which were conducted by the Cancer and Leukemia Group B and the U.S. Breast Intergroup, considered estrogen status or whether women had received tamoxifen, largely because the diagnostic importance of estrogen status for chemotherapy was not recognized at the time the trials were designed, Berry says.

Accumulated evidence indicates, however, that improvements in chemotherapy disproportionately benefit women with ER- tumors, Berry says; so the research team decided to statistically model the relative contribution of chemotherapy treatment given estrogen receptor status.

They found the absolute benefits due to chemotherapy were greater for patients with ER- tumors compared to those with ER+ tumors. Specifically, 22.8 percent more ER- patients were disease-free after five years if they received chemotherapy versus 7 percent of ER+ patients. The corresponding improvements for overall survival were 16.7 percent versus 4 percent.

The researchers also compared the different chemotherapy regimens tested in the trials, and found the latest chemotherapy combination studied - biweekly doxorubicin/cyclophosphamide plus paclitaxel - lowered the rate of recurrence and death in ER- patients by more than 50 percent, compared to the low-dose regimen used in the first study.

"This tells us that breast oncology has made enormous strides in treating patients with ER- tumors, a finding which contradicts the prevailing wisdom that with the development of tamoxifen and newer selective estrogen receptor modulator drugs, the benefits of medical science have been primarily focused on ER+ tumors," Berry says.

"It is true that tamoxifen changed the landscape for ER+ tumors, but the playing field has now been leveled somewhat given the fact that ER- tumors respond well to modern improvements in chemotherapy regimens," he says.

The study was funded by the National Cancer Institute through its support of the national cooperative oncology groups: the Cancer and Leukemia Group B, the Southwest Oncology Group, the Eastern Cooperative Oncology Group, and the North Central Cancer Treatment Group.

Co-authors include Constantine Cirrincione with the Cancer and Leukemia Group B Statistical Center; I. Craig Henderson, M.D., from the University of California at San Francisco; Marc Citron, M.D., from Albert Einstein College of Medicine; Daniel Budman, M.D., North Shore University Hospital; Lori Goldstein, M.D., from Fox Chase Cancer Center; Silvana Martino, D.O., from the Los Angeles Clinic and Research Institute; Edith Perez, M.D., from the Mayo Clinic and Mayo Foundation; Hyman Muss, M.D., from the Vermont Cancer Center; Larry Norton, M.D. and Clifford Hudis, M.D., from Memorial Sloan-Kettering Cancer Center; and Eric Winer, from the Dana-Farber Cancer Institute.
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Postby cas145 » Sun Mar 02, 2008 1:28 pm

Thanks Nav good read :hugs: Cas

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Postby yowyow » Sun Mar 02, 2008 8:13 am

More good stuff...................


Clinical trials for TRAIL warranted in triple-negative breast cancer By Andrew Czyzewski22 February 2008Breast Cancer Res Treat 2008; Advance online publicationMedWire News: Scientists have discovered that the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) selectively kills triple-negative breast cancer (estrogen receptor [ER]-, progesterone [PR]-, HER2-) cells grown in vitro.

Stanley Lipkowitz and colleagues from the National Cancer Institute in Bethesda, Maryland, USA, say their data "provide a basis for designing clinical studies using TRAIL and similar acting agents in women with triple-negative breast cancer."

Approximately 15-20% of patients with breast cancer have tumors that do not express ER or PR and do not have amplification of HER-2.

The identification of novel, treatments for patients with this subtype of disease is thus of paramount importance.

Studies have shown that the TRAIL protein induces apoptosis in a variety of cancer cell lines; however, breast cancer cells tested in these studies were generally resistant to such treatment.

Noting that breast cancer is a heterogenous group of diseases, Lipkowitz and colleagues decided to systematically test the TRAIL protein in a panel of 20 different breast cancer cell lines representing different subtypes of the disease.

Upon treatment with TRAIL protein, eight of 11 triple-negative cell lines in the panel showed a 10-fold increase in apoptosis as evidenced by an increase in the amount of fragmented DNA following cell lysis.

By contrast, three of the triple-negative cell lines showed a three-fold increase in apoptosis while the remaining nine non-triple-negative cell lines did not show any sensitivity to TRAIL.

Performing gene microarray analysis, Lipkowitz et al found that the eight triple-negative cells lines sensitive to TRAIL had a signature consistent with the basal "B" or mesenchymal type of breast cancer, while the three triple-negative cell lines that were more resistant to TRAIL had a basal "A" or epithelial signature.

In addition, mesenchymal-triple-negative cell lines upregulated the epidermal growth factor receptor (EGFR) gene.

The researchers note that treating these mesenchymal-triple-negative cell lines with a small molecule tyrosine kinase to inhibit EGFR and TRAIL increased apoptosis 14-fold - greater than the effect seen with TRAIL alone.

Commenting on the treatment implications of their findings for patients with triple-negative breast cancer, Lipkowitz and colleagues write: "The data here provide a strong rationale for testing TRAIL receptor agonists in this population - especially those with tumors that have mesenchymal features."

They add: "In addition, combination of EGFR inhibitors with TRAIL may be particularly effective for the treatment of triple-negative breast cancers with mesenchymal features."

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Postby ozzie » Sat Jan 26, 2008 3:10 pm

Also this is the US site for trials etc...but if its happening in OZ it will also be shown here and where the trial is in OZ ..hope this is of help also..

http://clinicaltrials.gov/ct2/home


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Postby ozzie » Sat Jan 26, 2008 3:06 pm

Not sure if this link will be of any help re trials in Aus and NZ ... but worth a look see..

http://www.anzctr.org.au/default.aspx


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