Possible Tripple Negative ?

Mom42July2007

Hi Everyone...I was dx on July 18th and onc visit on July 24th says...IDC, tumor size 3.0,Grade 3, Er/Pr neg and Her2 Equivocal....awaiting retest of HER2. Twink thanks for directing me to this Tripple Negative area. I have been reading through all the differnt information and following the links to understand more.

My first HER2 done via FISH says 1.8 Equivocal...says on a website FISH results are Negative if less then 1.8, Equivocal between 1.8 to 2.2, then positive if greater then 2.2. IF retest still at 1.8, an article form Canada says this would be treated as Negative; equivocal results of 2.0 or greater can be considered positive and treated with Herceptin.

Anyone else out there diagnosed tripple from a Equivocal FISH result?

Also the information on the MGH study about Cisplatin was very interesting...Does anyone know what the test is called to determine your P63 and P73 levels? I actaully live about 10 miles North of Boston but working with our local cancer center (they are great!)...I'm going to find out more about this, so I'll keep everyone updated!

I've already sent my NP a number of emails...today's email is going to be questioning this MGH study!!!

Thanks to all for the wonderful information posted....I feel like I'm becoming a medical professional from all your great advise and information which I guess is good...I don't have to feel as guilty about lieing on my Adjuvant online log in!!!!

ravdeb

Interesting post...I didn't know about the equivocal FSH results. I thought the FSH would establish if it was pos or neg. My HER2 test was equivocal and that's why they did the FSH test, or at least that's what I understood.

If it's equivocal, is there a chance that herceptin would be an option?

Mom42July2007

I have asked that question via email yesterday to NP at onc office...interesting article from another thread showing herceptin could help her2 neg also(link below)...but looks like it could be the test itself to determine her2 status that is the problem. My firt test was done via FISH which is surpose to be the best test. My understanding was they were going to retest original tumor using FISH again and then also use the test IHC. Had additional surgery on the 27th which did find more cancer cells in my breast but they did get a clean margin...I've asked if this new sample can also be tested! Sending many of emails to them, but also scheduled to talk with them on August 10th again! Hopefully I can some information soon!http://www.nytimes.com/2007/06/12/health...abf&ei=5070

TenderIsOurMight

"Also the information on the MGH study about Cisplatin was very interesting...Does anyone know what the test is called to determine your P63 and P73 levels? I actaully live about 10 miles North of Boston"

Well, I haven't learned how to quote as yet on this system....

How wonderful that you found this open study at Massachusetts General Hospital, and so close to you at that. I've taken license to post the entire study here for the benefit of other Triple Negative patients who may be interested, as well as to demonstrate how diligently the researchers and doctors are searching now for ways to better treat receptor negative cancers. The p63 and p73 protein signature test is not commercially available as yet, I believe, but rather in available only through such a clinical trial.

This is exciting news and sustains our hope that a solution to triple negative disease may soon be forthcoming. Thank you for posting on it!

Molecular signature may identify cisplatin-sensitive breast tumors :Protein interaction underlies treatment-resistant tumor, findings lead to new clinical trial

BOSTON - April 19, 2007 - Researchers at the Massachusetts General Hospital (MGH) Cancer Center have identified a subgroup of hard-to-treat breast cancers that may be sensitive to the drug cisplatin, rarely used in the treatment of breast tumors. They also have discovered the molecular basis of this sensitivity, which may help identify patients most likely to benefit from cisplatin treatment. The findings will be tested in a clinical trial anticipated to begin at the MGH Gillette Center for Breast Cancer and collaborating institutions later this spring.

"This paper describes a specific molecular pathway that makes these tumors sensitive to a therapy infrequently used for breast cancer," says Leif Ellisen, MD, PhD, of the MGH Cancer Center, senior author of the study to appear in the May 2007 Journal of Clinical Investigation and receiving early online release. "We're excited that this work has led to the design of a clinical trial for women with a very difficult to treat form of breast cancer."

About two thirds of breast cancers contain receptor molecules for the hormones estrogen or progesterone, and in recent years antiestrogen drugs like tamoxifen have improved outcomes for women with those tumors. About 20 to 30 percent of tumors, some with hormone receptors, have elevated levels of a growth-promoting protein called HER2, and those tumors are candidates for treatment with the monoclonal antibody Herceptin. The third major subtype is the 15 to 20 percent of breast tumors that have neither estrogen nor progesterone receptors and also do not overexpress HER2.

Since these so-called "triple-negative" tumors are treatable with neither Herceptin nor antiestrogen drugs, the prognosis for patients with the tumors has been poor. Triple-negative tumors are the most common subtype found in patients with mutations in the BRCA1 gene, but they also appear in women without alterations in the so-called "breast cancer gene." There have been reports that BRCA1-associated, triple-negative tumors might be sensitive to cisplatin, a drug used to treat several other types of cancer, but whether the more common sporadic triple-negative tumors shared that sensitivity was unknown. The current study was designed to answer that question and to investigate the mechanism underlying cisplatin sensitivity.

The research team focused on the function of p63, a protein that plays a role in normal breast development and is related to the common tumor suppressor p53. They analyzed tissue samples from triple-negative breast tumors and normal breast tissues for the expression of several forms of p63 and another related protein called p73, known to promote the cell-death process called apoptosis.

The researchers found that a significant number of triple-negative tumors overexpress particular forms of p63 and p73, a pattern not seen in other types of breast cancers. Using an RNA interference system to inhibit the action of p63, they showed that the protein stimulates tumor growth by interfering with p73's normal ability to induce cell death. Cisplatin was found to break up the binding of p63 to p73 and reactivate the cell-death process.

"The most important finding was that, if the tumor cells did not express both p63 and p73, the cells were not sensitive to cisplatin," says Ellisen. "These results suggest that testing p63 and p73 levels in patients' tumors might help predict whether they would benefit from cisplatin therapy." Ellisen is an assistant professor of Medicine at Harvard Medical School.

The clinical trial to investigate the role of p63/p73 expression in determining cisplatin sensitivity will be led by MGH researchers through the Dana-Farber/Harvard Cancer Center. Starting in Boston in the coming weeks, the trial will be open to patients with advanced triple-negative breast cancer and eventually will be offered at other U.S. cancer research centers. Patients or physicians interested in the trial should call Karleen Habin at (617) 726-1922 and ask about the cisplatin trial for breast cancer.

Additional authors of the Journal of Clinical Investigation paper are first author Chee-Onn Leong, PhD; Nick Vidnovic, Maurice DeYoung, and Dennis Sgroi, MD, all of the MGH Cancer Center. The study was supported by grants from the Mary Kay Ash Charitable Foundation, the National Institute of Dental and Craniofacial Research, the Tracey Davis Memorial Fund, and the Avon Foundation.

Massachusetts General Hospital, established in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of nearly $500 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, transplantation biology and photomedicine. MGH and Brigham and Women's Hospital are founding members of Partners HealthCare HealthCare System, a Boston-based integrated health care delivery system.

Media Contact: Sue McGreevey, MGH Public Affairs
Physician Referral Service: 1-800-388-4644
Information about Clinical Trials

All the best,
Tender

FloridaLady

MD Anderson Houston said to me they would let me try the Her2 tx...even the new vaccine. Than they back out completely... sdaying " that they were not going to tx triple negs with there protocol???????" I'm Her2++ Fish negative. No mets