Switch on Estrogen Receptors!
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defeatbc
Member Posts: 53
This might help us Triple Negatives:
Changes us from ER- PR- HER2- to ---> ER+ PR- HER2- so we can use Tamoxifen or AI's.
How cool is that! Now, if only they can hurry up with the research so we can benefit from it.
Hoa (defeatbc)
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AGREE!!! Just read the article and am hopeful they get this ball rolling.
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Found this on the San Antonio Breast Cancer Site, thought maybe it might give some hope, I was diagnosed as TN and then found out a year later they lost a report and I was Her2 positive, now on herceptin. I just really hope this will give any of you ladies on this board some ideas or questions to ask your onc about this. God Bless, Determination of HER2 Status Using Both Serum HER2 Levels and Circulating Tumor Cells in Patients With Recurrent Breast Cancer Whose Primary Tumor was HER2 Negative or of Unknown HER2 Status Breast Cancer Research. 2007 Oct 20;9(5)R74, T. Fehm, S. Becker, S. Duerr-Stoerzer, K. Sotlar, V. Mueller, D. Wallwiener, N. Lane, E. Solomayer, J. UhrApproximately 20% to 25% of patients with invasive primary breast cancer have amplification of the tyrosine kinase growth receptor protein, , HER2. These patients are candidates for treatment with the anti-HER2 monoclonal antibody-derived agent, trastuzumab. Determination of HER2 status in a patient with metastatic breast cancer can provide valuable information. This study aims for a noninvasive method to assess HER2 status in the metastatic setting and evaluates the possibility of checking both the serum HER2 status and the HER2 status of circulating tumor cells (CTCs). In addition, this study attempts to identify those patients who might benefit from HER2-targeted therapy by identifying HER2 positivity in the metastatic setting. Inclusion criteria required that patients with breast cancer have a first-time diagnosis of metastatic or progressive disease. In addition, the primary tumor was to be of either unknown or negative HER2 status. Only a select group of tumor cells are able to cause metastasis. Genetic alterations may also occur in these tumor cells. This constellation of changes together with the cell selection process of metastasis may cause the metastatic tumor to have a different phenotype than that of the primary lesion. The performance of metastatic lesion biopsies currently is not a routine practice. Alternative methods for detecting HER2 status, such as described in this study, can be of significant clinical value. Previous studies have suggested that the changes in serum HER2 status correlate to the expected response of trastuzumab.Patients were identified at either the Department of Gynecology and Obstetrics in Tuebingen, Germany, or the Department of Cancer Immunobiology at UT Southwestern in Dallas, Texas. A total of 77 patients met the inclusion criteria, of whom 25 had visceral metastases, 13 had bone metastases, and 39 had multiple sites of metastatic disease. The primary tumor was HER2 negative in 44 of the patients, with the remaining 33 patients having primary tumors with unknown HER2 status.The serum HER2 levels were found to be above cutoff values in 26% of the patients, of whom 45% initially had a negative HER2 status. The HER2 levels were not influenced by the tumor size of the primary lesion, status of estrogen receptor or progesterone receptor, and location of the metastasis. Of the 67 patients who could be evaluated for the presence of CTCs, 31% had evidence of CTCs. Of these, 38% had evidence of HER2 amplification. When the serum HER2 vs CTC HER2 status results were compared, a concordance rate of 71% was found. Therefore, HER2 status in serum, CTCs, or both is detectable in this group of patients with initially negative or unknown HER2 status. The 28% lack of concordance between these detection methods may indicate different mechanisms of HER2 shedding. Additional studies are recommended to identify the response to HER2-targeted therapy based on serum or CTC HER2 status. This important information may provide this group of patients with access to HER2-targeted therapy.View this article via PubMed »
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