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Dee1987 View Drop Down
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    Posted: Jun 26 2019 at 7:41am
hey there Im hoping someone can help me . I was operated for a stage 1 (1.5cm) node neg last October and im nearing  the end of treatment and Im still learning about this disease. Lately I paid to have my tumour profiled to see if my chemo taxol and carboplatin would have been successful. I feel like Ive been bumped 😪 the lab I used here in Italy is bioscience and the test was called helixafe genomics test on solid tumours. I was told it was 50/59 my chemo had worked and they proposed immunetherapy atezolizumab after chemo 🤔 I showed my oncologist and she told me I waisted money that these tests are for lungs etc however by googling my way about I noticed there is a little truth to it. I had vegfr expression in my tumour and ercc1 expression which seem to be bad 
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123Donna View Drop Down
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Insights into Molecular Classifications of Triple-Negative Breast Cancer: Improving Patient Selection for Treatment



Researchers reveal potential for exploring new treatment options for triple-negative breast cancer

Researchers from Caris Life Sciences and Fox Chase Cancer Center Temple Health announced the presentation of two studies revealing the potential for exploring new therapeutic options for triple-negative breast cancer (TNBC) at the 2015 San Antonio Breast Cancer Symposium (SABCS).

Researchers used Caris Molecular Intelligence, Caris's panomic, comprehensive tumor profiling service, to assess biomarker profiles in subsets of patients with TNBC, an aggressive type of breast cancer in which the cancer cells lack estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor (HER2). In the studies, multiplatform tumor profiling confirmed molecular differences between rare and aggressive subsets of TNBC, which can potentially lead to new treatment options and clinical trial strategies.

"Triple-negative breast cancer remains challenging because of its aggressive and complex nature, its high rate of recurrence and propensity to become a metastatic disease, and the lack of an effective targeted therapy," said Elias Obeid, MD, MPH, assistant professor in the Departments of Clinical Genetics and Medical Oncology at Fox Chase. "With the advancement of comprehensive molecular profiling technology and our partnership with Caris Life Sciences, our understanding of the differences in the subtypes of triple negative breast cancer is unfolding, as well as our understanding of the molecular drivers of the disease that may serve as potential targets for new therapies."

The first study compared the biomarker profiles of patients with quadruple-negative breast cancer (QNBC) a subgroup of TNBC that lacks androgen receptor (AR) expression against those of patients with TNBC who are AR-positive (AR+), confirming the molecular heterogeneity of TNBC. In the second study, researchers identified differences in the molecular profiles of BRCA1/2-mutated and BRCA1/2-non-mutated TNBCs, providing insights into potential targeted treatment strategies for these tumor subtypes.

Both studies utilized Caris Molecular Intelligence's multi-technology approach, which included protein expression analysis (immunohistochemistry [IHC]), gene copy number analysis (chromogenic or fluorescence in situ hybridization [CISH or FISH]), and gene sequencing (SEQ, using Next-Generation or Sanger sequencing).

http://www.news-medical.net/news/20151207/Researchers-reveal-potential-for-exploring-new-treatment-options-for-triple-negative-breast-cancer.aspx

https://robertanagourney.wordpress.com/2015/07/01/chemosensitivity-testing-what-it-is-and-what-it-isnt-2/

From the post, a brief overview

1.    Cancer patients are highly individual in their response to chemotherapies. This is why each patient must be tested to select the most effective drug regimen.
2.    Today we realize that cancer doesnt grow too much it dies too little. This is why older growth-based assays didnt work and why cell-death-based assays do.
3.    Cancer must be tested in their native state with the stromal, vascular and inflammatory elements intact. This is why we use microspheroids isolated directly from patients and do not grow or subculture our specimens.
4.    Predictions of response are not based on arbitrary drug concentrations but instead reflect the careful calibration of in vitro findings against patient outcomes the all-important clinical database.
5.    We do not conduct drug resistance assays. We conduct drug sensitivity assays. These drug sensitivity assays have been shown statistically significantly to correlate with response, time to progression and survival.
6.    We do not conduct genomic analyses for there are no genomic platforms available today that are capable of reproducing the complexity, cross-talk, redundancy or promiscuity of human tumor biology.
7.    Tumors manifest plasticity that requires iterative studies. Large biopsies and sometimes multiple biopsies must be done to construct effective treatment programs.
8.    With chemotherapy, very often more is not better.
9.    New drugs are not always better drugs.
10. And finally, cancer drugs do not know what diseases they were invented for.



Gene Expression Profiling for Diagnosis of Triple-Negative Breast Cancer: A Multicenter, Retrospective Cohort Study


Background: Triple-negative breast cancer (TNBC) accounts for 1220% of all breast cancers. Diagnosis of TNBC is sometimes quite difficult based on morphological assessment and immunohistochemistry alone, particularly in the metastatic setting with no prior history of breast cancer.

Methods: Molecular profiling is a promising diagnostic approach that has the potential to provide an objective classification of metastatic tumors with unknown primary. In this study, performance of a novel 90-gene expression signature for determination of the site of tumor origin was evaluated in 115 TNBC samples. For each specimen, expression profiles of the 90 tumor-specific genes were analyzed, and similarity scores were obtained for each of the 21 tumor types on the test panel. Predicted tumor type was compared to the reference diagnosis to calculate accuracy. Furthermore, rank product analysis was performed to identify genes that were differentially expressed between TNBC and other tumor types.

Results: Analysis of the 90-gene expression signature resulted in an overall 97.4% (112/115, 95% CI: 0.920.99) agreement with the reference diagnosis. Among all specimens, the signature correctly classified 97.6% of TNBC from the primary site (41/42) and lymph node metastasis (41/42) and 96.8% of distant metastatic tumors (30/31). Furthermore, a list of genes, including AZGP1, KRT19, and PIGR, was identified as differentially expressed between TNBC and other tumor types, suggesting their potential use as discriminatory markers.

Conclusion: Our results demonstrate excellent performance of a 90-gene expression signature for identification of tumor origin in a cohort of both primary and metastatic TNBC samples. These findings show promise for use of this novel molecular assay to aid in differential diagnosis of TNBC, particularly in the metastatic setting.

https://www.frontiersin.org/articles/10.3389/fonc.2019.00354/full





Edited by 123Donna - Jun 26 2019 at 8:12am
DX IDC TNBC 6/09 age 49, Stage 1,Grade 3, 1.5cm,0/5Nodes,KI-67 48%,BRCA-,6/09bi-mx, recon, T/C X4(9/09)
11/10 Recur IM node, Gem,Carb,Iniparib 12/10,MRI NED 2/11,IMRT Radsx40,CT NED11/13,MRI NED3/15

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