Ritwik Ghosh
Vanderbilt University
9 Papers
60 Citations
Ritwik Ghosh is an academic researcher from Vanderbilt University. The author has contributed to research in topics: PI3K/AKT/mTOR pathway & Receptor tyrosine kinase. The author has an hindex of 7, co-authored 9 publications. Previous affiliations of Ritwik Ghosh include Vanderbilt University Medical Center.
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Papers
Trastuzumab-Resistant Cells Rely on a HER2-PI3K-FoxO-Survivin Axis and Are Sensitive to PI3K Inhibitors
Anindita Chakrabarty,Neil E. Bhola,Cammie R. Sutton,Ritwik Ghosh,Maria G. Kuba,Bhuvanesh Dave,Jenny C. Chang,Carlos L. Arteaga +7 more
TL;DR: Together, the results suggest that survivin blockade is required for therapeutic responses to trastuzumab and that by combining trASTuzumAB and PI3K inhibitors, CSCs can be reduced within HER2(+) tumors, potentially preventing acquired resistance to anti-HER2 therapy.
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Increased expression and differential phosphorylation of stathmin may promote prostate cancer progression.
Ritwik Ghosh,Guangyu Gu,Erin Tillman,Erin Tillman,Jialing Yuan,Yongqing Wang,Ladan Fazli,Paul S. Rennie,Susan Kasper,Susan Kasper +9 more
TL;DR: It is postulate that proteins, which regulate prostate growth also promote prostate cancer (PCa) progression through dysregulation of these functions.
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Inhibition of PI3K and MEK: it is all about combinations and biomarkers.
TL;DR: A small molecule inhibitor of MAP/ERK kinase (MEK) was effective against human breast cancer cells with a basal-like gene expression signature but activity was limited by both feedback upregulation and loss of the phosphatase PTEN.
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Abstract 3: HER2 gene-amplified human breast cancer cells harboring a gatekeeper T768M mutation in HER2 overexpress EGFR ligands and are sensitive to dual therapeutic blockade of EGFR and HER2
TL;DR: Dual blockade of Her2 and EGFR might be effective at trumping the development of HER2-overexpressing cancers bearing a gatekeeper mutation in T768M, and allelic dilution will render it difficult to identify this drug resistant mutation with conventional sequencing techniques in patients with HER2 gene-amplified breast cancer.
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Differential Signaling by ErbB Receptor (HER) Dimers: Implications for Response to Anti-HER2 Therapies in Breast Cancer.
TL;DR: The data suggest that because of their inability to activate Akt, cells dependent on HER2-containing homodimers are less able to bypass trastuzumab action and may represent a biomarker predictive of response to anti-HER2 therapies.
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