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Argun Akcakanat

Researcher at University of Texas MD Anderson Cancer Center

Publications -  57
Citations -  3084

Argun Akcakanat is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Breast cancer & Cancer. The author has an hindex of 28, co-authored 48 publications receiving 2474 citations. Previous affiliations of Argun Akcakanat include Niigata University & Mayo Clinic.

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PD-L1 Expression in Triple-Negative Breast Cancer

TL;DR: Using tissue microarrays containing 105 triple-negative breast cancer specimens, Mittendorf and colleagues show that 20% of the TNBC specimens express PD-L1, half have lost PTEN, and inhibitors of PI3K pathway decrease PD- l1 expression, providing a rationale for therapeutic targeting of PD- L1 for TNBC.
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PIK3CA/PTEN Mutations and Akt Activation As Markers of Sensitivity to Allosteric mTOR Inhibitors

TL;DR: Rapamycin-mediated Akt activation is greater in RS cells, with a similar observation in patients with clinical responses on exploratory biomarker analysis; thus feedback loop activation of Akt is not a marker of resistance but rather may function as an indicator of rapamycin activity.
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Targeting the PI3-kinase/Akt/mTOR signaling pathway.

TL;DR: An overview of the PI3K/Akt/mTOR signaling pathway is presented, as a central regulator of cell growth, protein translation, survival, and metabolism, activation of this signaling pathway contributes to the pathogenesis of many tumor types.
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Biomarkers of Response to Akt Inhibitor MK-2206 in Breast Cancer

TL;DR: In vitro, MK-2206 showed a synergistic interaction with paclitaxel in MK- 2206–sensitive cell lines, and this combination had significantly greater antitumor efficacy than either agent alone in vivo.
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Antitumor activity of rapamycin and octreotide as single agents or in combination in neuroendocrine tumors

TL;DR: Rapamycin causes significant growth inhibition in carcinoid tumor cell lines in vitro and in vivo, thus mTOR is a promising therapeutic target for neuroendocrine tumors and octreotide does not enhance the efficacy of rapamycin's antiproliferative effects in the models tested.