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Review
. 2018 Jan 20;21(1):63-66.
doi: 10.3779/j.issn.1009-3419.2018.01.09.

Targeting of the AKT/m-TOR Pathway: Biomarkers of Resistance to Cancer Therapy-- AKT/m-TOR Pathway and Resistance to Cancer Therapy

Liudmila V Spirina  1   2 , Irina V Kondakova  1 , Natalia V Tarasenko  3   4 , Elena M Slonimskaya  5   6 , Evgeny A Usynin  5 , Alexey K Gorbunov  5 , Zahar A Yurmazov  5 , Svetlana Yu Chigevskaya  5
Affiliations
Review

Targeting of the AKT/m-TOR Pathway: Biomarkers of Resistance to Cancer Therapy-- AKT/m-TOR Pathway and Resistance to Cancer Therapy

Liudmila V Spirina et al. Zhongguo Fei Ai Za Zhi. .

Abstract

Resistance to cancer therapy continues to be a major limitation for the successful treatment of cancer. There are many published studies on therapy resistance in breast and prostate cancers; however, there are currently no data on molecular markers associated with resistance. The conflicting data were reported regarding the AKT/m-TOR signaling pathway components as markers predicting resistance. The AKT/m-TOR signaling pathway is involved in the development of many human cancers; its activation is related to cell proliferation, angiogenesis, apoptosis, as well as to therapy resistance. Molecular alterations in the AKT/m-TOR signaling pathway provide a platform to identify universal markers associated with the development of resistance to cancer therapy.

Keywords: AKT/m-TOR signaling pathway; Molecular markers; Resistance to cancer therapy.

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References

    1. Robbins HL, Hague A. The PI3K/Akt pathway in tumors of endocrine tissues. Front Endocrinol (Lausanne) 2016,;Jan 11, 6:188. doi: 10.3389/fendo.2015.00188.eCollection2015. - DOI - PMC - PubMed
    1. Dodd KM, Yang J, Shen MH, et al. mTORC1 drives HIF-1α and VEGF-A signalling via multiple mechanisms involving 4E-BP1, S6K1 and STAT3. Oncogene. 2015;34(17):2239–2250. doi: 10.1038/onc.2014.164. - DOI - PMC - PubMed
    1. Hager M, Haufe H, Alinger B, et al. pS6 expression in normal renal parenchyma, primary renal cell carcinomas and their metastases. Pathol Oncol Res. 2012;18(2):277–283. doi: 10.1007/s12253-011-9439-y. - DOI - PubMed
    1. Thangavelu K, Pan CQ, Karlberg T, et al. Structural basis for the allosteric inhibitory mechanism of human kidney-type glutaminase (KGA), its regulation by Raf-Mek-Erk signaling in cancer cell metabolism. Proc Natl Acad Sci U S A. 2012;109(20):7705–7710. doi: 10.1073/pnas.1116573109. - DOI - PMC - PubMed
    1. Figlin RA, Kaufmann I, Brechbiel J. Targeting PI3K and mTORC2 in metastatic renal cell carcinoma: New strategies for vercoming resistance to VEGFR and mTORC1 inhibitors. Int J Cancer. 2013;133(4):788–796. doi: 10.1002/ijc.28023. - DOI - PubMed

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