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mTOR in Lung Neoplasms

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  • Published:
Pathology & Oncology Research

Abstract

With the discovery of rapamycin 45 years ago, studies in the mechanistic target of rapamycin (mTOR) field started 2 decades before the identification of the mTOR kinase. Over the years, studies revealed that the mTOR signaling is a master regulator of homeostasis and integrates a variety of environmental signals to regulate cell growth, proliferation, and metabolism. Deregulation of mTOR signaling, particularly hyperactivation, frequently occurs in human tumors. Recent advances in molecular profiling have identified mutations or amplification of certain genes coding proteins involved in the mTOR pathway (eg, PIK3CA, PTEN, STK11, and RICTOR) as the most common reasons contributing to mTOR hyperactivation. These genetic alterations of the mTOR pathway are frequently observed in lung neoplasms and may serve as a target for personalized therapy. mTOR inhibitor monotherapy has met limited clinical success so far; however, rational drug combinations are promising to improve efficacy and overcome acquired resistance. A better understanding of mTOR signaling may have the potential to help translation of mTOR pathway inhibitors into the clinical setting.

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Acknowledgments

Research work of authors from 1st Department of Pathology and Experimental Cancer Research, Semmelweis University was supported by the National Bionics Program of National Research, Development and Innovation Fund of Hungary (ED_17-1-2017-0009), and grants of the Hungarian National Research, Development and Innovation Office (NKFI-FK-128404 and NVKP_16-1-2016-0004).

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Krencz, I., Sebestyen, A. & Khoor, A. mTOR in Lung Neoplasms. Pathol. Oncol. Res. 26, 35–48 (2020). https://doi.org/10.1007/s12253-020-00796-1

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