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Combined targeting of AKT and mTOR synergistically inhibits proliferation of hepatocellular carcinoma cells.

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Combined targeting of AKT and mTOR synergistically inhibits proliferation of hepatocellular carcinoma cells. / Grabinski, Nicole; Ewald, Florian; Hofmann, Bianca T.; Staufer, Katharina; Schumacher, Udo; Nashan, Björn; Jücker, Manfred.

In: MOL CANCER, Vol. 11, 2012, p. 85.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Grabinski, N, Ewald, F, Hofmann, BT, Staufer, K, Schumacher, U, Nashan, B & Jücker, M 2012, 'Combined targeting of AKT and mTOR synergistically inhibits proliferation of hepatocellular carcinoma cells.', MOL CANCER, vol. 11, pp. 85. https://doi.org/10.1186/1476-4598-11-85

APA

Grabinski, N., Ewald, F., Hofmann, B. T., Staufer, K., Schumacher, U., Nashan, B., & Jücker, M. (2012). Combined targeting of AKT and mTOR synergistically inhibits proliferation of hepatocellular carcinoma cells. MOL CANCER, 11, 85. https://doi.org/10.1186/1476-4598-11-85

Vancouver

Grabinski N, Ewald F, Hofmann BT, Staufer K, Schumacher U, Nashan B et al. Combined targeting of AKT and mTOR synergistically inhibits proliferation of hepatocellular carcinoma cells. MOL CANCER. 2012;11:85. https://doi.org/10.1186/1476-4598-11-85

Bibtex

@article{549388118e49418dbe81ce710d4194a9,
title = "Combined targeting of AKT and mTOR synergistically inhibits proliferation of hepatocellular carcinoma cells.",
abstract = "Due to the frequent dysregulation of the PI3K/AKT/mTOR signaling pathway, mTOR represents a suitable therapeutic target in hepatocellular carcinoma (HCC). However, emerging data from clinical trials of HCC patients indicate that mTOR inhibition by RAD001 (Everolimus) alone has only moderate antitumor efficacy which may be due to the feedback activation of AKT after mTOR inhibition. In this study, we analyzed the effects of dual inhibition of mTOR and AKT on the proliferation of HCC cell lines. In addition, we measured the feedback activation of each of the AKT isoforms after mTOR inhibition in HCC cell lines and their enzymatic activity in primary samples from HCC patients.",
author = "Nicole Grabinski and Florian Ewald and Hofmann, {Bianca T.} and Katharina Staufer and Udo Schumacher and Bj{\"o}rn Nashan and Manfred J{\"u}cker",
year = "2012",
doi = "10.1186/1476-4598-11-85",
language = "English",
volume = "11",
pages = "85",
journal = "MOL CANCER",
issn = "1476-4598",
publisher = "BioMed Central Ltd.",

}

RIS

TY - JOUR

T1 - Combined targeting of AKT and mTOR synergistically inhibits proliferation of hepatocellular carcinoma cells.

AU - Grabinski, Nicole

AU - Ewald, Florian

AU - Hofmann, Bianca T.

AU - Staufer, Katharina

AU - Schumacher, Udo

AU - Nashan, Björn

AU - Jücker, Manfred

PY - 2012

Y1 - 2012

N2 - Due to the frequent dysregulation of the PI3K/AKT/mTOR signaling pathway, mTOR represents a suitable therapeutic target in hepatocellular carcinoma (HCC). However, emerging data from clinical trials of HCC patients indicate that mTOR inhibition by RAD001 (Everolimus) alone has only moderate antitumor efficacy which may be due to the feedback activation of AKT after mTOR inhibition. In this study, we analyzed the effects of dual inhibition of mTOR and AKT on the proliferation of HCC cell lines. In addition, we measured the feedback activation of each of the AKT isoforms after mTOR inhibition in HCC cell lines and their enzymatic activity in primary samples from HCC patients.

AB - Due to the frequent dysregulation of the PI3K/AKT/mTOR signaling pathway, mTOR represents a suitable therapeutic target in hepatocellular carcinoma (HCC). However, emerging data from clinical trials of HCC patients indicate that mTOR inhibition by RAD001 (Everolimus) alone has only moderate antitumor efficacy which may be due to the feedback activation of AKT after mTOR inhibition. In this study, we analyzed the effects of dual inhibition of mTOR and AKT on the proliferation of HCC cell lines. In addition, we measured the feedback activation of each of the AKT isoforms after mTOR inhibition in HCC cell lines and their enzymatic activity in primary samples from HCC patients.

U2 - 10.1186/1476-4598-11-85

DO - 10.1186/1476-4598-11-85

M3 - SCORING: Journal article

VL - 11

SP - 85

JO - MOL CANCER

JF - MOL CANCER

SN - 1476-4598

ER -