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Iriana S, Ahmed S, Gong J, et al. Targeting mTOR in Pancreatic Ductal Adenocarcinoma. Front Oncol. 2016;6:99doi: 10.3389/fonc.2016.00099.
Iriana, S., Ahmed, S., Gong, J., Annamalai, A. A., Tuli, R., & Hendifar, A. E. (2016). Targeting mTOR in Pancreatic Ductal Adenocarcinoma. Frontiers in oncology, 699. https://doi.org/10.3389/fonc.2016.00099
Iriana, Sentia, et al. "Targeting mTOR in Pancreatic Ductal Adenocarcinoma." Frontiers in oncology vol. 6 (2016): 99. doi: https://doi.org/10.3389/fonc.2016.00099
Iriana S, Ahmed S, Gong J, Annamalai AA, Tuli R, Hendifar AE. Targeting mTOR in Pancreatic Ductal Adenocarcinoma. Front Oncol. 2016 Apr 25;6:99. doi: 10.3389/fonc.2016.00099. eCollection 2016. PMID: 27200288; PMCID: PMC4843105.
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Front Oncol. 2016 Apr 25;6:99. doi: 10.3389/fonc.2016.00099. eCollection 2016.

Targeting mTOR in Pancreatic Ductal Adenocarcinoma.

Frontiers in oncology

Sentia Iriana, Shahzad Ahmed, Jun Gong, Alagappan Anand Annamalai, Richard Tuli, Andrew Eugene Hendifar

Affiliations

  1. Department of Medicine, Cedars-Sinai Medical Center , Los Angeles, CA , USA.
  2. Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Department of Medical Oncology, City of Hope National Medical Center, Duarte, CA, USA.
  3. Department of Surgery, Cedars-Sinai Medical Center , Los Angeles, CA , USA.
  4. Department of Radiation Oncology, Cedars-Sinai Medical Center , Los Angeles, CA , USA.
  5. Department of Medicine, Division of Medical Oncology, Cedars-Sinai Medical Center , Los Angeles, CA , USA.

PMID: 27200288 PMCID: PMC4843105 DOI: 10.3389/fonc.2016.00099

Abstract

Treatment options for advanced pancreatic ductal adenocarcinoma (PDAC) are limited; however, new therapies targeting specific tumor-related molecular characteristics may help certain patient cohorts. Emerging preclinical data have shown that inhibition of mammalian target of rapamycin (mTOR) in specific KRAS-dependent PDAC subtypes leads to inhibition of tumorigenesis in vitro and in vivo. Early phase II studies of mono-mTOR inhibition have not shown promise. However, studies have shown that combined inhibition of multiple steps along the mTOR signaling pathway may lead to sustained responses by targeting mechanisms of tumor resistance. Coordinated inhibition of mTOR along with specific KRAS-dependent mutations in molecularly defined PDAC subpopulations may offer a viable alternative for treatment in the future.

Keywords: KRAS; clinical trials; mTOR; pancreatic ductal adenocarcinoma; preclinical

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