Resistance to dual blockade of the kinases PI3K and mTOR in KRAS -mutant colorectal cancer models results in combined sensitivity to inhibition of the receptor tyrosine kinase EGFR

Author:

Belmont Peter J.1,Jiang Ping1,McKee Trevor D.2,Xie Tao1,Isaacson Jason1,Baryla Nicole E.3,Roper Jatin4,Sinnamon Mark J.4,Lee Nathan V.1,Kan Julie L. C.1,Guicherit Oivin1,Wouters Bradly G.23,O’Brien Catherine A.5,Shields David1,Olson Peter1,VanArsdale Todd1,Weinrich Scott L.1,Rejto Paul1,Christensen James G.1,Fantin Valeria R.1,Hung Kenneth E.6,Martin Eric S.1

Affiliation:

1. Oncology Research Unit, Pfizer Global Research and Development, San Diego, CA 92121, USA.

2. Departments of Radiation Oncology and Medical Biophysics, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario M5G 2M9, Canada.

3. Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada.

4. Division of Gastroenterology, Department of Medicine, Tufts Medical Center, Boston, MA 02111, USA.

5. University Health Network, University of Toronto, Toronto, Ontario M5G 2M9, Canada.

6. Pfizer Biotherapeutics Clinical Research, Cambridge, MA 02140, USA.

Abstract

Combination therapy with EGFR inhibitors may overcome acquired resistance to PI3K pathway inhibitors in some colorectal cancer patients.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Cell Biology,Molecular Biology,Biochemistry

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