2014 Sackler Cancer Biology Award Recipients Named

The recipients of the 2014-2015 Sackler Families Collaborative Cancer Biology Awards have been selected. These awards support a student stipend and provide monies to supplement research costs for one year. These awards are designed to provide support for innovative studies in cancer biology that will advance our knowledge of this disease and have the potential for translation and an eventual impact on patient care.

This year's recipients are Kevin Goncalves, CMP student and Guo-fu Hu, PhD, Adviser for their project “Role of Angiogenin/Plexin B2 in Leukemic Stem Cell Quiescence and Chemoresistance” and Laura Stransky, CMP student and Michael Forgac, PhD, Adviser for their project “Elucidating the Mechanism of mTORC1 Activation by Amino Acids”.

Goncalves and Hu

Guo-fu Hu, PhD and his Cellular & Molecular Physiology student Kevin Goncalves received a Sackler Family Collaborative Cancer Biology Research Award this year for their application “Role of Angiogenin/Plexin B2 in Leukemic Stem Cell Quiescence and Chemoresistance”. This team is focused on Angiogenin (ANG), an angiogenic ribonuclease that has been shown to promote cancer cell proliferation by stimulating growth and survival pathways. They are particularly interested in the way this molecule functions in leukemic stem cells, cells that are extremely resistant to current therapies and drive relapse in patients. The pair will test the idea that the normal function of ANG in hematopoietic stem cells where it regulates quiescence is disrupted in leukemic stem cells. A long range goal of the work is to test the possibility that targeting ANG would expand therapeutic options for leukemia patients by targeting the leukemic stem cell.

Stransky and Forgac

Michael Forgac, PhD and his Cellular & Molecular Physiology student Laura Stransky received a Sackler Family Collaborative Cancer Biology Research Award this year for their application “Elucidating the Mechanism of mTORC1 Activation by Amino Acids”. Their work focuses on understanding the ways in which the vacuolar H+-ATPase (V-ATPase) proton pump influences rapamycin complex 1 (mTORC1) signaling. mTORC1 is a key signaling node responsible for integration of growth factor and nutrient sufficiency signals and is frequently deregulated in breast cancer. The pair will build on work showing that V-ATPase is necessary for amino acid-mediated activation of mTORC1 and study how the underlying mechanisms are subverted in cancer. These results should enhance our understanding of regulatory mechanisms important in breast cancer homeostasis and could eventually provide new approaches to therapeutic intervention.

Research Spotlight

Read up on the research of our featured PhD student and faculty member in our Research Spotlight.