American Cancer Society Professor

Tony Hunter

Molecular and Cell Biology Laboratory

Renato Dulbecco Chair

Tony Hunter

Current Research

The Problem

Cells are like creatures of habit—they follow the same cellular cycle over and over, coordinating the timing of gene and protein activation with growth and division. If this cycle is broken, things start to fall apart: cells begin copying the wrong genes, turning on proteins at the wrong times or dividing too fast or too slowly. All of these disruptions can lead to cancer. Understanding how a healthy cell controls its growth cycle can help researchers get a better grasp on what goes wrong in tumor cells when their growth spirals out of control—and how to fix it. But it’s hard to pinpoint which individual genes and proteins are most important.

The Approach

Tony Hunter made the seminal discovery, more than three decades ago, that the addition and subtraction of phosphate molecules to proteins on tyrosine, one of the 20 amino acids, allows cells to control when key proteins are on standby and when they are active. In cancers, he went on to show that growth was switched into an always-on mode by the malfunctions of these phosphates. Since then, his lab has led the field in understanding how chemical additions to proteins control the cell cycle and growth. Hunter uses cutting-edge molecular, genetic and cell biology techniques to probe how these programs interact with each other, what effect they have on cells and how cancers disrupt them to encourage uninhibited growth.

Already, cancer drugs—such as the leukemia therapy Gleevec—have been designed based on Hunter’s discoveries. Gleevec turns off an enzyme that normally adds phosphates to proteins, preventing cancers from growing. As Hunter continues to discover other ways in which cells use chemical additions to proteins to control their growth, he aims to find potential therapeutic targets for cancers.

The Innovations and Discoveries

Hunter demonstrated that a mechanism called tyrosine phosphorylation (the addition of phosphate molecules to an amino acid) acts as a master on/off switch for a number of key proteins. This discovery has led to new, successful cancer therapies.

Hunter helped to explain precisely how cells mobilize their repair crews to fix damaged DNA, an important mechanism for preventing cells from turning cancerous.

He showed how some cancers find a loophole in the cellular security system that should destroy them, which helps them to recover and resume dividing after treatment with DNA-damaging cancer drugs.

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BA, First Class Honors, University of Cambridge, England
PhD, University of Cambridge, England
Postdoctoral Fellow, The Salk Institute and University of Cambridge

Awards & Honors

  • 2013 Fellow, AACR Academy
  • 2013 Einstein Professor, Chinese Academy of Sciences
  • 2012 Thomson-Reuters Citation Laureate
  • 2011 Signal Transduction Society Honorary Medal
  • 2011 Lifetime Achievement in Cancer Research Award, Jefferson Kimmel Cancer Center
  • 2007 Clifford Prize for Cancer Research
  • 2006 Robert J. and Claire Pasarow award for Cancer Research
  • 2006 Daniel Nathan's Memorial Award
  • 2005 Wolf Prize in Medicine
  • 2004 Louisa Gross Horwitz Prize
  • 2004 Prince of Asturias Award for Scientific and Technical Research
  • 2004 Kirk A. Landon-AACR Prize for Basic Cancer Research
  • 2004 American Cancer Society Medal of Honor
  • 2003 City of Medicine Award
  • 2003 Sergio Lombroso Award in Cancer Research
  • 2001 Keio Medical Science Prize
  • 2000 J. Allyn Taylor International Prize in Medicine
  • 1994 Gairdner Foundation International Award
  • 1994 General Motors Cancer Research Foundation Prize
  • American Cancer Society Research Professorship
  • Member of the American Philosophical Society
  • Member of the National Academy of Medicine
  • Member of the National Academy of Medicine
  • Fellow of the American Academy of Arts and Sciences
  • Member of the United States National Academy of Sciences
  • Fellow of the Royal Society of London

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