Our Mission

The Jane Coffin Childs Memorial Fund for Medical Research is dedicated to providing financial support to offer highly qualified scientists the opportunity to pursue research into the causes and origins of cancer.

The goal of the Fund is to provide support to the brightest individual scientists pursuing careers in cancer research while promoting and emphasizing the value and contribution of the individual in keeping with the spirit of the conception of the Fund.

FINANCIAL REPORTS

2008 FINANCIAL REPORT >
2007 FINANCIAL REPORT >

JCC FUND NEWSLETTERS
Check out our current and past newletters to find out about the newest JCCF fellows and what they are researching, details on our annual retreats, and other interesting articles.

2011 JCC FUND NEWSLETTER >

2010 JCC FUND NEWSLETTER >
2009 JCC FUND NEWSLETTER >
2008 JCC FUND NEWSLETTER >
2007 JCC FUND NEWSLETTER >
2006 JCC FUND NEWSLETTER >
2005 JCC FUND NEWSLETTER >

We will accept referee and sponsor letters either through the website or by email until February 28. Referees may send letters and ratings (from A to E) directly to us at letters@jccfund.org. Sponsor letters may also be sent to the same address. Please paste the contents of your letter inside the body of your email.

Elia

Andrew Elia

Massachusetts General Hospital Harvard Medical School, Boston, MA

The cellular machinery of the DNA damage response (DDR) consists of a dynamic network of multiprotein complexes whose hierarchical assembly relies upon an array of posttranslational modifications. I am studying novel mechanisms by which such post-translational modifications regulate the DDR.


I obtained my bachelor’s degree in chemistry from Stanford University before entering an MD/PhD program at Harvard Medical School. I subsequently subsequently completed a residency in radiation oncology at Harvard and am now working in the laboratory of Stephen Elledge. I am interested in genomic instability and how it influences the progression and treatment of cancer.  Numerous cancer susceptibility syndromes arise from the mutation of DNA repair genes, whose loss undermines genomic integrity. The modulation of such DNA repair pathways can also affect tumor sensitivity to radiation and chemotherapy. I am interested in studying how synthetic lethal interactions between such DNA repair pathways might be exploited in the treatment of cancer.

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