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FINDING CURES TOGETHER<sup>SM</sup>

The 2015 Phillip A. Sharp Awards for Innovation in Collaboration

Genetic Heterogeneity of Pancreatic Cancer

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Hans Clevers, MD, PhD (Sta Op Tegen Kanker (SU2C-KWF) Tumor Organoids Dream Team), Hubrecht Institute, Netherlands

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David A. Tuveson, MD, PhD (SU2C Scientific Advisory Committee), Cold Spring Harbor Laboratory

Grant Term: June 2015 - May 2017
Total Funding: $250,000

Accomplishments
The team has shared the ability to culture pancreatic organoids with several research groups including SU2C Dream Teams such as the SU2C-LF Pancreatic Dream Team led by Drs. Jaffee and Vonderheide. Dr. Vonderheide has been able to use the organoid models to pursue the identification of tumor antigen in his studies. The team has also shared their organoid resources with Dr. Evans, co-leader of the SU2C-Cancer Research UK-Lustgarten Foundation Pancreatic Cancer Dream Team. The Evans lab is using the organoid models for drug discovery studies.

Currently, Dr. Tuveson is advising the SU2C-LF Pancreatic Interception Research Team who are using organoids to possibly predict the response of patients to a particular treatment regimen.

Targeting Epigenetic Plasticity and Drug Resistance in Pediatric Cancer

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Kimberly Stegmaier, MD (SU2C 2009 IRG Recipient), Dana-Farber Cancer Institute


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Adolfo A. Ferrando, MD, PhD (SU2C 2011 IRG Recipient), Columbia University



Grant Term: July 2015 - June 2016
Total Funding: $250,000

Project Summary

Treatment options for patients whose cancer returns are often limited because their cancer cells have become resistant to chemotherapy. It is thought that distinct subgroups of cells in the primary tumor are differentially sensitive to chemotherapy and that cells can become drug-resistant through epigenetic changes (modifications in the DNA that activate or inactivate genes). Drs. Stegmaier and Ferrando worked to define the factors involved in chemotherapy resistance in acute lymphoblastic leukemia and Ewing sarcoma.

Accomplishments
They analyzed 57 diagnostic, relapse, and remission leukemia DNA samples. They observed the high prevalence of mutations in the RAS signaling pathway, and recurrent mutations in epigenetic factors in relapse leukemia.