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Frederick W. Alt, PhD, Honored With 2021 AACR Award for Lifetime Achievement in Cancer Research


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The American Association for Cancer Research (AACR) is recognizing geneticist Frederick W. Alt, PhD, with the 18th AACR Award for Lifetime Achievement in Cancer Research.

Frederick W. Alt, PhD

Frederick W. Alt, PhD

Dr. Alt is a Howard Hughes Medical Institute investigator, Director of the Program in Cellular and Molecular Medicine at Boston Children’s Hospital, and the Charles A. Janeway Professor of Pediatrics and Professor of Genetics at Harvard Medical School. He is being honored for his discovery of gene amplification in mammalian cancer cells. His research established oncogene amplification as a mechanism of tumor progression and elucidated nonhomologous DNA end joining, a pathway that repairs double-strand breaks in DNA. His findings have revolutionized scientific understanding of how genomic rearrangements occur and how they contribute to cancer.

Early Discovery

Dr. Alt received his doctorate in biology from Stanford University in 1977 and did his postdoctoral training at the Massachusetts Institute of Technology with Nobel Laureate David Baltimore, PhD.

Early in his career, Dr. Alt made a discovery that would have a long-lasting impact on the cancer biology field. His finding of dihydrofolate reductase gene amplification provided the first molecular demonstration of genomic instability in mammalian cancer cells. His work also provided a molecular basis for considering cancer genomes as distinctly different from normal cell genomes. His subsequent discovery of N-myc, based on observed amplification rates in human neuroblastomas, was critical in establishing oncogene amplification as a fundamental tumor progression mechanism and provided several examples of cancer genomic instability. His discoveries revealed both a mechanism for how cancer cells acquire drug resistance and a mechanism for how they develop more potent oncogenes.

Dr. Alt’s later discovery of key nonhomologous DNA end joining played a major part in establishing its critical role in suppressing the rearrangements and amplifications that cause cancer. 


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