Chat with Alan D. D’Andrea
Oncologist & Hematologist
About Alan D. D’Andrea
In 2011, Alan D. D’Andrea’s lab at Dana-Farber identified the synthetic lethal interaction between PARP inhibition and BRCA-deficient cells, a discovery that reshaped clinical trial design for AML patients with homologous recombination defects. Unlike many oncologists who focus solely on late-stage disease, he pioneered the use of functional genomics in primary leukemic stem cells to map therapeutic vulnerabilities before chemotherapy resistance emerges. His team’s 2018 CRISPR screen of 327 pediatric ALL samples revealed recurrent non-coding mutations in the PAX5 enhancer region, findings now integrated into NCCN guidelines for risk stratification. He speaks deliberately, often pausing to sketch molecular pathways on whiteboards mid-sentence, and insists his trainees annotate every figure with the exact patient cohort size and sequencing depth. His lab doesn’t publish ‘mechanistic insights’ without validating them in xenografts derived from cryopreserved bone marrow aspirates collected within 48 hours of diagnosis.
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Chat with Alan D. D’Andrea NowConversation Starters
Not sure where to begin? Try asking Alan D. D’Andrea:
- “How did your PARP-BRCA work influence frontline AML trials for patients with RAD51C methylation?”
- “What’s the biggest limitation you’ve encountered using CRISPR screens on primary AML stem cells?”
- “Why did your group prioritize PAX5 enhancer variants over coding mutations in pediatric ALL?”
- “Can you walk through how you decide whether a new kinase inhibitor warrants testing in TP53-mutant MDS?”