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Molly Hammell

Assistant Professor
Ph.D., Dartmouth College, 2003

(516) 367-5009 (p)
  Hammell Lab Website
To ensure that cells function normally, tens of thousands of genes must be turned on or off together.  To do this, regulatory molecules - transcription factors and non-coding RNAs – simultaneously control hundreds of genes.  My group studies how the resulting gene networks function and how they adapt to changes, such as when cells become cancerous.”
Many of the best cancer drugs are highly toxic chemotherapeutics that kill normal and malignant cells alike. In contrast, targeted compounds that recognize cancer-specific pathways represent a kind of silver bullet that would be able to distinguish tumor cells from their healthy counterparts. A few targeted drugs have been identified, such as the BRAF inhibitor vemurafenib for melanoma, and initially these agents were highly promising. But patients rapidly relapsed as their cancers became resistant to treatment.

Molly Hammell
is working to tackle this problem, known as “acquired resistance,” in melanoma. Her lab, in collaboration with the Wistar Institute, combines the power of systems-level, high-throughput data analysis with patient-derived tumor samples. Hammell has developed computational algorithms for the integration of multiple types of high-throughput sequencing data into gene regulatory circuits. She is now applying these methods to explore the global changes in gene regulation that enable melanoma cells to bypass inhibitors of the BRAF signaling pathway, including DNA mutations and epigenetic modifications. Her work will identify the most clinically relevant pathways of interest for additional therapeutic approaches to inhibit tumor growth in melanoma. In addition to her work on melanoma, Hammell is using her expertise in bioinformatics in collaboration with other members of the CSHL community (including Marja Timmermans, Josh Dubnau, and Greg Hannon) to understand gene regulation in diverse systems, from maize to Drosophila.

Rozhkov, N. V. and Hammell, M. and Hannon, G. J. (2013) Multiple roles for Piwi in silencing Drosophila transposons. Genes and Development 27(4) pp. 400-412.

Li, W. H. and Jin, Y. and Prazak, L. and Hammell, M. and Dubnau, J. (2012) Transposable Elements in TDP-43-Mediated Neurodegenerative Disorders. PLoS ONE 7(9)

Hammell, M. (2010) Computational methods to identify miRNA targets. Seminars in Cell & Developmental Biology 21(7) pp. 738-44.

Hong, X. and Hammell, M. and Ambros, V. and Cohen, S. M. (2009) Immunopurification of Ago1 miRNPs selects for a distinct class of microRNA targets. Proceedings of the National Academy of Sciences of the United States of America 106(35) pp. 15085-90.

Hammell, M. and Long, D. and Zhang, L. and Lee, A. and Carmack, C. S. and Han, M. and Ding, Y. and Ambros, V. (2008) mirWIP: microRNA target prediction based on microRNA-containing ribonucleoprotein-enriched transcripts. Nature Methods 5(9) pp. 813-9.

Additional materials of the author at
CSHL Institutional Repository
2014 Rita Allen Foundation Scholar