Ph.D., University of Turin, 1998
firstname.lastname@example.org | (516) 367-5052
Two challenges in cancer biology guide my work: first, how do tumors become addicted to certain gene products, and second, how do tumors develop resistance to anti-cancer drugs. I focus on the epidermal growth factor receptor (EGFR), which is both addictive when mutated and a common source of drug resistance. We are also identifying new targets for the treatment of lung cancer.
Despite their large variety of genetic abnormalities, cancer cells have been found to be extremely sensitive to the reversal of certain mutations. Raffaella Sordella and colleagues study why cells in certain cancers are responsive to the inhibition of one particular gene or gene product. Why, for instance, do non-small-cell lung cancer (NSCLC) cells that have a particular mutation in the epidermal growth factor receptor (EGFR) respond dramatically to its inhibition by the drug Tarceva? This occurs in 15%–20% of patients, the great majority of whom, within 1–3 years, develop resistance. Various mutations have been implicated in about half of resistant patients. Sordella and colleagues have discovered a new resistance mechanism in a subpopulation of NSCLC cells that are intrinsically resistant to Tarceva. These tumor cells were observed to secrete elevated amounts of a growth factor called transforming growth factor-β (TGF-β), which in turn increases secretion of interleukin-6 (IL-6), an immune signaling molecule. Significantly, these effects were independent of the EGFR pathway. The team therefore hypothesizes that inflammation is one of the factors that can render a tumor cell resistant to treatment with Tarceva. In other work, Sordella collaborates with the Krainer lab to study whether alternative splicing has a role in the failure of p53-mediated senescence to halt oncogenesis in certain lung cancers.
New research explains why even targeted therapies eventually fail in lung cancer
March 29, 2017
Dr. Sordella and her team propose a novel theory of how some cancers circumvent the killing power of targeted therapies.
Researchers identify potentially druggable mutant p53 proteins that promote cancer growth
December 9, 2016
Truncated p53 proteins, presumed unimportant, now point to new drug targets for some of "the hardest cancers"
5th Graders spend a day as young scientists
December 16, 2015
Students from the West Side Elementary School learn about the history and workings of Cold Spring Harbor Laboratory.
Swim Across America fundraiser supports lung cancer research at CSHL
August 12, 2015
Swim Across America held its annual "Cove to Sound" swim at Morgan's Park in Glen Cove, NY on August 8, 2015.
Cancer metabolism and country music with first-year student Jackie Giovanniello
March 9, 2015
Student Jackie Giovanniello works to develop better treatment options for patients.
Experts convene at CSHL to scrutinize, assess low-dose CT screening for lung cancer
October 17, 2014
Nearly two dozen physicians and researchers took a close scientific view of lung cancer progression for diagnostic purposes.
Research may explain how the body’s foremost anti-cancer ‘guardian’ protein learned to switch sides
July 29, 2014
Researchers have discovered a new function of the body’s most important tumor-suppressing protein.
CSHL lung cancer researcher receives $70,000 from Swim Across America-Nassau Suffolk
March 3, 2014
Swim Across America (SAA) Nassau Suffolk Committee distributed the net proceeds of its 2013 Swims to six Long Island and metro area beneficiaries.
Long Island foundation presents check for $15,000 to support CSHL lung cancer research
October 1, 2013
The Elisabeth R. Woods Foundation gave $15,000 to support lung cancer research of CSHL Associate Professor Raffaella Sordella
Elisabeth R. Woods Foundation marks inaugural year
February 26, 2013
Local foundation makes an impact in their first year.
Smolen, G. A. and Sordella, R. and Muir, B. and Mohapatra, G. and Barmettler, A. and Archibald, H. and Kim, W. J. and Okimoto, R. A. and Bell, D. W. and Sgroi, D. C. and Christensen, J. G. and Settleman, J. and Haber, D. A. (2006) Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752. Proceedings of the National Academy of Sciences of the United States of America, 103(7) pp. 2316-21.
Kwak, E. L. and Sordella, R. and Bell, D. W. and Godin-Heymann, N. and Okimoto, R. A. and Brannigan, B. W. and Harris, P. L. and Driscoll, D. R. and Fidias, P. and Lynch, T. J. and Rabindran, S. K. and McGinnis, J. P. and Wissner, A. and Sharma, S. V. and Isselbacher, K. J. and Settleman, J. and Haber, D. A. (2005) Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib. Proceedings of the National Academy of Sciences of the United States of America, 102(21) pp. 7665-70.
Haber, D. A. and Bell, D. W. and Sordella, R. and Kwak, E. L. and Godin-Heymann, N. and Sharma, S. V. and Lynch, T. J. and Settleman, J. (2005) Molecular targeted therapy of lung cancer: EGFR mutations and response to EGFR inhibitors. Cold Spring Harbor Symposia on Quantitative Biology, 70 pp. 419-26.
Sordella, R. and Bell, D. W. and Haber, D. A. and Settleman, J. (2004) Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathways. Science, 305(5687) pp. 1163-7.
Lynch, T. J. and Bell, D. W. and Sordella, R. and Gurubhagavatula, S. and Okimoto, R. A. and Brannigan, B. W. and Harris, P. L. and Haserlat, S. M. and Supko, J. G. and Haluska, F. G. and Louis, D. N. and Christiani, D. C. and Settleman, J. and Haber, D. A. (2004) Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. The New England Journal of Medicine, 350(21) pp. 2129-39.Additional materials of the author at
CSHL Institutional Repository