McCormick Lab

McCormick Lab, UCSF
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Research Profile

(415) 502-1868 (lab)
(415) 502-1712 (fax)

1450 3rd St., MC 0128; PO Box 589001
San Francisco, CA 94158-9001

deliveries: 1450 3rd Street, HD-450; San Francisco, CA 94158

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Full Biosketch
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Frank McCormick, PhD, FRS, DSc (Hon)
Professor, UCSF Helen Diller Family Comprehensive Cancer Center

David A. Wood Distinguished Professorship of Tumor Biology and Cancer Research

My research is focused on signal transduction pathways in cancer cells, and ways of treating cancer based on these pathways. The Ras pathway has been my primary interest, although we are also interested in metabolic differences between cancer cells and normal cells, and defects in cancer proteins related to mitotic checkpoints. My lab is attempting to understand how oncogenic Ras alters cell growth and survival in cancer cells, and in cells from patients suffering from neurofibromatosis. The latter disease is caused by loss of a negative regulator of Ras of the Ras GAP family, a family of enzymes that was discovered in my lab. Loss of the neurofibromin protein leads to hyperactivation of Ras in cells of neural crest origin: as a result patients expressing defective neurofibromin suffer from learning defects, multiple benign lesions and an increased risk of certain cancers. We are using a combination of yeast genetics and biochemistry to understand more about the function of neurofibromin and how it is regulated, as well as new ways of treating this terrible disease.

The Ras pathway is negatively regulated by intrinsic pathways that are not well understood, including those involving ephrins and sprout proteins. We are using biochemical methods to elucidate these pathways at the molecular level, and hope that this will lead to new ways of blocking Ras activity for therapeutic purposes.

My lab has worked extensively on viruses that kill cancer cells selectively. We are developing this concept using self-amplifying plasmids that replicate in cancer cells specifically, and encode proteins that kill neighboring cancer cells. Plasmid amplification is driven by DNA replication proteins coded by the plasmid itself, and an origin of DNA replication also encoded in the plasmid. The replication protein has been modified to prevent amplification in normal cells, in which RB and p53 block activity.



Latest News


Recent Publications

  1. McCormick F. The potential of targeting Ras proteins in lung cancer. Expert Opin Ther Targets. 2015 Apr; 19(4):451-4.
    View on PubMed
  2. Martins MM, Zhou AY, Corella A, Horiuchi D, Yau C, Rakshandehroo T, Gordan JD, Levin RS, Johnson J, Jascur J, Shales M, Sorrentino A, Cheah J, Clemons PA, Shamji AF, Schreiber SL, Krogan NJ, Shokat KM, McCormick F, Goga A, Bandyopadhyay S. Linking Tumor Mutations to Drug Responses via a Quantitative Chemical-Genetic Interaction Map. Cancer Discov. 2015 Feb; 5(2):154-67.
    View on PubMed
  3. Phuchareon J, Overdevest JB, McCormick F, Eisele DW, van Zante A, Tetsu O. Fatty Acid binding protein 7 is a molecular marker in adenoid cystic carcinoma of the salivary glands: implications for clinical significance. Transl Oncol. 2014 Dec; 7(6):780-7.
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  4. Guinney J, Dienstmann R, Ferté C, Friend S, McCormick F. Social interactomes for enabling research communities. Cancer Discov. 2014 Nov; 4(11):1265-8.
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  5. Phuchareon J, van Zante A, Overdevest JB, McCormick F, Eisele DW, Tetsu O. c-Kit Expression is Rate-Limiting for Stem Cell Factor-Mediated Disease Progression in Adenoid Cystic Carcinoma of the Salivary Glands. Transl Oncol. 2014 Oct; 7(5):537-45.
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  6. Sos ML, Levin RS, Gordan JD, Oses-Prieto JA, Webber JT, Salt M, Hann B, Burlingame AL, McCormick F, Bandyopadhyay S, Shokat KM. Oncogene mimicry as a mechanism of primary resistance to BRAF inhibitors. Cell Rep. 2014 Aug 21; 8(4):1037-48.
    View on PubMed
  7. >Full list of publications here