Martin McMahon
Professor of Dermatology and Adjunct Professor of Oncological Sciences
Translational Cancer Research, Mouse Models, Melanoma, Lung Cancer, Thyroid Cancer, RAF Kinase, PI3 Kinase, Experimental Therapeutics
Molecular Biology Program
Biological Chemistry Program
Education
B.Sc. University of Glasgow
Ph.D. King's College, London
Research
Dr. McMahon’s translational cancer research program focuses on the mechanisms underlying the development of metastatic melanoma, lung and thyroid cancer. Although these malignancies are derived from distinct cell types, they share a striking number of common genetic alterations especially activating mutations in KRAS, BRAF, PIK3CA or CTNNB1 (b-catenin). In addition, many of these tumors display alterations in tumor suppressors such as CDKN2A, PTEN or TP53. To do this, Dr. McMahon’s laboratory works with cultured human cancer-derived cells and with genetically engineered mouse models of human cancer. Such model systems have demonstrated considerable value in the design and evaluation of new diagnostic, prognostic, and therapeutic tools to treat patients with cancer.
References
- Shai A, Dankort D, Juan J, Green S, McMahon M (05/22/15). TP53 silencing bypasses growth arrest of BRAFV600E-induced lung tumor cells in a two-switch model of lung tumorigenesis. Cancer Res, 75(15), 3167-3180.
- PI3'-kinase inhibition forestalls the onset of MEK1/2 inhibitor resistance in BRAF-mutated melanoma.Deuker MM, Marsh Durban V, Phillips WA, McMahon M (2015). PI3'-kinase inhibition forestalls the onset of MEK1/2 inhibitor resistance in BRAF-mutated melanoma. Cancer Discov, 5(2), 143-53.
- Activating BRAF and PIK3CA mutations cooperate to promote anaplastic thyroid carcinogenesis.Charles RP, Silva J, Iezza G, Phillips WA, McMahon M (2014). Activating BRAF and PIK3CA mutations cooperate to promote anaplastic thyroid carcinogenesis. Mol Cancer Res, 12(7), 979-86.
- Diminished WNT -> beta-catenin -> c-MYC signaling is a barrier for malignant progression of BRAFV600E-induced lung tumors.Juan J, Muraguchi T, Iezza G, Sears RC, McMahon M (2014). Diminished WNT -> beta-catenin -> c-MYC signaling is a barrier for malignant progression of BRAFV600E-induced lung tumors. Genes Dev, 28(6), 561-75.
- BRAFV600E cooperates with PI3K signaling, independent of AKT, to regulate melanoma cell proliferation.Silva JM, Bulman C, McMahon M (2014). BRAFV600E cooperates with PI3K signaling, independent of AKT, to regulate melanoma cell proliferation. Mol Cancer Res, 12(3), 447-63.
- Modelling vemurafenib resistance in melanoma reveals a strategy to forestall drug resistance.Das Thakur M, Salangsang F, Landman AS, Sellers WR, Pryer NK, Levesque MP, Dummer R, McMahon M, Stuart DD (2013). Modelling vemurafenib resistance in melanoma reveals a strategy to forestall drug resistance. Nature, 494(7436), 251-5.
- Differential AKT dependency displayed by mouse models of BRAFV600E-initiated melanoma.Marsh Durban V, Deuker MM, Bosenberg MW, Phillips W, McMahon M (2013). Differential AKT dependency displayed by mouse models of BRAFV600E-initiated melanoma. J Clin Invest, 123(12), 5104-18.
- Mutationally activated PIK3CA(H1047R) cooperates with BRAF(V600E) to promote lung cancer progression.Trejo CL, Green S, Marsh V, Collisson EA, Iezza G, Phillips WA, McMahon M (2013). Mutationally activated PIK3CA(H1047R) cooperates with BRAF(V600E) to promote lung cancer progression. Cancer Res, 73(21), 6448-61.
- A central role for RAF-->MEK-->ERK signaling in the genesis of pancreatic ductal adenocarcinoma.Collisson EA, Trejo CL, Silva JM, Gu S, Korkola JE, Heiser LM, Charles RP, Rabinovich BA, Hann B, Dankort D, Spellman PT, Phillips WA, Gray JW, McMahon M (2012). A central role for RAF-->MEK-->ERK signaling in the genesis of pancreatic ductal adenocarcinoma. Cancer Discov, 2(8), 685-93.
- Braf(V600E) cooperates with Pten loss to induce metastatic melanoma.Dankort D, Curley DP, Cartlidge RA, Nelson B, Karnezis AN, Damsky WE Jr, You MJ, DePinho RA, McMahon M, Bosenberg M (2009). Braf(V600E) cooperates with Pten loss to induce metastatic melanoma. Nat Genet, 41(5), 544-52.
- A new mouse model to explore the initiation, progression, and therapy of BRAFV600E-induced lung tumors.Dankort D, Filenova E, Collado M, Serrano M, Jones K, McMahon M (2007). A new mouse model to explore the initiation, progression, and therapy of BRAFV600E-induced lung tumors. Genes Dev, 21(4), 379-84.