Education & Training
- Graduate School – Vanderbilt University – PhD – Molecular Physiology
- Medical School – Vanderbilt University – MD
- Residency – University of Michigan – Pediatrics
- Fellowship – University of Michigan – Pediatric Hematology Oncology
NIH Grants: R01
Dr. McAllister-Lucas investigates the mechanisms by which dysregulated intracellular signaling promotes inflammation and neoplasia. She focuses on a complex of signaling proteins referred to as the CARMA-Bcl10-MALT1 (CBM) signalosome. She and others discovered this complex because the genes encoding its components are targeted by the mutation in lymphoid malignancy. This CBM signalosome functions in normal lymphocyte function by mediating antigen receptor-dependent activation of the pro-inflammatory, pro-survival NF-kappaB transcription factor. Her group discovered that the API2-MALT1 fusion oncoprotein possesses unique gain-of-function MALT1 proteolytic activity that drives the proliferation and survival of malignant B-cells. Additionally, she discovered that a CBM signalosome is activated by specific G protein-coupled receptors to augment the pathogenesis of solid tumors. Dr. McAllister-Lucas is an outstanding mentor and has served in leadership roles in the MSTP at the University of Michigan and now at the University of Pittsburgh. Her laboratory is an ideal environment for fellows in Bone Marrow Transplantation and Hematology-Oncology.
- McAuley JR, Freeman TJ, Ekambaram P, Lucas PC, McAllister-Lucas LM. CARMA3 Is a Critical Mediator of G Protein-Coupled Receptor and Receptor Tyrosine Kinase-Driven Solid Tumor Pathogenesis. Front Immunol. 2018 Aug 15;9:1887. doi: 10.3389/fimmu.2018.01887. eCollection 2018. Review. PubMed PMID: 30158935; PubMed Central PMCID: PMC6104486.
- Ekambaram P, Lee JL, Hubel NE, Hu D, Yerneni S, Campbell PG, Pollock N, Klei LR, Concel VJ, Delekta PC, Chinnaiyan AM, Tomlins SA, Rhodes DR, Priedigkeit N, Lee AV, Oesterreich S, McAllister-Lucas LM, Lucas PC. The CARMA3-Bcl10-MALT1 Signalosome Drives NFκB Activation and Promotes Aggressiveness in Angiotensin II Receptor-Positive Breast Cancer. Cancer Res. 2018. 78(5): 1225-1240.
- Klei LR, Hu D, Panek R, Alfano DN, Bridwell RE, Bailey KM, Oravecz-Wilson KI,Concel VJ, Hess EM, Van Beek M, Delekta PC, Gu S, Watkins SC, Ting AT, Gough PJ, Foley KP, Bertin J, McAllister-Lucas LM, Lucas PC. MALT1 Protease Activation Triggers Acute Disruption of Endothelial Barrier Integrity via CYLD Cleavage. Cell Rep. 2016 17(1):221-232.
- Rosebeck S, Rehman AO, Apel IJ, Kohrt D, Appert, A, O’Donnell MA, Ting AT, Du MQ, Baens M, Lucas PC, McAllister-Lucas LM. The API2-MALT1 fusion exploits TNFR pathway-associated RIP1 ubiquitination to promote oncogenic NF-kappaB signaling. Oncogene. 2014 33 (19): 2520-30.
- McAllister-Lucas LM, Baens M, Lucas PC. MALT1 protease: a new therapeutic target in B lymphoma and beyond? Clin. Cancer Res. 2011 17(21): 6623-31.
- Rosebeck S, Madden L, Jin X, Gu S, Apel IJ, Appert A, Hamoudi RA, Noels H, Sagaert X, Van Loo P, Baens M, Du MQ, Lucas PC, McAllister-Lucas LM. Cleavage of NIK by the API2-MALT1 fusion oncoprotein leads to noncanonical NFkappaB activation. Science 2011 331(6016):468-72.