Quilliam Lab

Under the direction of Lawrence Quilliam, PhD, the Quilliam Lab is interested in delineating signal transduction pathways induced by growth-stimulatory factors, and in determining the mechanisms by which these pathways are aberrantly activated during the course of malignant transformation. Many of the genes that become mutated in human cancers encode for mitogenic signaling proteins. Characterization of the enzymes and protein-protein interactions involved in mitogenic signaling forms the basis for the rational design of novel anti-cancer therapeutics.

Much of the focus of Quilliam’s research is centered on Ras family GTPases and the pathways they control. Ras proteins normally act as molecular switches to relay growth stimulatory signals but become constitutively activated in many cancers, leading to uncontrolled proliferation. The Ras onco-proteins are frequently mutated in pancreatic cancer, a malignancy with a dismal survival rate. Therefore, current lab efforts are addressing ways to combat Ras-induced transformation in pancreatic ductal adenocarcinoma cells through the simultaneous inhibition of pathways activated by Ras along with those, e.g. Yap/Taz transcriptional co-activators, that compensate for loss of Ras activity.

Independently, mouse models have been developed to understand the molecular and biological roles of Rap1, one of over 30 Ras-related proteins. Rap1A and 1B contribute to leukocyte (myeloid) and endothelial cell pathologies and also impact tumor growth and metastasis.

Research Updates

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Research Updates

Current Research Funding

Current research funding within the Quilliam Lab includes a biomedical research grant to support research targeting YAP to prevent resistance of pancreatic cancer to KRAS inhibition. The PI of this research is Lawrence Quilliam, PhD.

Recent Publications

  • Crk proteins transduce FGF signaling to promote lens fiber cell elongation
    Collins TN, Mao Y, Li H, Bouaziz M, Hong A, Feng GS, Wang F, Quilliam LA, Chen L, Park T, Curran T, Zhang X

    Elife. 2018 Jan 23;7. pii: e32586. doi: 10.7554/eLife.32586. PMID:29360039

  • Novel HRAS Mutation Independently Contributes to Left Ventricular Hypertrophy in a Family with a Known MYH7 Mutation
    Sana ME, Quilliam LA, Spitaleri A, Pezzoli L, Marchetti D, Lodrini C, Candiago E, Lincesso AR, Ferrazzi P, Iascone M. A

    PLoS One. 2016 Dec 21;11(12):e0168501. doi: 10.1371/journal.pone.0168501. PMID: 28002430

  • Small GTPase Rap1 Is Essential for Mouse Development and Formation of Functional Vasculature
    Chrzanowska-Wodnicka M, White GC 2nd, Quilliam LA, Whitehead KJ.

    PLoS One. 2015 Dec 29;10(12):e0145689. doi: 10.1371/journal.pone.0145689 PMID: 25545047

  • LKB1 tumor suppressor regulates AMP kinase/mTOR-independent cell growth and proliferation via the phosphorylation of Yap
    Nguyen HB, Babcock JT, Wells CD, Quilliam LA.

    Oncogene, 2013 Aug 29;32(35):4100-9. doi: 10.1038/onc.2012.431 PMID: 23027127

  • Mammalian target of rapamycin complex 1 (mTORC1) enhances bortezomibinduced death in tuberous sclerosis complex (TSC)-null cells by a cMYCdependent induction of the unfolded protein response
    Babcock JT, Nguyen HB, He Y; Hendricks JW, Wek RC, Quilliam LA.

    J Biol Chem. 2013 May 31;288(22):15687-98. doi: 10.1074/jbc.M112.431056. PMID: 23612979

Additional publications can be found on PubMed.