Alana L. Welm, PhD

Research Interests

  • Neoplasm Metastasis
  • Breast Cancer
  • Tumor Immunology

Labs

Lab Website

Languages

  • English

Academic Information

  • Departments: Oncological Sciences - Associate Professor
  • Cancer Center Programs: Cell Response & Regulation

Academic Office Information

  • Huntsman Cancer Institute
    2000 Circle of Hope
    Salt Lake City, UT 84112

Academic Bio

Alana Welm, PhD, is an Associate Professor in the Department of Oncological Sciences at the University of Utah, an Investigator at the Huntsman Cancer Institute, and Co-Leader of the Cell Response and Regulation Program at HCI. Welm's laboratory studies breast cancer metastasis.

Dr. Welm completed her PhD in Cell and Molecular Biology at Baylor College of Medicine in Houston, TX under the supervision of Gretchen Darlington, PhD. She then went on to conduct postdoctoral training in Dr. J. Michael Bishop’s laboratory at the University of California, San Francisco where her work focused on developing new models of breast cancer metastasis. Dr. Welm started her laboratory at the University of Utah’s Huntsman Cancer Institute in 2007, and was promoted to Associate Professor with tenure in 2013.

The research in Dr. Welm’s laboratory is focused on solving the problem of breast cancer metastasis using in vivo modeling of mouse and human breast cancers. Dr. Welm’s group discovered that the Ron kinase pathway is an important facilitator of breast cancer metastasis through its unique dual function in tumor cells and in resident macrophages. Current areas of research include (1) pre-clinical studies of various Ron inhibitors for treatment and prevention of metastatic breast cancer; (2) pre-clinical and early clinical studies of Ron/Met inhibitors in bone metastatic cancers; (3) discovering molecular mechanisms by which Ron kinases promote metastasis through cell-autonomous and non cell-autonomous pathways; and (4) refining “precision medicine” for metastatic breast cancer using functional assays in patient-derived breast tumor grafts.

Education History

Type School Degree
Postdoctoral Fellowship University of California, San Francisco
Cancer Biology
Postdoctoral Fellow
Doctoral Training Baylor College of Medicine
Cell and Molecular Biology
Ph.D.
Undergraduate University of Montana
Microbiology
B.S.

Selected Publications

Journal Article

  1. The RON Receptor Tyrosine Kinase Promotes Metastasis by Triggering MBD4-Dependent DNA Methylation Reprogramming.Cunha S, Lin YC, Goossen EA, Devette CI, Albertella MR, Thomson S, Mulvihill MJ, Welm AL (2014). The RON Receptor Tyrosine Kinase Promotes Metastasis by Triggering MBD4-Dependent DNA Methylation Reprogramming. Cell Rep, 6(1), 141-54.
  2. Inhibition of ron kinase blocks conversion of micrometastases to overt metastases by boosting antitumor immunity.Eyob H, Ekiz HA, Derose YS, Waltz SE, Williams MA, Welm AL (2013). Inhibition of ron kinase blocks conversion of micrometastases to overt metastases by boosting antitumor immunity. Cancer Discov, 3(7), 751-60.
  3. Survivin promotion of melanoma metastasis requires upregulation of alpha5 integrin.McKenzie JA, Liu T, Jung JY, Jones BB, Ekiz HA, Welm AL, Grossman D (2013). Survivin promotion of melanoma metastasis requires upregulation of alpha5 integrin. Carcinogenesis, 34(9), 2137-44.
  4. RON promotes the metastatic spread of breast carcinomas by subverting antitumor immune responses.Eyob H, Ekiz HA, Welm AL (2013). RON promotes the metastatic spread of breast carcinomas by subverting antitumor immune responses. Oncoimmunology, 2(9), e25670.
  5. Protein arginine methyltransferase 5 accelerates tumor growth by arginine methylation of the tumor suppressor programmed cell death 4.Powers MA, Fay MM, Factor RE, Welm AL, Ullman KS (2011). Protein arginine methyltransferase 5 accelerates tumor growth by arginine methylation of the tumor suppressor programmed cell death 4. Cancer Res, 71(16), 5579-87.
  6. Tumor grafts derived from women with breast cancer authentically reflect tumor pathology, growth, metastasis and disease outcomes.DeRose YS, Wang G, Lin YC, Bernard PS, Buys SS, Ebbert MT, Factor R, Matsen C, Milash BA, Nelson E, Neumayer L, Randall RL, Stijleman IJ, Welm BE, Welm AL (2011). Tumor grafts derived from women with breast cancer authentically reflect tumor pathology, growth, metastasis and disease outcomes. Nat Med, 17(11), 1514-20.
  7. Short-Form Ron Promotes Spontaneous Breast Cancer Metastasis through Interaction with Phosphoinositide 3-Kinase.Liu X, Zhao L, Derose YS, Lin YC, Bieniasz M, Eyob H, Buys SS, Neumayer L, Welm AL (2011). Short-Form Ron Promotes Spontaneous Breast Cancer Metastasis through Interaction with Phosphoinositide 3-Kinase. Genes Cancer, 2(7), 753-62.
  8. Phosphorylation of the SRC epithelial substrate Trask is tightly regulated in normal epithelia but widespread in many human epithelial cancers.Wong CH, Baehner FL, Spassov DS, Ahuja D, Wang D, Hann B, Blair J, Shokat K, Welm AL, Moasser MM (2009). Phosphorylation of the SRC epithelial substrate Trask is tightly regulated in normal epithelia but widespread in many human epithelial cancers. Clin Cancer Res, 15(7), 2311-22.
  9. Six1 expands the mouse mammary epithelial stem/progenitor cell pool and induces mammary tumors that undergo epithelial-mesenchymal transition.McCoy EL, Iwanaga R, Jedlicka P, Abbey NS, Chodosh LA, Heichman KA, Welm AL, Ford HL (2009). Six1 expands the mouse mammary epithelial stem/progenitor cell pool and induces mammary tumors that undergo epithelial-mesenchymal transition. J Clin Invest, 119(9), 2663-77.

Review

  1. Mouse models of breast cancer metastasis to bone.Kretschmann KL, Welm AL (2012). Mouse models of breast cancer metastasis to bone. [Review]. Cancer and Metastasis Reviews, 31(3-4), 579-83.
  2. The macrophage stimulating protein/Ron pathway as a potential therapeutic target to impede multiple mechanisms involved in breast cancer progression.Kretschmann KL, Eyob H, Buys SS, Welm AL (2010). The macrophage stimulating protein/Ron pathway as a potential therapeutic target to impede multiple mechanisms involved in breast cancer progression. [Review]. Curr Drug Targets, 11(9), 1157-68.