- Kalamazoo College
- Johns Hopkins University School of Medicine
- The Wistar Institute
Memberships & Activities
- Women in Bio
- 500 Women Scientists
- American Association for Cancer Research
- Association for Women in Science
- Women in Cancer Research
- American Society for Cell Biology
- Society for Melanoma Research
- American Association for the Advancement of Science
- American Chemical Society
Awards & Honors
- 2019–present Associate Editor of Cancer Molecular Targets and Therapeutics
- 2017 – Fitzpatrick Medal for Pigment Cell and Melanoma Research
- 2016 – NIH K99 Pathway to Independence Award
- 2013–2015 Wistar NCI Training Grant
- 2010 – Scheinberg Travel Award
- 2004–2005 – NIH Postbaccalaureate Fellowship
- 2002 – Howard Hughes Medical Institute Summer Research Grant
- 2002 – Dalton/Zannoni Summer Research Fellowship
- 1999 – Michigan Competitive Scholarship
The Webster lab is interested in delineating the underlying mechanisms of phenotype plasticity that lead to therapy resistance and disease progression in melanoma. Current projects in the lab include investigating the role of Wnt signaling and slow cycling cells in melanoma progression and epigenetic changes that occur in highly metastatic cells that promote survival following multiple types of stress.
Metastatic melanoma is highly therapy resistant. Patients who receive targeted therapy and chemotherapy often relapse due to the emergence of resistant populations. Resistant populations, which emerge following several types of stress, exhibit characteristics of a more invasive phenotype. We have observed that highly invasive melanoma cells undergo a senescent-like adaptive response following multiple types of stress. This response includes cell cycle arrest, beta-gal positivity, increased PML bodies, increased heterochromatic foci, increase in histone methylation as well as senescence associated secretory phenotype (SASP; Webster et al., PMCR). However, these cells are highly invasive and retain clonogenic properties. Understanding the mechanisms that allow these cells to survive, invade and proliferate may lead to new therapeutic strategies.
Age-related changes in HAPLN1 increases lymphatic permeability and affect routes of melanoma metastasis. Ecker B, Kaur A, Douglass SM, Webster MR, et al. Cancer Discov, 2019;9(1):82-95.
Remodeling of the collagen matrix in aging skin promotes melanoma metastasis and affects immune cell motility. Kaur A, Ecker B, Douglass SM, Kugel III CH, Webster MR, et al. Cancer Discov, 2019;9(1):64-81.
Age correlates with response to Anti-PD- 1, reflecting age-related differences in intratumoral effector and regulatory T-Cell populations. Kugel III CH, Douglass SM, Webster MR, et al. Clin Cancer Res, 2018;24(21):5347-56.
A feedback loop between Wnt signaling and autophagy in melanoma. Ndoye, A, Budina A, Kugel III CH, Webster MR, et al. Cancer Res 2017;77(21):5873-85.
Inhibition of age-related therapy resistance in melanoma by rosiglitazone-mediated induction of Klotho. Behera R, Kaur A, Webster MR, et al. Clin Cancer Res 2017;23(12):3181-90.
Modeling the two-way feedback between contractility and matrix realignment reveals a nonlinear mode of cancer cell invasion. Ahmadzadeh H, Webster MR, Behera R, et al. Proc Natl Acad Sci USA 2017;114(9):E1617-26.
HSP70 inhibition limits FAK-dependent invasion and enhances the durability of BRAF inhibitor treatment in melanoma. Budina AK, Webster MR, Julia IJL, et al. Cancer Res 2016;76(9):2720.
sFRP2 in the aged microenvironment drives metastasis and resistance to targeted therapy. Kaur A, Webster MR, Marchbank K, et al. Nature 2016;532(7598):250-4.
Wnt5A promotes an adaptive senescent-like stress response, while continuing to drive invasion in melanoma cells. Webster MR, Xu M, et al. Pigment Cell Melanoma Res 2015;28(2):184-95.
Bisphosphonamidate clodronate prodrug exhibits selective cytotoxic activity against melanoma cell lines. Webster MR, Kamat C, et al. Mol Cancer Ther 2014;3(12):1378-93.