MD/PhD candidate Boris Dimitrov has received the Ruth L. Kirschstein National Research Service F30 Award from the National Cancer Institute.
Congrats Boris on this well deserved achievement!!
UMass Chan Commencement Celebration with Emmet!!
This past weekend, Emmet Karner, PhD, joined the UMass Chan Class of 2026 in commencement ceremonies after successfully defending his thesis on “Integrin Regulation of Ferroptosis in the Context of Tumor Heterogeneity. “
We are so happy and proud to have had the opportunity to celebrate with Dr. Karner and his family on this major milestone, and wish him all the best in the next chapter of his life!!
Congratulations to Dr. Karner and all members of the Class of 2026!!
Prajakta Presents her Poster at AACR Annual Meeting!
Last week, graduate student Prajakta Ambegaokar presented her exciting research on folate receptor alphas’s role in ferroptosis resistance in breast cancer at the 2026 annual American Associate for Cancer Research meeting in San Diego, CA.
Mandy's Paper on PD-L1 Targeting Nanogel Conjugates Inducing Ferroptosis is Highlighted by Cell Chemical Biology!
Cell Chemical Biology highlights studies in the ever growing field of ferroptosis, including exciting work led by our very own Mandy Wang!
You can read Mandy’s paper here, and explore additional research projects on ferroptosis from Cell Chemical Biology here!
Boris's Paper on Ferroptosis Impeding Metastasis is Published in Cell Reports!
Abstract
We investigated a potential function of transient receptor potential cation channel 6 (TRPC6) in enabling breast cancer cells to resist stimuli that induce ferroptosis. A minority population of quiescent cells was isolated from triple-negative breast cancer (TNBC) cell lines that exhibit increased TRPC6 expression and resistance to ferroptosis compared to proliferating cells. These quiescent cells are also more metastatic than the proliferating cells, supporting the hypothesis that metastasis requires the ability of cells to evade ferroptosis. In pursuit of the mechanism, we discovered that the ability of TRPC6 to repress c-Myc is essential because its repression sustains levels of glutathione that are sufficient to impede ferroptosis. Importantly, treatment of TNBC cells with a TRPC6 inhibitor reduces metastasis significantly, an effect that is mitigated by a ferroptosis inhibitor. These results indicate that a sub-population of TNBC cells characterized by TRPC6 expression has the potential to form metastases by evading ferroptosis.
Dimitrov BS, Mukhopadhyay D, Goel HL, Karner ER, Silva CA, Kumar A, Peterson C, Wang M, Mercurio AM. Inducing ferroptosis to impede metastasis by inhibiting the calcium channel TRPC6. Cell Rep. 2025 Nov 25.