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Grants, Honors, Awards & Recognitions

  • May 30, 2025

    Former MCCB student Kevin O’Connor receives inaugural Satish & Sudha Gupta Award for Cancer Research

    Congratulations to Kevin O’Connor, an MD/PhD student in his final year of the medical program, on being the first recipient of the Satish & Sudha Gupta Award! The new award was established to support UMass Chan MD/PhD students who are actively engaged in cancer research and who have been recognized by their peers and faculty for their promise as oncology physician-scientists. The award was presented to O’Connor at the T.H. Chan School of Medicine Awards Ceremony on May 30th.

    O’Connor completed his PhD thesis in the lab of Michelle Kelliher, PhD, where his research centered on investigating the mechanisms underlying treatment resistance and relapse in T-cell acute lymphoblastic leukemia, a type of pediatric cancer. His research was published last year in the journal Leukemia.

    Read more about the award, and Dr. O'Connor's research, from UMass Chan’s Stories of Giving.  

  • May 12, 2025

    MCCB student Nate MacGilvary receives NIH fellowship to investigate mechanisms of chemoresistance in BRCA mutant cancers

    Nate MacGilvary, a PhD student in the lab of Sharon Cantor, PhD, has received an NIH National Research Service Award predoctoral training fellowship from the National Cancer Institute (NCI) to investigate replication gap suppression in distinct models of chemoresistant BRCA mutant cancers.

    The study will build upon recent groundbreaking research in the Cantor lab showing that small nicks (or gaps) in one strand of the DNA, rather than complete double-strand breaks as previously thought, are a key vulnerability in hereditary breast and ovarian cancers (HBOCs, most often caused by a mutation in the BRCA1 or BRCA2 gene) that renders them sensitive to chemotherapy. MacGilvary’s research will investigate whether chemoresistance, which poses a major challenge to the treatment of HBOCs, develops because a cancer cell acquires the ability to repair these small gaps—a mechanism called gap suppression.

    The results of the study will identify biological pathways that contribute to chemoresistance in HBOC, paving the way for future development of therapeutic strategies that target these pathways as a means of resensitizing chemoresistant HBOCs to therapy.

  • May 1, 2025

    Grad student Bradley Class receives NIH fellowship to advance understanding of rare neurodegenerative disorder

    Bradley Class, a 3rd year PhD student in the lab of Michael Lodato, PhD, has received an NIH predoctoral training fellowship from the National Institute of Neurological Disorders and Stroke (NINDS) to explore single-cell analysis of somatic mutation rates, mechanisms, and impacts in human ataxia telangiectasia cerebellum.

    Ataxia telangiectasia is a rare, inherited disorder that primarily affects the cerebellum—the part of the brain that controls muscle movement—resulting in loss of coordination (ataxia) and other neurological symptoms. The disease is caused by mutations in the ATM gene, which encodes a protein that plays a pivotal role in coordinating the repair of DNA double-strand breaks. Mutations in ATM lead to the progressive loss of Purkinje cells (PCs), a rare population of neurons in the cerebellum that are difficulty to study due to their low abundance. Exactly how loss of ATM function affects PC genome stability, and thus PC function, is not well known.

    To answer these questions, Class will leverage a protocol he recently developed for isolating PCs from frozen brain samples, and apply single-cell multi-omics to simultaneously analyze both the genome (DNA) and transcriptome (RNA). Using this approach, he will generate a catalog of DNA mutations in PCs to identify mutation “signatures”, and study the relationship between DNA damage and transcriptional changes. The results of the study will provide insight into the changes that occur in PCs in ataxia telangiectasia and the mechanisms that drive PC death—important stepping stones to finding a cure for the disease.

    Read the related story from UMass Chan News.

  • May 1, 2025

    Lucio Castilla receives NIH grant to explore therapeutic approach to delay onset of blood cancer

    Lucio Castilla, PhDLucio Castilla, PhD, has received NIH funding from the National Cancer Institute (NCI) to study tyrosine kinase inhibitors as preventive therapy in RUNX1-familial platelet disorder (RUNX1-FPD)—a type of hereditary blood disease, caused by mutations in the RUNX1 gene, that increases the lifetime risk of developing blood cancer. The grant will explore whether imatinib, a drug that is used to treat chronic myelogenous leukemia, can prevent or delay the development of blood cancer in a mouse model of RUNX1-FPD. The results of the study may support the use of imatinib in a phase-II clinical trial as preventive therapy in patients with RUNX1-FPD.

  • Feb 28, 2025

    MD/PhD student Ayush Kumar wins 2024 AMA Research Challenge

    Ayush KumarAyush Kumar, an MD/PhD student in his third year of dissertation research in the lab of Art Mercurio, PhD, was selected as the winner of the 2024 AMA Research Challenge—a national competition hosted by the American Medical Association in which medical students and residents showcase their research, culminating in presenting their work to an elite panel of judges. The AMA Research Challenge is the largest multi-specialty medical research conference in the nation. Mr. Kumar will be awarded the grand prize of $10,000.

    Watch a video of the finals and read the related story from UMass Chan News.

  • Oct 1, 2024

    Scot Wolfe receives funding for collaborative research to develop gene editing therapy for muscular dystrophy

    Scot Wolfe, PhDScot Wolfe, PhD, and collaborator Charles Emerson, Jr. (professor of neurology and Director of the Wellstone Muscular Dystrophy Program at UMass Chan) have received a three-year grant from the Muscular Dystrophy Association to develop a precise genome editing therapy to correct a common mutation in the TCAP gene, which leads to the R7 subtype of limb girdle muscular dystrophy. The project, which combines the use of stem cell, nanoparticle, mouse model and genome editing technologies, will provide a versatile platform to develop correction therapies for other gene mutations that cause other types of muscular dystrophy.

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