Grants, Honors, Awards & Recognitions

Heidi Tissenbaum, PhD, recently appeared on Longevity Roadmap, a podcast hosted by Dr. Buck Joffrey, MD, that features conversations with leading scientists in the field of aging research.

In the episode, “Molecular Secrets of Aging Told Through Worms,” Dr. Tissenbaum discusses why the tiny nematode Caenorhabditis elegans is such a powerful model organism for studying longevity, and how seminal research in C. elegans uncovered an evolutionarily conserved biological pathway—the insulin/IGF-1 signaling pathway—that ultimately led to the identification of a key gene associated with human longevity. She also emphasizes the importance of measuring healthspan (healthy aging), not just lifespan, and shares her perspective as a basic scientist on the future of aging research.

Listen to the episode of Longevity Roadmap on Spotify or Apple Podcast to hear more about Dr. Tissenbaum’s insights into the science of aging.

Craig Ceol, PhD, has received a two-year Established Investigator Award from the Melanoma Research Foundation to investigate inhibiting ligand-driven bone morphogenetic protein (BMP) signaling to overcome immunotherapy resistance.

This work builds on previous findings from the Ceol Lab identifying GDF6, a BMP ligand, as a melanoma oncoprotein. GDF6 is highly expressed in 75–80% of melanomas and drives tumor formation by suppressing cell differentiation and apoptosis. Blocking GDF6 disrupts BMP signaling, causing melanoma cells to differentiate and die, highlighting its potential as a therapeutic target. Importantly, GDF6 is not expressed in normal melanocytes or in adult tissues, making it a selective and attractive target for treatment.

The proposed research aims to determine whether targeting GDF6 could provide an effective therapy for immunotherapy-resistant melanoma, a persistent and major clinical challenge. To advance this work, Dr. Ceol is collaborating with Michael Brehm, PhD, Professor of Molecular Medicine and Co-Director of the UMass Chan Humanized Mouse Core. Together, they will investigate whether therapeutic monoclonal antibodies targeting GDF6, developed by the Ceol Lab in partnership with MassBiologics, can both directly attack immunotherapy-resistant tumor cells and enhance the effectiveness of existing immunotherapies. If successful, this two-pronged approach could deliver a powerful new treatment for patients with immunotherapy-resistant melanoma.

Groundbreaking work from the laboratory of Michael Lodato, PhD, has been spotlighted in The Scientist. The article highlights Lodato’s recent study, published in Nature, that offers new insights into the genomic and transcriptomic changes that occur in the human brain during the normal aging process. The study, conducted in collaboration with UMass Chan researcher and computational biologist Zhiping Weng, PhD, sheds light on how these changes may impact neuron function and cognitive health, even in the absence of disease.

Read the story in The Scientist.

New research from the lab of Sharon Cantor, PhD, has identified a targetable vulnerability in BRCA1-deficient cells—a finding with potential implications for the treatment of inherited breast and ovarian cancers.

The study builds upon the lab’s prior work demonstrating that single-stranded DNA replication gaps, rather than double-stranded DNA breaks, are the key cytotoxic lesions underlying BRCA1 deficiency. In their latest findings, published in Molecular Cell, Cantor’s group shows that these single-stranded gaps are enriched for RAD51, a DNA-binding protein involved in genome maintenance, and that RAD51 plays an essential protective function at these sites—rendering BRCA1-deficient cells dependent on RAD51 to prevent catastrophic genome instability. Importantly, pharmacological inhibition of RAD51 selectively reduces survival of BRCA1-deficient cells but not BRCA1-proficient cells, highlighting a vulnerability that can be exploited for therapeutic benefit.

Read more about the study here. 

A new study from the lab of Michael Lodato, PhD, published in Nature, sheds light on the molecular changes that occur in the human brain during the normal aging process at an extraordinary level of detail.

For the study, the Lodato lab obtained brain samples (specifically, prefrontal cortex) from 19 human donors, ranging in age from 0.4 to 104 years, from the National Institutes of Health NeuroBioBank repository. Using a trifecta of single-cell analysis technologies—single-nucleus RNA-sequencing, single-cell whole genome sequencing, and spatial transcriptomics—they generated a comprehensive catalog of age-related, cell-type specific changes in the transcriptomic and genomic landscape, creating an unprecedented map of the transformations that occur in the human brain across the lifespan.

The study identified cell clusters specifically in the infant brain that are enriched for the expression of neurodevelopmental genes, consistent with the idea that brain development continues after birth. They also found, unexpectedly, that expression of neuron-specific genes remains unchanged throughout life. However, they observed widespread downregulation of certain housekeeping genes during aging, with short, highly expressed housekeeping genes exhibiting high mutation rates, suggesting that a combination of gene length, gene function, and genome damage shapes the transcriptome of the aging brain.

Read the full article in Nature.

Jennifer Benanti, PhD, has renewed her NIH Maximizing Investigators’ Research Award (MIRA) from the National Institute of General Medical Sciences (NIGMS) to investigate the molecular mechanisms of cell cycle control.

The proposed research will investigate key aspects of cell cycle regulation, focusing on how multisite phosphorylation by cyclin-dependent kinases modulates the activity of transcription factors to drive cell cycle progression, and exploring the role of cell cycle control in cellular adaptation to environmental stress.

By elucidating the pathways and mechanisms that govern these processes, the study aims to provide critical insights into how disruption of cell cycle regulation contributes to uncontrolled proliferation and the development of cancer.