Novel mRNA treatment developed at UMass Chan Medical School eliminates pancreatic cancer tumors in 50 percent of treated mice.

Pancreatic ductal adenocarcinoma (PDAC) displays dismal immunotherapy outcomes in part through a lack of cytokine and antigen signals needed for anti-tumor immunity. The authors here develop a cocktai...

AbstractPatients with castration-resistant prostate cancer (CRPC) are generally unresponsive to tumor-targeted treatments and immunotherapies. Genetic alterations acquired during the evolution of CRPC...

AbstractPatients with castration-resistant prostate cancer (CRPC) are generally unresponsive to tumor-targeted treatments and immunotherapies. Genetic alterations acquired during the evolution of CRPC...

Abstract. Cellular senescence is a well-established tumor-suppressive cell cycle arrest program. However, chronic inflammation through the senescence-associated secretory phenotype (SASP) can alternat...

Proceedings of the National Academy of Sciences (PNAS), a peer reviewed journal of the National Academy of Sciences (NAS) - an authoritative source of high-impact, original research that broadly spans...

Nature - Basal cells, rather than neuroendocrine cells, have been identified as the probable origin of small cell lung cancer and other neuroendocrine–tuft cancers, explaining...

Researchers at academic institutions nationwide say that U.S. science is being dismantled.

Understanding the impact of senescence on disease is limited by the lack of tools to lineage label senescent cells. In a recent Cell issue, Zhao et al. create mouse models to genetically manipulate and trace p16+ cells, identifying contrasting roles for senescent macrophages and endothelial cells (ECs) in liver fibrosis.

Chronic damage following oncogene induction or cancer therapy can produce cellular senescence. Senescent cells not only exit the cell cycle but communicate damage signals to their environment that can trigger immune responses. Recent work has revealed that senescent tumor cells are highly immunogenic, leading to new ways to activate antitumor immunosurveillance and potentiate T cell-directed immunotherapies. However, other studies have determined that heterogeneous senescent stromal cell populations contribute to immunosuppression and tumor progression, sparking the development of senotherapeutics to target senescent cells that evade immune detection. We review current findings that provide deeper insights into the mechanisms contributing to the dichotomous role of senescence in immune modulation and how that can be leveraged for cancer immunotherapy.

Large extrachromosomal DNAs are engineered using a CRISPR- and Cre–loxP-based approach and shown to drive cancer in mouse models, with potential applications in determining the role of oncogene a...

Cancer cells rely on macropinocytosis to survive in a nutrient-deprived environment. Here, Lambies et al. identified various members of the cell polarity protein network as essential regulators of mac...