New study shows that cancer damages its own DNA by pushing key genes to work too hard. Researchers found that the most powerful genetic “on switches” in cancer cells, called super-enhancers, drive unusually intense gene activity. That high gear creates stress on the DNA and can cause dangerous breaks. Cancer cells can often repair this damage, but the process is frequently error-prone, the repeated cycle of breaking and repairing can make these regions more prone to accumulating mutations over time. In short, the same mechanisms that help cancer grow quickly may also make its DNA more fragile, helping explain how tumors continue to evolve and, in some cases, become more aggressive over time.

A small number of cancer cells with the ability to change their identities and behaviors appear to be a key driver of cancer progression and its ability to evolve resistance to treatment, Memorial Sloan Kettering Cancer Center researchers have found in a laboratory study of lung cancer.

54 compounds affecting pancreas development: Using an image-based screen and a robust analysis pipeline, researchers screened hundreds of molecules and identified 54 compounds that change pancreas organoids shape and/or cell types.

Generating functional human pancreatic acinar cells: Researchers focused on the compounds that inhibit the GSK3A/B protein and drive pancreatic progenitor cells to differentiate into pancreatic acinar cells. A further optimization of the growth media enabled the progenitor cells to develop into fully functional acinar cells.

Possibilities for pancreatic cancer research: The ability to generate acinar organoids is valuable for future studies on pancreatic exocrine function and cancer initiation in humans, as acinar cells are thought to be an important cell of origin for pancreatic cancer.

A new study led by researchers at the Johns Hopkins Kimmel Cancer Center, its Bloomberg~Kimmel Institute for Cancer Immunotherapy and the Johns Hopkins Bloomberg School of Public Health found that an enzyme involved in protein translation is essential for circulating immune cells, called monocytes, to mature into tissue-resident macrophages, a specialized population of immune cells that maintain organ health by clearing dead cells and debris. Without this enzyme, monocytes enter tissues but fail to fully differentiate, leading to impaired tissue maintenance and persistent immune cell infiltration that causes inflammation instead of repair.

Researchers at the Johns Hopkins Kimmel Cancer Center and its Bloomberg~Kimmel Institute for Cancer Immunotherapy found that an oral bacterium commonly associated with periodontal disease can promote breast cancer initiation, tumor growth and spread by inducing DNA damage and altering cancer cell behavior.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is now the most common chronic liver disease in the Western world, driven by obesity, insulin resistance, and systemic inflammation. Its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), can culminate in cirrhosis and hepatocellular carcinoma (HCC). While lifestyle modification remains central to MASLD management, there is growing interest in pharmacological interventions, particularly nutrient-stimulated hormone-based therapies (NuSHs), such as GLP-1 receptor agonists. NuSHs exert metabolic and anti-inflammatory effects primarily via weight loss and improved insulin sensitivity. Emerging clinical data support their efficacy in resolving MASH without worsening fibrosis. However, benefits in cirrhotic patients are less evident, suggesting greater utility in early intervention. Observational studies and clinical trials suggest a reduction in liver-related morbidity with GLP-1 receptor agonist use, though fibrosis regression remains inconsistent. Preclinical models indicate that NuSHs may also reduce MASH-related HCC incidence and tumor burden, likely through systemic metabolic improvements rather than direct antineoplastic action. Observational human data following bariatric surgery reinforce this link, suggesting that weight loss itself plays a key preventive role. Herein, we propose that NuSHs are promising candidates for MASH-related HCC prevention. We provide mechanistic suggestions for how this may occur. Furthermore, incorporating NuSHs into the post-locoregional treatment pathway for HCC may delay the need for systemic anti-cancer therapies, improve immunotherapy synergy and transplant eligibility, and even slow disease progression through reversal of carcinogenic drivers. Future studies are needed to target oncological endpoints and clarify immunometabolic mechanisms to guide the integration of NuSHs into MASLD treatment algorithms.

This study introduces a dual-scale CapCell microscope, a novel imaging system to dynamically visualize metabolic and vascular adaptations in vivo. The platform reveals subregional features associated with treatment that are often missed by bulk analyses.