Even for killer T cells—specialized immune cells—seeking and destroying cancer cells around the clock can be exhausting. In a new study, Professor Susan Kaech, first author Anna-Maria Globig, and colleagues discovered that the body’s sympathetic stress response (“fight-or-flight”) hormones can exhaust killer T cells in varying cancer types in mouse and human tissue samples—and that exhaustion can be inhibited with beta-blockers. Their discovery demonstrates the potential benefit of pairing beta-blockers with existing immunotherapies to improve cancer treatment by bolstering killer T cell function.
Cancer
Rewiring tumor mitochondria enhances the immune system’s ability to recognize and fight cancer
Immunotherapy, which uses the body’s own immune system to fight cancer, is an effective treatment option, yet many patients do not respond to it. Thus, cancer researchers are seeking new ways to optimize immunotherapy so that it is more effective for more people. Now, Professors Susan Kaech and Gerald Shadel, co-first authors Kailash Chandra Mangalhara and Karthik Varanasi, and colleagues have found that manipulating an early step in energy production in mitochondria—the cell’s powerhouses—reduces melanoma tumor growth and enhances the immune response in mice. In the future, this manipulation of mitochondrial energy production may be leveraged to create new cancer therapeutics that are less harmful for mitochondria and cells.
How drugs can target the thick “scar tissue” of pancreatic cancer
Pancreatic cancer is one of the deadliest cancers—only about one in eight patients survives five years after diagnosis. Those dismal statistics are in part due to the thick, nearly impenetrable wall of fibrosis, or scar tissue, that surrounds most pancreatic tumors and makes it hard for drugs to access and destroy the cancer cells. Professor Ronald Evans, Senior Staff Scientists Michael Downes and Annette Atkins, first author Gaoyang Liang, and colleagues have now discovered how a class of anti-cancer drugs called HDAC inhibitors can help treat pancreatic cancer by modulating the activation of fibroblasts—the cells that make up that wall of scar tissue.
Featured Stories
- Interaction + Infrastructure = Innovations in Healthy AgingSalk formula recalculates aging research, shifting focus to overall resilience and health span.
- Professor Jan Karlseder named Salk’s Chief Science OfficerOn February 1, Jan Karlseder started as Salk’s new senior vice president and chief science officer (CSO).
- Salk mourns the loss of Nobel Laureate Roger GuilleminThe Institute remembers the “father of neuroendocrinology” for his many contributions to science and friendship to all.
- Daniel Hollern–Turning a cancer diagnosis into a career in basic researchAssistant Professor Daniel Hollern pivoted his career trajectory after a family member’s life-changing diagnosis pushed his already-curious mind off a cliff of questions—starting with, “What can I do to help him?”
- Jerry Sheehan–Collaborating shoulder to shoulder with scientistsWhen you think about a person who heads an information technology department, you might not envision them working shoulder to shoulder with research scientists. But that’s exactly the approach Jerry Sheehan is taking as Salk’s new chief information officer (CIO).
- Laura Mainz–Taking control after a cancer diagnosisLaura Mainz grew up in a tiny village in midwestern Germany, with just as many cows as people. But the sweeping landscape speckled with farms never swayed her toward plant biology—instead, her interest in the human body grew.
- Black Association affinity group cultivates welcoming environmentThe Black Association at Salk (BAS) was one of the first affinity groups formed at Salk in 2020. Since that time, it has established itself as a welcoming space and go-to for resources for all Black Salk community members.