{"id":641282,"date":"2026-05-13T20:34:10","date_gmt":"2026-05-13T20:34:10","guid":{"rendered":"https:\/\/www.newsbeep.com\/us\/641282\/"},"modified":"2026-05-13T20:34:10","modified_gmt":"2026-05-13T20:34:10","slug":"totally-unexpected-scientists-discover-pancreatic-cancers-fatal-addiction","status":"publish","type":"post","link":"https:\/\/www.newsbeep.com\/us\/641282\/","title":{"rendered":"\u201cTotally Unexpected\u201d \u2013 Scientists Discover Pancreatic Cancer\u2019s Fatal Addiction"},"content":{"rendered":"

\"Exploding<\/a>A new study found that pancreatic cancer cells depend on inflammation triggered by damaged mitochondria and the TLR3\/TRAF6 pathway. Inhibiting this pathway killed cancer cells and halted tumor growth in mice. Credit: Stock<\/p>\n

Researchers have uncovered an unexpected weakness in pancreatic cancer involving damaged mitochondria and a powerful inflammatory signal.<\/p>\n

Researchers at The Wistar Institute and ChristianaCare\u2019s Helen F. Graham Cancer Center & Research Institute have identified a weakness in pancreatic cancer that may open the door to new treatments. Their study, published in the Proceedings of the National Academy of Sciences, found that damaged mitochondria inside cancer cells trigger inflammation that tumors rely on to survive and grow. When that inflammatory process is blocked, the cancer cells die.<\/p>\n

The findings point to a signaling pathway called TLR3\/TRAF6 as a possible treatment target for pancreatic cancer, according to senior author Dario Altieri, M.D., president and CEO of The Wistar Institute, director of the Ellen and Ronald Caplan Cancer Center, and Robert and Penny Fox Distinguished Professor. He said this is the first time the mechanism has been linked to cancer development.<\/p>\n

\u201cIt\u2019s been known that mitochondria could release double-stranded RNA and generate inflammation, but not in cancer, and not as a cancer driver,\u201d Altieri explained. \u201cSimilarly, this pair of molecules, TLR3 and TRAF6, were known to act as a sensor for double-stranded RNA, but again, not in cancer. So this could be a therapeutic target for pancreatic cancer, where we are in desperate need of therapeutic targets, but perhaps also for other types of cancers.\u201d<\/p>\n

\"DarioThe Wistar Institute\u2019s Dr. Dario Altieri. Credit: The Wistar Institute<\/p>\n

\u201cFor pancreatic cancer patients, options remain far too limited and the prognosis far too often devastating,\u201d said coauthor Nicholas Petrelli, M.D., director of the Cawley Center for Translational Cancer Research at ChristianaCare\u2019s Helen F. Graham Cancer Center & Research Institute. \u201cWhat makes this finding so exciting is that it points us toward a genuine vulnerability in the cancer itself\u2014one we may be able to exploit therapeutically.\u201d<\/p>\n

Why Pancreatic Cancer Is So Deadly<\/p>\n

Pancreatic cancer is among the deadliest forms of cancer and is notoriously difficult to treat. The disease is often diagnosed only after it has spread to other parts of the body, leaving patients with very limited treatment options and poor survival rates.<\/p>\n

Mitochondria are structures inside cells that produce energy from nutrients. Earlier research showed that many tumor cells contain mitochondria with low levels of a structural protein called Mic60. Although heavily damaged, these mitochondria remain inside the cell. Scientists previously observed that these so-called \u201cghost mitochondria\u201d acted as major sources of inflammatory signaling, but the reason was unclear.<\/p>\n

The new study explains how that happens.<\/p>\n

Healthy mitochondria are enclosed by a protective membrane. Researchers discovered that when Mic60 levels drop, the membrane becomes damaged and begins leaking double-stranded RNA into the cell. The cell\u2019s defense system interprets the leaked material as a sign of infection.<\/p>\n

Inflammation Pathway Fuels Tumor Survival<\/p>\n

Altieri said the team identified two proteins that detect the escaped double-stranded RNA and trigger a strong inflammatory response. Cancer cells then use that inflammation to support their growth.<\/p>\n

The researchers also found that pancreatic cancer cells become highly dependent on this inflammatory state for survival. When drugs were used to block the sensor proteins, cancer cells died while healthy cells remained unaffected. In mouse models, the treatment stopped pancreatic tumors from growing.<\/p>\n

Altieri said the findings were unexpected.<\/p>\n

\u201cThe idea that the reduction of a structural protein could play a role in the damaged mitochondria becoming hubs for stress response signaling, which would translate to a very potent inflammatory response\u2014that was totally unexpected,\u201d he said. \u201cWe had no idea that this was a possibility.\u201d<\/p>\n

Researchers now plan to investigate exactly how Mic60 damage causes mitochondrial membranes to release double-stranded RNA and whether that process can be interrupted. They also aim to continue developing inhibitors that target the TLR3\/TRAF6 pathway as a possible treatment for pancreatic cancer.<\/p>\n

Reference: \u201cMitochondrial double-stranded RNA fuels pancreatic cancer growth via RIG-I\/TLR3 inflammation\u201d by Andrew T. Milcarek, Minjeong Yeon, Camilla Esposito, Prerna Kulkarni, Andrew V. Kossenkov, Jozef Madzo, Anneliese M. Faustino, Hsin-Yao Tang, Alessandra M. Storaci, Alessandro Palleschi, Marco Locatelli, Valentina Vaira, Mary V. Iacocca, Andrea Ward, Arvind Sabesan, Nicholas J. Petrelli, Michela Perego and Dario C. Altieri, 28 April 2026, Proceedings of the National Academy of Sciences.
DOI: 10.1073\/pnas.2528281123<\/a><\/p>\n

Work supported by National Institutes of Health (NIH) grants R35 CA220446, R50 CA221838, and R50 CA211199; the Cotswold Foundation; and National Cancer Institute grant P30 CA10815.<\/p>\n

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