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Patient Daily | Jun 23, 2026

Scientists identify fat tissue's role in triple-negative breast cancer spread

Scientists at the Hackensack Meridian Center for Discovery and Innovation, along with colleagues from Georgetown University's Lombardi Comprehensive Cancer Center, announced on June 23 that they have identified how fat tissue may drive the spread of triple-negative breast cancer (TNBC). The findings are published in npj Breast Cancer, a Nature Portfolio journal.

The research team demonstrated that tumor cells can hijack fat tissue to aid their spread through the body using adipomes—small extracellular vesicles released by fat tissues. These adipomes help the cancer move from the breast to other organs. The study was led by Jyothi Nagajyothi, Ph.D., and Hariprasad Thangavel, Ph.D., with contributions from Robert Glazer, Ph.D., and other investigators.

"The findings of this study establish adipomes as potent and previously unrecognized regulators of the metastatic cascade in TNBC," write the authors. They also state, "This work challenges the traditional view of tumor-adjacent adipocytes as passive lipid reservoirs, and reveals instead their active and dynamic role as key orchestrator of the mammary TME (tumor microenvironment)."

Prior scientific understanding held that metastasis begins when cancer cells invade supportive tissues in the breast via invadopodia—protein structures that degrade bodily defenses. The new research focused on earlier phases leading up to this process by examining how adipomes act as cellular messengers initiating cancer growth cycles.

To conduct their study, Nagajyothi's team used human clinical samples from Hackensack Meridian Health Network Biorepository and preclinical models. They developed a purification technique capable of isolating pure adipomes from tissues, blood, and fluids—a method currently under patent application (US Patent App. 19/233,485) by Hackensack Meridian Health.

According to their results, these adipomes deliver a 'lipid code' reprogramming cancer cells through stress-response signaling and boosting protein synthesis. This activity supports invadopodia formation in TNBC. The researchers suggest future therapies could target this process: "Together, these findings establish adipocyte-derived adipomes as potent regulators of TNBC investigation and metastasis and reveal a previously unrecognized tumor-adipocyte signaling axis that may present new opportunities for therapeutic targeting," they conclude.

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