Scientists at UCSF have uncovered a novel mechanism in triple-negative breast cancer (TNBC), where cancer cells exploit nearby fat cells by forming gap junctions to siphon lipids, fueling tumor growth and metastasis.

Blocking these gap junctions in human tissue and mouse models has been shown to halt tumor growth, pointing to this pathway as a promising target for new therapies.

This discovery sheds light on the complex interactions within the tumor microenvironment, suggesting that disrupting this fat-extraction process could be an effective therapeutic strategy.

The research, supported by the NIH and the U.S. Department of Defense, emphasizes its significance and collaborative backing.

Triple-negative breast cancer, which accounts for about 15% of cases, is particularly aggressive, more common in Black women and women under 40, and is characterized by limited treatment options due to its lack of estrogen, progesterone, and HER2 receptors.

This form of breast cancer tends to recur more frequently and has a poorer prognosis, making new treatment avenues critically important.

The immediate clinical implication of this discovery is the potential to develop strategies that cut off the energy supply to tumors by targeting the gap junctions, offering hope for more effective treatments.

This research broadens our understanding of the tumor microenvironment, highlighting that tumors function as complex ecosystems that co-opt normal tissues like adipose tissue to sustain their growth.

Additionally, these findings suggest that lifestyle modifications aimed at maintaining a healthy weight could potentially reduce the risk of aggressive breast cancers such as TNBC.

The process, often described as 'energy theft,' appears crucial for the survival of certain breast cancer types and reveals an underexplored interaction between cancer cells and adipose tissue.

Experts consider these findings groundbreaking because they reveal a new way cancer can grow and feed itself, opening up promising avenues for therapies that starve tumors by disrupting lipid transfer.

This research highlights a novel aspect of tumor-host interaction, where cancer cells hijack normal energy pathways, and suggests that targeting intercellular channels like gap junctions could improve treatment outcomes for TNBC.

The study also notes that similar mechanisms involving gap junctions are present in other cancers, including brain tumors, which could be exploited for developing treatments for aggressive cancers like TNBC.