A fluid that women with advanced ovarian cancer know all too well — ascites, the buildup of liquid in the belly — may be doing more than causing discomfort. A federally funded Duke University School of Medicine study finds this fluid helps cancer cells survive and spread – and that a decades-old cholesterol drug may be able to disrupt that protection.

A new study by the Garvan Institute of Medical Research has uncovered a hidden mechanism explaining why breast cancer can return many years after successful treatment. Published in Nature Communications, the research revealed rogue cells that change their programming to allow them to divide at a remarkably slow pace, meaning they could form microscopic tumours that silently tick away in distant organs, evading detection for decades.

Alterations in the bacterial composition in various anatomical sites of the human body have been associated with tumorigenesis and the progression of multiple cancers; however, divergent results regarding enriched bacteria have been reported across studies of the same disease, indicating cohort-dependent bacterial compositional variance. To move beyond this inconsistency, a research team led by Professor Na Liu from Sun Yat-sen University Cancer Center proposes a fundamental shift in perspective. The team argues that it is the functional repertoire of bacterial communities, rather than their taxonomic identity, that serves as the core driver of tumor progression. The team proposes the unified nomenclature of bacterial functional constituents as “tumor-associated bacterial effectors” (TABEs), categorizing them into six functional classes according to their chemical nature, conserved structural features, and analogous mechanisms of action in regulating host cells. The researchers believe that exploring the mechanisms of TABEs in cancer represents a critical step toward harnessing their biological potential in real-life clinical settings.