Tumor myco-environment.

One thing we all probably underestimate is the extent to which our cells and those of commensal microorganisms “know” each other. C’mon, they spend their entire microscopic lives together. This study suggests that there’s something going on between the commensal fungus, Malassezia, and pancreatic ductal adenocarcinoma (PDA) cells. In both mice and humans with PDA, they found a much higher abundance of fungi, particularly Malassezia. What’s more, eradication of this mycobiome with amphotercin B enhanced the effects of chemo and halted PDA progression in mice. Repopulation of the gut with Malassezia (but not other fungal species such as Candida or Aspergillus) resulted in accelerated tumor growth. How? The authors postulate that oncogenic KRAS promotes inflammation and mycobiome dysbiosis. The increased amount of Malassezia then activates the complement cascade via something called mannose-binding lectin resulting in pro-inflammatory tumor growth. TBL: If your dandruff wasn’t reason enough, add pancreatic cancer progression to the list of reasons to get your Malassezia in check. | Aykut, Nature 2019


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