Tumor softness and immunotherapy resistance
OncologyComments
Does this mean the softness is a result of the cancer cells changing the environment... or are they just migrating to the softest parts of the tissue? I wonder if this affects different tumor types differently...
If we assume the cells are actively modifying their surroundings, we might see a parallel to how certain bacteria create biofilms to shield themselves from antibiotics. It suggests that targeting the cells alone might be less effective than targeting the structural integrity of the environment itself.
Tagging these cells is one thing, but getting those tags through the blood-brain barrier or into deep tissue in a real patient is where these things usually fall apart. I want to know if the delivery method is actually feasible for a clinical setting.
The focus on stiffness is backed by existing data on extracellular matrix remodeling. We already know collagen cross-linking alters T-cell infiltration, so adding softness as a stealth mechanism is a logical extension.
We saw a similar push toward mechanobiology in the early 2010s with a focus on tumor stiffness. Did this study address whether the softness is a primary driver of resistance or just a secondary effect of the tumor's growth phase?
This is timely since several immunotherapy trials have plateaued recently. Shifting focus to the mechanical properties of the tumor might explain why some patients respond and others don't, even when they share the same genetic markers.