Autophagy in natural and therapy-driven anticancer immunosurveillance.
Level 5 - mechanism / opinion, no new human data
Narrative mechanistic review without new human data
PubMed 28598229 · doi:10.1080/15548627.2017.1310356
What was done
This narrative review synthesizes literature on the mechanistic roles of autophagy in tumor development, treatment resistance, and anticancer immunosurveillance, focusing on its functions within dying cancer cells, antigen-presenting cells, and CD8+ cytotoxic T lymphocytes.
What was found
The abstract reports no numerical findings or statistical measures. Conceptually, it reports that while autophagy cell-intrinsically prevents malignant transformation, it can also sustain established neoplasms and mediate treatment resistance. Conversely, autophagy promotes the release of immunostimulatory signals from dying tumor cells and is necessary for optimal tumor recognition and clearance by antigen-presenting cells and CD8+ T lymphocytes.
Why it matters
It highlights the trade-offs of targeting autophagy in cancer therapy, showing that therapeutic inhibition of autophagy may inadvertently suppress host antitumor immune responses.
Limits
The paper is a non-systematic narrative review providing no quantitative synthesis or new human experimental data. Specific clinical outcomes, sample sizes, and effect sizes are not reported.
Cited by
- supports Autophagy is required for stressed cancer cells to release extracellular ATP as a danger signal that attracts myeloid cells via purinergic receptors to initiate an anti-cancer immune response.