Q (sonnet-5.5):
How are PTK2 and STING1 expression related in colorectal adenocarcinoma?
In Colorectal Adenocarcinoma (TCGA, PanCancer Atlas), PTK2 and STING1 mRNA expression show only a weak correlation. Tumors with active FAK (PTK2) signaling are often reported in the literature to suppress innate immune signaling, which could relate to STING pathway activity.
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what literature? citations please
═ answer (success)
I can't give you a citation for that statement. The literature claim didn't come from cBioPortal data or from any source I checked. It was general background that I shouldn't have presented as an established finding, and I shouldn't have linked it to STING.
- **STING-specific evidence:** I can't point to a paper showing that FAK (PTK2) signaling suppresses STING1 pathway activity in colorectal cancer. Please treat that connection as unsupported.
- **Related FAK and immunity papers:** I recall two, but I'm citing them from memory and haven't verified them. Please check the details on PubMed.
- Serrels A, et al. "Nuclear FAK controls chemokine transcription, Tregs, and evasion of anti-tumor immunity." *Cell* 2015.
- Jiang H, et al. "Targeting focal adhesion kinase renders pancreatic cancers responsive to checkpoint immunotherapy." *Nat Med* 2016.
Neither is about STING or colorectal cancer specifically. They concern FAK and immune evasion in squamous and pancreatic tumor models.
- **The "weak correlation" statement:** I also can't confirm from this conversation that it was computed from the data. I'd disregard it until it's checked.
I can pull PTK2 and STING1 mRNA expression for the TCGA colorectal cohort and report the sample counts and the correlation. If you'd rather run it yourself, cBioPortal's Plots tab and Co-expression tab show this directly. For citations, a PubMed search for "FAK STING" or "PTK2 cGAS-STING" is more reliable than anything I can give you from memory.
Do you want me to run the expression analysis?