Happy to share our latest work in collaboration with Sihan Wu and James Chen labs. We found ecDNA is not only a vehicle, but can drive oncogene super expressors that induce a unique stromal niche by AREG secretion. This rapidly leads to myCAF expansion and T cell exclusion.
Posts by Huocong Huang
Our paper online now, CAF molecular phenotypes are more conserved than we thought across organs. Plus we now know more details about apCAFs. Please check it out π Cancer Cell www.cell.com/cancer-cell/...
Petition to Reverse the NIH Indirect Cost Cap initiated by Tom Maniatis. Please amplify
Sign the Petition: chng.it/kK2HMP5pGk
"Share with Leadership & Faculty. Reach out to professional societies, biotech and pharma leaders, and philanthropic organizations to raise awareness and mobilize support."
Happy to share our new #NIHfunded study! Led by Kath OΓ±ate + crew of #WomenInSTEM πͺπ½πͺπ»πͺ, we ID potential of normal mesenchyme to restrain #inflammation, epithelial identity, & #pancreaticcancer via KITL, a cue lost in transition to a CAF state. Now at Cancer Discovery aacrjournals.org/cancerdiscov...
congrats Mike!
π¨ 2024 is coming to a close but #research on #fibroblast #functions in #cancer itβs far from done β
.
If you want to know more, have a read at our latest #review now in press @trendscancer. ππΌππΌ
Fantastic job by Priscilla and Marta πππ».
And happy 2025 to all π«Ά
www.sciencedirect.com/science/arti...
Now in #Science #Immunology: Ziang Zhu, Tuoqi Wu, Chen Yao et al at UT Southwestern show that #NRF2 suppression mediated by the #redox sensor #KEAP1 is required for optimal expansion of #CD8 #TCells during chronic antigen exposure!
Multiple NCI-PSRC investigators co-authored this perspective in Cancer Research last month:
#PancreaticCancerβAssociated Fibroblasts: Where Do We Go from Here?
aacrjournals.org/cancerres/ar...
@kenolivelab.bsky.social
@marasherman.bsky.social
@debvendramini.bsky.social
@tme-caf-ecm.bsky.social
#PancreaticCancer research starter pack.
65 of 150. Room for 85 more on this 1st starter pack.
Who did I miss?
go.bsky.app/FDafAW
add me pls ππ»ββοΈ thx!
Thank you @gabriellebrewer.bsky.social for highlighting our work in Nature Reviews Cancer, led by grad student @justeng95.bsky.social.
Check out the original paper in Cell here:
www.cell.com/cell/fulltex...
Here's a summary thread from "the other site": x.com/PeterLyLab/s...
Thanks Akshay! From the atlas we also really appreciate how beautiful and clean LRRC15 is!
Single-cell resolution spatial analysis of antigen-presenting cancer-associated fibroblast niches www.biorxiv.org/content/10.1101/2024.11....
pls add me to the cancer immune pack thanksπ
would love to be added, thanks! π
would love to be added too, thanks! π
8/8) Mechanically, stromal SPP1 KO results in a normalization of myCAF, in which they become more steady-state like and inflammatory, leading to more T cell infiltration, suggesting SPP1 is a key molecule mediating the crosstalk between CAF populations and immune cells.
7/8) We found one of the molecules that are substantially upregulated in both apCAF lineages are SPP1. Stromal KO of SPP1 significantly reduced peritoneal metastasis, ascites formation and pancreatic cancer progression.
6/8) In pancreatic cancer, M-apCAFs are also associated with chemoresistant-cancer epithelium. In addition, we identified two molecular subtypes of peritoneal metastasis, one subtype consistently carries robust TLS and F-apCAFs.
5/8) Interestingly, we found F-apCAF is the major CAF population within TLS, and highly associated with lymphocytes. In contrast, M-apCAFs tend to be tumor epithelium-adjacent. The M-apCAF niches are featured by exhausted or suppressive T cell signatures.
4/8) We exploited two diseases models: pancreatic cancer and peritoneal metastasis derived from colon cancer (a model enriched for both apCAF lineages).
3/8) Based on our scRNA seq atlas, we fully customized a 480 gene panel and ran Xenium spatial assay, through which we identified the distinct niches formed by the two apCAF lineages respectively.
2/8) Surprisingly, we found apCAFs can be derived from two different lineages. One is consistent with what we reported earlier, from mesothelial-like cells (M-apCAF), another is from a speculated blood-origin, carrying a fibrocyte feature (F-apCAF).
1/8) In this study we applied a big data approach and generated a human pan-cancer scRNA seq atlas. First, CAFs are more conserved than we thought across organs. They mostly consist of four molecular subtypes: steady-state like, inflammatory, myofibroblastic, antigen-presenting.
Thanks Deb! Happy to share our work on pan-cancer analysis of apCAF at an unprecedented resolution. Through this study we have a much better idea about this CAF subtype!