Huocong Huang

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.

Single-cell resolution spatial analysis of antigen-presenting cancer-associated fibroblast niches Chen et al. identify two distinct antigen-presenting cancer-associated fibroblast (apCAF) populations across multiple cancer types. Mesothelial-related apCAFs locate near cancer cells while fibrocyte-...

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 👉 Cancer Cell www.cell.com/cancer-cell/...

Sign the Petition Petition to Reverse the NIH Indirect Cost Cap (NOT-OD-25-068)

Petition to Reverse the NIH Indirect Cost Cap initiated by Tom Maniatis. Please amplify
Sign the Petition: chng.it/kK2HMP5pGk
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Stromal KITL/SCF maintains pancreas tissue homeostasis and restrains tumor progression Abstract. Components of normal tissue architecture serve as barriers to tumor progression. Inflammatory and wound-healing programs are requisite features of solid tumorigenesis, wherein alterations to...

Happy to share our new #NIHfunded study! Led by Kath Oñate + crew of #WomenInSTEM 💪🏽💪🏻💪, 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!

Functional heterogeneity of fibroblasts in primary tumors and metastases Cancer-associated fibroblasts (CAFs) are abundant components of the tumor microenvironment (TME) of most solid malignancies and have emerged as key re…

🚨 2024 is coming to a close but #research on #fibroblast #functions in #cancer it’s far from done ✅.

If you want to know more, have a read at our latest #review now in press @trendscancer. 👇🏼👇🏼

Fantastic job by Priscilla and Marta 🌟👏🏻.

And happy 2025 to all 🫶

www.sciencedirect.com/science/arti...

The redox sensor KEAP1 facilitates adaptation of T cells to chronic antigen stimulation by preventing hyperactivation KEAP1 promotes persistent T cell immunity and a stem-like T cell response during chronic antigen stimulation by repressing NRF2.

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:
#PancreaticCancer–Associated 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 🙋🏻‍♂️ 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 https://www.biorxiv.org/content/10.1101/2024.11.15.623232v1 Recent studies have identified a unique subtype of cancer-associated fibroblasts (CAFs) termed antig

Single-cell resolution spatial analysis of antigen-presenting cancer-associated fibroblast niches https://www.biorxiv.org/content/10.1101/2024.11.15.623232v1

pls add me to the cancer immune pack thanks🙏

would love to be added, thanks! 🙏

would love to be added too, thanks! 🙏

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!