Evidence map›Paper›PMID 39289380›Full record

ArticleNature communications2024

Basal-to-inflammatory transition and tumor resistance via crosstalk with a pro-inflammatory stromal niche.

Nancy Yanzhe Li, Weiruo Zhang, Daniel Haensel, Anna R Jussila, Cory Pan, Sadhana Gaddam, Sylvia K Plevritis, Anthony E Oro

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Observational
  6. Cancer therapy resistance from a spatial-omics perspective.Clinical and translational medicine · 2025
    Review
  7. Article
  8. Review
  9. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Nancy Yanzhe LiProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0001-6217-5234
Weiruo ZhangDepartment of Biomedical Data Science, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-3680-7562
Daniel HaenselProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0001-5168-4068
Anna R JussilaProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-5451-1813
Cory PanProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-1808-6239
Sadhana GaddamProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA.
Sylvia K PlevritisDepartment of Biomedical Data Science, Stanford University School of Medicine, Stanford, CA, USA.
Anthony E OroProgram in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA. oro@stanford.edu.ORCID 0000-0002-6261-138X

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Melanie Funes · 1994 to 2026
$57.9M
Spatial-Genomic Integrative Multi-Species Analysis of Lymph Node MetastasisU54CA209971 · NCI · STANFORD UNIVERSITY · PI NOLAN, GARRY P, PLEVRITIS, SYLVIA KATINA · 2016 to 2021
$11.0M
Systems Biology of Tumor-Immune-Stromal Interactions in Metastatic ProgressionU54CA274511 · NCI · STANFORD UNIVERSITY · PI EDGAR G. ENGLEMAN, SYLVIA KATINA PLEVRITIS · 2023 to 2026
$9.5M
STROMAL REGULATION OF BASAL CELL CARCINOMA FORMATIONR01AR046786 · NIAMS · STANFORD UNIVERSITY · PI Anthony E Oro · 2001 to 2026
$9.5M
Postgraduate Training Program in Epithelial BiologyT32AR007422 · NIAMS · STANFORD UNIVERSITY · PI PAUL KHAVARI · 1986 to 2026
$5.0M
REGULATING GLI FUNCTION IN HAIR FOLLICLE PROGENITORSR01AR054780 · NIAMS · STANFORD UNIVERSITY · PI ORO, ANTHONY E · 2007 to 2017
$4.3M
Regulating Gli Function in Hair Follicle ProgenitorsR37AR054780 · NIAMS · STANFORD UNIVERSITY · PI Anthony E Oro · 2019 to 2026
$3.7M
Ultra high throughput sequencer for sustaining and enhancing multi-scale genomic studiesS10OD025212 · OD · STANFORD UNIVERSITY · PI SNYDER, MICHAEL P. · 2018 to 2018
$600k
Four Laser, 18 Color Cell Sorter in the SSFFS10RR025518 · NCRR · STANFORD UNIVERSITY · PI HERZENBERG, LEONARD A · 2009 to 2009
$500k
Computer ClusterS10OD021763 · OD · STANFORD UNIVERSITY · PI JI, HANLEE P · 2016 to 2016
$481k
Nikon A1Rsi resonant spectral confocal microscopeS10OD010580 · OD · STANFORD UNIVERSITY · PI FULLER, MARGARET T · 2013 to 2013
$377k
BD Canto II RUO CytometerS10RR027431 · NCRR · STANFORD UNIVERSITY · PI NOLAN, GARRY P · 2010 to 2010
$236k
NCI NIH HHS F32 CA254434NCI NIH HHS P30 CA062203NCI NIH HHS U54 CA209971NCI NIH HHS U54 CA274511NCRR NIH HHS S10 RR025518NCRR NIH HHS S10 RR027431NIAMS NIH HHS R01 AR046786NIAMS NIH HHS R01 AR054780NIAMS NIH HHS R37 AR054780NIAMS NIH HHS T32 AR007422NIH HHS S10 OD010580NIH HHS S10 OD021763NIH HHS S10 OD025212U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) 2R37-ARO54780U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) RO1 ARO46786
6 · The paper itself

Abstract

Cancer-associated inflammation is a double-edged sword possessing both pro- and anti-tumor properties through ill-defined tumor-immune dynamics. While we previously identified a carcinoma tumor-intrinsic resistance pathway, basal-to-squamous cell carcinoma transition, here, employing a multipronged single-cell and spatial-omics approach, we identify an inflammation and therapy-enriched tumor state we term basal-to-inflammatory transition. Basal-to-inflammatory transition signature correlates with poor overall patient survival in many epithelial tumors. Basal-to-squamous cell carcinoma transition and basal-to-inflammatory transition occur in adjacent but distinct regions of a single tumor: basal-to-squamous cell carcinoma transition arises within the core tumor nodule, while basal-to-inflammatory transition emerges from a specialized inflammatory environment defined by a tumor-associated TREM1 myeloid signature. TREM1 myeloid-derived cytokines IL1 and OSM induce basal-to-inflammatory transition in vitro and in vivo through NF-κB, lowering sensitivity of patient basal cell carcinoma explant tumors to Smoothened inhibitor treatment. This work deepens our knowledge of the heterogeneous local tumor microenvironment and nominates basal-to-inflammatory transition as a drug-resistant but targetable tumor state driven by a specialized inflammatory microenvironment.

Indexed as

InflammationTumor MicroenvironmentAnimalsBasal Cell CarcinomaCarcinoma, Squamous CellCell Line, TumorDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMiceNF-kappa BSingle-Cell AnalysisStromal CellsTriggering Receptor Expressed on Myeloid Cells-1NF-kappa BTriggering Receptor Expressed on Myeloid Cells-1

Identifiers

PMID39289380
PMCPMC11408617

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.