Evidence map›Paper›PMID 41674835›Full record

ArticleResearch square2026

Immune Niche Formation Reveals Mechanisms of Tumor Dormancy and Targeting Opportunities.

Abdul Ahad, Feng Leng, Hiroshi Ichise, Edward Schrom, Jae Young So, Carter Sellner, Yang Gu, Wenjuan Wang, Celine Kieu, Woo Yong Park and 10 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

20 authors.

Abdul AhadLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.ORCID https://orcid.org/0000-0002-9609-3103
Feng LengLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Hiroshi IchiseCenter for Advanced Tissue Imaging, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892.
Edward SchromCenter for Advanced Tissue Imaging, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892.
Jae Young SoLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Carter SellnerLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Yang GuLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Wenjuan WangLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Celine KieuLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Woo Yong ParkLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Rachel YangLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Karen WolcottLaboratory of Genome Integrity, Flow Cytometry Core, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Ferenc LivakLaboratory of Genome Integrity, Flow Cytometry Core, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Michael KruhlakLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.ORCID https://orcid.org/0000-0003-3976-6233
Olga AprelikovaLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Justin GrayLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Vishal N KopardéBioinformatics, CCBR (CCR Collaborative Bioinformatics Resource), National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.ORCID https://orcid.org/0000-0001-8978-8495
Yasuhiro MoriwakiDepartment of Pharmacology, Keio University, Faculty of Pharmacy, Tokyo, Japan.
Ronald N GermainCenter for Advanced Tissue Imaging, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892.ORCID https://orcid.org/0000-0003-1495-9143
Li YangLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.ORCID https://orcid.org/0000-0002-0930-206X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Residual tumor cells can persist in a dormant state during clinical remissions that may last decades. The mechanisms leading to such growth control vs. eventual macroscopic metastases remain unclear. Here, we report abrogation of myeloid TGF-β RII resulted in an IFN-γ rich microenvironment. IFN-γ in turn elevated KLF4-mediated SLURP1 production in malignant cells, which is critical to their quiescent state through interruption of fibronectin-integrin pathways. The dormant tumor lesions were found in spatially localized immune niches rich in NK cells, cDCs, monocytes, and neutrophils, concomitant with tumor cell inactivation of NK cell immune surveillance through CD200-CD200R1. Our studies identify the IFN-γ-KLF4-SLURP1 and CD200-CD200R1 axes as critical molecular drivers in tumor dormancy regulated by immune-tumor crosstalk. Targeting the CD200-mediated dormant niche in combination with chemotherapy and immune check point blockade (ICB) significantly eradicated the dormant tumor cells. These insights provide mechanistic understanding of tumor dormancy and treatment options for ICB relapse.

Indexed as

immunemetastasisnicherelapseTGF-βTumor dormancy

Identifiers

PMID41674835
PMCPMC12889818

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.