Evidence map›Paper›PMID 28813659›Full record

ArticleImmunity2017

The DNA Methylcytosine Dioxygenase Tet2 Sustains Immunosuppressive Function of Tumor-Infiltrating Myeloid Cells to Promote Melanoma Progression.

Wen Pan, Shu Zhu, Kun Qu, Katrina Meeth, Jijun Cheng, Kaixin He, Hongdi Ma, Yan Liao, Xizhi Wen, Christine Roden and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
5.6field-weighted citation impact, top 3% of its field
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

137 citing papers in PubMed, 182 citations in OpenAlex.

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  14. TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
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  17. Immunity and Beyond: Emerging Roles of Monocytes and Macrophages in Cancer.Advances in experimental medicine and biology · 2026
    Review
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  19. Article
  20. Article

77 more citing papers are in PubMed but not listed here.

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 at 5 institutions in 2 countries.

Wen PanDepartment of Genetics, Yale University School of Medicine, New Haven, CT 06520, USA; Yale Stem Cell Center, Yale Cancer Center, Yale Cooperative Center of Excellence in Hematology, Yale University, New Haven, CT 06520, USA.
Shu ZhuDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA; Institute of Immunology, University of Science and Technology of China, Hefei 230027, China; CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.
Kun QuCAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.
Katrina MeethDepartment of Pathology, Yale University School of Medicine, New Haven, CT 06519, USA; Department of Dermatology, Yale University School of Medicine, New Haven, CT 06519, USA.
Jijun ChengDepartment of Genetics, Yale University School of Medicine, New Haven, CT 06520, USA; Yale Stem Cell Center, Yale Cancer Center, Yale Cooperative Center of Excellence in Hematology, Yale University, New Haven, CT 06520, USA.
Kaixin HeInstitute of Immunology, University of Science and Technology of China, Hefei 230027, China; CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.
Hongdi MaInstitute of Immunology, University of Science and Technology of China, Hefei 230027, China; CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.
Yan LiaoCenter for Stem Cell Biology and Tissue Engineering, Key Laboratory for Stem Cells and Tissue Engineering, Ministry of Education, Sun Yat-Sen University, Guangzhou 510060, China.
Xizhi WenBiotherapy Center, Sun Yat-Sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Christine RodenDepartment of Genetics, Yale University School of Medicine, New Haven, CT 06520, USA; Yale Stem Cell Center, Yale Cancer Center, Yale Cooperative Center of Excellence in Hematology, Yale University, New Haven, CT 06520, USA.
Zuzana TobiasovaDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Zheng WeiDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Jun ZhaoDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Jun LiuDepartment of Genetics, Yale University School of Medicine, New Haven, CT 06520, USA; Yale Stem Cell Center, Yale Cancer Center, Yale Cooperative Center of Excellence in Hematology, Yale University, New Haven, CT 06520, USA.
Ji ZhengDepartment of Genetics, Yale University School of Medicine, New Haven, CT 06520, USA; Yale Stem Cell Center, Yale Cancer Center, Yale Cooperative Center of Excellence in Hematology, Yale University, New Haven, CT 06520, USA; Department of Urology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
Bo GuoDepartment of Genetics, Yale University School of Medicine, New Haven, CT 06520, USA; General Hospital of People's Liberation Army, Beijing, China.
Sajid A KhanDepartment of Surgery, Yale University School of Medicine, New Haven, CT 06519, USA.
Marcus BosenbergDepartment of Pathology, Yale University School of Medicine, New Haven, CT 06519, USA; Department of Dermatology, Yale University School of Medicine, New Haven, CT 06519, USA.
Richard A FlavellDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Jun LuDepartment of Genetics, Yale University School of Medicine, New Haven, CT 06520, USA; Yale Stem Cell Center, Yale Cancer Center, Yale Cooperative Center of Excellence in Hematology, Yale University, New Haven, CT 06520, USA. Electronic address: jun.lu@yale.edu.
Yale University · USUniversity of Science and Technology of China · CNSun Yat-sen University · CNYale Cancer Center · USPeople's Liberation Army No. 150 Hospital · CN

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Cooperative Hematology Specialized Core CenterU54DK106857 · NIDDK · YALE UNIVERSITY · PI JOHN HWA, Diane S Krause · 2015 to 2026
$9.7M
GENETICS AND GENOMICS OF HUMAN DISEASET32HD007149 · NICHD · YALE UNIVERSITY · PI James P Noonan · 1985 to 2026
$8.2M
The role of microRNAs in leukemic initiation and maintenanceR01CA149109 · NCI · YALE UNIVERSITY · PI LU, JUN · 2011 to 2015
$1.7M
Howard Hughes Medical InstituteNCATS NIH HHS UL1 TR001863NCI NIH HHS R01 CA149109NICHD NIH HHS T32 HD007149NIDDK NIH HHS U54 DK106857
6 · The paper itself

Abstract

Ten-Eleven-Translocation-2 (Tet2) is a DNA methylcytosine dioxygenase that functions as a tumor suppressor in hematopoietic malignancies. We examined the role of Tet2 in tumor-tissue myeloid cells and found that Tet2 sustains the immunosuppressive function of these cells. We found that Tet2 expression is increased in intratumoral myeloid cells both in mouse models of melanoma and in melanoma patients and that this increased expression is dependent on an IL-1R-MyD88 pathway. Ablation of Tet2 in myeloid cells suppressed melanoma growth in vivo and shifted the immunosuppressive gene expression program in tumor-associated macrophages to a proinflammatory one, with a concomitant reduction of the immunosuppressive function. This resulted in increased numbers of effector T cells in the tumor, and T cell depletion abolished the reduced tumor growth observed upon myeloid-specific deletion of Tet2. Our findings reveal a non-cell-intrinsic, tumor-promoting function for Tet2 and suggest that Tet2 may present a therapeutic target for the treatment of non-hematologic malignancies.

Indexed as

CarcinogenesisAnimalsDioxygenasesDNA-Binding ProteinsFemaleHumansMaleMelanomaMelanoma, ExperimentalMiceMice, Inbred C57BLMice, KnockoutMyeloid-Derived Suppressor CellsProto-Oncogene ProteinsSkin NeoplasmsT-LymphocytesDioxygenasesDNA-Binding ProteinsProto-Oncogene ProteinsTET2 protein, humanTet2 protein, mouse5hmC5mCArg1BMDMHSCIl1bMDSCTAMTet3YUMM1.7

Identifiers

PMID28813659
PMCPMC5710009
OpenAlexW2748041212

What OpenQuestion holds

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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.