Evidence map›Paper›PMID 35133065›Full record

ArticleCancer science2022

CHIP-associated mutant ASXL1 in blood cells promotes solid tumor progression.

Xiaoxiao Liu, Naru Sato, Yuko Shimosato, Teh-Wei Wang, Tamami Denda, Yu-Hsuan Chang, Tomohiro Yabushita, Takeshi Fujino, Shuhei Asada, Yosuke Tanaka and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Clonal Hematopoiesis of Indeterminate Potential Influences Breast Cancer Outcomes in a Genotype-Specific Manner.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

16 authors at 5 institutions in 1 country.

Xiaoxiao LiuDivision of Molecular Oncology, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0002-0023-4013
Naru SatoDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yuko ShimosatoDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Teh-Wei WangDivision of Cancer Cell Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Tamami DendaDepartment of Pathology, The Institute of Medical Science Research Hospital, The University of Tokyo, Tokyo, Japan.
Yu-Hsuan ChangDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Tomohiro YabushitaDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Takeshi FujinoDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Shuhei AsadaDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yosuke TanakaDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Tomofusa FukuyamaDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yutaka EnomotoDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yasunori OtaDepartment of Pathology, The Institute of Medical Science Research Hospital, The University of Tokyo, Tokyo, Japan.
Takeharu SakamotoDepartment of Cancer Biology, Institute of Biomedical Science, Kansai Medical University, Osaka, Japan.
Toshio KitamuraDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Susumu GoyamaDivision of Molecular Oncology, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan.
Tokyo Medical University · JPShiga University of Medical Science Hospital · JPThe University of Tokyo · JPKansai Medical University · JPThe Cancer Institute Hospital · JP

Funding

Japan Society for the Promotion of Science 19H03685Japan Society for the Promotion of Science 19K22554Koyanagi Foundation
6 · The paper itself

Abstract

Clonal hematopoiesis of indeterminate potential (CHIP) is an age-associated phenomenon characterized by clonal expansion of blood cells harboring somatic mutations in hematopoietic genes, including DNMT3A, TET2, and ASXL1. Clinical evidence suggests that CHIP is highly prevalent and associated with poor prognosis in solid-tumor patients. However, whether blood cells with CHIP mutations play a causal role in promoting the development of solid tumors remained unclear. Using conditional knock-in mice that express CHIP-associated mutant Asxl1 (Asxl1-MT), we showed that expression of Asxl1-MT in T cells, but not in myeloid cells, promoted solid-tumor progression in syngeneic transplantation models. We also demonstrated that Asxl1-MT-expressing blood cells accelerated the development of spontaneous mammary tumors induced by MMTV-PyMT. Intratumor analysis of the mammary tumors revealed the reduced T-cell infiltration at tumor sites and programmed death receptor-1 (PD-1) upregulation in CD8

Indexed as

Clonal HematopoiesisNeoplasmsRepressor ProteinsAnimalsCD8-Positive T-LymphocytesHematopoiesisMiceMutationTranscription FactorsTumor MicroenvironmentAsxl1 protein, mouseRepressor ProteinsTranscription FactorsASXL1CHIPmouse solid-tumor modelsT celltumor immunity

Identifiers

PMID35133065
PMCPMC8990791
OpenAlexW4210943139

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.