Evidence map›Paper›PMID 35921533›Full record

ArticleBlood2022

Genome-wide CRISPR screens identify CD48 defining susceptibility to NK cytotoxicity in peripheral T-cell lymphomas.

Masahiro Chiba, Joji Shimono, Takashi Ishio, Norio Takei, Kohei Kasahara, Reiki Ogasawara, Takahide Ara, Hideki Goto, Koh Izumiyama, Satoko Otsuguro and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. SLAM family-mediated crosstalk between tumor and immune cells in the tumor microenvironment: a promising biomarker and a potential therapeutic target for immune checkpoint therapies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Deletion of theProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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

19 authors at 7 institutions in 2 countries.

Masahiro ChibaDepartment of Hematology, Hokkaido University, Sapporo, Japan.ORCID 0000-0003-2731-6091
Joji ShimonoDepartment of Hematology, Hokkaido University, Sapporo, Japan.ORCID 0000-0003-1044-1654
Takashi IshioDepartment of Hematology, Hokkaido University, Sapporo, Japan.
Norio TakeiInstitute for Animal Experimentation, Faculty of Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0003-0403-8332
Kohei KasaharaDepartment of Hematology, Sapporo Hokuyu Hospital, Sapporo, Japan.
Reiki OgasawaraDepartment of Hematology, Aiiku Hospital, Sapporo, Japan.ORCID 0000-0002-1136-5035
Takahide AraDepartment of Hematology, Hokkaido University, Sapporo, Japan.ORCID 0000-0001-9609-3202
Hideki GotoDepartment of Hematology, Hokkaido University, Sapporo, Japan.
Koh IzumiyamaDepartment of Hematology, Aiiku Hospital, Sapporo, Japan.ORCID 0000-0002-0762-6255
Satoko OtsuguroCenter for Research and Education on Drug Discovery, Faculty of Pharmaceutical Science, Hokkaido University, Sapporo, Japan.
Liyanage P PereraLymphoid Malignancies Branch, National Cancer Institute, NIH, Bethesda, MD.
Hiroo HasegawaDepartment of Laboratory Medicine, Nagasaki University Hospital, Nagasaki, Japan.ORCID 0000-0002-1822-5692
Michiyuki MaedaInstitute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan.
Satoshi HashinoHealth Care Center, Hokkaido University, Sapporo, Japan.
Katsumi MaenakaCenter for Research and Education on Drug Discovery, Faculty of Pharmaceutical Science, Hokkaido University, Sapporo, Japan.ORCID 0000-0002-5459-521X
Takanori TeshimaDepartment of Hematology, Hokkaido University, Sapporo, Japan.ORCID 0000-0002-0941-271X
Thomas A WaldmannLymphoid Malignancies Branch, National Cancer Institute, NIH, Bethesda, MD.
Yibin YangBlood Cell Development and Function Program, Fox Chase Cancer Center, Philadelphia, PA.
Masao NakagawaDepartment of Hematology, Hokkaido University, Sapporo, Japan.ORCID 0000-0002-8602-6054
Hokkaido University · JPKisarazu Hospital · JPNational Cancer Institute · USFox Chase Cancer Center · USKyoto University · JPNagasaki University Hospital · JPSapporo Hokuyu Hospital · JP

Funding

Investigating the IL-1R Pathway in Anaplastic Large Cell Lymphoma for Targeted TherapyR01CA259188 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Yibin Yang · 2021 to 2026
$2.5M
Analysis and Therapeutic Targeting of the Linear-Ubiquitination Pathway in Hodgkin LymphomaR01CA251674 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI YANG, YIBIN · 2021 to 2025
$2.1M
NCI NIH HHS R01 CA251674NCI NIH HHS R01 CA259188
6 · The paper itself

Abstract

Adult T-cell leukemia/lymphoma (ATLL) is one of the aggressive peripheral T-cell neoplasms with a poor prognosis. Accumulating evidence demonstrates that escape from adaptive immunity is a hallmark of ATLL pathogenesis. However, the mechanisms by which ATLL cells evade natural killer (NK)-cell-mediated immunity have been poorly understood. Here we show that CD48 expression in ATLL cells determines the sensitivity for NK-cell-mediated cytotoxicity against ATLL cells. We performed unbiased genome-wide clustered regularly interspaced short palindromic repeat (CRISPR) screening using 2 ATLL-derived cell lines and discovered CD48 as one of the best-enriched genes whose knockout conferred resistance to YT1-NK cell line-mediated cytotoxicity. The ability of CD48-knockout ATLL cells to evade NK-cell effector function was confirmed using human primary NK cells with reduced interferon-γ (IFNγ) induction and degranulation. We found that primary ATLL cells had reduced CD48 expression along with disease progression. Furthermore, other subgroups among aggressive peripheral T-cell lymphomas (PTCLs) also expressed lower concentrations of CD48 than normal T cells, suggesting that CD48 is a key molecule in malignant T-cell evasion of NK-cell surveillance. Thus, this study demonstrates that CD48 expression is likely critical for malignant T-cell lymphoma cell regulation of NK-cell-mediated immunity and provides a rationale for future evaluation of CD48 as a molecular biomarker in NK-cell-associated immunotherapies.

Indexed as

Leukemia-Lymphoma, Adult T-CellLymphoma, T-Cell, PeripheralAdultCD48 AntigenClustered Regularly Interspaced Short Palindromic RepeatsHumansKiller Cells, NaturalCD48 Antigen

Identifiers

PMID35921533
PMCPMC9837448
OpenAlexW4289653953

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.