Evidence map›Paper›PMID 27452524›Full record

ArticleOncogene2017

CD84 mediates CLL-microenvironment interactions.

A Marom, A F Barak, M P Kramer, H Lewinsky, I Binsky-Ehrenreich, S Cohen, A Tsitsou-Kampeli, V Kalchenko, Y Kuznetsov, V Mirkin and 9 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Article
  6. SLAM Family Receptors in B Cell Chronic Lymphoproliferative Disorders.International journal of molecular sciences · 2024
    Review
  7. Review
  8. Leukaemia: a model metastatic disease.Nature reviews. Cancer · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. CD74 is a novel transcription regulator.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  20. 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 5 institutions in 2 countries.

A MaromDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
A F BarakDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
M P KramerDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
H LewinskyDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
I Binsky-EhrenreichDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
S CohenDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
A Tsitsou-KampeliDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
V KalchenkoDepartment of Veterinary Resources Weizmann Institute of Science, Rehovot, Israel.
Y KuznetsovDepartment of Veterinary Resources Weizmann Institute of Science, Rehovot, Israel.
V MirkinHematology Institute, Kaplan Medical Center, Rehovot, Israel.
N DezorellaDepartment of Hematology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.
M ShapiroDepartment of Hematology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.
P L SchwartzbergNational Human Genome Research Institute, National Institutes of Health, Bethesda, MA, USA.
Y CohenDepartment of Hematology, Sanz medical Center, Laniado Medical Center, Netanya, Israel.
L ShvidelHematology Institute, Kaplan Medical Center, Rehovot, Israel.
M HaranHematology Institute, Kaplan Medical Center, Rehovot, Israel.
S Becker-HermanDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Y HerishanuDepartment of Hematology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.
I ShacharDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Weizmann Institute of Science · ILKaplan Medical Center · ILTel Aviv Sourasky Medical Center · ILLaniado Hospital · ILNational Human Genome Research Institute · US

Funding

Genetic and Biochemical Approaches to Tyrosine Kinase FunctionZIAHG000123 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI SCHWARTZBERG, PAMELA · 2009 to 2018
$20.8M
6 · The paper itself

Abstract

Chronic lymphocytic leukemia (CLL) is a malignant disease of small mature lymphocytes. Signals from the CLL microenvironment promote progression of the disease and induce drug resistance. This phenomenon is largely dependent on direct contact between the malignant B cells and stromal cells. CD84 belongs to the signaling lymphocyte activation molecule family of immunoreceptors, which self-associates, forming an orthogonal homophilic dimer. We therefore hypothesized that CD84 may bridge between CLL cells and their microenvironment, promoting cell survival. Our in vitro results show that CD84 expressed on CLL cells interact with CD84 expressed on cells in their microenvironment, inducing cell survival in both sides. Blocking CD84 in vitro and in vivo disrupt the interaction of CLL cells with their microenvironment, resulting in induced cell death. Thus, our findings suggest novel therapeutic strategies based on the blockade of this CD84-dependent survival pathway.

Indexed as

AnimalsCell Line, TumorFemaleHumansLeukemia, Lymphocytic, Chronic, B-CellMiceMice, Inbred C57BLMice, KnockoutSignaling Lymphocytic Activation Molecule FamilyTumor MicroenvironmentCD84 protein, humanCd84 protein, mouseSignaling Lymphocytic Activation Molecule Family

Identifiers

PMID27452524
OpenAlexW2504648136

What OpenQuestion holds

Textmetadata
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.