Evidence map›Paper›PMID 37226083›Full record

ArticleCellular & molecular biology letters2023

Deletion of CD36 exhibits limited impact on normal hematopoiesis and the leukemia microenvironment.

Yiting Meng, Mateusz Pospiech, Atham Ali, Ritu Chandwani, Mary Vergel, Sandra Onyemaechi, George Yaghmour, Rong Lu, Houda Alachkar

Open access · goldAbstract readLetter
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular & molecular biology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Yiting MengDepartment of Clinical Pharmacy, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, USA.
Mateusz PospiechDepartment of Clinical Pharmacy, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, USA.
Atham AliDepartment of Clinical Pharmacy, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, USA.
Ritu ChandwaniDepartment of Pharmacology and Pharmaceutical Science, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, USA.
Mary VergelKeck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA.
Sandra OnyemaechiDepartment of Pharmacology and Pharmaceutical Science, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, USA.
George YaghmourDivision of Hematology, Department of Medicine, University of Southern California Norris Comprehensive Cancer Center, Los Angeles, CA, 90033, USA.
Rong LuKeck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA.
Houda AlachkarDepartment of Clinical Pharmacy, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, USA. alachkar@usc.edu.ORCID http://orcid.org/0000-0001-5567-5521
University of Southern California · US

Funding

NIH HHS R01
6 · The paper itself

Abstract

backgroundCD36 has been identified as a potential therapeutic target both in leukemic cells and in the tumor immune microenvironment. In acute myeloid leukemia (AML), we found that APOC2 acts with CD36 to promote leukemia growth by activating the LYN-ERK signaling. CD36 also plays a role in lipid metabolism of cancer associated T-cells leading to impaired cytotoxic CD8

methodsDifferential expression data of CD36 during human and mouse normal hematopoiesis were examined and compared. Cd36 knockout (Cd36-KO) mice were evaluated for blood analysis, hematopoietic stem cells and progenitors (HSPCs) function and phenotype analyses, and T cells in vitro expansion and phenotypes in comparison with wild type (WT) mice. In addition, MLL-PTD/FLT3-ITD leukemic cells were engrafted into Cd36-KO and WT mice, and leukemia burden was compared between groups.

resultsRNA-Seq data showed that Cd36 expression was low in HSPCs and increased as cells matured. Phenotypic analysis revealed limited changes in blood count except for a slight yet significantly lower red blood cell count and hemoglobin and hematocrit levels in Cd36-KO mice compared with WT mice (P < 0.05). In vitro cell proliferation assays of splenocytes and HSPCs from Cd36-KO mice showed a similar pattern of expansion to that of cells from WT mice. Characterization of HSPCs showed similar percentages of the different progenitor cell populations between Cd36-KO with WT mice. However, Cd36-KO mice exhibited ~ 40% reduction of the number of colonies developed from HSPCs cells compared with WT mice (P < 0.001). Cd36-KO and WT mice presented comparably healthy BM transplant in non-competitive models and developed similar leukemia burden.

conclusionsAlthough the loss of Cd36 affects the hematopoietic stem cell and erythropoiesis, limited detrimental overall impact was observed on normal Hematopoietic and leukemic microenvironments. Altogether, considering the limited impact on normal hematopoiesis, therapeutic approaches to target CD36 in cancer are unlikely to result in toxicity to normal blood cells.

Indexed as

LeukemiaAnimalsCD8-Positive T-LymphocytesCell CycleHematopoiesisHematopoietic Stem CellsHumansMiceTumor MicroenvironmentAcute myeloid leukemiaCD36HematopoiesisKnockoutMouseT Cells

Identifiers

PMID37226083
PMCPMC10210361
OpenAlexW4378172295

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.