Evidence map›Paper›PMID 38964473›Full record

ReviewProgress in lipid research2024

Leveraging altered lipid metabolism in treating B cell malignancies.

Jaewoong Lee, Arya Mani, Min-Jeong Shin, Ronald M Krauss

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Progress in lipid research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  3. NADPharmaceutical science advances · 2026
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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

4 authors.

Jaewoong LeeSchool of Biosystems and Biomedical Sciences, College of Health Science, Korea University, Seoul 02841, Republic of Korea; Department of Integrated Biomedical and Life Science, Korea University, Seoul 02841, Republic of Korea; Interdisciplinary Program in Precision Public Health, Korea University, Seoul 02841, Republic of Korea; Center of Molecular and Cellular Oncology, Yale University, New Haven, CT 06511, USA. Electronic address: jaewoong.lee.jl3663@yale.edu.
Arya ManiDepartment of Internal Medicine, Section of Cardiovascular Medicine, Yale University, New Haven, CT 06511, USA; Department of Genetics, Yale University, New Haven, CT 06511, USA.
Min-Jeong ShinSchool of Biosystems and Biomedical Sciences, College of Health Science, Korea University, Seoul 02841, Republic of Korea; Department of Integrated Biomedical and Life Science, Korea University, Seoul 02841, Republic of Korea; Interdisciplinary Program in Precision Public Health, Korea University, Seoul 02841, Republic of Korea.
Ronald M KraussDepartment of Pediatrics and Medicine, University of California San Francisco, San Francisco, CA 94143, USA. Electronic address: ronald.krauss@ucsf.edu.

Funding

The characterization of Cela2a, a novel disease gene for metabolic syndrome in health and diseasesR01DK134329 · NIDDK · YALE UNIVERSITY · PI Arya Mani · 2023 to 2026
$2.6M
The transcriptional regulation of smooth muscle genes by PRDM6 in vascular health and diseasesR01HL171054 · NHLBI · YALE UNIVERSITY · PI Arya Mani · 2024 to 2026
$2.5M
NHLBI NIH HHS R01 HL171054NIDDK NIH HHS R01 DK134329
6 · The paper itself

Abstract

B cell malignancies, comprising over 80 heterogeneous blood cancers, pose significant prognostic challenges due to intricate oncogenic signaling. Emerging evidence emphasizes the pivotal role of disrupted lipid metabolism in the development of these malignancies. Variations in lipid species, such as phospholipids, cholesterol, sphingolipids, and fatty acids, are widespread across B cell malignancies, contributing to uncontrolled cell proliferation and survival. Phospholipids play a crucial role in initial signaling cascades leading to B cell activation and malignant transformation through constitutive B cell receptor (BCR) signaling. Dysregulated cholesterol and sphingolipid homeostasis support lipid raft integrity, crucial for propagating oncogenic signals. Sphingolipids impact malignant B cell stemness, proliferation, and survival, while glycosphingolipids in lipid rafts modulate BCR activation. Additionally, cancer cells enhance fatty acid-related processes to meet heightened metabolic demands. In obese individuals, the obesity-derived lipids and adipokines surrounding adipocytes rewire lipid metabolism in malignant B cells, evading cytotoxic therapies. Genetic drivers such as MYC translocations also intrinsically alter lipid metabolism in malignant B cells. In summary, intrinsic and extrinsic factors converge to reprogram lipid metabolism, fostering aggressive phenotypes in B cell malignancies. Therefore, targeting altered lipid metabolism has translational potential for improving risk stratification and clinical management of diverse B cell malignancy subtypes.

Indexed as

Lipid MetabolismAnimalsB-LymphocytesHumansLeukemia, B-CellLymphoma, B-CellB cell malignancyB cell receptorLeukemiaLipid metabolismLymphomaObese

Identifiers

PMID38964473
PMCPMC11347096

What OpenQuestion holds

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Registered trials

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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.