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December 8, 2025BloodOpen Access

SMARCD1 subunit of SWI/SNF chromatin remodeling complexes collaborates with p53 to exert an oncogenic role in B-ALL by maintaining high metabolic activity

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Authors

APAlexandre PolsinelliGAGabriel AlzialJLJulie Lessard

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Overview

Analysis reveals oncogenic collaboration between SMARCD1 and p53 in B-ALL, enhancing cell proliferation and survival.

Key Points

  • B-ALL cells exhibit decreased survival and proliferation when SMARCD1 is inactivated, highlighting its role in oncogenesis.
  • Inactivation of p53 similarly impairs cell proliferation, indicating a cooperative dependency on both proteins in B-ALL.
  • Utilizing techniques such as coimmunoprecipitation and RNA sequencing, metabolic pathways linked to cell survival and proliferation were analyzed.
  • Targeting the SMARCD1-WTp53 axis may provide novel therapeutic strategies for treating resistant B-ALL cases.

Cite This Study

Polsinelli et al. (2025) studied this question.

synapsesocial.com/papers/69362f604fa91c937236dcd7https://doi.org/10.1182/blood-2025-1486
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Also Consider

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  1. 1Chromatin remodeler SATB2 thorough Bmi1/PRC1 activity controls transformation and reprogramming of ph+ B-cell progenitors2025
  2. 2SMARCC1 loss impairs differentiation and enhances self-renewal in ASXL1-mutant hematopoietic cells2025
  3. 3Targeting TP53 promotes anti-leukemia immunity and enhances CD70 CAR-T efficacy in AML by transcriptionally upregulating CD702025
  4. 4Lipid uptake via FATP2 enhances CAR-t therapy resistance in B-cell acute lymphoblastic leukemia2025
  5. 5MYC-dependent permissiveness of PI3K hyperactivation renders metabolic vulnerability in R/R b-ALL2025