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December 8, 2025BloodOpen Access

MYC-dependent permissiveness of PI3K hyperactivation renders metabolic vulnerability in R/R b-ALL

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Authors

JJJian‐Ping JinHHHe HuangMMMarkus Müschen

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Overview

Analysis shows NADH accumulation enhances redox homeostasis, indicating therapeutic strategy using glutamine in R/R B-ALL.

Key Points

  • NADH accumulation impairs redox homeostasis in relapsed B-ALL, leading to enhanced cell vulnerability.
  • Targeting glutamine metabolism improved survival in xenograft models with concurrent PI3K and MYC activation.
  • Observational analysis indicates that PI3K and MYC activities serve as prognostic markers for patient outcomes.
  • Combining therapies like Pegaspargase and complex I inhibitors targets metabolic adaptation in B-ALL cells.

Cite This Study

Jin et al. (2025) studied this question.

synapsesocial.com/papers/69362f604fa91c937236dcc3https://doi.org/10.1182/blood-2025-1475
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