ArticleBlood advances2022
Inflammation accelerates BCR-ABL1+ B-ALL development through upregulation of AID.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- CD19-targeted HSP90 inhibitor nanoparticle combined with TKIs reduces tumor burden and enhances T-cell immunity in murine B-cell malignancies.Theranostics · 2025Article
- B-Acute Lymphoblastic Leukemia/Lymphoblastic Lymphoma Mimicking Fibrosing Mediastinitis: A Case Report and Diagnostic Insight.The American journal of case reports · 2024Article
- Inflammation as a driver of hematological malignancies.Frontiers in oncology · 2024Review
- Co-targeting HSP90 alpha and CDK7 overcomes resistance against HSP90 inhibitors in BCR-ABL1+ leukemia cells.Cell death & disease · 2023Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation contributes to the initiation and disease progression of several lymphoid malignancies. BCR-ABL1-positive B-cell acute lymphoblastic leukemia (BCR-ABL1+ B-ALL) is triggered by the malignant cloning of immature B cells promoted by the BCR-ABL1 fusion gene. However, it is unclear whether the mechanism driving the disease progression of BCR-ABL1+ B-ALL involves inflammatory stimulation. Here, we evaluate BCR-ABL1+ B-ALL cells' response to inflammatory stimuli lipopolysaccharide (LPS) in vitro and in vivo. The results indicate that LPS promotes cell growth and genomic instability in cultured BCR-ABL1+ B-ALL cells and accelerates the BCR-ABL1+ B-ALL development in a mouse model. We show that the LPS-induced upregulation of activation-induced deaminase (AID) is required for the cell growth and disease progression of BCR-ABL1+ B-ALL. Moreover, AID modulates the expression of various genes that are dominated by suppressing apoptosis genes and upregulating DNA damage-repair genes. These genes lead to facilitation for BCR-ABL1+ B-ALL progression. The heat shock protein 90 (Hsp90) inhibitors significantly reduce AID protein level and delay the disease progression of BCR-ABL1+ B-ALL upon inflammatory stimulation. The present data demonstrate the causative role of AID in the development and progression of BCR-ABL1+ B-ALL during inflammation, thus highlighting potential therapeutic targets.
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