ArticlePloS one2019
Bacterial translocation in acute lymphocytic leukemia.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- The gastrointestinal microbiome and constituent short-chain fatty acids: a narrative review of an underexplored axis in acute lymphoblastic leukemia.Gut pathogens · 2026Review
- Evaluation of biomarkers for intestinal damage in pediatric acute lymphoblastic leukemia.Scientific reports · 2025Article
- Causal Relationship Between Gut Microbiota and Leukemia: Future Perspectives.Oncology and therapy · 2024Review
- The gut microbiome: an important factor influencing therapy for pediatric acute lymphoblastic leukemia.Annals of hematology · 2024Review
- Potential role of short-chain fatty acids in the pathogenesis and management of acute lymphocytic leukemia.Annals of translational medicine · 2024Review
- Article
- Microbial and host factors contribute to bloodstream infection in a pediatric acute lymphocytic leukemia mouse model.Heliyon · 2022Article
- Microbiota changes in a pediatric acute lymphocytic leukemia mouse model.MicrobiologyOpen · 2020Article
- The Microbiota in Hematologic Malignancies.Current treatment options in oncology · 2020Review
- Bidirectional interaction between intestinal microbiome and cancer: opportunities for therapeutic interventions.Biomarker research · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bloodstream infection (BSI) is the major cause of mortality in acute lymphocytic leukemia (ALL). Causative pathogens in BSI originate from the gut microbiota due to an increase in intestinal permeability, a process known as bacterial translocation (BT). The gut microbiota in physiological conditions is controlled by a large number of immune cells as part of the gut-associated lymphoid tissue (GALT).The aim of the current study was to investigate the mechanism of bacterial translocation in leukemia by identifying and characterizing alterations in the GALT in leukemic mouse model. Our studies revealed a severe impairment of the GALT characterized by a loss of lymphatic cells in ALL, which eventually led to BSI. We identified differentially expressed genes in the intraepithelium and the lamina propria, which may contribute to BT and to the impairment of lymphocyte migration.
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Registered trials
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