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Most childhood leukemias are pregenital B-cell acute lymphoblastic leukemia (pB-ALL), caused by pre-birth genetic susceptibility and post-birth carcinogenic events.
although genetic susceptivity is common in children, less than 1% of genetic susceptible carriers develop pB-ALL.
that although infectious stimuli are thought to play a major role in the development of leukemia, the key determinants are not yet clear.
In this study, researchers used pB-ALL mouse models to demonstrate that microbiome disorders caused by early-life antibiotic treatment were sufficient to induce leukemia in genetically susceptible mice, even without infection stimulation and independent of T-cells.
by sequencing V4 and full-length 16SrRNA in a series of fecal samples, the researchers found that mice with pB-ALL genetic susceptivity (Pax5 hybrid or ETV6-RUNX1 fusion variant) had a different gut microbiome than mice without genetic susceptivity.
machine learning (treatment of the survival of Pax5 hybrid mice by antibiotics (abx); CF, traditional breeding; SPF, sterile feeding) accurately predicted genetic susceptivity (96.8%) using 40 of the 3,983 amplification sequence variants (ASVs) as alternatives to bacterial species.
the wild type (WT) or Pax5 plus/- hematocyte bone marrow cells were transplanted to the WT recipient mice, and the microbiome of the recipient mice was gradually changed to the microbiome of the donor mice.
gas chromatography-mass spectrometrometromety (GC-MS) analysis of serums in WT and Pax5 plus/- mice showed the existence of a unique metabolic spectrum specific to genotypes.
, this study shows that in mice with genetic susceptibleness, there is a lack of symbic microbiomes, rather than the presence of specific bacteria, contributing to the development of leukemia.
large-scale longitudinal studies are needed in the future to determine whether targeted microbiome adjustment for children at risk of PB-ALL can be an effective prevention strategy.
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