Are submicroscopic chromosomal inversions predisposing factors for the t(9;22)(q34;q11.2) translocation in chronic myeloid leukemia?

A complex chromosomal rearrangement observed in a patient with chronic myeloid leukemia was explained as the consequence of a multistep process. The explanation involved an initial t(9;22) translocation with breakpoints distant from the BCR and ABL1 genes followed by genomic deletions that produced the BCR-ABL1 hybrid gene. We present an alternative model that fits the origin of the patient’s rearrangement better. The present model links submicroscopic inversions with the occurrence of the t(9;22) translocation and opens a new approach on the research on the disease.

• Publication year

  2015

• Venue

  Molecular Cytogenetics

• Publication date

  2015-02-22

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1186/s13039-015-0116-9PMID 25741382PMCID 4348163
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• International System for Human Cytogenetic Nomenclature

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