A novel method of amplified fluorescent in situ hybridization for detection of chromosomal microdeletions in B cell lymphoma

Int J Hematol. 2019 May;109(5):593-602. doi: 10.1007/s12185-019-02617-x. Epub 2019 Mar 4.

Abstract

Chromosomal microdeletions frequently cause loss of prognostically relevant tumor suppressor genes in hematologic malignancies; however, detection of minute deletions by conventional methods for chromosomal analysis, such as G-banding and fluorescence in situ hybridization (FISH), is difficult due to their low resolution. Here, we describe a new diagnostic modality that enables detection of chromosomal microdeletions, using CDKN2A gene deletion in B cell lymphomas (BCLs) as an example. In this method, which we refer to as amplified-FISH (AM-FISH), a 31-kb fluorescein isothiocyanate (FITC)-conjugated DNA probe encoding only CDKN2A was first hybridized with the chromosome, and then labeled with Alexa Fluor 488-conjugated anti-FITC secondary antibody to increase sensitivity. CDKN2A signals were equally identifiable by AM-FISH and conventional FISH in normal mononuclear blood cells. In contrast, when two BCL cell lines lacking CDKN2A were analyzed, CDKN2A signals were not detected by AM-FISH, whereas conventional FISH yielded false signals. Furthermore, AM-FISH detected CDKN2A deletions in two BCL patients with 9p21 microdeletions, which were not detected by conventional FISH. These results suggest that AM-FISH is a highly sensitive, specific, and simple method for diagnosis of chromosomal microdeletions.

Keywords: Amplified-FISH; CDKN2A; Fluorescence in situ hybridization (FISH); Hematologic malignancy; Microdeletion.

MeSH terms

  • Cell Line, Tumor
  • Chromosome Deletion*
  • Chromosomes, Human / genetics*
  • Chromosomes, Human / metabolism*
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • Cyclin-Dependent Kinase Inhibitor p16 / metabolism
  • Humans
  • In Situ Hybridization, Fluorescence / methods*
  • Lymphoma, B-Cell / genetics*
  • Lymphoma, B-Cell / metabolism*
  • Lymphoma, B-Cell / pathology

Substances

  • CDKN2A protein, human
  • Cyclin-Dependent Kinase Inhibitor p16