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Identified hidden genomic changes in mantle cell lymphoma using high-resolution single nucleotide polymorphism

Norihiko Kawamata¹, Seishi Ogawa, Saskia Gueller

¹Hematology/Oncology, Cedars-Sinai Medical Center/UCLA School of Medicine, Los Angeles, Calif., USA.

Experimental Hematology

|May 30, 2009

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Single nucleotide polymorphism genomic microarrays (SNP-chip) offer high-resolution analysis of mantle cell lymphoma (MCL) genomic abnormalities, including acquired uniparental disomy (aUPD). This advanced technique detects subtle genetic changes missed by conventional methods, improving understanding of MCL pathogenesis.

Area of Science:

Genomics
Oncology
Hematology

Background:

Mantle cell lymphoma (MCL) is characterized by CCND1/cyclin D1 activation and genetic abnormalities.
Conventional methods like cytogenetics and comparative genomic hybridization have identified genomic alterations in MCL.
Single nucleotide polymorphism genomic microarrays (SNP-chip) provide higher resolution for cancer genomics analysis, detecting subtle changes like acquired uniparental disomy (aUPD).

Purpose of the Study:

To investigate genomic abnormalities in mantle cell lymphoma (MCL) using high-resolution single nucleotide polymorphism genomic microarrays (SNP-chip).
To identify novel genomic alterations and refine the characterization of known regions in MCL.
To evaluate the utility of SNP-chip technology in detecting small genomic gains/losses and aUPDs in MCL.

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Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients

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Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

Main Methods:

Analysis of 33 MCL samples (28 primary, 5 cell lines) using Affymetrix 250,000 SNP-chip arrays.
High-resolution detection of genomic gains, losses, and copy-neutral loss of heterozygosity (acquired uniparental disomy - aUPD).

Main Results:

Confirmed known MCL alterations (e.g., deletions in INK4A/ARF, ATM, TP53; MYC amplification).
Identified novel or refined regions of genomic abnormality, including 13q duplication involving miR17-92, cyclin D1 amplification, del(1p), del(6q), dup(3q), and dup(18q).
Detected various aUPD sites, including whole chromosome 9 and 9p aUPD, and a homozygous deletion of TNFSF genes on 19p.

Conclusions:

SNP-chip analysis provides high-resolution detection of genomic alterations in MCL.
This technique identifies small genomic gains/losses and aUPDs not discernible by conventional methods.
SNP-chip analysis enhances the understanding of MCL genomic landscape and potential therapeutic targets.