ArticleHematology reports2012
Translocation t(11;14) (q13;q32) and genomic imbalances in multi-ethnic multiple myeloma patients: a Malaysian study.
Article in Hematology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 16 citations in OpenAlex.
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- The Transcriptional Co-factor IRF2BP2: A New Player in Tumor Development and Microenvironment.Frontiers in cell and developmental biology · 2021Review
- TRPM2 promotes the proliferation and invasion of pancreatic ductal adenocarcinoma.Molecular medicine reports · 2018Article
- Genome-wide screening for genomic aberrations in Kazakh patients with esophageal squamous cell cancer by comparative genomic hybridization.International journal of clinical and experimental pathology · 2018Article
- Myelomatous plasma cells display an aberrant gene expression pattern similar to that observed in normal memory B cells.American journal of cancer research · 2015Article
- RPL24: a potential therapeutic target whose depletion or acetylation inhibits polysome assembly and cancer cell growth.Oncotarget · 2014Article
- SAMSN1 is a tumor suppressor gene in multiple myeloma.Neoplasia (New York, N.Y.) · 2014Article
- Nicotinamide phosphoribosyltransferase in malignancy: a review.Genes & cancer · 2013Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
More than 50% of myeloma cases have normal karyotypes under conventional cytogenetic analysis due to low mitotic activity and content of plasma cells in the bone marrow. We used a polymerase chain reaction (PCR)-based translocation detection assay to detect BCL1/JH t(11;14) (q13;q32) in 105 myeloma patients, and randomly selected 8 translocation positive samples for array comparative genomic hybridization (aCGH) analysis. Our findings revealed 14.3% of myeloma samples were positive for BCL1/JH t(11;14) (q13;q32) translocation (n=15 of 105). We found no significant correlation between this translocation with age (P=0.420), gender (P=0.317), ethnicity (P=0.066) or new/relapsed status of multiple myeloma (P=0.412) at 95% confidence interval level by χ(2)test. In addition, aCGH results showed genomic imbalances in all samples analyzed. Frequent chromosomal gains were identified at regions 1q, 2q, 3p, 3q, 4p, 4q, 5q, 7q, 9q, 11q, 13q, 15q, 21q, 22q and Xq, while chromosomal losses were detected at 4q and 14q. Copy number variations at genetic loci that contain NAMPT, IVNS1ABP and STK17B genes are new findings that have not previously been reported in myeloma patients. Besides fluorescence in situ hybridization, PCR is another rapid, sensitive and simple technique that can be used for detecting BCL1/JH t(11;14)(q13;q32) translocation in multiple myeloma patients. Genes located in the chromosomal aberration regions in our study, such as NAMPT, IVNS1ABP, IRF2BP2, PICALM, STAT1, STK17B, FBXL5, ACSL1, LAMP2, SAMSN1 and ATP8B4 might be potential prognostic markers and therapeutic targets in the treatment and management of multiple myeloma patients positive for BCL1/JH t(11;14) (q13;q32) translocation.
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