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Blood Res. 2018 Dec;53(4):320-324. English. Original Article. https://doi.org/10.5045/br.2018.53.4.320
Ahmadi A , Kaviani S , Yaghmaie M , Pashaiefar H , Ahmadvand M , Jalili M , Alimoghaddam K , Eslamijouybari M , Ghavamzadeh A .
Department of Hematology, Faculty of Medical Sciences, Tarbiat Modarres University, Tehran, Iran. kavianis@modares.a.ir
Hematology-Oncology and Stem Cell Transplantation Research Center, Tehran, Iran. m-yaghmaie@sina.tums.ac.ir
Cell Therapy and Hematopoietic Stem Cell Transplantation Research Center, Tehran, Iran.
Hematologic Malignancies Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Comprehensive Cancer Research Center, Mazandaran University of Medical Science, Sari, Iran.
Abstract

Background

Recent studies have devoted much attention to non-protein-coding transcripts in relation to a wide range of malignancies. MALAT1, a long non-coding RNA, has been reported to be associated with cancer progression and prognosis. Thus, we here determined MALAT1 gene expression in chronic lymphocytic leukemia (CLL), a genetically heterogeneous disease, and explored its possible relationships with cytogenetic abnormalities.

Methods

MALAT1 expression level was evaluated using real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) on blood mononuclear cells from 30 non-treated CLL patients and 30 matched healthy controls. Cytogenetic abnormalities were determined in patients by fluorescence in situ hybridization (FISH).

Results

MALAT1 expression level was up-regulated in the CLL group compared to healthy controls (P=0.008). Del13q14, followed by Del11q22, were the most prevalent cytogenetic abnormalities. We found no association between the FISH results and MALAT1 expression in patients.

Conclusion

Altered expression of MALAT1 is associated with CLL development. Further investigations are required to assess the relationship between this long non-coding RNA and CLL patient survival and prognosis.

Copyright © 2019. Korean Association of Medical Journal Editors.