Cytogenetic profiles of 2806 patients with acute myeloid leukemia—a retrospective multicenter nationwide study View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2016-08

AUTHORS

Ja Min Byun, Young Jin Kim, Hwi-Joong Yoon, Si-Young Kim, Hee-Je Kim, Jaeho Yoon, Yoo Hong Min, Jun-Won Cheong, Jinny Park, Jae Hoon Lee, Dae Sik Hong, Seong Kyu Park, Hyeoung-Joon Kim, Jae-Sook Ahn, Ho-Jin Shin, Joo Seop Chung, Won Sik Lee, Sang Min Lee, Yong Park, Byung Soo Kim, Je-Hwan Lee, Kyoo-Hyung Lee, Chul Won Jung, Jun Ho Jang, Woo-Sung Min, Tae Sung Park, on behalf of the AML/MDS working party of Korean Society of Hematology

ABSTRACT

The cytogenetic and molecular data is recognized as the most valuable prognostic factor in acute myeloid leukemia (AML). Our aim was to systemically analyze the cytogenetics of Korean AML patients and to compare the cytogenetic profiles of various races to identify possible geographic heterogeneity. We retrospectively reviewed medical records of 2806 AML patients diagnosed at 11 tertiary teaching hospitals in Korea between January 2007 and December 2011. The most common recurrent chromosomal abnormality was t(8;21) (8.8 %, 238/2717), but t(15;17) showed an almost same number (8.6 %,235/2717). Among de novo AML, the most frequent aberrations were t(15;17), observed in 229 (10.7 %). The most common French-American-British (FAB) classification type was M2 (32.2 %), and recurrent cytogenetic abnormalities correlated with the FAB subtypes. Among 283 secondary AML cases, myelodysplastic syndrome was the most common predisposing factor. About 67.1 % of the secondary AML cases were associated with chromosomal aberrations, and chromosome 7 abnormalities (n = 45, 15.9 %) were most common. The incidence of FLT3 internal tandem duplication mutation was relatively low at 15 %. Our study reports certain similarities and differences in comparison to previous reports. Such discrepancies call for extensive epidemiological studies to clarify the role of genetic as well as geographic heterogeneity in the pathogenesis of AML. More... »

PAGES

1223-1232

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00277-016-2691-1

DOI

http://dx.doi.org/10.1007/s00277-016-2691-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1038746252

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27230620


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