News Column

Reports from Institute of Genetic Engineering Add New Data to Findings in Acute Myeloid Leukemia

June 4, 2014



By a News Reporter-Staff News Editor at Biotech Week -- Research findings on Oncology are discussed in a new report. According to news reporting from Guangdong, People's Republic of China, by NewsRx journalists, research stated, "It is known that chemoresistance is a major cause of treatment failure in acute myeloid leukemia (AML). Substantial data indicate that the CD44 adhesion molecule is strongly expressed on AML blasts and that it can also inhibit apoptosis."

The news correspondents obtained a quote from the research from the Institute of Genetic Engineering, "Our study shows that drug resistance of the AML cell line HL60/ADM is due to overexpression of CD44. In an in vitro study, we knocked down CD44 in the HL60/ADM cell line using small interfering RNA (siRNA). Cell proliferation and the 50 % inhibitory concentrations (IC50) were determined by Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis and intracellular ADM accumulation were detected by flow cytometry. Expression of CD44, Bcl-2, c-Myc were assayed by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. The results indicate that the expression of CD44 in HL60/ADM cell line was much higher than in HL60 cell, and siRNA targeted CD44 (siRNA/CD44) could silence its expression in both mRNA and protein levels effectively. siRNA/CD44 substantially induces cell apoptosis, inhibits cell proliferation, enhances susceptibility to ADM and Ara-C, and at the same time increases intracellular ADM accumulation even reverses chemoresistance to ADM and Ara-C. Furthermore, by qRT-PCR and Western blot, we found that siRNA/CD44 decreases Bcl-2 and c-Myc synthesis. Our study provides a novel clue that CD44 plays a significant role in the chemoresistance of AML cells to Ara-C and ADM."

According to the news reporters, the research concluded: "Moreover, this provides a new direction to the approaches that combination therapy including targeting CD44 may overcome drug resistance and improve treatment effects."

For more information on this research see: Knockdown of CD44 enhances chemosensitivity of acute myeloid leukemia cells to ADM and Ara-C. Tumor Biology, 2014;35(4):3933-3940. Tumor Biology can be contacted at: Springer, Van Godewijckstraat 30, 3311 Gz Dordrecht, Netherlands. (Springer - www.springer.com; Tumor Biology - www.springerlink.com/content/1010-4283/)

Our news journalists report that additional information may be obtained by contacting N.S. Wang, Southern Med Univ, Inst Genet Engn, Guangzhou 510515, Guangdong, People's Republic of China. Additional authors for this research include M. Wei, W.L. Ma, W. Meng and W.L. Zheng (see also Oncology).

Keywords for this news article include: Asia, Oncology, Guangdong, Apoptosis, Hematology, Combination Therapy, Acute Myeloid Leukemia, People's Republic of China

Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2014, NewsRx LLC


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Source: Biotech Week


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