Publications by authors named "Yuan-mao Huang"

To investigate the prognostic value of the circulating peripheral blood cell counts changes in acute myeloid leukemia (AML) at different time points during induction chemotherapy.We retrospectively analyzed the clinical and laboratory data of 237 newly diagnosed AML patients admitted to Fujian Medical University Union Hospital from January 2011 to December 2014.1.

View Article and Find Full Text PDF

Genetic heterogeneity is the basis of clinical heterogeneity among different subtypes of AML. We have successfully cloned a gene related to AML termed from a FAB-M2 patient's sample of a second largest AML pedigree. Then we revealed at least three splice variants, named as , and , and found miR181a1/b1 in the second intron of FAMLF gene family.

View Article and Find Full Text PDF

The role of , a newly identified DEAH-box RNA helicase, in leukemogenesis remains elusive. Here, we identified a recurrent mutation in (NM_001358:c.664C>G: p.

View Article and Find Full Text PDF

Objective: To investigate the significance of serum interleukin-35 level and the new regulatory T cells -iTR35 cells in patients with myelodysplastic syndrome (MDS).

Methods: Twenty three cases of newly diagnosed MDS were enrolled in this study from January 2014 to January 2016 in Department of Hematology of The First Hospital of Quanzhou in Fujian Province. According to MDS International Prognostic Scoring System (IPSS), the 23 patients were divided into 4 groups: high-risk (n=4), intermediate risk-2 (n=10), intermediate risk-1 (n=5) and low-risk group(n=4).

View Article and Find Full Text PDF

Objective: To study the expression and its mechamisms of microRNA let-7b in adult acute lymphoblastic leukemia (ALL), so as to provide the basis for searching a new targeted therapy.

Methods: Firstly, methylation-specific polymerase chain reaction (MSP) was used to analyze the methylation status of CpG islands in microRNA let-7b promoter of bone marrow mononuclear cells in the patients with ALL and patients with non-hematologic malignancies as control, the real-time fluorescence quantitative polymerase chain reaction (qPCR) was used to detect the expression levels of microRNA let-7b in this 2 groups; and then 5-aza-2'-deoxycytidine (5-Aza-dC, DAC) was used to treat ALL cell line MOLT-4; after drug treatment, MSP was used to analyze the methylation status of the CpG islands in microRNA let-7b promoter; the qPCR was used to detect the expression levels of microRNA let-7b, and further explore the regulatory mechanism of microRNA let-7b expression.

Results: Hypermethylation of CpG islands in microRNA let-7b promoter in ALL patients was significantly higher than that in patients with non-hematologic malignancies, and the relative expression level of microRNA let-7b was significantly reduced in ALL patients; 5-aza-dC could significantly inhibit the growth of MOLT-4 cells and arrest the cells in G1 phase, thus biosynthesis of RNA and protein was suppressed, and the apoptosis was promoted, meanwhile, 5-Aza-dC could increase the expression of microRNA let-7b.

View Article and Find Full Text PDF

An inherited predisposition to acute myeloid leukaemia (AML) is exceedingly rare, but the investigation of these families will aid in the delineation of the underlying mechanisms of the more common, sporadic cases. Three AML predisposition genes, RUNX1, CEBPA and GATA2, have been recognised, but the culprit genes in the majority of AML pedigrees remain obscure. We applied a combined strategy of linkage analysis and next-generation sequencing (NGS) technology in an autosomal-dominant AML Chinese family with 11 cases in four generations.

View Article and Find Full Text PDF

This study was purposed to investigate the expression of RPL36A (ribosomal protein 36a) in the newly diagnosed acute myeloid leukemia (AML) cells and its mechanism at the molecular level. The RPL36A mRNA expression in the newly diagnosed AML cells, U937 cells and normal MNCs was determined by RT-PCR. Small interfering RNA (siRNA) targeting to RPL36A was transfected into U937 cells by Lipofectamine 2000 system.

View Article and Find Full Text PDF

Objective: To clone the full-length cDNA of a novel gene related to familial acute myelogenous leukemia (AML) and to demonstrate its molecular mechanisms on the gene level.

Methods: Bone marrow specimen was obtained from a patient of familial AML, male, aged 11, and peripheral blood samples were obtained from 23 AML patients outside this family, 9 normal persons in this family, and 23 normal persons outside this family. Based on the EST sequence zywb87 (GenBank accession number: CV973101) from a subtractive cDNA library of differential expressed genes constructed in familial AML, SMART-rapid amplification of cDNA ends (SMART-RACE) was applied to clone the full-length cDNA of the novel gene, and bioinformatics was used to predict its biological function, the expression of the novel gene in AML was detected by One-Step RT-PCR.

View Article and Find Full Text PDF