Tung-Huei Lin
Chang Gung University
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Tung-Huei Lin.
Blood | 2013
Der-Cherng Liang; Hsi-Che Liu; Chao-Ping Yang; Tang-Her Jaing; Iou-Jih Hung; Ting-Chi Yeh; Shih-Hsiang Chen; Jen-Yin Hou; Ying-Jung Huang; Yu-Shu Shih; Yu-Hui Huang; Tung-Huei Lin; Lee-Yung Shih
Gene mutations involving epigenetic regulators recently have been described in adult acute myeloid leukemia (AML). Similar studies are limited in children. We analyzed gene mutations and cooperation in pediatric AML with special reference on mutated epigenetic regulators. Nineteen gene mutations, including 8 class I genes, 4 class II genes, WT1 and TP53 (class III), and 5 epigenetic regulator genes (class IV), were analyzed in 206 children with de novo AML. Mutational analysis was performed with polymerase chain reaction-based assay followed by direct sequencing. One hundred seventeen of 206 patients (56.8%) had at least one mutation: 51% class I, 13% class II, 6.8% class III, and 5.6% class IV. FLT3-internal tandem duplication was most frequent, and 29% of patients had more than one gene mutation. Two patients carried ASXL1 mutations, both with t(8;21), 2 had DNMT3A mutations, 2 had IDH1 mutations, 1 had IDH2 mutation, and 3 had TET2 mutations. Both patients with IDH1 mutations had AML-M0 subtype and MLL-partial tandem duplication. Cooperating mutations with mutated epigenetic regulators were observed in 8 of 10 patients. We conclude that mutated epigenetic regulators were much less than those in adult AML but with frequent cooperating mutations. ASXL1, TET2, and IDH1 mutations were associated with specific genetic subtypes.
Haematologica | 2014
Tung-Liang Lin; Yasunobu Nagata; Hsiao-Wen Kao; Masashi Sanada; Yusuke Okuno; Chein-Fuang Huang; Der-Cherng Liang; Ming-Chung Kuo; Chang-Liang Lai; En-Hui Lee; Yu-Shu Shih; Hiroko Tanaka; Yuichi Shiraishi; Kenichi Chiba; Tung-Huei Lin; Jin-Hou Wu; Satoru Miyano; Seishi Ogawa; Lee-Yung Shih
Somatic mutations of TET2, IDH1, and IDH2 have been described in myelodysplastic syndrome. The impact of these mutations on outcome of myelodysplastic syndrome and their progression to secondary acute myeloid leukemia remains unclear. Mutation status of TET2, IDH1 and IDH2 was investigated in a cohort of 46 paired myelodysplastic syndrome/acute myeloid leukemia samples and 122 non-paired cases with de novo myelodysplastic syndrome, to clarify their roles in the evolution of myelodysplastic syndrome to acute myeloid leukemia. Among the 168 de novo myelodysplastic syndrome patients, the frequency of TET2, IDH1, and IDH2 mutations was 18.5%, 4.2% and 6.0%, respectively. TET2/IDH mutations had no impact on survivals, while TET2 mutations were significantly associated with rapid progression to acute myeloid leukemia. Seventeen of the 46 paired myelodysplastic syndrome/secondary acute myeloid leukemia samples harbored TET2/IDH mutations; none acquired these mutations in acute myeloid leukemia phase. Progression to acute myeloid leukemia was accompanied by evolution of a novel clone or expansion of a minor pre-existing subclone of one or more distinct mutations in 12 of the 17 cases with TET2/IDH mutations. A minor subclone in 3 cases with biallelic TET2 inactivation subsequently expanded, indicating biallelic TET2 mutations play a role in acute myeloid leukemia progression. Twelve patients acquired other genetic lesions, and/or showed increased relative mutant allelic burden of FLT3-ITD, N/K-RAS, CEBPA or RUNX1 during acute myeloid leukemia progression. Our findings provide a novel insight into the role of TET2/IDH mutation in the pathogenesis of myelodysplastic syndrome and subsequent progression to acute myeloid leukemia.
Neoplasia | 2014
Hsiao-Wen Kao; Der-Cherng Liang; Jin-Hou Wu; Ming-Chung Kuo; Po-Nan Wang; Chao-Ping Yang; Yu-Shu Shih; Tung-Huei Lin; Yu-Hui Huang; Lee-Yung Shih
Minimally differentiated acute myeloid leukemia (AML-M0) is a rare subtype of AML with poor prognosis. Although genetic alterations are increasingly reported in AML, the gene mutations have not been comprehensively studied in AML-M0. We aimed to examine a wide spectrum of gene mutations in patients with AML-M0 to determine their clinical relevance. Twenty gene mutations including class I, class II, class III of epigenetic regulators (IDH1, IDH2, TET2, DNMT3A, MLL-PTD, ASXL1, and EZH2), and class IV (tumor suppressor genes) were analyzed in 67 patients with AML-M0. Mutational analysis was performed with polymerase chain reaction–based assays followed by direct sequencing. The most frequent gene mutations from our data were FLT3-ITD/FLT3-TKD (28.4%), followed by mutations in IDH1/IDH2 (28.8%), RUNX1 (23.9%), N-RAS/K-RAS (12.3%), TET2 (8.2%), DNMT3A (8.1%), MLL-PTD (7.8%), and ASXL1 (6.3%). Seventy-nine percent (53/67) of patients had at least one gene mutation. Class I genes (49.3%) were the most common mutated genes, which were mutually exclusive. Class III genes of epigenetic regulators were also frequent (43.9%). In multivariate analysis, old age [hazard ratio (HR) 1.029, 95% confidence interval (CI) 1.013-1.044, P = .001) was the independent adverse factor for overall survival, and RUNX1 mutation (HR 2.326, 95% CI 0.978-5.533, P = .056) had a trend toward inferior survival. In conclusion, our study showed a high frequency of FLT3, RUNX1, and IDH mutations in AML-M0, suggesting that these mutations played a role in the pathogenesis and served as potential therapeutic targets in this rare and unfavorable subtype of AML.
Oncotarget | 2015
Hsiao-Wen Kao; Der-Cherng Liang; Ming-Chung Kuo; Jin-Hou Wu; Po Dunn; Po-Nan Wang; Tung-Liang Lin; Yu-Shu Shih; Sung-Tzu Liang; Tung-Huei Lin; Chen-Yu Lai; Chun-Hui Lin; Lee-Yung Shih
The mutational profiles of acute myeloid leukemia (AML) with partial tandem duplication of mixed-lineage leukemia gene (MLL-PTD) have not been comprehensively studied. We studied 19 gene mutations for 98 patients with MLL-PTD AML to determine the mutation frequency and clinical correlations. MLL-PTD was screened by reverse-transcriptase PCR and confirmed by real-time quantitative PCR. The mutational analyses were performed with PCR-based assays followed by direct sequencing. Gene mutations of signaling pathways occurred in 63.3% of patients, with FLT3-ITD (44.9%) and FLT3-TKD (13.3%) being the most frequent. 66% of patients had gene mutations involving epigenetic regulation, and DNMT3A (32.7%), IDH2 (18.4%), TET2 (18.4%), and IDH1 (10.2%) mutations were most common. Genes of transcription pathways and tumor suppressors accounted for 23.5% and 10.2% of patients. RUNX1 mutation occurred in 23.5% of patients, while none had NPM1 or double CEBPA mutation. 90.8% of MLL-PTD AML patients had at least one additional gene mutation. Of 55 MLL-PTD AML patients who received standard chemotherapy, age older than 50 years and DNMT3A mutation were associated with inferior outcome. In conclusion, gene mutations involving DNA methylation and activated signaling pathway were common co-existed gene mutations. DNMT3A mutation was a poor prognostic factor in MLL-PTD AML.
Pediatric Blood & Cancer | 2018
Der-Cherng Liang; Shih-Hsiang Chen; Hsi-Che Liu; Chao-Ping Yang; Ting-Chi Yeh; Tang-Her Jaing; Iou-Jih Hung; Jen-Yin Hou; Tung-Huei Lin; Chun-Hui Lin; Lee-Yung Shih
We aimed to investigate the frequencies and the association with genetic/cytogenetic abnormalities as well as prognostic relevance of RAS pathway mutations in Taiwanese children with B‐precursor acute lymphoblastic leukemia (ALL), the largest cohort in Asians.
Blood | 2014
Der-Cherng Liang; Lee-Yung Shih; Ming-Chung Kuo; Chao-Ping Yang; Hsi-Che Liu; Tang-Her Jaing; Jen-Fen Fu; Yu-Shu Shih; Tung-Huei Lin
Blood | 2013
Lee-Yung Shih; Hung Chang; Ming-Chung Kuo; Tung-Huei Lin; Chen-Yu Lai; Yu-Shu Shih; Yu-Hui Huang; Tung-Liang Lin; Po-Nan Wang; Jin-Hou Wu
Blood | 2009
Tung-Liang Lin; Lee-Yung Shih; Der-Cherng Liang; Chein-Fuang Huang; Chia-Hui Chang; Ming-Chung Kuo; Chang-Liang Lai; Tung-Huei Lin
Blood | 2005
Der-Cherng Liang; Lee-Yung Shih; Chang-Liang Lai; Tung-Huei Lin; Jen-Fen Fu; Huei-Ying Li; Hsiu-I. Wang; Iou-Jih Hung; Chao-Ping Yang; Tang-Her Jaing; Shu-Huey Chen; Hsi-Che Liu; Lin-Yen Wang
Archive | 2013
Lee-Yung Shih; Shih-Hsiang Chen; Jen-Yin Hou; Ying-Jung Huang; Yu-Shu Shih; Yu-Hui Huang; Tung-Huei Lin; Der-Cherng Liang; Hsi-Che Liu; Chao-Ping Yang; Tang-Her Jaing; Iou-Jih Hung; Ting-Chi Yeh