Liang‐In Lin

National Taiwan University

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Hwei‐Fang Tien

National Taiwan University Hospital

Da‐Liang Ou

National Taiwan University

Hsin‐An Hou

National Taiwan University Hospital

Wen‐Chien Chou

National Taiwan University Hospital

Jih‐Luh Tang

Sir Run Run Shaw Hospital

Jeng‐Wei Lu

University of Copenhagen

Chiun Hsu

National Taiwan University Hospital

Ming Yao

National Taiwan University Hospital

Shang‐Ju Wu

Taichung Veterans General Hospital

Chien‐Yuan Chen

Kaohsiung Chang Gung Memorial Hospital

Cooperative Institutions

National Taiwan University

230

National Taiwan University Hospital

189

National Yang Ming Chiao Tung University

Chinese Academy of Medical Sciences & Peking Union Medical College

Shanghai Jiao Tong University

China Medical University

Sun Yat-sen University

Stanford University

Peking University

Capital Medical University

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In Alzheimer disease, increased wake fragmentation found in those with lower hypocretin-1

Neurology (2007)

Leah Friedman Jamie M. Zeitzer Liang‐In Lin Dag Arne Lihaug Hoff E. Mignot

Regulation of wakefulness is often disturbed in Alzheimer disease (AD). We examined CSF concentrations of hypocretin-1, a wake-stimulating peptide, in 16 patients with AD and simultaneously recorded a week of at-home sleep. Although hypocretin-1 concentrations were normal, fragmentation of daytime wake was elevated in those with low hypocretin-1 levels ( r = −0.64, p < 0.05, number of naps; r = −0.62, p < 0.05, napping hours; r = −0.63, p < 0.05, locomotor rhythm amplitude). Lower hypocretin-1 levels may be permissive for, or a consequence of, increased wake fragmentation in AD. Sleep disruption is commonly observed in older individuals with Alzheimer disease (AD)1 and may predict rapidity of cognitive decline. The biologic basis for sleep dysregulation is unknown but may be related to the degeneration of the cholinergic fibers critical to both cognition and control of sleep. A recently discovered hypothalamic neuropeptide, hypocretin-1, has been hypothesized to be involved in consolidation of wakefulness into a single daily episode2 or in consolidation of both nocturnal sleep and diurnal wake.3 Failure of this consolidation process may underlie some sleep disturbances observed in AD.1 Although previous studies have determined that there may be normal levels of hypocretin-1 in AD,4,5 we sought to determine whether there were associations between …

Fragmentation

10.1212/01.wnl.0000256731.57544.f9

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Citations (54)

Analysis of genetic variants in four children with congenital hyperinsulinemia

Liang‐In Lin Fei Shen Qi Yang Shang Yi Zailong Qin

OBJECTIVE To explore the genetic basis of four children with congenital hyperinsulinemia (CHI). METHODS The four children were subjected to high-throughput whole exome sequencing (WES). Candidate variants were validated by Sanger sequencing. RESULTS WES analysis has identified 4 variants in the ABCC8 gene and 1 variant in GLUD1, including a ABCC8 c.382G>A variant in case 1, compound heterozygous c.698T>C and c.4213G>A variants of the ABCC8 gene concomitant with a de novo 14.9 Mb microduplication of chromosome 15 in case 2, and ABCC8 c.331G>A variant in case 3, and de novo c.955T>C variant of the GLUD1 gene in case 4. Of these, c.698T>C of the ABCC8 gene and c.955T>C of the GLUD1 gene were unreported previously. Based on the American College of Medical Genetics and Genomics guidelines, the c.382G>A(p.Glu128Lys), c.698T>C(p.Met233Thr) and c.4213G>A(p.Asp1405Asn) variants of ABCC8 gene and c.955T>C(p.Tyr319His) variant of GLUD1 gene were predicted to be likely pathogenic(PM1+PM2+PP3+PP4, PM1+PM2+PM5+PP3+PP4, PM1+PM2+PP3+PP4 and PS1+PM1+PM2+PP3), and the c.331G>A (p.Gly111Arg) variant of ABCC8 gene was predicted to be uncertain significance(PM1+PM2+PP4). CONCLUSION The variants of the ABCC8 and GLUD1 genes probably underlay the pathogenesis of CHI in the four patients. Above results have facilitated clinical diagnosis and genetic counseling for the affected families.

Sanger sequencing

Compound heterozygosity

Proband

10.3760/cma.j.cn511374-20200520-00358

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Citations (2)

Data from Cyclin E1 Inhibition can Overcome Sorafenib Resistance in Hepatocellular Carcinoma Cells Through Mcl-1 Suppression

Chiun Hsu Liang‐In Lin Yu‐Che Cheng Zi-Rui Feng Yu‐Yun Shao

<div>AbstractPurpose: To clarify the effects of cyclin E1 suppression on antitumor efficacy of sorafenib in hepatocellular carcinoma cells and to explore the potential of combining sorafenib with cyclin-dependent kinase (CDK) inhibition in therapy.Experimental Design: The effects of cyclin E1 suppression on sorafenib-induced apoptosis were tested in both sorafenib-sensitive (Huh-7 and HepG2, IC50 5–6 μmol/L) and sorafenib-resistant (Huh-7R and HepG2R, IC50 14–15 μmol/L) hepatocellular carcinoma cells. The activity of pertinent signaling pathways and the expression of cell cycle and apoptosis-related proteins were measured using Western blotting. Efficacy of sorafenib combined with the pan-CDK inhibitor flavopiridol was tested both in vitro and in xenograft experiments. The pertinent downstream mediators of antitumor efficacy were tested in transient transfection and RNA interference experiments.Results: Cyclin E1 mRNA and protein expressions were suppressed after sorafenib treatment in sorafenib-sensitive but not in sorafenib-resistant hepatocellular carcinoma cells. Changes in cyclin E2 or D1 were not correlated with sorafenib sensitivity. The knockdown of cyclin E1 expression reversed the resistance of hepatocellular carcinoma cells to sorafenib in terms of cell growth and apoptosis induction, whereas the overexpression of cyclin E1 increased the resistance to sorafenib. The growth-inhibitory and apoptosis-inducing effects of sorafenib were enhanced by flavopiridol, and Mcl-1 suppression was determined to play a critical role in mediating this enhancing effect.Conclusions: The cyclin E1 suppression in hepatocellular carcinoma cells may serve as a pharmacodynamic biomarker for predicting sorafenib efficacy. The combination of sorafenib and CDK inhibitors may improve the efficacy of sorafenib in hepatocellular carcinoma. Clin Cancer Res; 22(10); 2555–64. ©2015 AACR.</div>

Cyclin E1

Cyclin E

10.1158/1078-0432.c.6524096.v1

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Supplementary Table 1 from Nucleophosmin Mutations in De novo Acute Myeloid Leukemia: The Age-Dependent Incidences and the Stability during Disease Evolution

Wen‐Chien Chou Jih‐Luh Tang Liang‐In Lin Ming Yao Woei Tsay

Supplementary Table 1 from Nucleophosmin Mutations in De novo Acute Myeloid Leukemia: The Age-Dependent Incidences and the Stability during Disease Evolution

Nucleophosmin

10.1158/0008-5472.22365572.v1

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Detection of p53 Gene Abnormality by Sequence Analysis of Archival Paraffin Tissue

Diagnostic Molecular Pathology (1996)

Mehrdad Nadji Lou Meng Liang‐In Lin Mehdi Nassiri Azorides R. Morales

Log in or Register Subscribe to journalSubscribe Get new issue alertsGet alerts Enter your Email address: Wolters Kluwer Health may email you for journal alerts and information, but is committed to maintaining your privacy and will not share your personal information without your express consent. For more information, please refer to our Privacy Policy. Subscribe to eTOC Secondary Logo Journal Logo All Articles Images Videos Podcasts Blogs Advanced Search Toggle navigation Subscribe Register Login Articles & Issues Current IssuePrevious IssuesPublished Ahead-of-Print For Authors Information for AuthorsLanguage Editing Services Journal Info About the JournalEditorial BoardAffiliated SocietyAdvertisingOpen AccessSubscription ServicesReprintsRights and PermissionsMobileNew Features All Articles Images Videos Podcasts Blogs Advanced Search

10.1097/00019606-199612000-00009

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Characterization of CEBPA Mutations in Acute Myeloid Leukemia: Most Patients with CEBPA Mutations Have Biallelic Mutations and Show a Distinct Immunophenotype of the Leukemic Cells

Clinical Cancer Research (2005)

Liang‐In Lin Chien‐Yuan Chen Dong‐Tsamn Lin Woei Tsay Jih‐Luh Tang

Abstract Purpose: The transcription factor CCAAT/enhancer binding protein α, encoded by the CEBPA, is crucial for the differentiation of immature granulocytes. Mutation of the CEBPA may play an important role in leukemogenesis and prognosis. We sought to characterize the CEBPA mutation in acute myeloid leukemia (AML) and to clarify if there is a distinct immunophenotype for leukemic cells with the mutation. Experiment Design: One hundred and four patients with de novo AML were evaluated for the CEBPA mutation and immunophenotype of the leukemic cells. Results: Twenty-two distinct mutations were identified in 16 (15%) of 104 AML patients. Fourteen patients had biallelic mutations, mostly involving both the NH2-terminal TAD1 region and the COOH-terminal basic leucine zipper domain (bZIP). The mutations in the bZIP region were always tandem duplications and were located at hot-spot regions for topoisomerase II sites. Sequential study of the CEBPA mutations showed that the mutations disappeared at complete remission but the same mutations reappeared at relapse. None of the patients developed novel mutations during the follow-up period. Patients with CEBPA mutations had significantly higher incidences of CD7 (73%), CD15 (100%), CD34 (93%), and HLA-DR (93%) expression on the leukemic cells. Conclusion: These data revealed that most AML with CEBPA mutations were associated with an immunophenotype of HLA-DR+CD7+CD13+CD14−CD15+CD33+CD34+. The close relationship of CEBPA mutations with the leukemia status of the patients and the concordance of mutation in presenting and relapse samples implicate the CEBPA mutation as a potential marker for monitoring minimal residue disease.

CEBPA

Immunophenotyping

NPM1

10.1158/1078-0432.ccr-04-1816

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Citations (218)

Cell Type-Specific Protein-DNA Interactions in the Human ζ-Globin Upstream Promoter Region: Displacement of Sp1 by the Erythroid Cell-Specific Factor NF-E1

Molecular and Cellular Biology (1990)

Chun-Yuan Yu Julia Chen Liang‐In Lin Ming F. Tam C.‐K. James Shen

The protein-DNA interactions of the upstream promoter region of the human embryonic zeta-globin gene in nuclear extracts of erythroid K562 cells and nonerythroid HeLa cells were analyzed by DNase I footprinting, gel mobility shift assay, methylation interference, and oligonucleotide competition experiments. There are mainly two clusters of nuclear factor-binding sites in the zeta promoter. The proximal cluster spans the DNA sequence from -110 to -60 and consists of binding sites for CP2, Sp1, and NF-E1. NF-E1 binding is K562 specific, whereas CP2 binding is common to both types of cells. Overlapping the NF-E1- and CP2-binding sites is a hidden Sp1-binding site or CAC box, as demonstrated by binding studies of affinity-purified Sp1. In the distal promoter region at -250 to -220, another NF-E1-binding site overlaps a CAC box or Sp1-binding site. Extract-mixing experiments demonstrated that the higher affinity of NF-E1 binding excluded the binding of Sp1 in the K562 extract. NF-E1 factors could also displace prebound Sp1 molecules. Between the two clusters of multiple-factor-binding sites are sequences recognized by other factors, including zeta-globin factors 1 and 2, that are present in both HeLa and K562 extracts. We discuss the cell type-specific, competitive binding of multiple nuclear factors in terms of functional implications in transcriptional regulation of the zeta-globin gene.

DNA binding site

K562 cells

Sp1 transcription factor

10.1128/mcb.10.1.282-294.1990

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Expression of angiopoietins and vascular endothelial growth factors and their clinical significance in acute myeloid leukemia

Leukemia Research (2007)

Hsin‐An Hou Wen‐Chien Chou Liang‐In Lin Jih‐Luh Tang Mei‐Hsuan Tseng

Clinical Significance

10.1016/j.leukres.2007.08.010

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