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Ng C.S.,Academia Sinica, Taiwan | Chen C.-K.,Academia Sinica, Taiwan | Chen C.-K.,National Taiwan University | Fan W.-L.,Academia Sinica, Taiwan | And 20 more authors.
BMC Genomics | Year: 2015

Background: Feathers have diverse forms with hierarchical branching patterns and are an excellent model for studying the development and evolution of morphological traits. The complex structure of feathers allows for various types of morphological changes to occur. The genetic basis of the structural differences between different parts of a feather and between different types of feather is a fundamental question in the study of feather diversity, yet there is only limited relevant information for gene expression during feather development. Results: We conducted transcriptomic analysis of five zones of feather morphologies from two feather types at different times during their regeneration after plucking. The expression profiles of genes associated with the development of feather structure were examined. We compared the gene expression patterns in different types of feathers and different portions of a feather and identified morphotype-specific gene expression patterns. Many candidate genes were identified for growth control, morphogenesis, or the differentiation of specific structures of different feather types. Conclusion: This study laid the ground work for studying the evolutionary origin and diversification of feathers as abundant data were produced for the study of feather morphogenesis. It significantly increased our understanding of the complex molecular and cellular events in feather development processes and provided a foundation for future studies on the development of other skin appendages. © 2015 Ng et al. Source


Su K.-J.,Academia Sinica, China | Ho C.-C.,Chung Shan Medical University | Lin C.-W.,Chung Shan Medical University | Chen M.-K.,Chung Shan Medical University | And 6 more authors.
Tumor Biology | Year: 2015

In humans, fucosyltransferase-2 (FUT2) plays an important role in α1,2- linkage of fucose and participates in complex cellular processes such as fertilization, embryogenesis, and immune responses. However, little information is available concerning the FUT2 expression in tumorigenesis. The aim of this work was to investigate the combined effect of FUT2 gene polymorphisms and exposure to environmental carcinogens on the susceptibility and clinic pathological characteristics of oral cancer. Four SNPs of the FUT2 gene (rs281377, rs1047781, rs601338, and rs602662) from 1200 non-cancer controls and 700 oral squamous cell carcinoma (OSCC) patients were analyzed by real-time polymerase chain reaction (PCR). The samples were further analyzed to clarify the associations between these gene polymorphisms and the risk of OSCC, and the impact of these SNPs on the susceptibility and clinic pathological characteristics of OSCC. After adjusting for other covariant, we observed that betel quid chewing among 1255 smokers who carrying at least one C genotype (TC and CC) at rs281377 and least one T genotype (TA and TT) at rs1047781 were exhibited synergistic effects of environmental factors (betel quid and cigarette use) on the susceptibility of oral cancer. Taken together, our results support gene–environment interactions of FUT2 polymorphisms with smoking and betel quid chewing habits possibly altering oral cancer susceptibility. Furthermore, to our knowledge, this is the first study of association between FUT2 gene variants and OSCC risk. © 2015 International Society of Oncology and BioMarkers (ISOBM) Source


Chung W.-H.,Drug Hypersensitivity Clinical and Research Center | Chung W.-H.,Chang Gung University | Chung W.-H.,Whole Genome Research Core Laboratory of Human Diseases | Wang C.-W.,Drug Hypersensitivity Clinical and Research Center | And 2 more authors.
Journal of Dermatology | Year: 2016

The clinical manifestations of drug eruptions can range from mild maculopapular exanthema to severe cutaneous adverse drug reactions (SCAR), including drug-induced hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms, Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) which are rare but occasionally fatal. Some pathogens may induce skin reactions mimicking SCAR. There are several models to explain the interaction of human leukocyte antigen (HLA), drug and T-cell receptor (TCR): (i) the “hapten/prohapten” theory; (ii) the “p-i concept”; (iii) the “altered peptide repertoire”; and (iv) the “altered TCR repertoire”. The checkpoints of molecular mechanisms of SCAR include specific drug antigens interacting with the specific HLA loci (e.g. HLA-B*15:02 for carbamazepine-induced SJS/TEN and HLA-B*58:01 for allopurinol-induced SCAR), involvement of specific TCR, induction of T-cell-mediated responses (e.g. granulysin, Fas ligand, perforin/granzyme B and T-helper 1/2-associated cytokines) and cell death mechanism (e.g. miR-18a-5p-induced apoptosis; annexin A1 and formyl peptide receptor 1-induced necroptosis in keratinocytes). In addition to immune mechanism, metabolism has been found to play a role in the pathogenesis of SCAR, such as recent findings of strong association of CYP2C9*3 with phenytoin-induced SCAR and impaired renal function with allopurinol SCAR. With a better understanding of the mechanisms, effective therapeutics and prevention for SCAR can be improved. © 2016 Japanese Dermatological Association Source


Su C.-W.,Chung Shan Medical University | Huang Y.-W.,Chung Shan Medical University | Huang Y.-W.,Pulmonary and Critical Care Unit | Chen M.-K.,Chung Shan Medical University | And 4 more authors.
Medicine (United States) | Year: 2015

Oral cancer, the fourth most common cancer among men in Taiwan, is associated with environmental carcinogens. Tissue inhibitor of metalloproteinase-3 (TIMP3), a member of the TIMP family, is the only protein that binds to the extracellular matrix for suppressing cancer cell growth, angiogenesis, migration, and invasion. The association of TIMP3 polymorphism with oral cancer susceptibility, however, has not yet been reported. In this study, 1947 participants-1200 healthy male controls and 747 male patients with oral cancer-were recruited. Allelic discrimination of TIMP3 1296 T>C (rs9619311), TIMP3 C>T (rs9862), and TIMP3 C>T (rs11547635) polymorphisms were assessed through real-time polymerase chain reaction. The authors discovered that individuals carrying the polymorphic rs9862 allele are more susceptible to oral cancer [odds ratio (OR), 1.5; 95% confidence interval (CI), 1.2-1.9; adjusted OR (AOR), 1.6; 95% CI, 1.2-2.1] after adjustment for betel quid chewing, alcohol, and tobacco consumption. Among 601 betel quid chewers, the TIMP3 polymorphism rs9862 T/T carriers had a 32.2-fold (95% CI, 20.2-51.3) increased oral cancer risk compared with those carrying C/C and not chewing betel quid. In addition, the authors observed a significant association between rs9862 variants and large tumors (OR, 1.5; 95% CI, 1.0-2.3) development. Moreover, TIMP3 plasma levels significantly increased in oral cancer patients who have large tumor or carry T allele rs9862 polymorphism. In conclusion, these results suggest that gene-environment interactions between the TIMP3 rs9862 polymorphisms and betel quid may alter oral cancer susceptibility and tumor growth in Taiwanese men. © 2015 Wolters Kluwer Health, Inc. All rights reserved. Source


Yang J.-S.,Chung Shan Medical University | Lin C.-W.,Chung Shan Medical University | Chuang C.-Y.,Chung Shan Medical University | Su S.-C.,Drug Hypersensitivity Clinical and Research Center | And 4 more authors.
Tumor Biology | Year: 2015

Carbonic anhydrase IX (CAIX) is reportedly overexpressed in several types of carcinomas and is generally considered a marker of malignancy. The current study investigated the association between membrane expression of CAIX and the clinicopathological characteristics in oral squamous cell carcinoma (OSCC) patients. The study used immunohistochemistry to examine CAIX expression in 271 OSCC specimens by tissue microarray (TMA) and assessed the effect of CAIX overexpression and knockdown on migration of oral cancer cells in vitro. We found that CAIX expression was associated with more advanced clinical stages (p = 0.030) and positive lymph node metastasis (p = 0.026). Importantly, CAIX expression was correlated with a poorer patient prognosis in a univariate survival analysis (p = 0.025). Moreover, CAIX suppression by small interfering RNA (siRNA) significantly reduced cellular migration in OECM-1 oral cancer cell. In conclusion, our study showed that the expression of CAIX in OSCC samples can predict the progression of OSCC and survival of OSCC patients in Taiwan. © 2015, International Society of Oncology and BioMarkers (ISOBM). Source

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