Teh-Ying Chou

National Yang Ming University, T’ai-pei, Taipei, Taiwan

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Publications (89)423.9 Total impact

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    ABSTRACT: Colorectal cancer (CRC) is among the leading causes of cancer-related mortality worldwide. Emerging evidence suggests that human cytomegalovirus (HCMV) exists in the tumour tissue of CRC and is associated with disease outcome. To study whether tumoural HCMV is related to viral reactivation in blood, tumour specimens and pre- and post-operative blood samples from CRC patients were collected prospectively. PCR and quantitative PCR were performed to detect HCMV DNA. HCMV IgG and IgM antibodies were measured using microparticle enzyme immunoassay (MEIA). Transcription of a spliced HCMV UL73 gene transcript was analysed by quantitative RT-PCR. HCMV was detected in 42.2%(35/83) of the tumour samples, with a low median viral load (30.08, range 2.33-5704 copies per 500 ng of genomic DNA). Vast majority (80/81, 98.8%) of the CRC patients were seropositive for HCMV IgG. HCMV DNA was positive in 11.3% (22/194) of the pre-operative and 8.9% (15/168) of post-operative blood samples. However, presence of HCMV and its viral load in tumours were not associated with the detection or viral loads in blood samples. About 26.67% (8/30) of the HCMV-positive tumours with available RNA had detectable viral UL73 transcripts, while none of the blood samples were positive for viral RNA (p < 0.0001). Therefore, presence of HCMV in tumours does not correlate with the serologic or viraemic status of CRC patients. Active viral gene transcription occurred in the tumour but not in the blood of CRC patients. HCMV reactivation in CRC patients is possibly due to virus-cancer interactions in the CRC tumour microenvironment.
    Journal of General Virology 10/2015; DOI:10.1099/jgv.0.000315 · 3.18 Impact Factor
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    ABSTRACT: Human cytomegalovirus (HCMV) has been increasingly detected in colorectal cancer (CRC), and genetic polymorphisms in HCMV affect its pathogenesis. This study aimed to investigate HCMV genetic polymorphisms in CRC and its correlation with the clinical outcomes. We performed PCR and sequencing of a viral immunomodulatory gene, UL144, in clinical isolates and CRC specimens. The nucleotide and amino acid sequences were aligned, and a phylogenetic tree was constructed. The clinical, pathological, and survival data were compared among tumours with different UL144 genotypes. HCMV was detected in 49 (47.8%) of the tumour specimens. Genotype A predominated in 43 samples (22/43; 51.2%) with successful sequencing, followed by genotype B (13/43; 30.2%) and genotype C (8/43; 18.6%). The genotypic distribution was similar to that of the clinical isolates and those reported in other Asian populations. The amino acid sequence of genotype B was the most conserved. For stage II and III CRC patients with HCMV-positive tumours, disease-free survival (DFS) varied amongst the 3 major genotypes (p = 0.0046). The presence of genotype B virus in the tumours was associated with a shorter DFS and independently predicted tumour recurrence in a multivariate Cox proportional hazards model (hazard ratio, 5.79; 95% confidence interval, 1.30-25.81; p = 0.021). By reverse-transcription PCR, tumour samples with genotype B viruses had the highest rate of UL144 expression. Our results suggest that genetic polymorphisms of HCMV UL144 were associated with clinical outcome in CRC and that HCMV may plays an immunomodulatory role in the tumour microenvironment of CRC.
    Journal of General Virology 10/2015; DOI:10.1099/jgv.0.000308 · 3.18 Impact Factor
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    ABSTRACT: Recurrence after surgical resection is the most common cause of treatment failure in patients with non-small-cell lung cancer. The aim of the study is to investigate the prognostic factors of postrecurrence survival (PRS) in patients of resected lung adenocarcinoma. The clinicopathological characteristics of 179 patients with recurrence after complete resection of lung adenocarcinoma at Taipei Veterans General Hospital between 2004 and 2010 were retrospectively reviewed. The prognostic and predictive effects of these clinicopathological variables in PRS were analyzed. The pattern of recurrence included local only in 25 (15.4%), distant only in 56 (34.6%), and both local and distant in 81 (50.0%) of patients. The 2-year and 5-year PRS were 65.2% and 29.8%, respectively. The most common organ sites of metastasis were the contralateral lung (39.1%), followed by the brain (33.5%) and the bone (31.3%). Multivariate analysis revealed that micropapillary/solid predominant pattern group (versus acinar/papillary; hazard ratio = 2.615; 95% confidence interval: 1.395-4.901; p = 0.003) and no treatment for recurrence (p < 0.001) were significant prognostic factors of worse PRS. For patients receiving treatment for recurrence, micropapillary/solid predominant pattern group (versus acinar/papillary; hazard ratio = 2.570; 95% confidence interval: 1.357-4.865; p = 0.004) was a significant predictive factor of worse PRS. Treatment for recurrence with surgery (p = 0.067) tended to be a significant predictive factor of better PRS. In lung adenocarcinoma, micropapillary/solid predominant pattern group (versus acinar/papillary) was a significant poor prognostic factor for PRS.
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 09/2015; 10(9):1328-36. DOI:10.1097/JTO.0000000000000618 · 5.28 Impact Factor
  • Jung-Jyh Hung · Teh-Ying Chou · Yu-Chung Wu · Wen-Hu Hsu ·

    Cancer Research 08/2015; 75(15 Supplement):4356-4356. DOI:10.1158/1538-7445.AM2015-4356 · 9.33 Impact Factor
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    ABSTRACT: Colorectal polyps are generally believed to be the precursors of colorectal cancers (CRC); however, the proportion and speed of progression differed widely in different subsets of polyps. Using microarray-based comparative genomic hybridization (aCGH) platform and CD133 immunostaining, we characterized colon polyps according to their association with CRC that developed in the same individual. aCGH was performed to unveil genomic changes in 18 cancer-synchronous polyps (CSP), and 9 cancer-preceding polyps (CPP), together with their corresponding cancers and 16 cases of incidental polyps (IP), were examined for comparison. aCGH profiles were analyzed to determine the clonal relationship (CR) between the paired adenoma and carcinoma. CD133 expressions in each subset of polyps were quantified by immunohistochemistry (IHC) staining. Progressive genomic changes were observed from IP, CSP/CPP to CRC; they encompass an entire chromosomal region in IP and sub-chromosomal region in CSP/CPP and CRC. CR analyses demonstrated that 50 % of CSP and 67 % of CPP were clonally related to the concurrent or later developed carcinomas, respectively. The CD133 expression levels were significantly higher in CSP/CPP than those in IP (P < 0.0001) and even higher in CSP/CPP that were clonally related to their corresponding carcinomas than CSP/CPP that were unrelated (P < 0.05). There were more genomic changes in CSP/CPP than IP; more than half of the CSP/CPP were clonally related to the corresponding carcinomas. Genomic changes at sub-chromosomal regions and/or high CD133 expression were associated with CSP/CPP and highlighted their carcinogenic potential.
    International Journal of Colorectal Disease 07/2015; DOI:10.1007/s00384-015-2319-2 · 2.45 Impact Factor
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    ABSTRACT: The human C-type lectin 18 (clec18) gene cluster, which contains three clec18a, clec18b, and clec18c loci, is located in human chromosome 16q22. Although the amino acid sequences of CLEC18A, CLEC18B, and CLEC18C are almost identical, several amino acid residues located in the C-type lectin-like domain (CTLD) and the sperm-coating protein/Tpx-1/Ag5/PR-1/Sc7 (SCP/TAPS) domain, also known as the cysteine-rich secretory proteins/antigen 5/pathogenesis-related 1 proteins (CAP) domain, are distinct from each other. Genotyping by real-time PCR and sequencing further shows the presence of multiple alleles in clec18a/b/c loci. Flow cytometry analysis demonstrates that CLEC18 (CLEC18A, -B, and -C) are expressed abundantly in human peripheral blood cells. Moreover, CLEC18 expression is further up-regulated when monocytes differentiate into macrophages and dendritic cells. Immunofluorescence staining reveals that CLEC18 are localized in the endoplasmic reticulum, Golgi apparatus, and endosome. Interestingly, CLEC18 are also detectable in human sera and culture supernatants from primary cells and 293T cells overexpressing CLEC18. Moreover, CLEC18 bind polysaccharide in Ca(2+)-independent manner, and amino acid residues Ser/Arg(339) and Asp/Asn(421) in CTLD domain contribute to their differential binding abilities to polysaccharides isolated from Ganoderma lucidum (GLPS-F3). The Ser(339) (CLEC18A) → Arg(339) (CLEC18A-1) mutation completely abolishes CLEC18A-1 binding to GLPS-F3, and a sugar competition assay shows that CLEC18 preferentially binds to fucoidan, β-glucans, and galactans. Because proteins with the SCP/TAPS/CAP domain are able to bind sterol and acidic glycolipid, and are involved in sterol transport and β-amyloid aggregation, it would be interesting to investigate whether CLEC18 modulates host immunity via binding to glycolipids, and are also involved in glycolipid transportation and protein aggregation in the future.
    Journal of Biological Chemistry 07/2015; 290(35). DOI:10.1074/jbc.M115.649814 · 4.57 Impact Factor
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    ABSTRACT: Hypoxia-inducible factor (HIF) is a heterodimer transcription factor complex that monitors the cellular response to the oxygen levels in cells. Hypoxia-inducible factor-1α (HIF-1α) has been shown to be stabilized by ionizing radiation (IR) and its stabilization promotes tumor progression and metastasis. Nijmegen breakage syndrome protein 1 (NBS1), a component of the MRE11-RAD50-NBS1 complex, plays an important role in the cellular response to DNA damage but its overexpression contributes to transformation and has been found to correlate with metastasis. However, whether NBS1 participates in IR-induced metastasis needs to be further determined. The aim of this study is to investigate whether radiation-induced HIF-1α stabilization is regulated by NBS1 and thereby promotes tumor cell migration/invasion. Here, we show that both NBS1 and HIF-1α expression are up-regulated after exposure to IR, and NBS1 increases HIF-1α expression at the protein level. In addition, IR treatment promotes the epithelial-mesenchymal transition (EMT) and in vitro cell migration and invasion activity, which could be abolished by suppression of NBS1. Furthermore, NBS1 directly interacts with HIF-1α and reduces the ubiquitination of HIF-1α⋅ Co-expression of HIF-1α and NBS1 in primary tumors of patients with lung adenocarcinoma correlates with a worse prognosis. These results provide a new function of NBS1 in stabilizing HIF-1α under IR, which leads to enhanced cancer cell migration and invasion. Copyright © 2015. Published by Elsevier Ltd.
    The international journal of biochemistry & cell biology 05/2015; 64. DOI:10.1016/j.biocel.2015.04.015 · 4.05 Impact Factor
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    ABSTRACT: Influenza A virus (IAV) infects macrophages and stimulates innate immunity receptors and sensors to produce proinflammatory cytokines and chemokines, which are responsible for IAV-induced pulmonary inflammation and injury. Decoy receptor 3 (DcR3) is a soluble protein belonging to the tumor necrosis factor receptor superfamily (TNFRSF), and is able to skew macrophage differentiation into an M2 phenotype. We demonstrated that DcR3 attenuated IAV-induced secretion of proinflammatory cytokines and chemokine from macrophages, and mitigated pulmonary infiltration and reduce lethality. Proteome-wide phosphoproteomic mapping revealed that DcR3 not only activated STK10, a negative regulator of cell migration, but also inactivated PKC-α, which are crucial for the activation of ERK and JNK in human macrophages. Furthermore, less pulmonary infiltration with lower levels of proinflammatory cytokines and chemokine in bronchoalveolar lavage fluid (BALF) were observed in DcR3-transgenic mice. Moreover, recombinant DcR3.Fc and heparan sulfate proteoglycan binding domain of DcR3.Fc (HBD.Fc) fusion proteins attenuated weight loss and protected mice from IAV-induced lethality. Thus, DcR3-mediated protection is not only via suppression of proinflammatory cytokine and chemokine release, but also via activation of STK10 to inhibit cell infiltration. DcR3 fusion proteins may become therapeutic agents to protect host from IAV-induced lethality in the future. Key message • DcR3 suppresses IAV-induced cytokine secretion.• DcR3 inhibits IAV-induced JNK and ERK activation in human macrophages.• DcR3 downregulates TLR3 and 7 expressions in human macrophages.• DcR3 protects mice from IAV-induced lethality.
    Journal of Molecular Medicine 05/2015; 93(10). DOI:10.1007/s00109-015-1291-1 · 5.11 Impact Factor
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    ABSTRACT: Breast cancer resistance protein [BCRP/ATP-binding cassette subfamily G member 2 (ABCG2)] is a member of the ATP-binding cassette transporter family. The presence of ABCG2 on the plasma membrane in many kinds of human cancer cells contributes to multidrug resistance during chemotherapy, and it has been used as the side population marker for identifying cancer stem cells in lung cancers. We report here that, in addition to the membranous form, ABCG2 proteins are also found inside the nucleus, where they bind to the E-box of CDH1 (E-cadherin) promoter and regulate transcription of this gene. Increased expression of ABCG2 causes an increase of E-cadherin and attenuates cell migration, whereas knockdown of ABCG2 downregulates E-cadherin and enhances cell motility. In mice, xenografted A549 cells that have less ABCG2 are more likely to metastasize from the subcutaneous inoculation site to the internal organs. However, for the cancer cells that have already entered the blood circulation, an increased level of ABCG2, and correspondingly increased E-cadherin, may facilitate circulating cancer cells to colonize at a distant site and form a metastatic tumor. We propose a novel role for nuclear ABCG2 that functions as a transcription regulator and participates in modulation of cancer metastasis. Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.
    Neoplasia (New York, N.Y.) 03/2015; 55(3). DOI:10.1016/j.neo.2015.01.004 · 4.25 Impact Factor
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    ABSTRACT: Cancer stem cells (CSCs) are usually tolerant to chemotherapy and radiotherapy and associated with tumor relapse. Suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor (HDACI), is currently being used in clinical trials of lung cancer. However, SAHA facilitates the formation of induced pluripotent stem cells from somatic cells. We hypothesized that SAHA would mediate the CSCs properties and subsequently confer a more malignant phenotype in lung cancer. Transfected H1299 lung cancer cells, which stably expresses a triple fused reporter gene (DsRedm-Fluc-tTKsr39) under the control of CMV promoter was used to establish a xenograft mouse model. After the treatment of SAHA, H1299 cell line and tumor xenografts were sorted by fluorescence-activated cell sorting (FACS) based on aldehyde dehydrogenase (ALDH) activity. We found that SAHA could suppress the growth of xenografted H1299 tumors with decreased proportion of ALDHbr lung cancer cells indicating that SAHA may target CSCs. However, SAHA significantly enhanced the tumor initiating capacity and the expression of malignant genes such as KCNMA1, MORF4L2 and ASPM in the remaining living ALDH(br) cells. These findings suggested that SAHA treatment created a more drug-resistant state in residual ALDH(br) cells. The in vivo imaging technique may facilitate searching and characterization of CSCs.
    Oncotarget 03/2015; 6(11). DOI:10.18632/oncotarget.3536 · 6.36 Impact Factor
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    ABSTRACT: A significant fraction of patients with lung adenocarcinomas harboring activating epidermal growth factor receptor (EGFR) mutations do not experience clinical benefits from EGFR tyrosine kinase inhibitor (TKI) therapy. Using next-generation sequencing, we screened 739 mutation hotspots in 46 cancer-related genes in EGFR L858R-mutant lung adenocarcinomas from 29 patients who received EGFR-TKI therapy; 13 had short (< 3 months) and 16 had long (> 1 year) progression-free survival (PFS). We discovered MLH1 V384D as a genetic variant enriched in the group of patients with short PFS. Next, we investigated this genetic variation in 158 lung adenocarcinomas with the EGFR L858R mutation and found 14 (8.9%) patients had MLH1 V384D; available blood or non-tumor tissues from patients were also tested positive for MLH1 V384D. Patients with MLH1 V384D had a significantly shorter median PFS than those without (5.1 vs. 10.6 months; P= 0.001). Multivariate analysis showed that MLH1 V384D polymorphism was an independent predictor for a reduced PFS time (hazard ratio, 3.5; 95% confidence interval, 1.7 to 7.2; P= 0.001). In conclusion, MLH1 V384D polymorphism is associated with primary resistance to EGFR-TKIs in patients with EGFR L858R-positive lung adenocarcinoma and may potentially be a novel biomarker to guide treatment decisions.
    Oncotarget 03/2015; 6(10). DOI:10.18632/oncotarget.3511 · 6.36 Impact Factor
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    ABSTRACT: Introduction: The efficacy of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in EGFR mutation-positive non-small-cell lung cancer (NSCLC) patients necessitates accurate, timely testing. Although EGFR mutation testing has been adopted by many laboratories in Asia, data are lacking on the proportion of NSCLC patients tested in each country, and the most commonly used testing methods. Methods: A retrospective survey of records from NSCLC patients tested for EGFR mutations during 2011 was conducted in 11 Asian Pacific countries at 40 sites that routinely performed EGFR mutation testing during that period. Patient records were used to complete an online questionnaire at each site. Results: Of the 22,193 NSCLC patient records surveyed, 31.8% (95% confidence interval: 31.2%-32.5%) were tested for EGFR mutations. The rate of EGFR mutation positivity was 39.6% among the 10,687 cases tested. The majority of samples were biopsy and/or cytology samples (71.4%). DNA sequencing was the most commonly used testing method accounting for 40% and 32.5% of tissue and cytology samples, respectively. A pathology report was available only to 60.0% of the sites, and 47.5% were not members of a Quality Assurance Scheme. Conclusions: In 2011, EGFR mutation testing practices varied widely across Asia. These data provide a reference platform from which to improve the molecular diagnosis of NSCLC, and EGFR mutation testing in particular, in Asia.
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 11/2014; 10(3). DOI:10.1097/JTO.0000000000000422 · 5.28 Impact Factor
  • Jung-Jyh Hung · Teh-Ying Chou · Wen-Hu Hsu · Yu-Chung Wu ·

    Cancer Research 10/2014; 74(19 Supplement):4667-4667. DOI:10.1158/1538-7445.AM2014-4667 · 9.33 Impact Factor
  • Chao-Hua Chiu · Teh-Ying Chou · Chi-Lu Chiang · Chun-Ming Tsai ·
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    ABSTRACT: There is no argument over using epidermal growth factor receptor (EGFR) mutation status to guide the frontline treatment for advanced lung adenocarcinoma (LADC); however, the role of the testing in lung squamous cell carcinoma (LSQC) remains controversial. Currently, the guidelines/consensus statements regarding EGFR mutation testing in LSQC are not consistent among different oncology societies. American Society of Clinical Oncology recommends performing EGFR mutation testing in all patients; European Society for Medical Oncology, College of American Pathologists/International Association for the Study of Lung Cancer/Association for Molecular Pathology, and National Comprehensive Cancer Network suggest for some selected group. EGFR mutation is rarely found in LSQC; however, more importantly, it is not a valid predictive biomarker for EGFR tyrosine kinase inhibitors (EGFR-TKI) in LSQC as it has been shown in LADC. Available data showed that the response rate and progression-free survival in EGFR mutant LSQC patients treated with EGFR-TKI are not better than that observed in patients treated with platinum-doublet chemotherapy in the first-line setting. Therefore, in contrast to advanced LADC, EGFR mutation testing may not be necessarily performed upfront in advanced LSQC because not only the mutation rate is low, but also the predictive value is insufficient. For LSQC patients with known sensitizing-EGFR mutations, both conventional chemotherapy and EGFR-TKI are acceptable frontline treatment options.
    Cancer Chemotherapy and Pharmacology 07/2014; 74(4). DOI:10.1007/s00280-014-2536-3 · 2.77 Impact Factor
  • Chun-Yi Lee · Meng-Che Wu · Chi-Lin Ho · Chia-Chun Lai · Teh-Ying Chou · Yu-Jiun Chan ·
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    ABSTRACT: Human adenoviruses (HADVs) comprise at least 54 types and cause a wide spectrum of respiratory tract infections; early diagnosis and epidemiological monitoring of HADV infections requires a rapid and sensitive assay. The use of a real-time polymerase chain reaction (PCR) assay was evaluated with one set of in-house designed primers for respiratory adenoviral infections. The assay was first validated by detecting successfully 6 representative types and 100 clinical isolates. A concomitant prospective surveillance of viral aetiology using conventional cultures and PCR assays in 160 febrile children with acute respiratory tract symptoms was conducted between May 2010 and July 2011. Viral aetiologies were confirmed in 72 (45%) cases using conventional cultures, including 51 adenoviral infections. The concordance between the real-time PCR and culture was good (Kappa = 0.94), and two additional culture-negative adenovirus infections were identified. During the study period (January 2011), an adenoviral community epidemic occurred. Adenovirus B3 was the predominant type in this epidemic (69.8%), followed by C2 (5.7%), C1 (5.7%), C5 (1.9%), E4 (1.9%), C6 (1.9%), F41 (1.9%), and 4 unclassified species C (7.5%). Significantly prolonged duration of fever (>5 days), higher leukocyte counts, higher neutrophil counts, and higher C-reactive protein levels were in the adenoviral infected group (n = 53, P < 0.001), compared with the non-adenoviral infected group (n = 107). In conclusion, this in-house real-time PCR is capable of detecting adenoviral respiratory infections of various types in children; and patients with adenoviral aetiology suffered from more severe clinical manifestations. J. Med. Virol. © 2014 Wiley Periodicals, Inc.
    Journal of Medical Virology 06/2014; 86(12). DOI:10.1002/jmv.23940 · 2.35 Impact Factor
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    ABSTRACT: This study investigated the pattern of recurrence of lung adenocarcinoma and the predictive value of histologic classification in resected lung adenocarcinoma using the new International Association for the Study of Lung Cancer (IASLC)/American Thoracic Society (ATS)/European Respiratory Society (ERS) classification system. Histologic classification of 573 patients undergoing resection for lung adenocarcinoma was determined according to the IASLC/ATS/ERS classification system, and the percentage of each histologic component (lepidic, acinar, papillary, micropapillary, and solid) was recorded. The pattern of recurrence of those components and their predictive value were investigated. The predominant histologic pattern was significantly associated with sex (P < .01), invasive tumor size (P < .01), T status (P < .01), N status (P < .01), TNM stage (P < .01), and visceral pleural invasion (P < .01). The percentage of recurrence was significantly higher in micropapillary- and solid-predominant adenocarcinomas (P < .01). Micropapillary- and solid-predominant adenocarcinomas had a significantly higher possibility of developing initial extrathoracic-only recurrence than other types (P < .01). The predominant pattern group (micropapillary or solid v lepidic, acinar, or papillary) was a significant prognostic factor in overall survival (OS; P < .01), probability of freedom from recurrence (P < .01), and disease-specific survival (P < .01) in multivariable analysis. For patients receiving adjuvant chemotherapy, solid-predominant adenocarcinoma was a significant predictor for poor OS (P = .04). In lung adenocarcinoma, the IASLC/ATS/ERS classification system has significant prognostic and predictive value regarding death and recurrence. Solid-predominant adenocarcinoma was also a significant predictor in patients undergoing adjuvant chemotherapy. Prognostic and predictive information is important for stratifying patients for aggressive adjuvant chemoradiotherapy.
    Journal of Clinical Oncology 05/2014; 32(22). DOI:10.1200/JCO.2013.50.1049 · 18.43 Impact Factor
  • Yi-Chen Yeh · Teh-Ying Chou ·
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    ABSTRACT: Pulmonary neuroendocrine tumors have a prognostic spectrum including typical carcinoid (TC), atypical carcinoid (AC), small cell carcinoma (SCLC), and large cell neuroendocrine carcinoma (LCNEC). We conducted a retrospective study to compare their clinicopathological characteristics, immunophenotype, preoperative biopsy and frozen section diagnoses, and prognosis. Ninety cases of surgically treated pulmonary neuroendocrine tumors were studied. Immunohistochemical studies were performed using antibodies to chromogranin A, synaptophysin, and CD56. The preoperative biopsy and frozen section diagnoses were reviewed. The 5-year survival rates for TC, AC, SCLC, and LCNEC were 96.6%, 66.7%, 42.4%, and 38.0%, respectively. T stage and pleural status correlated with outcome of SCLC and LCNEC, but N-stage and overall TNM stage did not. In preoperative biopsy, accurate diagnosis was achieved in 5 of 11 TC, 2 of 4 AC, 6 of 15 SCLC, and 0 of 5 LCNEC cases. Using frozen sections, accurate diagnosis was achieved in 8 of 12 TC, 2 of 11 SCLC, and 0 of 11 LCNEC cases. LCNEC was the most difficult to diagnose using either preoperative biopsy or frozen sections. T stage and pleural status can predict outcome of SCLC and LCNEC. J. Surg. Oncol. © 2013 Wiley Periodicals, Inc.
    Journal of Surgical Oncology 03/2014; 109(3). DOI:10.1002/jso.23497 · 3.24 Impact Factor
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    ABSTRACT: Detection of epidermal growth factor receptor (EGFR) mutation has become the most critical molecular test in managing patients with advanced lung adenocarcinoma. Whether patients with discrepant EGFR mutation results determined by low- and high-sensitivity methods have different clinical outcomes with EGFR tyrosine kinase inhibitor (TKI) treatment needs to be further evaluated. Genomic DNA from serial lung adenocarcinoma samples that were EGFR wild-type determined by direct sequencing (DS) were reanalyzed using Scorpion/Amplification Refractory Mutation System (ARMS). The outcomes with EGFR-TKI treatment among patients with discrepant EGFR mutation results between DS and Scorpion/ARMS versus patients with EGFR mutations detected by DS were studied. Of the 130 tumors studied, 28 (21.5%) were found to have EGFR mutations by Scorpion/ARMS. Discrepant EGFR mutation testing results were more common in samples from nonsmokers than in samples from smokers (30.7% versus 9.1%; p = 0.003) and in pleural than in nonpleural samples (62.5% versus 18.9%; p = 0.012). There was no significant difference in the abundance of cancer cells in region(s) selected for testing (26.2% in tumor cell percentage ≤50 versus 16.9% in tumor cell percentage >50; p = 0.201). During EGFR-TKI treatment, the progression-free survival in patients with discrepant EGFR mutation results was similar to those with EGFR mutations detected by DS (median, 13.4 versus 10.9 months; p = 0.225). DS overlooked EGFR mutation in a significant number of lung adenocarcinoma patients. These patients could have obtained the same benefit from EGFR-TKI when a high-sensitivity method such as Scorpion/ARMS was applied.
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 01/2014; 9(1):91-96. DOI:10.1097/JTO.0000000000000041 · 5.28 Impact Factor
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    ABSTRACT: Although significant improvement in myasthenic symptoms has been reported following the removal of thymolipomas, information on surgical outcomes among patients with thymolipomatous myasthenia gravis (MG) is limited. This was a retrospective review of patients who underwent extended thymectomy for treatment of MG. From 1995 to 2010, 267 patients with MG underwent extended thymectomy, including 104 with thymomatous MG, 151 with non-thymomatous MG and 12 (4.4%) with thymolipoma. The mean duration of myasthenic symptoms before surgery was greatest in the thymolipomatous group (P < 0.001). The lowest mean age (36.1 years old, P < 0.001) and the lowest preoperative serum anti-acetylcholine receptor antibody titre (P = 0.015) occurred in the non-thymomatous group. More thymic and adipose tissue was removed from the thymolipomatous group compared with the non-thymomatous group (P < 0.001). Regarding surgical outcomes, the rate of stable remission was higher in the non-thymomatous (42.3%) and thymolipomatous (41.7%) groups compared with the thymomatous group (28.8%, P = 0.029). No instances of postoperative exacerbation of MG or tumour recurrence were noted during the postoperative follow-up of patients treated for thymolipoma. Our results suggest that patients with myasthenia thymolipomatous have surgical outcomes similar to those of patients with non-thymomatous MG and have a mean age at the time of surgery similar to that of patients with thymomatous MG.
    Interactive Cardiovascular and Thoracic Surgery 12/2013; 18(4). DOI:10.1093/icvts/ivt531 · 1.16 Impact Factor
  • Chao-Yu Liu · Yu-Chao You · Chih-Cheng Hsieh · Yeh-Han Wang · Teh-Ying Chou ·

    Thorax 12/2013; 69(11). DOI:10.1136/thoraxjnl-2013-203929 · 8.29 Impact Factor

Publication Stats

1k Citations
423.90 Total Impact Points


  • 2006-2015
    • National Yang Ming University
      • • Institute of Clinical Medicine
      • • Department of Pathology
      T’ai-pei, Taipei, Taiwan
  • 2006-2014
    • Taipei Veterans General Hospital
      • • Department of Laboratory Medicine
      • • Department of Pathology and Laboratory Medicine
      T’ai-pei, Taipei, Taiwan
  • 2011
    • Koo Foundation Sun Yat-Sen Cancer Center
      T’ai-pei, Taipei, Taiwan
  • 2008
    • Academia Sinica
      • Genomics Research Center
      T’ai-pei, Taipei, Taiwan