bluuebunny/crossref_metadata_2025_split huggingface dataset:
Molecular Epidemiology of G9 Rotaviruses in Taiwan between 2000 and 2002
Authors: Lin Yi-Pei , Chang Sui-Yuan , Kao Chuan-Liang , Huang Li-Min , Chung Ming-Yi , Yang Jyh-Yuan , Chen Hour-Young , Taniguchi Koki , Tsai Keh-Sung , Lee Chun-Nan 
Published: October 2006

ABSTRACT
Since the mid-1990s, novel G9 rotaviruses have been detected in many countries, suggesting that G9 is a globally important serotype. The molecular epidemiology of G9 rotaviruses in Taiwan from 2000 to 2002 was investigated in this study. G9 rotavirus first appeared in 2000 with 4 cases and constituted 33.8% and 54.8% of the rotavirus-positive samples in 2001 and 2002, respectively. These G9 strains belonged to P[8]G9, subgroup II, and long electropherotype, except one belonged to P[4]G9, subgroup II, and short electropherotype. Nucleotide sequencing and phylogenetic analysis of 52 Taiwanese G9 rotaviruses showed that the VP7 genes shared a high degree of identity to overseas G9 rotaviruses detected after 1993 and that the VP8* portions of the VP4 genes were more closely related to those of local rotaviruses of other G types. The two P[8]G9 strains with high nucleotide identities in the VP7 and the partial VP4 genes, 01TW591 of Taiwan from 2001 and 95H115 of Japan from 1995, varied in four genes, genes 2, 3, 7, and 8, which was revealed by RNA-RNA hybridization. Representative strains for different RNA patterns were also analyzed in the partial VP2 and VP3 genes; the nucleotide identities were high between Taiwanese G9 strains and local G3 or G2 strains. These results suggested that Taiwanese G9 rotaviruses possibly had evolved through reassortment between overseas G9 strains and circulating rotaviruses of other G types.
Coexpression of an unusual form of theEWS–WT1fusion transcript and interleukin 2/15 receptor βmRNA in a desmoplastic small round cell tumour
Authors: Nakanishi Y , Oinuma T , Sano M , Fuchinoue F , Komatsu K , Seki T , Obana Y , Tabata M , Kikuchi K , Shimamura M , Ohmori K , Nemoto N 
Published: October 2006

Background:The β chain of the interleukin 2/15 receptor (IL-2/15Rβ) is induced by the expression of theEWS–WT1. A case of desmoplastic small round cell tumour (DSRCT) expressing only an unusualEWS-WT1treated by us is reported here.Aim:To characterise an unusual form ofEWS–WT1.Methods:Frozen tissue sections of the axillary tumour were examined using a laser-assisted microdissection technique and reverse transcriptase polymerase chain reaction.Results:The novel fusion of exon 8 ofEWSand the defective exon 10 ofWT1(−KTS) was detected. Although it was an unusual form, the coexpression of the presentEWS–WT1,IL-2/15Rβand Janus kinase (JAK1) mRNA was detected in the tumour cells.IL-2and signal transducers and activators of transcription (STAT5) mRNA were detected in both tumour and stromal cells.Conclusion:The induction of the IL-2/15 receptor signalling pathway may contribute to tumorigenesis in DSRCT through a paracrine or an autocrine system, even though theEWS–WT1was an unusual form.
CD56-positive haematological neoplasms of the skin: a multicentre study of the Cutaneous Lymphoma Project Group of the European Organisation for Research and Treatment of Cancer
Authors: Assaf Chalid , Gellrich Sylke , Whittaker Sean , Robson Alistair , Cerroni Lorenzo , Massone Cesare , Kerl Helmut , Rose Christian , Chott Andreas , Chimenti Sergio , Hallermann Christian , Petrella Tony , Wechsler Janine , Bagot Martine , Hummel Michael , Bullani-Kerl Katrin , Bekkenk Marcel W , Kempf Werner , Meijer Chris J L M , Willemze Rein , Sterry Wolfram 
Published: October 2006

Background:Cutaneous lymphomas expressing CD56, a neural cell adhesion molecule, are characterised in most cases by a highly aggressive clinical course and a poor prognosis. However, prognostic subsets within the CD56+ group have been difficult to identify due to the lack of uniform clinicopathological and immunophenotypical criteria.Methods:A multicentre study was conducted by the Cutaneous Lymphoma Task Force of the European Organisation for Research and Treatment of Cancer to define prognostic parameters and establish diagnostic and therapeutic guidelines for CD56+ haematological neoplasms presenting primarily in the skin.Results:Four different subtypes of lymphoproliferations with CD56 expression were identified: (1) haematodermic neoplasm; (2) skin infiltration as the first manifestation of CD56+ acute myeloid leukaemia; (3) nasal-type extranodal natural killer/T-cell lymphoma; and (4) “classical” cases of cutaneous T-cell lymphoma (CTCL) with co-expression of the CD56 molecule. Patients in the first three groups had a poor outcome (93% died) with a median survival rate of 11 months (95% CI 2–72 months), whereas all patients with CD56+ CTCL were alive at the last follow-up.Conclusion:Results show that CD56+ cutaneous lymphoproliferative disorders, with the exception of CD56+ CTCL have a very poor prognosis. It is therefore clinically important to separate CD56+ CTCL from the remaining CD56+ haematological disorders.
Increased Expression of Wiskott-Aldrich Syndrome Protein Family Verprolin-Homologous Protein 2 Correlated with Poor Prognosis of Hepatocellular Carcinoma
Authors: Yang Lian-Yue , Tao Yi-Ming , Ou Di-Peng , Wang Wei , Chang Zhi-Gang , Wu Fan 
Published: October 2006

Abstract
Purpose: Because of its role in cell migration, the Wiskott-Aldrich syndrome protein family verprolin-homologous protein (WAVE) 2 has been implicated in cancer metastasis. Evidence to support such a role of WAVE2 in human cancer, however, is lacking. We thus examined the expression of WAVE2 in hepatocellular carcinoma (HCC) tissues to test whether the levels of WAVE2 expression correlated to the progression of HCC.
Experimental Design: Samples of 112 HCC patients were determined immunohistochemically for WAVE2 expression and the correlation of WAVE2 levels with prognosis was analyzed. Among the 112 cases, 31 paired HCC and paracarcinomatous liver tissue specimens were analyzed for WAVE2 levels by reverse transcription-PCR and Western blotting, respectively.
Results: Among 112 cases of HCCs, the immunohistochemistry data indicated significant increase of WAVE2 expression levels in 71 cases. Importantly, the increased WAVE2 expression correlated with the multiple tumor nodules (P = 0.008), the absence of capsular formation (P = 0.035), Edmondson-Steiner grade (P = 0.009), vein invasion (P = 0.023), and a shortened median survival time (326 versus 512 days; P = 0.003). Multivariable Cox regression analysis revealed the WAVE2 expression level was an independent factor for prognosis. The immunohistochemistry data were further confirmed by results of reverse transcription-PCR and Western analysis of 31 HCC cases, in which the WAVE2 mRNA and protein in HCC tissues were significantly elevated when compared with paracarcinomatous liver tissue (P &lt; 0.001).
Conclusions: WAVE2 expression is elevated in HCC tissues, which correlates with a poor prognosis, suggesting WAVE2 as a candidate prognostic marker of HCC.
Identification of α-Enolase as an Autoantigen in Lung Cancer: Its Overexpression Is Associated with Clinical Outcomes
Authors: Chang Gee-Chen , Liu Ko-Jiunn , Hsieh Chia-Ling , Hu Tsai-Shu , Charoenfuprasert Suparat , Liu Hsiung-Kun , Luh Kwen-Tay , Hsu Li-Han , Wu Chew-Wen , Ting Chou-Chik , Chen Chih-Yi , Chen Kun-Chieh , Yang Tsung-Ying , Chou Teh-Ying , Wang Wen-Hua , Whang-Peng Jacqueline , Shih Neng-Yao 
Published: October 2006

Abstract
Purpose: Although existence of humoral immunity has been previously shown in malignant pleural effusions, only a limited number of immunogenic tumor-associated antigens (TAA) have been identified and associated with lung cancer. In this study, we intended to identify more TAAs in pleural effusion–derived tumor cells.
Experimental Design: Using morphologically normal lung tissues as a control lysate in Western blotting analyses, 54 tumor samples were screened with autologous effusion antibodies. Biochemical purification and mass spectrometric identification of TAAs were done using established effusion tumor cell lines as antigen sources. We identified a p48 antigen as α-enolase (ENO1). Semiquantitative immunohistochemistry was used to evaluate expression status of ENO1 in the tissue samples of 80 patients with non–small cell lung cancer (NSCLC) and then correlated with clinical variables.
Results: Using ENO1-specifc antiserum, up-regulation of ENO1 expression in effusion tumor cells from 11 of 17 patients was clearly observed compared with human normal lung primary epithelial and non-cancer-associated effusion cells. Immunohistochemical studies consistently showed high level of ENO1 expression in all the tumors we have examined thus far. Log-rank and Cox's analyses of ENO1 expression status revealed that its expression level in primary tumors was a key factor contributing to overall- and progression-free survivals of patients (P &lt; 0.05). The same result was also obtained in the early stage of NSCLC patients, showing that tumors expressing relatively higher ENO1 level were tightly correlated with poorer survival outcomes.
Conclusions: Our data strongly support a prognostic role of ENO1 in determining tumor malignancy of patients with NSCLC.
Prognostic Significance of the Epstein-Barr Virus, p53, Bcl-2, and Survivin in Nasopharyngeal Cancer
Authors: Yip Kenneth W. , Shi Wei , Pintilie Melania , Martin Joseph D. , Mocanu Joseph D. , Wong Derek , MacMillan Christine , Gullane Pat , O'Sullivan Brian , Bastianutto Carlo , Liu Fei-Fei 
Published: October 2006

Abstract
Purpose: Nasopharyngeal cancer (NPC) is a malignant epithelial carcinoma which is intimately associated with EBV. The latent presence of EBV affects the function of p53, Bcl-2, and survivin. We thus investigated the relationship between EBV status, p53, Bcl-2, and survivin in biopsy specimens from patients with primary NPC.
Experimental Design: Archival formalin-fixed, paraffin-embedded NPC biopsies were evaluated in 80 patients treated with curative radiation from a single institution. The presence of EBV was determined using EBER in situ hybridization, whereas p53, Bcl-2, and survivin were assessed using immunohistochemistry.
Results: The majority of NPC specimens in this patient cohort were EBER-positive (64 of 78, or 82%), which in turn, was significantly associated with ethnicity (P = 0.0007), and WHO subtype 2A/2B (P = 0.04). EBER-positive tumors were also associated with p53 (P = 0.002), Bcl-2 (P = 0.04), and nuclear survivin (P = 0.03) expression. Patients with EBER-positive NPC fared better, with a 10-year overall survival of 68% versus 48% for EBER-negative patients (P = 0.03). For nuclear survivin, patients with either low or high nuclear survivin fared worse than patients with intermediate survivin expression (P = 0.05), suggesting that there is an optimal proportion of survivin-expressing cells for best function and clinical outcome.
Conclusions: With an extended median follow-up time of 11.4 years, EBV status remains a strong predictor for overall survival in NPC. EBV-positive NPC has strong molecular associations with p53, Bcl-2, and survivin expression. Furthermore, we provide clinical data revealing the potentially dual nature of survivin in predicting clinical outcome.
Phase I Study of Decitabine-Mediated Gene Expression in Patients with Cancers Involving the Lungs, Esophagus, or Pleura
Authors: Schrump David S. , Fischette Maria R. , Nguyen Dao M. , Zhao Ming , Li Xinmin , Kunst Tricia F. , Hancox Ana , Hong Julie A. , Chen G. Aaron , Pishchik Vitaliy , Figg William D. , Murgo Anthony J. , Steinberg Seth M. 
Published: October 2006

Abstract
Purpose: The DNA methylation paradox, manifested as derepression of cancer-testis antigens, and silencing of tumor suppressors during malignant transformation, provides the rationale for the utilization of chromatin remodeling agents for cancer therapy. A phase I trial was done to examine pharmacokinetics, toxicities, and gene expression mediated by 5-aza-2′-deoxycytidine (DAC) in patients with thoracic malignancies.
Experimental Design: Thirty-five patients with cancers refractory to standard therapy received continuous 72-hour DAC infusions using a phase I dose-escalation schema. Each full course of therapy consisted of two identical 35-day cycles. Plasma DAC levels were evaluated by liquid chromatography-mass spectrometry techniques. Quantitative reverse transcription-PCR, methylation-specific PCR, and immunohistochemical techniques were used to evaluate NY-ESO-1, MAGE-3, and p16 expression in tumor biopsies. Long oligonucleotide arrays were used to evaluate gene expression profiles in laser-captured tumor cells before and after DAC exposure.
Results: Thirty-five patients were evaluable for toxicities; 25 were evaluable for treatment response. Myelosuppression constituted dose-limiting toxicity. The maximum tolerated dose of DAC was 60 to 75 mg/m2 depending on the number of prior cytotoxic chemotherapy regimens. No objective responses were observed. Plasma DAC concentrations approximated thresholds for gene induction in cultured cancer cells. Target gene induction was observed in 36% of patients. Posttreatment antibodies to NY-ESO-1 were detected in three patients exhibiting NY-ESO-1 induction in their tumor tissues. Complex, heterogeneous gene expression profiles were observed in pretreatment and posttreatment tissues.
Conclusion: Prolonged DAC infusions can modulate gene expression in primary thoracic malignancies. These findings support further evaluation of DNA-demethylating agents alone or in combination with other regimens targeting induced gene products for the treatment of these neoplasms.
Analysis of Epidermal Growth Factor Receptor Gene Mutation in Patients with Non–Small Cell Lung Cancer and Acquired Resistance to Gefitinib
Authors: Kosaka Takayuki , Yatabe Yasushi , Endoh Hideki , Yoshida Kimihide , Hida Toyoaki , Tsuboi Masahiro , Tada Hirohito , Kuwano Hiroyuki , Mitsudomi Tetsuya 
Published: October 2006

Abstract
Purpose: Non–small cell lung cancers carrying activating mutations in the gene for the epidermal growth factor receptor (EGFR) are highly sensitive to EGFR-specific tyrosine kinase inhibitors. However, most patients who initially respond subsequently experience disease progression while still on treatment. Part of this “acquired resistance” is attributable to a secondary mutation resulting in threonine to methionine at codon 790 (T790M) of EGFR.
Experimental Design: We sequenced exons 18 to 21 of the EGFR gene to look for secondary mutations in tumors with acquired resistance to gefitinib in 14 patients with adenocarcinomas. Subcloning or cycleave PCR was used in addition to normal sequencing to increase the sensitivity of the assay. We also looked for T790M in pretreatment samples from 52 patients who were treated with gefitinib. We also looked for secondary KRAS gene mutations because tumors with KRAS mutations are generally resistant to tyrosine kinase inhibitors.
Results: Seven of 14 tumors had a secondary T790M mutation. There were no other novel secondary mutations. We detected no T790M mutations in pretreatment specimens from available five tumors among these seven tumors. Patients with T790M tended to be women, never smokers, and carrying deletion mutations, but the T790M was not associated with the duration of gefitinib administration. None of the tumors had an acquired mutation in the KRAS gene.
Conclusions: A secondary T790M mutation of EGFR accounted for half the tumors with acquired resistance to gefitinib in Japanese patients. Other drug-resistant secondary mutations are uncommon in the EGFR gene.
Overexpression of Caspase-3s Splice Variant in Locally Advanced Breast Carcinoma Is Associated with Poor Response to Neoadjuvant Chemotherapy
Authors: Végran Frédérique , Boidot Romain , Oudin Claire , Riedinger Jean-Marc , Bonnetain Franck , Lizard-Nacol Sarab 
Published: October 2006

Abstract
Purpose: CASP-3 gene gives rise, by alternative splicing to a caspase-3s variant, to the antagonist apoptotic property of caspase-3. Deregulation of splicing in tumor cells favoring the expression of antiapoptotic variants has been reported to contribute to both tumorigenesis and chemoresistance. Thus, we investigated the role of caspase-3 and its splice variant in breast cancer cells.
Experimental Design: Breast tumor cell lines deficient (MCF-7) and proficient (HBL100) for CASP-3 gene were transfected with each transcript and were characterized for their apoptotic response to cyclophosphamide. Expression of the two transcripts were measured by reverse transcription-PCR in 130 breast carcinomas, including 90 locally advanced tumors treated with neoadjuvant chemotherapy containing cyclophosphamide, epirubicine, and 5-fluorouracil.
Results: Overexpression of caspase-3s variant in caspase-3–transfected cell lines significantly inhibits apoptosis induced by cyclophosphamide (P &lt; 0.0001 for both cell lines). In breast tissues, only caspase-3 levels were higher in carcinomas than in corresponding adjacent normal tissues (P = 0.0396). Locally advanced carcinomas with high levels of caspase-3 (P &lt; 0.0001) and weak levels of caspase-3s (P = 0.0248) were more sensitive to treatment. Therefore, increase in caspase-3s/caspase3 ratio expression was significantly associated with chemoresistance (P = 0.01). Logistic univariate and multivariate analyses realized according to pathologic response confirm that increased caspase-3s expression was indicative of chemoresistance (P = 0.012 and P = 0.026, respectively).
Conclusions: The results agree with an antagonist function between the two transcripts of caspase-3 and show that their ratio of expression levels may define a subset of locally advanced breast cancer patients who are more likely to benefit from neoadjuvant cyclophosphamide-containing chemotherapy.
Understanding the Influence of Climate Forecasts on Farmer Decisions as Planned Behavior*
Authors: Artikov Ikrom , Hoffman Stacey J. , Lynne Gary D. , Zillig Lisa M. Pytlik , Hu Qi , Tomkins Alan J. , Hubbard Kenneth G. , Hayes Michael J. , Waltman William 
Published: October 2006

Abstract
Results of a set of four regression models applied to recent survey data of farmers in eastern Nebraska suggest the causes that drive farmer intentions of using weather and climate information and forecasts in farming decisions. The model results quantify the relative importance of attitude, social norm, perceived behavioral control, and financial capability in explaining the influence of climate-conditions information and short-term and long-term forecasts on agronomic, crop insurance, and crop marketing decisions. Attitude, serving as a proxy for the utility gained from the use of such information, had the most profound positive influence on the outcome of all the decisions, followed by norms. The norms in the community, as a proxy for the utility gained from allowing oneself to be influenced by others, played a larger role in agronomic decisions than in insurance or marketing decisions. In addition, the interaction of controllability (accuracy, availability, reliability, timeliness of weather and climate information), self-efficacy (farmer ability and understanding), and general preference for control was shown to be a substantive cause. Yet control variables also have an economic side: The farm-sales variable as a measure of financial ability and motivation intensified and clarified the role of control while also enhancing the statistical robustness of the attitude and norms variables in better clarifying how they drive the influence. Overall, the integrated model of planned behavior from social psychology and derived demand from economics, that is, the “planned demand model,” is more powerful than models based on either of these approaches alone. Taken together, these results suggest that the “human dimension” needs to be better recognized so as to improve effective use of climate and weather forecasts and information for farming decision making.
Risk-adapted BEACOPP regimen can reduce the cumulative dose of chemotherapy for standard and high-risk Hodgkin lymphoma with no impairment of outcome
Authors: Dann Eldad J. , Bar-Shalom Rachel , Tamir Ada , Haim Nissim , Ben-Shachar Menachem , Avivi Irit , Zuckerman Tzila , Kirschbaum Mark , Goor Odelia , Libster Diana , Rowe Jacob M. , Epelbaum Ron 
Published: October 2006

AbstractTherapy of Hodgkin disease (HD) is designed to prolong progression-free survival and minimize toxicity. The best regimen to achieve this has not yet been defined. A total of 108 patients with newly diagnosed HD and adverse prognostic factors were prospectively studied between 1999 and 2004. They were assigned to therapy according to defined risk stratification. Patients were defined depending on the International Prognostic Score (IPS). Those with IPS of 3 or higher received 2 cycles of escalated therapy, including bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone (BEACOPP [EB]). All others received 2 cycles of standard BEACOPP (SB). Subsequent therapy was prospectively assigned following 2 cycles according to results of early interim 67Ga or positron emission tomography/computed tomography (PET/CT). Following a positive interim scan, 4 cycles of EB were administered, whereas 4 cycles of SB were given to patients with a negative scan. The complete remission rate, the 5-year event-free survival (EFS), and overall survival (OS) rates were 97%, 85% and 90%, respectively. Relapse or progression occurred in 27% of patients with interim positive PET/CT versus 2.3% of negative scans (P < .02). Early interim fluorine-18 2-fluoro-2-deoxy-d-glucose (FDG)–PET/CT is a useful tool for adjustment of chemotherapy on an individual basis. Similar EFS and OS rates were observed for patients in both risk groups.
Dendritic-cell maturation alters intracellular signaling networks, enabling differential effects of IFN-α/β on antigen cross-presentation
Authors: Longman Randy S. , Braun Deborah , Pellegrini Sandra , Rice Charles M. , Darnell Robert B. , Albert Matthew L. 
Published: October 2006

AbstractThe broad and often contrasting effects of type I interferons (IFNs) in innate and adaptive immunity are belied by the signaling via a single receptor, IFN-α receptor (IFNAR). Here, we show that IFN-α/β induces opposing effects on the immunologic outcome of antigen cross-presentation depending on dendritic cell (DC) maturation status. Despite equivalent IFNAR expression, immature conventional DCs (cDCs) activate STAT1 in response to IFN-α/β, whereas exposure of mature DCs to IFN-α/β results in signaling via STAT4. Microarray analysis revealed numerous transcriptional changes resulting from the altered signaling. Importantly, STAT1 signaling resulted in significant inhibition of CD40L-induced IL-12 production, accounting for the inhibition of CD8+ T-cell activation. These data provide evidence for a molecular switch in signaling pathways concomitant with DC maturation that offers a novel mechanism by which DCs modulate the integration of signals from the surrounding environment.