tbuckley/cabot-search huggingface dataset:
Abstract 723: Detection of TIMP3 promoter hypermethylation in salivary rinse as an independent predictor of local recurrence-free survival in head and neck cancer
Authors: Wenyue Sun, David Zaboli, Hao Wang, Yan Liu, Demetri Arnaoutakis, Tanbir Khan, Zubair Khan, Wayne Koch, Joseph Califano
Journal: Cancer Research (2012)

Abstract Objective: To validate a panel of methylation-based salivary rinse biomarkers (P16, CCNA1, DCC, TIMP3, MGMT, DAPK, and MINT31) previously shown to be independently associated with poor overall survival and local recurrence in a larger, separate cohort of patients with head and neck squamous cell carcinoma (HNSCC). Methods: One hundred ninety-seven patients were included. All pre-treatment saliva DNA samples were evaluated for the methylation status of the gene promoters by quantitative methylation-specific PCR. The main outcome measures were overall survival, local recurrence-free survival and disease-free survival. Results: In univariate analyses, the detection of hypermethylation of CCNA1, MGMT, and MINT31 was significantly associated with poor overall survival; the detection of hypermethylation of TIMP3 was significantly associated with local recurrence-free survival; and the detection of hypermethylation of MINT31 was significantly associated with poor disease-free survival. In multivariate analyses, detection of hypermethylation at any single marker was not predictive of overall survival in patients with HNSCC; detection of hypermethylation of TIMP3 in salivary rinse had an independent, significant association with local recurrence-free survival (Hazard Ratio, 2.51, 95% CI, 1.10 to 5.68); and none of the studied markers was significantly associated with disease-free survival. Conclusions: The detection of promoter hypermethylation of the seven genes in salivary rinse as an independent prognostic indicator of overall survival in patients with HNSCC was not validated. Detection of promoter hypermethylation of TIMP3 in pretreatment salivary rinse is independently associated with local recurrence-free survival in patients with HNSCC and may be a valuable salivary rinse biomarker for HNSCC recurrence. Such a test could potentially refine our ability to identify HNSCC patients at a high risk for recurrence. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 723. doi:1538-7445.AM2012-723
P321 HEPATIC FIBROSIS AND APOPTOSIS INDUCED BY ETHANOL ADMINISTRATION ARE EXACERBATED IN HUMAN NEUTROPHIL PEPTIDE-1 TRANSGENIC MICE
Authors: R. Ibusuki, H. Uto, M. Kozono, K. Oda, A. Oshige, K. Kumagai, S. Mawatari, T. Tamai, A. Moriuchi, M. Oketani, A. Ido, H. Tsubouchi
Journal: Journal of Hepatology (2014)
Abstract LB-108: Formation and maintenance of mesenchymal and stem-cell states in the breast by paracrine and autocrine signals
Authors: Christina Scheel, Elinor NgEaton, Sophia Hsin-Jung Li, Christine L. Chaffer, Ferenc Reinhardt, Kong-Jie Kah, George Bell, Wenjun Guo, Jeffrey Rubin, Andrea Richardson, Robert A. Weinberg
Journal: Cancer Research (2011)

Abstract Passage through an epithelial-mesenchymal transition (EMT) is associated with the acquisition of migratory and self-renewal abilities in human mammary epithelial cells (MECs). The signaling mechanisms that induce and then maintain these properties have remained unclear. We describe three signaling pathways, involving Transforming Growth Factor (TGF)-beta as well as canonical and non-canonical Wnt signaling, that collaborate to induce epithelial MECs to enter into a mesenchymal and SC-like state. Acting as autocrine signaling loops, these pathways then maintain migratory and self-renewal abilities in normal MECs and control tumorigenicity and metastasis in their transformed derivatives. Autocrine signaling is enabled, at least in part, through downregulation of secreted Wnt antagonists and Bone Morphogenetic Proteins. Like immortalized and transformed MECs, the maintenance of migratory and self-renewal abilities in primary human MECs is dependent on these autocrine loops, suggesting that similar mechanisms regulate biological properties of normal tissue stem cells and tumor-initiating cells in the breast Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-108. doi:10.1158/1538-7445.AM2011-LB-108
AB1334 Multimodal treatment in a day clinic effects the pain experience in patients with rheumatic diseases
Authors: G. Weiland, B. Goldberg, K. Geißler, H. Ernst
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Rheumatic diseases require high healthcare recourses. The pain associated with these inflammatory or degenerative conditions require a multidisciplinary and continuous therapeutic approach. Due to cost restraints the value of day clinics for patients with rheumatic disorders is under debate. <h3>Objectives</h3> Therefore we measured the Pain Experience Scale before and after treatment of patients with rheumatic diseases using the multimodal treatment programme of our specialised day clinic. <h3>Methods</h3> From 1.1.2010 until 12.11.2011 199 consecutive patients scheduled for our day clinic were asked to fill out a the Pain Experience Scale ("Schmerzempfindungsskala"-SES; Geissner E.: Rehabilitation (Stuttg). 1995 Nov; 34 (4)), which measures two dimensions of subjectively felt pain, the affective characterization as well as modes of sensory characterization of pain. Multimodal treatment consisted of 15 days of treatment with physiotherapy (structured approach, assessment, treatment and evaluation), psychological pain management approaches and adjustment of medical treatment. For statistical analysis a Students t-test for paired samples was performed. <h3>Results</h3> 127 patients (47 with rheumatoid arthritis; 21 with SpA, 32 with osteoarthritis, 14 with psoriasis and SpA, 5 with fibromyalgia, 8 with various rheumatic disorders) filled out the questionnaire before entering the day clinic and 103 patients returned the questionnaire 14 days after completion of the treatment. The affective felt pain after completion of a 3 week treatment program in our day clinic was sign. improved (p=0.001). In contrast the sensory felt pain did not change after treatment (p=0.264). <h3>Conclusions</h3> Multidisciplinary treatment in a day clinic is useful to change the course of pain in patients with rheumatic diseases. A long term follow up is needed. <h3>References</h3> Geissner E.: Rehabilitation (Stuttg). 1995 Nov; 34 (4) <h3>Disclosure of Interest</h3> None Declared
Abstract 1997: A gene expression profiling and molecular pathway analysis in early recurrence of patients with early stage lung adenocarcinoma.
Authors: Hisashi Saji, Masahiro Tsuboi, Yoshihisa Shimada, Yasufumi Kato, Wakako Hamanaka, Koichi Yoshida, Jitsuo Usuda, Tatsuo Ohira, Norihiko Ikeda
Journal: Cancer Research (2013)

Abstract Background: Clinico-histopathological staging is insufficient to predict disease progression and clinical outcome in lung carcinoma. Here, we show that gene expression profiles and molecular pathways based on microarray and functional analysis can be used to predict early relapse in patients with early-stage lung adenocarcinoma. Methods and Results: Based on the results of principal component analysis of a series of 24 samples of early-stage lung adenocarcinoma, there were two subgroups within the early-relapse group. The histological classification of all of group A was poorly differentiated, whereas only one of three cases in group B was classified as such. DAVID functional annotation analysis revealed 16 and 17 enriched pathways in groups A and B, respectively. Clusters of genes related to oncological or immunological functional signaling were found enriched in group A as were pathways such as cell adhesion molecules (CAMs), cell cycle, and antigen processing and presentation, whereas in group B the pathways were CAMs, T cell receptor signaling, cytokine-cytokine receptor interaction, toll-like receptor signaling, chemokine signaling, primary immunodeficiency, and natural killer cell mediated cytotoxicity. The CAMs pathway was found to be enriched in both groups.Conclusions: In this study, we present a comprehensive gene expression analysis and functional pathway analysis of early-stage lung adenocarcinoma, wherein we identified a distinct molecular pathway category, CAMs that correlated with early relapse of early-stage lung adenocarcinoma subclasses. This prognostic signature could be used to identify patients with early-stage high-risk NSCLC who might benefit from adjuvant therapy following surgery. Citation Format: Hisashi Saji, Masahiro Tsuboi, Yoshihisa Shimada, Yasufumi Kato, Wakako Hamanaka, Koichi Yoshida, Jitsuo Usuda, Tatsuo Ohira, Norihiko Ikeda. A gene expression profiling and molecular pathway analysis in early recurrence of patients with early stage lung adenocarcinoma. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1997. doi:10.1158/1538-7445.AM2013-1997 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Interactions of Natural Killer (NK) Cells and Surfactant Protein D (SP-D) in Regulation of Ozone Induced Airway Inflammation: Involvement of NKp46
Authors: Moyar Q. Ge, Jin Hwang, Imre Redai, Blerina Kokalari, David M. Kemeny, Kerry S. Campbell, Angela Haczku
Journal: Journal of Allergy and Clinical Immunology (2013)
OP0101 First Report of IL-38 in Systemic Lupus Erythematosus (SLE)
Authors: J. Godsell, I. Rudloff, A. Hoi, M. Nold, E. Morand
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> The cytokine IL-38 (IL-1F10) is a member of the IL-1 superfamily, which binds to IL-36R. IL-38 polymoprhisms have been associated with spondylitis and rheumatoid arthritis, and while IL-38 function is poorly understood, it has been reported to inhibit Th17 responses. <h3>Objectives</h3> Clinical associations of serum IL-38 have not been reported. Here, we investigated associations of serum IL-38 in SLE. <h3>Methods</h3> Serum was obtained from patients with SLE (≥ACR 4) followed in a longitudinal cohort in which disease activity (SLEDAI-2k) and drug treatment details were recorded with each sample. IL-38 was quantified by ELISA. <h3>Results</h3> 142 SLE patients (median age 42 (20-80) years, disease duration 103 (18-439) months) were studied at baseline, 115 of whom were also studied in two consecutive subsequent clinic visits. 28 age- and gender-matched healthy control individuals were also studied. IL-38 (0-5928 pg/ml) was detectable in 128 (13.4%) baseline SLE samples. Mean serum IL-38 was significantly higher in SLE compared with controls (p=0.0031). Significantly higher IL-38 was observed in patients with active disease (SLEDAI ≥4, n=84, p=0.0438). Baseline IL-38 was significantly higher in patients with subsequent persistently active disease (PAD; Nikpour 2009) (p=0.0057), and time-adjusted mean IL-38 measured longitudinally was also significantly higher in patients with PAD (p=0.0226). Detectable IL-38 was associated with a 1.7 fold increased risk of PAD (RR=1.669, 95%CI 1.255-1.938, p=0.0096). Mean serum IL-38 was increased in patients with renal (p=0.0170) or CNS (p=0.0189) lupus, and detectable IL-38 was associated with increased risk of renal disease (RR=1.605, 95%CI 1.153-2.234, p=0.0280) and CNS disease (RR=2.233, 95%CI 1.174-4.249, p=0.0349). <h3>Conclusions</h3> These data are the first report of IL-38 in SLE. Serum IL-38 is strongly associated with markers of adverse outcome including disease activity and renal and CNS disease. Further investigation of the role of IL-38 in SLE is justified. <h3>References</h3> Nikpour, M., Urowitz, M. B., Ibañez, D., &amp; Gladman, D.D. (2009). Frequency and determinants of flare and persistently active disease in systemic lupus erythematosus. Arthritis &amp; Rheumatism, 61(9), 1152–1158. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3594
Abstract 750: Negative regulation of <i>bcl-2</i> transcription by DNA damage-binding protein complex in human ovarian cancer cells.
Authors: Ran Zhao, Chunhua Han, Eric Eisenhauer, John Kroger, Li Gong, Qianzheng Zhu, Weiqiang Zhao, Jianhua Yu, Selvendiran Karuppaiyah, Xingluo Liu, Altaf Ahmad Wani, Qi-En Wang
Journal: Cancer Research (2013)

Abstract Elevated expression of the anti-apoptotic factor Bcl-2 is believed to be one of the contributing factors to an increased relapse rate associated with multiple cisplatin-resistant cancers. DNA damage-binding protein 2 (DDB2) has recently been revealed to play an important role in sensitizing human ovarian cancer cells to cisplatin-induced apoptosis through the down-regulation of Bcl-2, but the underlying molecular mechanism remains poorly defined. Here, we report that DDB2 functions as a transcriptional repressor for Bcl-2. DDB2 binds to a specific response element at the 5’-end of bcl-2 P1 promoter, concomitant with marked losses of histone H3 acetylation along the bcl-2 promoter and enhancer regions. Quantitative chromatin immunoprecipitation analysis revealed that HDAC1 was locally enriched in the bcl-2 P1 core promoter following DDB2 over-expression. Lysine 244 in DDB2 is essential for the transcriptional regulation of bcl-2, evidenced by the fact that the K244E mutant failed to inhibit bcl-2 promoter activity. Interestingly, the simultaneous DDB1 knock-down and DDB2 over-expression are required to potentiate bcl-2 promoter activity in the human ovarian cancer cell line CP70, while the knockdown of DDB1 alone failed to produce any significant effect. Furthermore, quantitative analysis of DDB2 and Bcl-2 expression in ovarian cancers provides clinical evidence that DDB2 and Bcl-2 are inversely correlated. Collectively, our data supports a model in which DDB2 and DDB1 function cooperatively in repressing bcl-2 transcription by recruiting HDAC1 to deacetylate histone H3 across bcl-2 regulatory regions, with DDB2 being responsible for binding to a specific cis-acting element in the bcl-2 P1 promoter. These findings have immediate implications for clinical trial designs of DDB2-based therapies for diverse cisplatin-resistant malignancies.(Supported by NIH grant CA151248 to QEW, and CA93413 to AAW) Citation Format: Ran Zhao, Chunhua Han, Eric Eisenhauer, John Kroger, Li Gong, Qianzheng Zhu, Weiqiang Zhao, Jianhua Yu, Selvendiran Karuppaiyah, Xingluo Liu, Altaf Ahmad Wani, Qi-En Wang. Negative regulation of bcl-2 transcription by DNA damage-binding protein complex in human ovarian cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 750. doi:10.1158/1538-7445.AM2013-750
Purging Tumor Cells From Bone Marrow by Use of Antibody and Complement: A Critical Appraisal
Authors: A. P. Gee, M. D. P. Boyle
Journal: JNCI Journal of the National Cancer Institute (1988)

This review highlighted several problems associated with the use of antibody and complement in the elimination of tumor cells from bone marrow that was to be used for transplantation, and it discussed some of the difficulties encountered in developing this approach in model systems. These problems should be seriously considered by any clinician contemplating this method for bone marrow purging. [J Natl Cancer Inst 1988;80:154-159]
THU0368 Dosage Reduction of Biological Therapy in Patients with Axial Spondyloarthritis in Persistent Clinical Remission.
Authors: M. Almirall, T. C. Salman, M. P. Lisbona, S. Iniesta, J. Maymó
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The effectiveness of TNF blockers in treating axial Spondyloarthritis patients is well know, but we don’t know most appropriate dosage for treatment of patients in persistent clinical remission. <h3>Objectives</h3> Our objective is to assess the clinical activity at 3 and 6 months in patients with axial Spondyloarthritis in persistent remission who received low dosages of biological therapy. <h3>Methods</h3> We performed a observational study with patients of our department with axial Spondyloarthritis including Ankylosing Spondylitis who received low dosages of TNF blockers until September 2012 by persistent remission (BASDAI≤2, absence of arthritis and enthesitis and normality of CRP values) for a minimum of 6 months without NSAIDs consume. Data analysed were: demographic characteristics, duration of clinical remission, diagnosis and disease duration, type and duration of biological agent used and at 3 and 6 months: percentage of patients who remained in remission (BASDAI≤2), percentage who had low disease activity (BASDAI between 2 and 4 units) and percentage who relapsed (BASDAI≥4) and required the previous dose of biological treatment. <h3>Results</h3> We included 40 patients (75% man) with a mean age of 43,7+/- 13 years and a mean time of remission of 28,7 +/- 18,5 months. The diagnoses were: 33 Ankylosing Spondylitis, 5 non-radiographic axial Spondyloarthritis and 2 Spondyloarthritis associated with bowel inflammatory disease. They had a mean duration of disease of 8,6+/- 6,1 years and 75% of patients had HLAB27 positive. 7 patients received Etanercept, 7 Infliximab and 26 Adalimumab and a mean duration of current biological therapy was 41,9 +/- 23,9 months. Used low dosages was 50 mg every 10 days or 25 mg every week for Etanercept, 3mg/kg every 8 weeks for Infliximab and 40 mg every 3 weeks for Adalimumab. All 40 patients had a minimum follow-up of 3 months after dosage reduction. At 3 months 85% of patients remained in remission, 10% had low disease activity and 5% relapsed (2). 24 patients were followed for 6 months after dosage reduction. At 6 months 71% remained in clinical remission, 12,5% had low disease activity and 16,5% relapsed (4), 2 at 3 months and 2 at 6 months. <h3>Conclusions</h3> Most of our patients with axial Spondylarthritis remained in clinical remission at 3 and 6 months after after dosage reduction of TNF blockers. Only a small percentage of the patients relapsed and required the previous dosage of biological treatment. <h3>Disclosure of Interest</h3> None Declared
PWE-214 Endoscopic mucosal resection for early neoplasia in Barrett's epithelium in patients on anticoagulation using warfarin: is it safe?
Authors: U Selvarajah, S Al-Mamari, A A Bailey, B Sgromo, R Marshall, N Maynard, B Braden
Journal: Gut (2012)

<h3>Introduction</h3> Endoscopic mucosal resection (EMR) has become an established treatment modality in the managment of patients with high grade dysplastic lesions and intramucosal cancer in Barrett oesophagus. The mucosal defect caused by the endoscopic resection usually takes several weeks to heal. There is no data whether this procedure is also safe for patients requiring anticoagulation. The aim of the study was to investigate the risk of acute and delayed bleeding in patients on anticoagulation undergoing EMR for treatment of early neoplasia in Barrett oesophagus. We compared the complication rate of EMR in patients taking warfarin as anticoagulants with that of a control group. <h3>Methods</h3> Warfarin was stopped 5 days before the planned EMR and restarted on the evening of the procedure day. Patients with high risk conditions such as recent pulmonary thromboemboli received bridging with low molecular weight heparin. All EMRs were performed when the INR was &lt;1.5. <h3>Results</h3> 34 EMRs were performed in nine patients requiring anticoagulation. 8 were on warfarin due to atrial fibrillation, one took warfarin after pulmonary embolism. One patient on warfarin was readmitted 10 days after EMR with haematemesis, melaena and an drop in haemoglobin &gt;5 g/dl caused by bleeding from an EMR resection ulcer; the bleeding had settled spontaneously at the time of endoscopy. Out of 138 EMRs in 35 controls, five acute bleeding events occurred during EMR which required treatment by clipping, coagulation grasper or heater probe. No delayed bleeding event occurred in the control group. The maximal diameter of the resected specimen did not differ between anticoagulated patients and controls (median 17 mm; 25%&gt;75% percentile: 15–18 mm vs 17 mm; 25%&gt;75% percentile: 15–20 mm; p=0.68). No perforations were observed in either groups. The number of bleeding events did not differ between groups (p=0.85), neither for acute (p=0.60) or delayed bleeding (p=0.46). <h3>Conclusion</h3> EMR of early oesophageal neoplasia can be safely performed in patients requiring anticoagulation when warfarin is discontinued 5 days before the endoscopic intervention and reinstituted on the evening of the procedure day. <h3>Competing interests</h3> None declared.
Androgen-Insensitivity Syndrome as a Possible Coactivator Disease
Authors: Masahiro Adachi, Ryoichi Takayanagi, Arihiro Tomura, Kyosuke Imasaki, Shigeaki Kato, Kiminobu Goto, Toshihiko Yanase, Shoichiro Ikuyama, Hajime Nawata
Journal: New England Journal of Medicine (2000)

Androgen-insensitivity syndromes in 46,XY fetuses result in various degrees of impairment in genital virilization.1 These syndromes are caused by mutations in the androgen receptor gene that result in decreased binding of androgen to the receptor.2–9 As a consequence, the transcriptional activity of the androgen–androgen-receptor complex is reduced, and therefore, genital virilization is reduced. The androgen receptor, like other steroid hormone receptors, has two major transactivation domains10 — activation function 1 (AF-1) in the N-terminal region11–13 and activation function 2 (AF-2) in the C-terminal ligand-binding domain14 — that interact with the target genes directly as well as indirectly by . . .
Scientists Show That Invasive Breast Cancer Develops From Early Cancer Cells
Authors: D. Holzman
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article Scientists Show That Invasive Breast Cancer Develops From Early Cancer Cells Get access David Holzman David Holzman Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 10, 17 May 1995, Pages 710–711, https://doi.org/10.1093/jnci/87.10.710 Published: 17 May 1995