tbuckley/cabot-search huggingface dataset:
Abstract 2571: Genetic variations in telomere maintenance pathway genes are associated with risk of esophageal cancer.
Authors: Yuanqing Ye, Jaffer Ajani, Xifeng Wu
Journal: Cancer Research (2013)

Abstract Many studies have shown the association of telomere dysfunction with aging and cancer development. We hypothesize that genetic variations in telomere maintenance genes may modulate esophageal cancer risk. To test this hypothesis, we comprehensively assessed the association of 616 SNPs in 45 telomere maintenance pathway genes in 602 esophageal adenocarcinoma cases and 1,512 healthy controls. Unconditional multivariate logistic regression was used to estimate odds ratio (OR) and 95% confidence interval (CI) while adjusting for age, gender, and smoking status. In single SNP analysis, a total of 77 SNPs had P value &amp;lt; 0.05. 5 SNPs remained significant after adjusting for multiple comparisons at FDR &amp;lt; 0.10 including 3 SNPs in PINX1 gene and 2 SNPs in TPP1 gene. The most significant association was observed for rs9657541 in PINX1 gene that exhibited a significantly reduced risk of esophageal cancer in dominant model (OR = 0.62, 95% CI = 0.50-0.77, P = 1.54×10−5, FDR = 0.020). Cumulative effects of SNPs were assessed by the number of unfavorable genotypes. Each subject was classified into low (zero unfavorable genotype), medium (one to three unfavorable genotypes), and high-risk groups (more than three unfavorable genotypes). Compared with the low-risk group, the OR was 1.58 (95% CI = 1.20-2.09) for the median-risk group and 2.57 (95% CI = 1.87-3.54) for the high-risk group. Classification and regression tree (CART) analysis was performed to identify genetic profiles that can classify individuals into differential risk of esophageal cancer. CART analysis identified 3 terminal nodes. Compared to terminal node 1, individuals in terminal nodes 2 and 3 had significantly increased risks of esophageal cancer with ORs of 1.43 (95% CI = 1.13-1.80) and 2.46 (95% CI = 1.81-3.34), respectively. We also performed gene-based analysis to determine the combined effect of SNPs within a gene region and identified four genes (TPP1, PINX1, TNKS, TERF1) significantly associated with the risk of esophageal cancer. In conclusion, our results suggest that genetic variants in telomere maintenance pathway genes may contribute to the altered risk of esophageal cancer, both individually and jointly. Citation Format: Yuanqing Ye, Jaffer Ajani, Xifeng Wu. Genetic variations in telomere maintenance pathway genes are associated with risk of esophageal cancer. [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 2571. doi:10.1158/1538-7445.AM2013-2571
Hematologic Neoplasia in Patients Treated for Hodgkin's Disease
Authors: C. Norman Coleman, Christopher J. Williams, Andrew Flint, Eli J. Glatstein, Saul A. Rosenberg, Henry S. Kaplan
Journal: New England Journal of Medicine (1977)

We studied 680 patients with Hodgkin's disease, treated at Stanford University Medical Center from July 1, 1968, through December 31, 1975, to determine the risk of development of hematologic neoplasia. Six cases of leukemia occurred in patients in clinical remission, one 7 1/2 years after diagnosis. Two additional cases occurred in patients with active Hodgkin's disease. No cases were seen in 320 patients treated with radiotherapy alone or in 30 treated with chemotherapy alone. A single case of subacute leukemia occurred in a patient treated initially with radiation therapy and colloidal gold. The actuarial probability of development of leukemia at five and seven years is 1.5 and 2.0 per cent for the entire group and 2.9 and 3.9 per cent for the 330 patients treated with combined radiation and chemotherapy. The medium survival after diagnosis is four months, with no patient living beyond six months.
Governing drug use through neurobiological subject construction: The sad loss of the sociocultural
Authors: Kevin Chien-Chang Wu
Journal: Behavioral and Brain Sciences (2011)

Abstract Based on their “drugs as instruments” framework, Müller &amp; Schumann (M&amp;S) propose a staged drug policy that matches well the neoliberal governance scheme. To mend the sad loss of the sociocultural dimension in their model, I propose three such considerations: first, sociocultural interactions with the brain; second, sociocultural context and justice of drug use; and third, sociocultural preparedness for implementing their drug policy.
Cardiac lesions induced by chemicals.
Authors: T Balazs, V J Ferrans
Journal: Environmental Health Perspectives (1978)

Chemically induced cardiomyopathies are frequently the consequences of a cardiac metabolic imbalance brought about by exaggerated functional affects. The infarctlike lesions induced by adrenergic beta-receptor stimulants and the vasodilating antihypertensives serve as examples of this phenomenon. Direct cardiotoxic mechanisms not related to cardiovascular functional effects are responsible for another class of toxic cardiomyopathy. An example of this is the cardiomyopathy produced by the anthracycline antineoplastic agents. The pathogenesis, morphological changes and toxicologic features of these cardiomyopathies are described with particular reference to their detection in preclinical toxicity studies.
Understanding Small Fiber Neuropathy
Authors: John T. Kissel, A. Gordon Smith
Journal: JAMA Neurology (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Neurology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Neurology journal
EVOLUCIÓN POST-OPERATORIA DESPUÉS DE UNA PERITONEOSCOPIA NOTES UTILIZANDO DIFERENTES VÍAS DE ACCESO (TRANSGÁSTRICA, TRANSRECTAL Y TRANSVAGINAL) VERSUS LAPAROSCOPIA. ESTUDIOALEATORIAZADO EN UN MODELO PORCINO DE SUPERVIVENCIA
Authors: C Guarner-Argente, H Córdova, G Martínez-Pallí, R Navarro-Ripoll, C Rodríguez de Miguel, M Beltrán, J Comas, MA Martínez, A Rodríguez D'Jesús, A Lacy, CC Thompson, À Ginès, M Pellisé, B González-Suárez, O Sendino, JM Bordas, J Llach, G Fernández-Esparrach
Journal: Endoscopy (2010)

Objetivo: Evaluar el impacto fisiológico e inmunológico de la NOTES utilizando diferentes rutas de acceso versus la laparoscopia tradicional.
Abstract 1223: Relief of feedback inhibition of RTK and RAS signaling in V600E BRAF melanomas exposed to RAF inhibitors buffers their effects on signaling
Authors: Christine A. Pratilas, Eric W. Joseph, Madhavi Tadi, Poulikos I. Poulikakos, Maytal Gabay, Piro Lito, Wai Wong, Elisa DeStanchina, Sarat Chandarlapaty, Neal Rosen
Journal: Cancer Research (2012)

Abstract Activation of ERK signaling causes feedback inhibition of receptor tyrosine kinase and RAS signaling by multiple mechanisms and limits the steady-state output of the pathway. The V600E BRAF mutant does not depend on RAS-dependent dimerization and is not susceptible to feedback inhibition of RAS. In V600E BRAF melanomas, ERK pathway output and the expression of ERK genes such as DUSP6 and members of the SPROUTY family are markedly elevated. In these tumors, RTK signaling and RAS activation are actively suppressed. In the context of elevated DUSP6, RAF inhibitors rapidly inhibit ERK phosphorylation and output. This relieves the feedback inhibition of various RTKs and induces RAS activity and the formation of activated wild type RAF dimers that are insensitive to RAF-inhibitors. This results in a rebound in ERK phosphorylation and output that is sensitive to MEK, but not RAF inhibitors and suggests that the latter cannot maximally inhibit ERK signaling in these tumors. In support of this idea, combined treatment with MEK and RAF inhibitors reduces ERK output and the growth of V600E BRAF melanoma xenografts to a greater degree than either alone. 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 1223. doi:1538-7445.AM2012-1223
Patient perception of choice in decision-making for early-stage breast cancer: do race and socioeconomic status matter?.
Authors: S Dhage, K Fei, J Weidman, AA Guth, N Bickell
Journal: Cancer Research (2009)

Abstract Abstract #5098 Background: It has been well-established that survival following breast conservation surgery(BCS) vs. mastectomy(MT) is equivalent. Therefore women with early-stage breast cancer should given a choice between BCS and MT. It has recently been recognized that women who have a choice of surgery type have better short term health status. Some studies suggest that there is treatment variation according to socioeconomic status and race. But little is known about whether there is a variance in a feeling of choice based on ethnicity/race and socioeconomic status. Do these factors affect women's sense of choice in her surgical treatment?&amp;#x2028; Methods: Women with a newly diagnosed Stage I/II breast cancer were identified from pathology databases of 6 participating NYC hospitals, including 3 municipal, 2 tertiary, and one community hospital. Patients were surveyed an average of 6 months after surgical treatment. Bivariate, logistic and factor analyses were conducted on the 258 participants. IRB approval was obtained at all 6 institutions.&amp;#x2028; Results: Despite high rates(88%) of reported discussion of surgery types, only 55% of women felt they had a choice of surgical treatment. Women who felt they had a choice were more likely to be younger(55 vs. 61; p=0.0009), more knowledgeable about equivalent survival outcomes(24% vs. 12%, p+0.0170), and shared decision making(Cronbach α=0.79) with their physician(92% vs. 88%, p=0.0066). When taking into account the patient's stage of cancer, there was no difference in the feeling of choice based on race/ethnicity, income level, or education level. This feeling of having a choice in the surgical procedure performed was not related to type of surgery: 57% of women with mastectomy felt they had a choice, while 56% of breast conservation surgery patients felt they had a choice.&amp;#x2028; Conclusions: There is a difference between mentioning treatment options during preoperative evaluations and counseling of women with newly diagnosed early-stage breast cancer, and shared decision-making. Shared-decision making is associated with a greater sense of choice, which can affect health status and may influence patients satisfaction with overall treatment. Surgeons should involve women in discussion of treatment options, regardless of education or race, as this can influence patient's sense of choice, which in turn, can affect health status. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 5098.
Reporting of potential immunogenicity with biologic drugs: clarity and accuracy required
Authors: Robert J Moots, Alejandro Balsa, Gertjan Wolbink
Journal: Annals of the Rheumatic Diseases (2016)

Reporting of potential immunogenicity with biologic drugs: clarity and accuracy requiredWe welcome the study from Emery et al 1 reporting the phase III trial comparing the biosimilar SB4 with originator etanercept.In this publication, the authors report comparable clinical efficacy and safety profile between both drugs, but an apparent difference in immunogenicity, with 'antidrug antibodies (ADAs)' reported in only 0.7% of patients taking SB4, compared with 13% with reference product, etanercept.While the development of ADAs clearly has the potential to translate into the clinical situation, the science underpinning their detection (and also extrapolation to potential clinical effect) is complex, highly dependent on the assay system employed and often poorly reported. 2 3We believe that the data on ADAs documented in this report to be confusing and, as presented, do not merit the headline conclusions drawn.In particular, we note only a minimal description of the assay system used to measure ADAs and sparse details of immunogenicity results (online supplementary appendix 9).We also note just one time point (week 4) with an apparent excess of ADAs in patients taking reference etanercept, with no or minimal detection of ADAs for either drug at any other time point.To correctly interpret the results of this important part of the study, we believe that additional details are required: What was the full protocol for measurement of ADAs?At what cut-off point was 'positivity' considered?What were the titres of ADAs?What were the drug trough plasma concentrations and did the presence of apparent ADA correlate with these or with reports of adverse events?What potential mechanism would explain the one-off measurement of ADAs at 4 weeks alone, with one drug?Where did the ADAs go after 4 weeks as they could not be measured after that period?What was the rationale for reporting a 'week 24 overall ADA incidence,' when analyses of weekly ADA incidence apparently showed one transient excess 'positive' ADAs for one drug at 1 week and, is it appropriate to present this as clear evidence for immunogenicity?We trust that further information able to address these important questions can soon be made available to allow the rheumatology and scientific community undertake a more suitable assessment of this important paper.
Adrenal Hyperplasia in Cushing’s Syndrome Demonstrated by FDG Positron Emission Tomographic Imaging
Authors: EUGENE C. LIN, ROBERT HELGANS
Journal: Clinical Nuclear Medicine (2002)

From the Department of Radiology, University of Colorado Health Sciences Center, Denver, Colorado Received for publication October 10, 2001. Revision accepted December 17, 2001. Reprint requests: Eugene C. Lin, University of Colorado Health Sciences Center, Department of Radiology, Box A-034, 4200 East Ninth Avenue, Denver, Colorado 80262. E-mail: [email protected]
The Scintigraphic Features of Giant-Cell Tumors in Relation to Other Imaging Modalities
Authors: M. O'REILLY, FELIX S. CHEW
Journal: Clinical Nuclear Medicine (1996)

Thirty-three patients with untreated giant-cell tumors of bone were studied with Tc-99m phosphate scintigraphy. The scintigraphic patterns of the tumors were varied and the tumors exhibited extended uptake of radioactivity in the majority of cases. The homogeneously diffuse pattern and the nonhomogeneous "doughnut" and "blob" patterns are described. The scintigraphic patterns of giant-cell tumors are considered in the light of the radiographic, angiographic, CT, and MR imaging studies and the histopathologic findings.
P3-06-03: Hypodiploidy, 1pter Loss and Inactive X Chromosome Retention Are Associated with BRCA1 Somatic or Germline Inactivation in Basal-Like Breast Carcinomas: Proposal for a New BRCAness Genomic Signature.
Authors: E Manié, T Popova, A Vincent-Salomon, T Dubois, O Delattre, X Sastre-Garau, D Stoppa-Lyonnet, M-H Stern
Journal: Cancer Research (2011)

Abstract Basal-Like Carcinomas (BLCs) are high grade ductal carcinomas identified by large scale transcriptomic analyses among carcinomas with triple-negative phenotype (ER- PR- HER2−). A particular relationship between this phenotype and the BRCA1 breast cancer susceptibility gene has been described based on several observations including high genomic similarities of sporadic and BRCA1 BLCs. BRCA1 mutated patients have been shown to strongly benefit from treatments using PARP inhibitors. However, significant benefit of this treatment was not demonstrated in sporadic triple-negative breast cancers in association to standard chemotherapy in phase III clinical trials, which emphasizes the necessity for a better selection of DNA repair deficient tumors. The goal of this study was to determine whether BRCA1 inactivation leads to particular genomic alterations that could be used to identify BRCA1 deficient sporadic BLCs. Genomic profiling was performed using SNP-arrays (Affymetrix and Illumina) and high quality profiles were obtained for 60 BLCs with more than 35% of tumor cells. The series contained 28 BRCA1 BLCs and 32 sporadic BLCs consisting in 10 sporadic BLCs with BRCA1 somatic inactivation by promoter methylation (BRCA1-like BLCs) and 22 sporadic tumors without BRCA1 methylation (nonBRCA1 BLCs). Genomic data was mined with GAP methodology (Popova et al, Genome Biol 2009), which allows absolute copy-number evaluation with DNA content calculation and clarification of Loss Of Heterozygosity (LOH) status. Genomic patterns of BLCs were characterized by frequent and highly recurrent allelic losses. Comparison between BRCA1, BRCA1-like and nonBRCA1 BLCs confirmed their overall similarity, and identified few significant differences enhanced when BRCA1 and BRCA1-like BLCs were considered as one group. Firstly, hypodiploidy characterized BLCs with BRCA1 germline and/or somatic inactivation. Secondly, the lpter region was found more often lost in BRCA1 and BRCA1-like BLCs than in nonBRCA1 BLCs. Thirdly, retention of inactive X chromosome was a characteristic of BLCs with BRCA1 germline and/or somatic inactivation. Finally, a BRCA1ness score based on the above described difference is proposed. In conclusion, despite a strong similarity of genomic patterns in BLCs, BRCA1 inactivation leads to few key genomic aberrations which constitute a new BRCA1 molecular signature namely hypodiploidy, 1pter loss and inactive X chromosome retention. This signature needs to be further evaluated in terms of response to PARP inhibitors in order to evaluate its capacity to identify patients that will benefit from this treatment. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P3-06-03.
Abstract 2115: REV1, DNA polymerase ≤ and the fanconi anemia proteins FANCD2 and FANCI function together during repair
Authors: Shilpy Sharma, Christine E. Canman
Journal: Cancer Research (2012)

Abstract Fanconi anemia (FA) is a chromosomal instability disorder characterized by bone marrow failure, congenital abnormalities and increased incidence of malignancies. Cells derived from FA patients exhibit cellular hypersensitivity to interstrand crosslink (ICL)-inducing agents, including mitomycin C (MMC) and cisplatin. ICLs are sensed and repaired by a complex process which involves multiple DNA repair proteins including the FA factors as well as proteins that function in nucleotide excision repair, translesion DNA synthesis and homologous recombination (HR). REV1 (a Y family translesion DNA polymerase) and DNA Polymerase ≤ (Polα, comprised of the catalytic REV3 protein and REV7 accessory subunit) play important roles in performing DNA replication across blocking lesions. Previous studies have demonstrated an epistatic relationship between Polα and genes encoding proteins comprising the Fanconi anemia core complex with regards to resistance to ICLs. Additionally, REV1, Polα, and the FANCD2/FANCI heterodimer have each been shown individually to be involved in promoting HR repair, although the reasons for their involvement remain unclear. Here, we show that human REV1 and REV3 exhibit an epistatic relationship with FANCD2 and FANCI in homology-directed repair of a defined DNA double-stranded break and cellular resistance to ICLs created by MMC. We also demonstrate that MMC-induced chromosomal anomalies are increased in REV1 or REV3-depleted cells and FANCD2 depletion does not further exacerbate this phenotype. Additionally, we demonstrate for the first time that full length human REV1 and REV3 interact with FANCD2 and FANCI in vivo as detected by co-immunoprecipitation studies. We therefore propose a model where replication fork stalling during HR repair DNA synthesis is resolved through Polα-dependent translesion DNA synthesis which is regulated by the Fanconi anemia pathway. 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 2115. doi:1538-7445.AM2012-2115
921 ALTERED BEHAVIOR OF PERIPHERAL BLOOD MONOCYTES FROM CHRONIC HEPATITIS C PATIENTS
Authors: Y. Rodrîguez-Munoz, S. Martín-Vílchez, M.J. Borque, R. López-Rodriguez, A. Hernande-Bartolome, M. Trapero-Marugan, L. García-Buey, R. Moreno-Otero, P. Sanz-Cameno
Journal: Journal of Hepatology (2012)
SAT0199 An estimate of the proportion of patients with sle receiving off-label treatment with rituximab in european countries
Authors: R. van Vollenhoven, M. Seddighzadeh, S. Jacobsen, T. Dörner, G. Ferraccioli, F. Houssiau, T. Huizinga, D. Isenberg, K. Lászlό, G. Ruiz-Irastorza, D. Squatrito, A. Voskuyl, A. Askanase, S. Bernatsky
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Rituximab (MabThera; RTX) has not been approved for use in SLE, but uncontrolled observations have suggested efficacy in some patients. There clearly is off-label use of this medication in practice in Europe, but the extent of it has not previously been analyzed. The International Registry for Biologics in SLE (IRBIS), initiated by the SLICC group provided the data for this study. <h3>Objectives</h3> To estimate the proportion of SLE patients treated with RTX in Europe. <h3>Methods</h3> Data previously submitted to the IRBIS registry by 28 centers in 11 European countries were complemented with additional clinical information from the participating sites and SLE prevalence estimates based on previously published data and data provided by direct contact with participating physicians. For the remaining countries in the European Union (EU) and European Economic Area-European Free Trade Association (EEA-EFTA), estimates were extrapolated on the assumption of regional similarities between countries. <h3>Results</h3> Most of the SLE-dedicated rheumatology specialty centers represented in this study had 200 to 300 SLE patients of whom generally &lt;5% were treated with RTX. In the 11 European countries and regions represented in this report the estimated calculated rate of exposure to RTX among SLE patients ranged from 0.6-1.6%. Extrapolating to all 30 EU-EEA-EFTA countries, with an overall population of around 416 million, and with published prevalence estimates for SLE between 3.6 and 7.3 per 10.000 adults, we calculated that between 0.5 and 1.3% of European patients with SLE currently have been treated, off-label, with RTX. <h3>Conclusions</h3> In Europe, RTX is estimated to be used off-label in 0.5-1.3% of SLE patients. This modest number suggests that it is chosen only for those patients in whom established therapeutic options have been exhausted. Limitations of the study include the use of extrapolations, and the fact that RTX use by non-rheumatologists was not ascertained. Although controlled evidence for the efficacy of RTX in SLE is lacking, the current usage of RTX in SLE may be considered conservative, given the high medical need in the larger SLE patient population. <b>Supported by a research grant from Roche</b> <h3>Disclosure of Interest</h3> None Declared