tbuckley/cabot-search huggingface dataset:
The Occupation of Fishing as a Risk Factor in Cancer of the Lip
Authors: Walter O. Spitzer, Gerry B. Hill, Larry W. Chambers, Barbara E. Helliwell, H. Bliss Murphy
Journal: New England Journal of Medicine (1975)

To study the role of commercial fishing and related factors in the development of lip cancer, a project that included a case-control study and a cohort analysis was undertaken in Newfoundland. Household survey data were linked with cancer-registry and census data. In comparison with other males, fishermen had a probability of development of lip cancer that was 1.5 times higher (by the case-control method, P less than 0.05) or 4.4 times higher (by cohort analysis, P less than 0.001). Despite the effect of pipe smoking, "outdoorness" and age on the development of lip cancer in general, the occupation of fishing was an additional, independent contribution to the risk. Unexpectedly, using the mouth as a third hand to handle tar-coated nets seemed to protect fishermen from the disease. It was not possible to attribute the higher risk to a particular work activity, nor was a specific responsible carcinogen identified.
Brief Report: Hypoglycemia Due to a Monoclonal Insulin-Binding Antibody in Multiple Myeloma
Authors: B Redmon, K L Pyzdrowski, M K Elson, N E Kay, A P Dalmasso, F Q Nuttall
Journal: New England Journal of Medicine (1992)

RECURRENT, severe hypoglycemia in the absence of exogenous insulin administration is uncommon. Reported causes include islet-cell adenomas or carcinomas, surreptitious use of insulin or sulfonylurea medications, stimulatory insulin-receptor antibodies, and various non—islet-cell tumors.1 2 3 4 The autoimmune insulin syndrome is another rare cause of hypoglycemia.5 , 6 This syndrome is characterized by late postprandial hypoglycemia and the presence of polyclonal insulin-binding autoantibodies, typically occurring in a patient with other autoimmune disease. Excess insulin is released in response to a meal because of binding to antibodies. Later, as the bound insulin is released, it causes hypoglycemia. We describe a patient who presented with a hypoglycemic . . .
La pose systématique d'une prothèse pancréatique après ampullectomie endoscopique réduit significativement le risque de pancréatite aiguë: étude rétrospective d'une série monocentrique de 107 patients
Authors: P Leclercq, D Ribeiro, R Gincul, F Mion, M Cambou, F Fumex, J Pialat, JY Scoazec, B Napoléon
Journal: Endoscopy (2011)

Introduction: La résection endoscopique est devenue le traitement de première intention des tumeurs débutantes de l'ampoule de Vater.La pancréatite aiguë (PA) représente le principal facteur de morbidité (18 à 21%) dans les séries multicentriques rétrospectives et prospectives françaises. Une étude de Harewood et al en 2005 était en faveur de la pose systématique d'une prothèse pancréatique (PP) à visée préventive. La série était cependant limitée (19 patients) et les résultats non significatifs en intention de traiter. Dans les séries françaises le seul facteur significatif de risque de PA était l'absence de symptômes. La question de l'intérêt de la pose systématique de PP après ampullectomie endoscopique reste donc posée.
Abstract A50: Loss of pVHL inactivates p53 by permission of interaction between p14/ARF and progerin
Authors: Su-Jin Lee, Youn-Sang Jung, Sun-Hye Lee, Ji-Yun Chung, Bum-Joon Park
Journal: Cancer Research (2011)

Abstract Renal cell carcinoma (RCC) is a common primary renal malignancy in adults. The typical feature is the nuclear irregularity which is a basis for grading. Moreover, resistance to chemotherapy and irradiation (IR) is also one of the characters of RCC. p53 inactivation without genetic mutation and pVHL mutation in early stage are shown in RCC. However, it is still remained the question about the mechanism of the nuclear deformation and chemotherapy resistance. Here we proposed that the effect of progerin on RCC. Progerin elevated in RCC and the elimination of progerin could ameliorate the nuclear morphology. Moreover, knockdown of progerin could recover DNA damage sensitivity and p53 activation in RCC. Loss of pVHL induces elevated progerin expression, which inhibit p14/ARF by direct interaction to suppress p53 activity. Moreover, forced enhancement of progerin is found in human leukemia sample. In this study, we provide that the novel mechanism for p53 suppression in RCC and the importance of progerin in cancer progression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the Second AACR International Conference on Frontiers in Basic Cancer Research; 2011 Sep 14-18; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2011;71(18 Suppl):Abstract nr A50.
PMO-145 Ethnicity has no impact on SVR rates in patients with HCV genotype 3 treated with pegylated interferon and ribavirin: Abstract PMO-145 Figure 1
Authors: A Evans, D Linzey, J Booth
Journal: Gut (2012)

<h3>Introduction</h3> Chronic Hepatitis C affects over 170 million people world wide. Of the 4 main genotypes, genotype 3 is common in South East Asia, particularly Pakistan, and in Europe represents up to 45% of newly diagnosed infections.<sup>1</sup> Although it is well established that ethnicity impacts on response rates (sustained virological response (SVR) rates) for Hepatitis C virus (HCV) Genotype 1 infections, there is controversy over whether ethnicity impacts on SVR rates in HCV genotype 3 infections.<sup>2 3</sup> In this study we performed a retrospective analysis of patients with genotype 3 HCV infections who had undergone treatment in a busy District General Hospital over the last 4 years to assess whether ethnicity impacted on SVR rates. <h3>Methods</h3> All patients treated with standard therapy (pegylated interferon and ribavirin) over the last 4 years were studied and factors which are known to influence response rates together with ethnicity were examined in patients with genotype 3 chronic hepatitis C infection. <h3>Results</h3> In total 630 patients were undergoing/had undergone standard treatment for chronic hepatitis C infection in our hospital over the last 4 years. Of these 147 were identified as being HCV genotype 3 infections. 80 of these patients had completed a course of treatment and had at least 6 months of follow-up (for assessment of SVR rates). These patients were divided into those from South East Asia (43 patients) and European patients (37 patients). Of the patients of Asian ethnicity 36 achieved an SVR (83.7%), six relapsed (13.9%) and one was a non-responder (2.4%). Of the patients of European ethnicity 31 achieved an SVR (83.8%), five relapsed (13.5%) and one was a non responder (2.7%). There was no significant statistical difference in SVR rates in patients from South East Asia (83.7% SVR) compared with patients of European origin (83.8%) (p&lt;0.01). <h3>Conclusion</h3> In this retrospective cohort study SVR rates in patients with genotype 3 chronic hepatitis C infection were not affected by ethnicity. Those patients who did not achieve SVR and failed standard therapy were predominantly relapsers as opposed to non-responders. <h3>Competing interests</h3> None declared. <h3>References</h3> 1. <b>Esteban J</b>, <i>et al</i>. The changing epidemiology of hepatitis C virus infection in Europe. <i>J Hepatol</i> 2008;<b>48</b>:148–62. 2. <b>Foster G</b>, <i>et al</i>. Response to antiviral therapy in patients with genotype 3 chronic hepatitis C: fibrosis but not race encourages relapse. <i>Eur J Gastroenterol Hepatol</i> 2011;<b>23</b>:747–53. 3. <b>Mutimer D</b>, <i>et al</i>. Inferior response of Asian versus non-Asian hepatitis C genotype 3 infection to combination antiviral therapy. <i>J Viral Hepat</i> 2008;<b>15</b>:115–19.
283 MIXED-PHENOTYPE HEPATOCELLULAR CARCINOMA IN LIVER TRANSPLANTS AFTER USE OF TRANSARTERIAL CHEMOEMBOLIZATION (TACE) IS ASSOCIATED WITH ACTIVATION OF MITOGEN-ACTIVATED PROTEIN KINASE (MAPK) SIGNALLING PATHWAY
Authors: V. Iansante, Y. Zen, A. Barbarulo, C. Starling, S. Chokshi, N. Heaton, R. Williams, C. Bubici, A. Quaglia, S. Papa
Journal: Journal of Hepatology (2012)
Predicting Obesity in Young Adulthood from Childhood and Parental Obesity
Authors: Robert C. Whitaker, Jeffrey A. Wright, Margaret S. Pepe, Kristy D. Seidel, William H. Dietz
Journal: New England Journal of Medicine (1997)

Childhood obesity increases the risk of obesity in adulthood, but how parental obesity affects the chances of a child's becoming an obese adult is unknown. We investigated the risk of obesity in young adulthood associated with both obesity in childhood and obesity in one or both parents.
MICROVESICLES REDUCE ARRHYTHMIAS AND IMPROVE THE ELECTRICAL CONDUCTION BY RECOVERING CONNEXIN 43 AND SODIUM CURRENTS IN A RAT ISCHEMIA REPERFUSION INJURY MODEL
Authors: Hyewon Park, Ilkwon Kim, Hyelim Park, Hyoeun Kim, Cui Shanyu, Hui-Nam Pak, Moon-Hyoung Lee, Boyoung Joung
Journal: Journal of the American College of Cardiology (2016)
A Case of Diffuse Large B-Cell Lymphoma in Association With Paraesophageal Leiomyoma: Highlighting False-Positivity of PET Scan and Importance of Tissue Diagnosis
Authors: Rajinder S Grover, Kemp Kernstine, Amrita Krishnan
Journal: Journal of the National Comprehensive Cancer Network (2012)

PET scan and PET/CT scans are being widely used for staging of diffuse large B-cell lymphoma (DLBCL) and Hodgkin lymphoma. They are sensitive and specific imaging techniques available for lymphoma. However, practicing hematologists must be aware of false-positive tests, which can upgrade the stage of the lymphoma significantly and may alter the treatment paradigm for an individual patient. This report describes a case of DLBCL that was upgraded with PET/CT scan to stage IVA from stage IA. Pursuit of tissue biopsy with minimally invasive surgery eventually confirmed it to be stage IA DLBCL and paraesophageal leiomyoma. This case highlights the potential pitfalls of modern imaging techniques and the need for histologic diagnosis.
Abstract 4326: The potential role of IMP-3 and PDPN in invadopodia formation and collective cancer invasion: Anti-invadopodia therapy as a therapeutic target
Authors: Young Sun Hwang, Kwang-Kyun Park, Won-Yoon Chung
Journal: Cancer Research (2012)

Abstract Better understanding the mechanisms underlying the metastatic process is essential to developing novel targeted therapeutics. Recently, invadopodia have been increasingly recognized as important drivers of local invasion in metastasis. Invadopodia are actin-rich structures that have the ability to degrade the underlying extracellular matrix (ECM) and promote cell invasion. However, many questions concerning the mechanisms of invadopodia formation, regulation and function remain open to debate. Meanwhile, invasion of cells into the surrounding tissue and destruction of normal tissue architecture are two hallmarks of malignant tumors. Morphologically, two patterns of tumor invasion can be distinguished; single cell and collective cell invasion. The invasion of single cells and collective cells is often correlated with dramatic changes in the expression and function of adhesive and regulatory proteins. These changes are reminiscent of early developmental processes when cells acquire a migratory, mesenchymal phenotype. Currently, the role of invadopodia in collective cancer invasion is completely unknown. In the present study, we reveal that insuline-like growth factor-II mRNA-binding protein-3 (IMP-3) associated with invadopodial infiltration and collective cancer invasion through podoplanin (PDPN) mRNA stabilization as a component of invadopodia, suggesting that invadopodia plays a pivotal role in invasive front of collective cancer invasion and thereby involved the cancer metastasis. This finding, combined with other investigations into the mechanisms of invadopodia formation, reveal clinically-relevant targets for intervention in invadopodia, including IMP-3 and PDPN. 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 4326. doi:1538-7445.AM2012-4326
PROGNOSTIC VALUE OF ANKLE-BRACHIAL INDEX IN PATIENTS UNDERWENT PERCUTANEOUS CORONARY INTERVENTION: IN-HOSPITAL AND MIDTERM OUTCOMES FROM SHINANO-REGISTRY
Authors: Naoto Hashizume, Takashi Miura, Yasushi Ueki, Tomoaki Mochidome, Mikiko Harada, Naoyuki Abe, Hitoshi Nishimura, Soichiro Ebisawa, Hirohiko Motoki, Ayako Okada, Yuji Shiba, Atsushi Izawa, Jun Koyama, Uichi Ikeda
Journal: Journal of the American College of Cardiology (2016)
Abstract 4306: KLF8 promotes human ovarian tumorigenesis in athymic mouse models
Authors: Heng Lu, Xianhui Wang, Alison M. Urvalek, Tianshu Li, Lin Yu, Jihe Zhao
Journal: Cancer Research (2011)

Abstract KLF8 is a dual transcription factor that plays a role in oncogenic transformation in mouse fibroblast cells and is highly over-expressed in human ovarian cancer. To test if KLF8 alone or together with each of the ovarian oncoprotein c-Myc, Stat3c or Akt plays a role in ovarian cell transformation, we used the immortalized normal human ovarian epithelial cell line T80 to generate stable cell lines that overexpress KLF8 alone or its combination with one of the other three oncoproteins. The Soft agar assay showed that T80/KLF8 formed significantly more colonies compared with the mock control cells, suggesting that KLF8 may play a role to transform T80 cells. Interestingly the cells expressing both KLF8 and c-Myc formed the largest amounts of colonies that were even greater than the sum of colonies formed by the cells expressing either KLF8 or c-Myc alone, suggesting a potential synergistic role of KLF8 with c-Myc. Surprisingly, however, overexpression of KLF8 alone was sufficient to induce tumorigenesis in athymic mice when the T80/KLF8 cells were injected subcutaneously (s.c.), intraperitoneally (i.p.) or orthotopically into the ovarian bursa. HE and IHC staining identified the tumors’ epithelial origin characteristic of human ovarian cancer. The s.c. growth rate of the T80/KLF8 tumors was greater than the T80/Stat3c tumors and similar to T80/Akt tumors although slower than the tumors formed by SKOV3ip1 and T80/c-Myc cells. The average survival time for the mice with the i.p. implantations was about six months for T80/KLF8 as compared to approximately two months for SKOV3ip1. These novel findings suggest that KLF8 plays a critical oncogenic role in synergy with c-Myc in the ovarian cancer progression. The mouse tumor models generated in this work provide important tools for the studies of mechanisms underlying human ovarian cancer progression. 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 4306. doi:10.1158/1538-7445.AM2011-4306
AB0474 Changes in T and B Lymphocyte Subsets with Tofacitinib do not Translate from Nonclinical Species to Humans
Authors: D.J. Ball, T.T. Kawabata, W.M. Vogel, R.J. Riese, S. Krishnaswami, M. Lamba, M.J. Brown, S.H. Zwillich
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Tofacitinib is an oral Janus kinase (JAK) inhibitor for the treatment of rheumatoid arthritis (RA). Cytokines involved in lymphocyte development, function and homeostasis (e.g., interleukin (IL)-2, -4, -7, -15, -21) signal through JAK. Repeat dose toxicology studies were conducted in rats and monkeys to support clinical development of tofacitinib. <h3>Objectives</h3> The objective of the nonclinical studies was to determine the potential toxicity of tofacitinib with a focus on the effects on lymphocyte subsets. Based on the results from these nonclinical studies, Phase 2 studies with RA patients included lymphocyte subset monitoring. <h3>Methods</h3> Absolute counts of total T cells (CD3+), CD4+ T cells, CD8+ T cells, B cells and natural killer (NK) cells were monitored in peripheral blood samples by flow cytometry. Changes from baseline values and changes relative to the vehicle/placebo treated groups were used to identify tofacitinib treatment related changes. <h3>Results</h3> Tofacitinib treatment decreased all subsets in rats (6-month study) whereas only T and NK cells were decreased in monkeys (4- and 39-week studies). In RA patients (6 and 24 weeks of exposure), NK cell counts decreased and B cell counts increased. There were transient increases in T cell counts after 2 weeks of treatment. However, at the end of studies, counts were variable but near baseline levels (Table 1). <h3>Conclusions</h3> The differences in directionality and magnitude of change, across different lymphocyte subsets, demonstrate that T cell generation and/or homeostasis is more sensitive to tofacitinib in monkeys than in humans. Based on the observed translational differences, any further studies to understand tofacitinib mechanism of action on lymphocyte subset and immune function should be conducted using human subjects rather than nonclinical species. <h3>Disclosure of Interest</h3> D. Ball Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, T. Kawabata Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, W. Vogel Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, R. Riese Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, S. Krishnaswami Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, M. Lamba Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, M. Brown Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, S. Zwillich Shareholder of: Pfizer Inc, Employee of: Pfizer Inc <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.2276
Abstract 2064: Regulation of the VHL tumor suppressor protein in hypoxia and through the cell cycle
Authors: James R. Gnarra, Julie Brown, Weijun Liu
Journal: Cancer Research (2011)

Abstract The von Hippel-Lindau (VHL) gene is a classical tumor suppressor and is inactivated in patients with von Hippel-Lindau disease, as well as the majority of patients with sporadic clear cell renal carcinoma (RCC). The VHL protein (pVHL) is an E3 ubiquitin ligase with many functions, including regulating the hypoxia response as well as microtubule stability. While the involvement of pVHL in targeting of HIF alpha subunits for ubiquitin-mediated degradation is well documented, less is understood about regulation of pVHL itself. We determined pVHL levels under normoxic (room air, 21% oxygen) and hypoxic (1% oxygen) conditions and found that pVHL levels decreased in hypoxia. VHL protein half-life was similar in cells cultured in normoxia or hypoxia, suggesting that pVHL expression is regulated through a post-transcriptional mechanism. Down regulation of pVHL in hypoxia suggests a novel and complementary mechanism to account for stabilization of HIF alpha subunits. While pVHL-negative RCC cells progress through the cell cycle when cultured in hypoxia, isogenic pVHL-expressing RCC exhibited hypoxia-induced arrest in G1 phase of the cell cycle. We also determined pVHL levels during cell cycle progression and found that pVHL levels were decreased levels during mitosis and G1. The anaphase promoting complex/cyclosome (APC/C) is an E3 ubiquitin ligase that is active during late M phase and G1 through the association with the activators, Cdh1 and Cdc20. Cdh1 and Cdc20 bind to APC/C target proteins through recognition of Destruction box consensus sequences. Such sequences are found in pVHL, suggesting that pVHL may be a target for APC/C ubiquitylation. We found that pVHL physically bound to Cdh1, that Cdh1 knockdown was associated with increased pVHL levels, that Cdh1 overexpression was associated with decreased pVHL levels and increased polyubiquitylation pVHL, and that these activities were dependent on pVHL Destruction box sequences. Our results indicate that pVHL is a novel substrate of APC/C-Cdh1. 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 2064. doi:10.1158/1538-7445.AM2011-2064
Studies in Myasthenia Gravis
Authors: Jerome J. Klein, Kermit E. Osserman
Journal: New England Journal of Medicine (1964)

RECENT interest in myasthenia gravis has centered around aspects of the disease that suggest an autoimmune pathogenesis.1 Abnormal binding of gamma globulin to muscle fibers in this disorder,2 fluctuation in serum complement level,3 presence of antinuclear antibodies in blood,4 apparent relation in some cases to polymyositis5 and to lupus erythe-matosus6 and association of myasthenia gravis with thymus abnormalities7 all support this autoimmune hypothesis. Inconsistent has been the observation made some time ago that ACTH (adrenocorticotropic hormone), administered to myasthenic patients,8 frequently results in exacerbation of muscle weakness during the period of administration9 , 10 and occasionally in improved muscle function after termination . . .
Abstract 1344: TGFß, an inflammation and immune suppressor in tumor microenvironment and progression
Authors: Li Yang, Yanli Pang, Hannah Yan, Zhaoyang Li, BR Achyut
Journal: Cancer Research (2010)

Abstract Alterations in TGFβ signaling have significant effects on tumor initiation and progression. TGFβ functions both as a tumor suppressor and as a tumor promoter. Most work so far to dissect mechanisms underlying this dual role of TGFβ has been largely focused on differential regulation of signaling pathways by tumor autonomous TGFβ signaling. Studies from our lab demonstrate that TGFβ significantly regulate inflammation in tumor microenvironment and host immune response. When TGFβ R2 receptor is deleted in mammary cancer epithelial cells, there was an increased inflammation and recruitment of Gr-1+CD11b+ myeloid cells, which leads to increased tumor invasion and metastasis. This infiltration of Gr-1+CD11b+ cells also results in increased abundance of TGFβ1 and metalloproteinase activity in tumors with Tgfbr2 deletion. Interestingly, Tumor-infiltrating Gr-1+CD11b+ cells exhibited significant elevated TGFß signaling including increased expression of RI and RII receptor, TGFß1 and TGFß3 ligands, as well as latent transforming growth factor ß binding protein when compared with normal myeloid cells. Genetic deletion of Tgfbr2 in myeloid cells significantly attenuated 4T1 breast carcinoma tumor growth and metastasis. This is accompanied with significantly increased IFNγ production in the lungs of tumor bearing mice. These data suggest that TGFß, the tumor suppressor, also functions as an inflammation and immune suppressor. TGFß signaling in host derived myeloid cells is an important mediator in tumor immune surveillance. This new understanding of TGFß in inflammation and immune response in the interface of tumor and host may provide insight information for TGFß switch from a tumor suppressor to a tumor promoter. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1344.
Case 27-1991
Authors: L. Dana DeWitt, David N. Louis
Journal: New England Journal of Medicine (1991)

Presentation of CaseA 75-year-old man was admitted to the hospital because of an impaired mental status, myoclonic jerks, and a tonic–clonic seizure.The patient was right-handed. There was a history of adult-onset diabetes mellitus that was managed with tolbutamide, peripheral neuropathy, and hypertension that was treated with diltiazem. He had discontinued smoking 30 years earlier and did not imbibe alcohol. Five years before admission the patient complained of smelling gas in his home, but representatives of the local gas company found no evidence of a leak. A computed tomographic (CT) cranial scan, performed at this hospital, showed a contrast-enhancing . . .