tbuckley/cabot-search huggingface dataset:
Abstract 3608: The effect of tobacco on prostate cancer cell aggressiveness.
Authors: Natalie Bodmer, Aishwarya Gokuldass, Theresa Kucynda, Virgilia Macias, Gnasekar Munirathinam, Andre Kajdacsy-Balla
Journal: Cancer Research (2013)

Abstract Studies have shown that smoking is associated with both greater incidence and worse outcomes of prostate cancer. The mechanism involved in this adverse effect of cigarette smoke on prostate cancer cells is not known. We hypothesized that cigarette smoke condensate (CSC) would have an effect on in vitro cell proliferation and motility. CSC is the tar phase of smoke particulate. We submitted PC-3 cells for proliferation assays after 4 and 24 hours exposure to varying concentrations of CSC. We also performed motility assays and probed for epithelial to mesenchymal transition (EMT) using immunohistochemistry on cells exposed to CSC to investigate how the action of cigarette smoke induces more aggressive behavior in cells. Results showed that CSC caused up to 83% increase in cell proliferation depending on dose and time of exposure. The antioxidant Ebselen, a scavenger of H2O2 and hydroperoxides, decreased but did not abrogate the proliferation caused by CSC. There was no effect of CSC on cell motility in Boyden chamber assays. There was also no effect of CSC on EMT, which was demonstrated by testing the immunohistochemical expression of vimentin, E-cadherin, and beta-catenin after cell exposure to CSC. In conclusion, CSC increases cell proliferation, but has no effect on motility. This action of CSC is at least in part mediated by H2O2, as shown by Ebselen inhibition of cell proliferation. The increase in proliferation could in part explain the worse prognosis of patients who smoke. Citation Format: Natalie Bodmer, Aishwarya Gokuldass, Theresa Kucynda, Virgilia Macias, Gnasekar Munirathinam, Andre Kajdacsy-Balla. The effect of tobacco on prostate cancer cell aggressiveness. [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 3608. doi:10.1158/1538-7445.AM2013-3608
Catastrophic Gastroduodenal Pneumatosis
Authors: Juan A Ramos, Emir Festic
Journal: New England Journal of Medicine (2014)

A 71-year-old man with advanced pancreatic carcinoma who was receiving chemoradiation therapy presented with diffuse abdominal pain and vomiting. An abdominal film and CT scans showed intestinal pneumatosis along the stomach and duodenum, portal venous gas, and bowel thickening.
High-level azithromycin-resistant Neisseria gonorrhoeae clinical isolate in France, March 2014
Authors: B Berçot, A Belkacem, A Goubard, F Mougari, P Sednaoui, G La Ruche, E Cambau
Journal: Eurosurveillance (2014)

We report the first case in France of a high-level azithromycin-resistant Neisseria gonorrhoeae (minimum inhibitory concentration (MIC)?=?96 mg/L) assigned to MLST7363 (NG-MAST ST6360), also resistant to ciprofloxacin and tetracycline but susceptible to ceftriaxone. The patient was a 51 year-old heterosexual man who returned following 1g azithromycin monotherapy. Mechanisms of azithromycin resistance were a C2599T mutation in the four copies of the rrl gene and a novel mutation in the promoter of the mtrR gene.
Abstract 3446: Inhibition of EZH2 suppresses medulloblastoma cell growth
Authors: Irina N. Alimova, Sujatha Venkataraman, Peter Harris, Rajeev Vibhakar
Journal: Cancer Research (2011)

Abstract EZH2 (enhancer of zeste homologue2) is a polycomb group protein that mediates repression of gene transcription through its Histone 3 Lysine 27methyltransferase activity. EZH2 is highly expressed in many cancers including metastatic prostate cancer, breast cancer, and glioblastoma multiform. EZH2 expression is associated with tumor cell proliferation, invasive growth and aggressive cancer phenotypes. The fact that EZH2 increases tumor cell proliferation and aggressive subgroups in several cancers may be of practical interest because the polycomb proteins have been suggested as candidates for targeted therapy. We found EZH2 expression to be increased in medulloblastoma when compared to normal cerebellum. Inhibition of EZH2 by RNAi in medulloblastoma cells resulted in suppression of cell growth. To further examine this phenotype we used a global histone methylation inhibitor, 3-Deazaneplanocin A (DZNep). DZNep preferentially inhibits H3 Lys27me via EZH2. DZNep showed a dose dependent, anti-proliferative and anti-clonogenic activity in medulloblastoma cells. Synergetic effect was shown in cells transfected with shEZH2 and treated with DZNEP. Furthermore DZNep treatment decreased EZH2 protein levels. We found that DZNep induced differentiation of mouse neural stem cells even when they are grown in proliferation medium. Most critically transformation of these neural stem cells was significantly attenuated by shEZH2 and DZNep. Our results suggest that EZH2 is a target for medulloblastoma treatment and that DZNep is an excellent candidate for further testing as a therapeutic candidate. 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 3446. doi:10.1158/1538-7445.AM2011-3446
Acute Lupus Erythematosus with Laryngeal Involvement
Authors: Dante G. Scarpelli, Francis W. McCoy, John K. Scott
Journal: New England Journal of Medicine (1959)

THE early clinical descriptions of lupus erythematosus by Biett1 in 1838 and Hebra2 in 1845 characterized the disease solely as a dermatologie entity. However, in 1872 Kaposi3 stressed the systemic nature of the disease and pointed out that it may terminate fatally. Since then the protean manifestations and gravity of lupus have been repeatedly emphasized by numerous authors.4 5 6 7 8 Although laryngeal edema is frequently seen in hyperergic diseases, to our knowledge laryngeal involvement by lupus erythematosus has not been previously described. The present report describes a patient with acute lupus erythematosus whose death was due to laryngeal edema as a result . . .
Suppression of Allergic Airway Inflammation by Low Dose, Intranasally Administered Der p 1 Derived Peptides, in a Murine Model of House Dust Mite Allergy
Authors: D.M. Moldaver, M.S. Bharhani, J. Wattie, R.P. Hafner, M. Inman, M. Larche
Journal: Journal of Allergy and Clinical Immunology (2012)
COSTS AND IN-HOSPITAL OUTCOMES OF TRANSCATHETER VERSUS SURGICAL AORTIC VALVE REPLACEMENT IN COMMERCIAL CASES USING A PROPENSITY SCORE MATCHED MODEL
Authors: Robert M. Minutello, Shing-Chiu Wong, Rajesh Swaminathan, Dmitriy Feldman, Arash Salemi, Harsimran Singh, Geoffrey Bergman, Luke Kim
Journal: Journal of the American College of Cardiology (2015)
1361 LACK OF ASSOCIATION BETWEEN METABOLIC SYNDROME AND NON-ALCOHOLIC FATTY LIVER DISEASE IN PATIENTS WITH PNPLA3 M148M GENE VARIANT
Authors: L. Polimeni, M. Del Ben, D. Salzano, A. Di Costanzo, L. D'Erasmo, F. Baratta, M. Arca, F. Angelico
Journal: Journal of Hepatology (2013)
The serum vitamin D level is inversely correlated with nonalcoholic fatty liver disease
Authors: Goh Eun Chung, Donghee Kim, Min-Sun Kwak, Jong In Yang, Jeong Yoon Yim, Seon Hee Lim, Mustafa Itani
Journal: Clinical and Molecular Hepatology (2016)

Background/Aims: A low vitamin D level has been associated with metabolic syndrome and diabetes. However, an association between a low vitamin D level and nonalcoholic fatty liver disease (NAFLD) has not yet been definitively established. This study aimed to characterize the relationship between a vitamin D level and NAFLD in Korea. Methods: A cross-sectional study involving 6,055 health check-up subjects was conducted. NAFLD was diagnosed on the basis of typical ultrasonographic findings and a history of alcohol consumption. Results: The subjects were aged 51.7±10.3 years (mean±SD) and 54.7% were female. NAFLD showed a significant inverse correlation with the vitamin D level after adjusting for age and sex [odds ratio (OR)=0.85, 95% confidence interval (CI)=0.75–0.96]. The age- and sex-adjusted prevalence of NAFLD decreased steadily with increasing vitamin D level [OR=0.74, 95% CI=0.60–0.90, lowest quintile (≤14.4 ng/mL) vs highest quintile (≥28.9 ng/mL), p for trend <0.001]. Multivariate regression analysis after adjusting for other metabolic factors revealed that NAFLD showed a significant inverse correlation with both the vitamin D level (>20 ng/mL) [OR=0.86, 95% CI=0.75-0.99] and the quintiles of the vitamin D level in a dose-dependent manner (p for trend=0.001). Conclusions: The serum level of vitamin D, even when within the normal range, was found to be inversely correlated with NAFLD in a dose-dependent manner. Vitamin D was found to be inversely correlated with NAFLD independent of known metabolic risk factors. These findings suggest that vitamin D exerts protective effects against NAFLD. Keywords: Fatty liver; Vitamin D; Metabolic factor
Incidental Detection of Skeletal Uptake on Tetrofosmin Cardiac Imaging in a Patient with Multiple Myeloma
Authors: MITSUYOSHI HADASE, TATSUYA KAWASAKI, YURI KAMITSUJI, TOMOHIKO SAKATANI, TADAAKI KAMITANI, SHINGO KAWASAKI, HIROKI SUGIHARA
Journal: Clinical Nuclear Medicine (2003)

HADASE, MITSUYOSHI M.D.; KAWASAKI, TATSUYA M.D.; KAMITSUJI, YURI M.D.; SAKATANI, TOMOHIKO M.D.; KAMITANI, TADAAKI M.D.; KAWASAKI, SHINGO M.D.; SUGIHARA, HIROKI M.D. Author Information
Industry and Government Meet in First Collaborative Forum
Authors: K. Smigel
Journal: JNCI Journal of the National Cancer Institute (1988)

Journal Article Industry and Government Meet in First Collaborative Forum Get access Kara Smigel Kara Smigel Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 80, Issue 20, 21 December 1988, Pages 1587–1588, https://doi.org/10.1093/jnci/80.20.1587 Published: 21 December 1988
Abstract 3368: Efficient delivery of prostate cancer gene therapy via adipose-derived mesenchymal stem cells <i>in vivo</i>
Authors: Olga Zolochevska, Marxa L. Figueiredo
Journal: Cancer Research (2012)

Abstract It is critical to develop new therapeutic approaches for prostate cancer, since there is no effective treatment for patients in the advanced stages of this disease. And although many gene therapy approaches have been evaluated to date, clinical responses unfortunately remain poor. We have examined the potential of developing more effective cell-based gene therapies for preventing prostate cancer progression, using adipose-derived mesenchymal stem cells (ASC) as vehicles. The present study reports promising preliminary observations using this novel gene therapy modality. ASCs can be isolated using simpler methods as compared to those involving bone marrow mesenchymal cells, and are much more easily expanded at early passage numbers to therapeutic quantities. And since current techniques allow isolation of ASCs from an individual's own adipose tissue, this could help prevent immune reaction, suggesting that ASCs could be far more efficient as a gene delivery vehicle than viral vectors currently in clinical trials. In this study we have examined the potential of new antiangiogenesis and proapoptotic therapies delivered by ASCs and evaluated their ability to reduce prostate tumor growth rate in vitro and in vivo. We expressed in ASCs several secreted antitumor gene therapies (PEDF, Mda7, or IFNb), and all were found to be highly effective in almost complete prevention of tumor progression in vivo using prostate cancer xenograft models. Overall, ASC-delivered PEDF prevented HUVEC tube formation in vitro and induced strong apoptosis of cocultured cancer cells, suggesting a potential bystander effect that might be useful for therapeutic applications. Similar antitumor findings were observed when Mda7 or IFNb were delivered by ASCs, with induction of strong cell cycle arrest, and viability reduction by an increase in the apoptosis of cocultured tumor cells as assessed by Caspase 3/7 detection. The transgene expression was overall non-toxic and did not appear to interfere with the normal differentiation potential of ASCs (osteogenesis or adipogenesis). Therefore, this novel cellular delivery method for gene therapy appears to be effective and highly promising for translational applications. 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 3368. doi:1538-7445.AM2012-3368
Sestamibi Uptake in Brown Tumor Simulating a Lung Mass
Authors: ILONA GINSBERG, ADAM FEDERMAN, HELEN KIM, LEONARD M. FREEMAN
Journal: Clinical Nuclear Medicine (1997)

A 28-year-old man with severe secondary hyperparathy-roidism and on hemodialysis for 11 years underwent a Tc-99m sestamibi study for preoperative localization of hyperfunctioning parathyroid glands. Laboratory data included a serum calcium of 10.8 mg/100 mL and a parathormone level of 1722 pg/mL. There were no palpable neck masses. In addition to bilateral localization of hyperplastic parathyroid glands, the scintigram showed an intense focus of uptake in the left hemithorax, suggesting a lung mass. Radiographic correlation revealed the MIBI uptake to be in a large expansile lytic lesion of the second rib consistent with a brown tumor.
A dual-design expandable colorectal stent for malignant colorectal obstruction: results of a multicenter study
Authors: H.-Y. Song, J. Kim, J. Shin, H.-C. Kim, C. S. Yu, J.-C. Kim, S.-G. Kang, C. Yoon, J. Lee, J. H. Koo, K.-H. Lee, J.-K. Kim, D. Kim, T.-B. Shin, G.-S. Jung, Y.-M. Han
Journal: Endoscopy (2007)

See also: Commentaire de travail de H.-Y. Song et al., pp. 448Endoscopy 2007; 39(05): 485-486DOI: 10.1055/s-0032-1306934
Abstract P3-06-22: Mechanisms behind trastuzumab resistance as neoadjuvant therapy in HER2-positive operable breast cancer
Authors: H Jinno, T Sato, T Hayashida, M Takahashi, S Hirose, Y Kitagawa
Journal: Cancer Research (2012)

Abstract Background: The development of trastuzumab has had a major impact in treatment of breast cancer patients with HER2 overexpression. Despite clinical usefulness, intrinsic or acquired resistance to trastuzumab is a common clinical phenomenon. However, the mechanisms of resistance to trastuzumab have not been fully elucidated. Potential mechanisms include aberrant downstream signaling caused by loss of PTEN and/or PIK3CA mutation, alternative signaling from IGF-1R and masking with MUC4. The objective of this study was to determine the possible mechanisms of resistance to trastuzumab as neoadjuvant therapy in women with HER2-overexpressing operable breast cancer. Patients &amp; methods: Patients with operable breast cancer received 12 cycles of weekly paclitaxel (80 mg/m2 IV) plus weekly trastuzumab (4mg/kg loading dose followed by 2 mg/kg IV) for 12 weeks before surgery. All tumors were HER2-positive by immunohistochemistry (IHC) or fluorescence in situ hybridization. Expressions of ER, PgR, Ki67, PTEN, phosphorylated IGF-1R (pIGF-1R) and MUC4 were performed by IHC in core needle biopsy samples at baseline. ER and PgR status was assessed using Allred score. For Ki67 labeling index, a total of 400 cells were counted from three consecutive high-power magnifications. PTEN, pIGF-1R and MUC4 expression level was scored semiquantitatively based on staining intensity. PIK3CA mutation status was evaluated by sequencing of PIK3CA exons 9 and 20 using PCR amplification and direct sequencing. pCR was defined as no residual invasive carcinoma in the breast. Results: Thirty-seven patients were enrolled and assessable for clinical and pathologic responses. ER and PgR were positive in 18 (48.6%) and 16 (43.2%) patients, respectively. The overall response rate was 86.5%, including a complete response in 21 patients and a partial response in 11 patients. The pCR rate was 48.6% (18/37). Negative, moderate and strong membranous expression of MUC4 was observed in 3 (8.1%), 18 (48.6%) and 12 (32.4%) patients, respectively. Membranous staining for pIGF1-R was negative in 24 (64.9%) patients. PTEN loss was observed in 33.3% (8/24) of the tumor examined. PIK3CA sequence analysis of the 13 tumors identified 2 mutations in exon 20 and 2 mutations in exon 9, corresponding to a PIK3CA mutation frequency of 30.8%. MUC4 and pIGF1-R status did not affect the pCR rate. PTEN loss and/or PIK3CA mutation were not significantly associated with pCR rate. pCR rate was significantly correlated with PgR negativity (p = 0.004) and higher Ki67 (p = 0.01). Conclusions: These data indicate that aberrant downstream signaling caused by loss of PTEN and/or PIK3CA mutation, alternative signaling from IGF-1R and masking with MUC4 were not important mechanisms of resistance to trastuzumab. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P3-06-22.
Abstract 158: Expression of miR-205 is significantly associated with prognosis of endometrial cancer
Authors: Mihriban Karaayvaz, Cecilia Zhang, Saira Mehmood, Penelope Georgakopoulos, Stephanie Burke, Kenneth Shroyer, Sharon Liang, Jingfang Ju
Journal: Cancer Research (2011)

Abstract Background: microRNAs (miRNAs) have emerged as key regulators of gene expression, and their altered expression has been associated with tumorigenesis and tumor progression. As a result, miRNAs represent important diagnostic biomarkers for the advancement of cancer and potential therapeutic approaches. They may be up-regulated or down-regulated in various tumor types, thus act as oncogenes or tumor suppressors. Although accumulating evidence suggests the role of aberrant miRNA expression in endometrial carcinogenesis, there is still limited data available about the endrometrial miRNAs. Endometrial cancer is characterized by frequently infiltrating tumors, and one of the most important molecular alterations in this process is through epithelial-mesencymal transition (EMT). Several studies implicated the role of miRNAs targeting the critical players during EMT. The goal of this study is to investigate the clinical utility of selected key miRNAs in archival FFPE tissue samples of patients with endometrial cancer. In this study, the expression of miR-26a, miR-205, miR-200c, miR-192, miR-215, let-7g, miR-21, miR-181b were quantified from 20 stage I, 2 stage II, 5 stage III, 8 stage IV endometrial cancer patients (endometrioid-type endometrial cancer (EEC), endometrial serous carcinoma(ESC), clear cell carcinoma(CCC) undifferentiated carcinoma (UDC), malignant mullerian mixed tumor (MMMT)) with up to 15 years clinical follow up information. Methods: Using archival FFPE tissues, areas of tumor and normal tissues were identified according to the corresponding hematoxylin and eosin stained sections, and cores of 1.5 mm in diameter were extracted. Total RNAs were isolated from 35 paired endometrial tumor and adjacent normal tissue specimens by using Trizol based approach. The expression levels of miRNAs were quantified by using real-time qRT-PCR analysis. Results: The expression of miR-205 (p=0.0002) and miR-200c (p&amp;lt;0.0001) were significantly elevated in endometrial cancer tissue specimens when compared to adjacent normal tissues. Kaplan-Meier survival analysis indicated that low levels of miR-205 expression (hazard ratio, 0.309; log rank test, p=0.018) is closely associated with better patient's overall survival. Conclusions: miR-205 holds a great potential as a prognostic biomarker in endometrial cancer. 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 158. doi:10.1158/1538-7445.AM2011-158
AB0551 The use and effectiveness of rituximab in patients with rheumatoid arthritis observational study: Corrona registry:
Authors: L. Harrold, A. John, G. Reed, W. Reiss, R. Magner, C.Y. Chung, K.C. Saunders, J.M. Kremer, J.D. Greenberg
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Little is known regarding the use and effectiveness of rituximab (RTX) in patients with rheumatoid arthritis (RA) in the United States. Using a cohort of 26,877 patients with RA from 28-Feb-2006– 05-Dec-2011 from a multicenter observational registry within the U.S. (Consortium of Rheumatology Researchers of North America: CORRONA) we evaluated the use and effectiveness of RTX. <h3>Methods</h3> Using data from CORRONA, we identified RA patients that initiated RTX with prior anti-TNF exposure (baseline visit) and were not in remission based on the Clinical Disease Activity Index (CDAI) at the time of initiation, with a follow-up visit at 1 year (±3 month) and at least 1 additional visit between baseline and 1 year visits. Outcomes assessed at 1 year included change in CDAI and the Disease Activity Score-28 joint (DAS-28), as well as achievement of remission (based on CDAI and DAS28). Rates of adverse events were identified. <h3>Results</h3> We identified 265 patients that used RTX and met study inclusion criteria. Most patients were female (80%), rheumatoid factor seropositive (75%) with a median age of 57 (IQR 50-65), median disease duration of 13 years (IQR 7-22), and moderate to severe disease activity (median CDAI 22; IQR 13-33) at baseline. Most had prior exposure to nonbiologic disease modifying anti-rheumatic medications (DMARDs) (median 3; IQR 2-5) and biologics (median 2; IQR 1-3). RTX was commonly prescribed with a nonbiologic DMARD (77%) and prednisone (42%). Over the 1-year follow-up (outcomes in Table 1), 67% were retreated with RTX and 17% received a subsequent non-RTX biologic. Rates of cardiovascular events, serious infection, and malignancy were 1.9 (95% CI 0.6-4.0), 1.6 (95% CI 0.5-4.9), and 1.5 (95% CI 0.6-4.0) per 100 person-years, respectively. <h3>Conclusions</h3> Patients initiating RTX had very active disease with prior exposure to several nonbiologic and biologic agents. Use of RTX was shown to be effective with a safety profile comparable to previous RTX clinical trials. <h3>Disclosure of Interest</h3> L. Harrold Consultant for: CORRONA, A. John Employee of: Genentech, Inc, G. Reed Grant/Research support from: CORRONA, Consultant for: CORRONA, Employee of: University of Massachusetts Medical School, Paid Instructor for: Harvard Medical School, W. Reiss: None Declared, R. Magner: None Declared, C. Chung: None Declared, K. Saunders Employee of: CORRONA, J. Kremer Shareholder of: CORRONA, Grant/Research support from: Abbott, Amgen, AstraZeneca, BMS, Genentech, Lilly, Pfizer, Consultant for: Amgen, Genentech, Lilly, Pfizer, Employee of: CORRONA, Speakers Bureau: Abbott, Amgen, BMS, Pfizer, J. Greenberg Shareholder of: CORRONA, Consultant for: AstraZeneca, Novartis, Pfizer, CORRONA