tbuckley/cabot-search huggingface dataset:
Abstract 3951: Expression of SIRT1 and p27 during progression of human cervical cancer
Authors: Sapna Singh, P. Uday Kumar, Suresh Thakur, Poongothai AR, Gayatri Ramakrishna
Journal: Cancer Research (2012)

Abstract Recent studies point to a close connection between cancer and ageing. Cellular senescence when initiated early in cancerous cells results in growth suppression due to permanent growth arrest. Sirtuins, belonging to family of the NAD-dependent deacetylases, play a crucial role in cellular metabolism and organismal ageing/ longevity. However, the role of human Sirtuin isoforms in malignancies and cellular senescence is still not clearly discernible. The present study is therefore designed to evaluate the correlation of SIRT1 expression with proliferation marker Ki-67, and growth arrest/senescence marker p27, during cervical cancer progression. The expression was evaluated by immunohistochemistry in 70 formalin fixed archival human cervical samples: normal/ASCUS (N= 20), squamous intraepithelial lesions (SIL N=20) and invasive squamous cell carcinoma (SCC, N= 30 samples). All the intraepithelial lesions and SCC cases were positive for human papilloma virus as detected by in-situ hybridization. The SIRT1 expression was either absent or feeble in cytoplasm of normal/ASCUS cervical epithelium, while a progressive increase in its expression was noted in 65% of preneoplastic lesions (SIL). Intriguingly, the invasive carcinoma showed heterogeneous pattern for both expression and localization of SIRT1: ranging from negative to strong expression levels and mixed localization pattern in cytoplasm only or both in nucleus and cytoplasm. The growth arrest/senescence marker p27 showed elevated level of expression in SIL cases compared to SCC (75%). Interestingly, the increased nucleo-cytoplasmic expression pattern of SIRT1 correlated well with the increased expression of p27 in the intraepithelial preneoplastic lesion. In conclusion, our results suggest activation of growth suppressive pathways by SIRT1-p27 regulation, atleast in the in preneoplastic lesions of cancer cervix which may help retard its progression to invasive cancer. 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 3951. doi:1538-7445.AM2012-3951
Corneal-Flap Dehiscence after Screwdriver Trauma
Authors: Nelson A Rodríguez, Francisco J Ascaso
Journal: New England Journal of Medicine (2013)

A 29-year-old man presented with blurred vision, photophobia, and pain after trauma to his left eye caused by a screwdriver. He had a history of moderate myopia (visual acuity, 20/25) and had undergone uneventful bilateral laser-assisted in situ keratomileusis (LASIK) 10 years previously. On examination, he had a 180-degree traumatic corneal flap dislocation with an inverted tear in the temporal cornea (Panel A, fluorescein dye). After repositioning of the flap, a disposable contact lens, used as a therapeutic bandage, was placed on the cornea. Topical antibiotics and glucocorticoids were administered. One month postoperatively, his previous visual acuity had recovered and . . .
P4-01-21: An Estrogen-Inducible Transcription Factor FOXP1 Promotes Estrogen-Dependent Cell Proliferation of Breast Cancer Cells and Is Associated with 5-Year Disease-Free Survival in Patients with Tamoxifen-Treated Breast Cancer.
Authors: T Shigekawa, N Ijichi, K Ikeda, K Horie-Inoue, C Shimizu, S Saji, K Aogi, H Tsuda, A Osaki, T Saeki, S Inoue
Journal: Cancer Research (2011)

Abstract Estrogen signaling pathways are involved in the growth and development of breast tumors through the activation of estrogen receptor a (ERα). ERα is expressed in most breast cancers and involves in estrogen-dependent proliferation by acting as transcription factors activating the expression of target genes. Various coregulators and transcription factors are associated with ERα-mediated transcriptional control of target genes. Therefore, a comprehensive understanding of estrogen signaling pathways in breast cancer is required for both treatment and diagnosis of the disease. Forkhead box P1 (FOXP1) is a member of the forkhead box transcription factor family and has been reported to be associated with various types of tumors. Here, we investigated the expression pattern of FOXP1 by immunohistochemistry in a series of 133 invasive breast cancers and compared it with clinicopathological factors. The expression of FOXP1 was detected in nuclei in 89 cases (67%) and correlated positively with tumor grade and hormone receptor status, including ERα and progesterone receptor (PgR), and negatively with pathological tumor size (pT). And in ERα-positive MCF-7 breast cancer cells, we demonstrated that FOXP1 mRNA was upregulated by estrogen and that ERα recruitment to ER binding sites within the FOXP1 gene region identified by ChIP-chip analysis was increased. We also demonstrated that proliferation of MCF-7 cells was increased by exogenously transfected FOXP1 and decreased by FOXP1-specific siRNA. Moreover, in MCF-7 cells, FOXP1 enhanced estrogen response element (ERE)-driven transcription. Finally, FOXP1 immunoreactivity was significantly more elevated in relapse-free breast cancer patients treated with tamoxifen than in relapse patients treated with it. Taken together, these results suggest that FOXP1 plays an important role in proliferation of breast cancer cells by modulating estrogen signaling and that FOXP1 immunoreactivity might be associated with the estrogen dependency of breast cancer clinically, which may predict favorable prognosis in the patients treated with tamoxifen. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P4-01-21.
615 EARLY USE OF TIPS DECREASES REBLEEDING AND IMPROVES THE SURVIVAL IN CIRRHOTIC PATIENTS OF EVL ULCER BLEEDING: A PROSPECTIVE STUDY
Authors: H.K. Garg, A. Chaudhary, A. Mukund, M. Kumar, R. Kumar, V. Bhatia, S.K. Sarin
Journal: Journal of Hepatology (2013)
TCTAP A-111 Development of an ECG-Independent Algorithm for the Calculation of Instantaneous Wave-Free Ratio (iFR): A Step Towards Further Simplification of Physiological Lesion Assessment
Authors: Ricardo Petraco, Sayan Sen, Sukhjinder Nijjer, Rasha Al-Lamee, Darrel Francis, Justin E. Davies
Journal: Journal of the American College of Cardiology (2015)
P14 Comparison of two interferon-gamma release assays (QuantiFERON-TB Gold In-Tube and T-SPOT.TB) in screening for latent tuberculosis infection (LTBI) among HIV-infected adults attending an inner London HIV clinic
Authors: R. F. Miller, T. Mahungu, M. Young, D. Mercey, S. Morris-Jones, P. Benn
Journal: Thorax (2011)

<h3>Background</h3> There is a paucity of data on the performance of interferon-gamma release assays (IGRAs) in screening HIV-infected patients for latent tuberculosis infection (LTBI). <h3>Methods</h3> Prospective evaluation of two IGRAs [QuantiFERON-TB Gold In-Tube (QuantiFERON) and T-SPOT.TB] for screening HIV-infected patients attending an inner city clinic with a high local prevalence of tuberculosis (TB). For each patient we recorded their gender, ethnicity, country of birth, BCG status and prior treatment for TB, CD4 count, plasma HIV load and receipt of antiretroviral therapy (ART). All patients had both IGRAs (results = positive, negative, or indeterminate) and a chest radiograph. <h3>Results</h3> Of 117 patients, 91 (78%) were men, 48 (41%) were white British, 29 (24.8%) black African, 21 (18%) European, 7 (6%) South American and 12 (10%) from other ethnic groups. Individuals born outside the UK had been resident in the UK for a median of 10 years (range 3–45). 91/117 (78%) had previously received BCG and 14/117 (12%) had been treated for TB a median of 9.5 years (range 3–13) previously. Of 106 (90.6%) receiving ART, 105 (99%) had an undetectable plasma HIV load) and the median CD4 count was 550 (range 30–1250). Among those not receiving ART the median (range) plasma HIV load and CD4 count was 21 000 copies/ml (590–160 000) and 520 (250–950) respectively. IGRA results are shown in the Abstract P14 table 1. Overall there was good concordance (92.3%) between the two IGRAs. Among 14 patients previously treated for TB, 10 (71.4%) had previously received BCG; 4/14 (28.6%) had a positive IGRA (3/4 both IGRAs were positive, 1/4 QuantiFERON was positive). Of those previously treated for TB with negative IGRAs (n=10) all had an undetectable HIV viral load, 9/10 had been on ART &gt;2 years and median CD4 count was 670 (range 180–1250). Five other patients with CD4 &lt;200 had negative IGRAs; all had previously received BCG. Mantoux testing, done in 2 of the 5, was negative. <h3>Conclusion</h3> Overall there was a high concordance between the two IGRAs. Four of the 12 with positive IGRA results had a past history of TB making interpretation uncertain. The low rate of indeterminate results likely reflects the high CD4 counts among this patient group.
Abstract 3689: Association of thymidylate synthase gene polymorphisms with efficacy and toxicity of oral fluoropyrimidine based chemotherapy in advanced gastric cancer
Authors: Gun Min Kim, Hei-Cheul Jeung, Woo Sun Kwon, Sun Young Rha, Hyo Song Kim, Inkyung Jung, Byung-Ho Nam, Kyung Hee Lee, Hyun Cheol Chung
Journal: Cancer Research (2012)

Abstract Purpose: Oral fluoropyrimidines (S-1 or capecitabine) are metabolized by different enzymes. We evaluated the association between polymorphisms of cytochrome P450 2A6 (CYP2A6), carboxylesterase 2(CES 2), thymidylate synthase (TS), and excision repair cross complementation group 1 (ERCC1) and toxicity of advanced gastric cancer patients treated with oral fluoropyrimidine based chemotherapy. Methods: A total of 123 patients received S-1 80mg/m2 or capecitabine 2000 mg/m2 plus oxaliplatin 130 mg/m2 for advanced gastric cancer. We analyzed polymorphisms of CYP2A6, CES 2, TS and ERCC1 by using genomic DNA extracted from prospectively collected peripheral blood sample. Associations between polymorphisms and toxicity of these patients treated with oral fluoropyrimidines based chemotherapy were evaluated individually. Results: Patients who were 2R/3R for the double repeat in the TS promoter region had more toxicity of oral fluoropyrimidines. Patients with a 2R/3R and 2R/2R or 3R/3R genotype had a grade 2 or more gastrointestinal toxicity rate of 50 and 22%, respectively (P = .049). Response rate was higher in patients with a 2R/3R than those with a 2R/2R or 3R/3R (50% vs. 32%, P = .082). Polymorphisms of CYP2A6, CES 2, and ERCC1 were not associated with efficacy and toxicity of oral fluoropyrimidine based chemotherapy for advanced gastric cancer. Conclusion. This study demonstrated that TS genotyping could be of help in predicting toxicity to oral fluoropyrimidine based chemotherapy in advanced gastric cancer patients. 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 3689. doi:1538-7445.AM2012-3689
Abstract 1972: Nicotine regulates DNA-binding protein inhibitor (Id1) through a Src-dependent pathway promoting tumorigenic properties and chemoresistance in pancreatic adenocarcinoma
Authors: José G. Treviño, Smitha R. Pillai, Sateesh S. Kunigal, Srikumar P. Chellappan
Journal: Cancer Research (2011)

Abstract Nicotine, an addicting component of an established risk factor (tobacco) for pancreatic cancer is identified as a tumor promoter potentially acting through activation of oncogenes such as Src, a non-receptor protein tyrosine kinase. Recent studies from our laboratory have shown that the Id1 transcription factor (inhibitor of DNA binding/Differentiation) is induced by nicotine in NSCLC cells. Id1 has been shown to play a role in tumor progression by promoting angiogenesis, invasion, and chemoresistance. Further, Src and its family of non-receptor protein tyrosine kinases (SFKs) play a role in angiogenesis, tumor progression, and chemoresistance. Based on our observations on NSCLC cells, we hypothesize nicotine-induces Id1 expression in a Src-dependent fashion and promotes tumorigenesis and chemoresistance. Protein analysis, mRNA expression, and further experiments were determined in a panel of pancreatic cancer cells, PANC-1, Mia-Paca-2, L3.6pl, and L3.6plGemRes by western blot analysis and RT-PCR respectively. Our results demonstrate that stimulation with nicotine (1 µM), and activation of nAChR, resulted in phosphorylation of Src, indicative of activation, and its family of kinases. Nicotine also induced Id1 expression at similar concentrations. Inhibition of SFK activity with Dasatinib (500nM) did not allow serum or nicotine-induced SFK activity and subsequent Id1 expression. Specific inhibition of c-Src expression with short-interfering RNA (siRNA) decreased constitutive and nicotine-induced Id1 expression and depletion of Id1 expression by siRNA or short-hairpin RNA (shRNA) significantly reduced the proliferative (80%) and invasive property (75%) of pancreatic cancer cells, a property often mediated by Src. Additionally, inhibition of Src and Id1 expression in innate or established gemcitabine resistant cancer cells resulted in gemcitabine sensitization at IC50, 250 ng/ml. To determine if nicotine contributes to gemcitabine chemoresistance potentially through a Src-dependent Id1 signaling axis, we exposed gemcitabine-sensitive cells to nicotine with subsequent exposure to gemcitabine. Nicotine promoted a 2-fold increase in cell proliferation and a 4.5-fold reduction in apoptosis. Further, nicotine induced phosphorylation of key Src-dependent signaling enzymes involved in proliferation and apoptosis, Erk1/2 and Akt respectively. We demonstrate that Id1, by a nicotine promoting Src-dependent pathway, contributes to signaling pathways involved in tumor progression and establishment of a chemoresistant phenotype in pancreatic 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 1972. doi:10.1158/1538-7445.AM2011-1972
Abstract 4797: A member of the SLC25 family is epigenetically inactivated in human gliomas and suppresses cell growth <i>in vitro</i>
Authors: Anke Waha, Jörg Felsberg, Matthias Simon, Wolfgang Hartmann, Torsten Pietsch, Andreas Waha
Journal: Cancer Research (2011)

Abstract In a genome-wide screen using DMH (differential methylation hybridization) we have identified a CpG rich fragment upstream of the coding region of a member of the solute carrier family 25 (SLC25) that showed hypermethylation in gliomas compared to normal white matter controls. Pyrosequencing analysis was performed to confirm the methylation status of this gene in 76 gliomas and 7 glioma cell lines. Hypermethylation was detected in 14% of primary glioblastomas, 62% of secondary glioblastomas, 27% of anaplastic astrocytomas, 0.7% low-grade diffuse astrocytomas and in 71% of glioma cell lines. None of three investigated white matter samples showed hypermethylation of the investigated region. Hypermethylation of the SLC25 member was significantly more frequent in secondary glioblastomas compared to primary glioblastomas (P = 0.0066). Furthermore, the investigation of matched low grade and high grade glioma tissues revealed that this hypermethylation was associated with progression. Expression of the SLC25 member was investigated by real-time reverse transcription-PCR and found to be down regulated in primary and secondary glioblastomas as well as in anaplastic and low-grade astrocytomas when compared to white matter and total brain tissue. After treatment of glioma cell lines with 5-aza-2’-deoxycytidine, the transcription was restored. In functional investigations overexpression of exogenous SLC25 family member in glioblastoma cell lines lead to a significant reduction in focus formation. In summary, we describe for the first time the epigenetic silencing of a nuclear encoded member of the mitochondrial transporter family (SLC25) in high grade malignant human brain tumors and provide functional proof for its growth suppressive activity on glioma cells in vitro. 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 4797. doi:10.1158/1538-7445.AM2011-4797
Implantable Left Ventricular Assist Devices
Authors: Daniel J. Goldstein, Mehmet C. Oz, Eric A. Rose
Journal: New England Journal of Medicine (1998)

Congestive heart failure affects about 1 percent of adults in the United States1 and is a contributing factor in over 250,000 deaths annually.2 It is diagnosed in 400,000 Americans each year3 and is the primary diagnosis for over 900,000 hospitalizations per year.4 In 1990 the age-adjusted death rate from congestive heart failure was 106.4 per 100,000,5 more than that from breast cancer and the acquired immunodeficiency syndrome combined.6,7 The median survival after diagnosis is 1.7 years in men and 3.2 years in women, with a 5-year survival rate of less than 50 percent.8 Even though medical therapies have improved . . .
ATM Mutations in Major Stereotyped CLL Subsets: Enrichment in Subset #2 is Associated with Unfavourable Outcome
Authors: Veronika Navrkalova, Emma Young, Panagiotis Baliakas, Lenka Radova, Karla Plevova, Lesley-Ann Sutton, Larry Mansouri, Viktor Ljungstrom, Stavroula Ntoufa, Zadie Davis, Gunnar Juliusson, Karin E Smedby, Chrysoula Belessi, Panagiotis Panagiotidis, Frederic Davi, Anton W. Langerak, Paolo Ghia, Jonathan C Strefford, David G Oscier, Kostas Stamatopoulos, Sarka Pospisilova, Richard Rosenquist, Martin Trbusek
Journal: Blood (2015)
Abstract 4280: Genome-wide expression and methylation analysis in CD31+ cells from African American and Caucasian American benign and malignant prostate tissue
Authors: Wei Luo, Kristin K. Deeb, Song Liu, Yingyu Ma, Carl D. Morrison, Donald L. Trump, Candace S. Johnson
Journal: Cancer Research (2012)

Abstract Prostate cancer exhibits striking racial disparity; African American (AA) men have a markedly higher risk of being diagnosed and of dying of prostate cancer compared to Caucasian American (CA) men. This disparity may be due to biologic differences associated with race or to sociologic factors, such as economic disparities or differences in access to care or interactions of all these factors. Differences in tumor gene expression and methylation might be associated with the poorer prognosis seen among AA men and may contribute to better understanding of these disparities and the delineation of new therapeutic targets. In order to study the effect of the tumor microenvironment on endothelial cells found in tissue from AA and CA patients with prostate cancer, we first established a method for the isolation of the endothelial cells from malignant and benign prostate tissue obtained at prostatectomy. We then conducted a pilot study of transcriptome and methylome analysis in 5 pairs of CD31+ endothelial cells isolated from paired samples of benign and malignant tissue from AA and CA patients with prostate cancer. We have identified 2,096 and 920 differentially expressed transcripts for the tumor versus normal in AA and CA group, respectively. However, only 140 transcripts are shared. Furthermore, a total of 2,248 transcripts show different level of expression change for tumor versus normal in samples with AA origin compared to samples with CA origin. Genome-wide DNA methylation profiling in the same endothelial samples have identified 18,093 differentially methylated loci in AA group, and 12,372 differentially methylated loci in CA group. Only a total of 1,324 loci are shared. Remarkably, there are a total of 20,164 loci with different level of methylation change for tumor versus normal in AA group compared to CA group. Integrative analysis of transcriptome and methylatome data showed that a large percentage of differentially expressed genes have loci whose methylation change is inversely correlated with gene expression change, and vice versa. Taken together, our pilot data, while preliminary, suggest the possibility that there is a potential racial difference in terms of differential expression and methylation between CA and AA endothelial cell populations. Future large studies are warranted to confirm our findings and further explore the role of race disparity in the delineation of novel therapeutic targets to be utilized clinically for prostate cancer. 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 4280. doi:1538-7445.AM2012-4280
Tc-99m HMPAO White Blood Cell SPECT of an Enterovesical Fistula Complicating Crohn’s Disease
Authors: Jeong-Ho Kim, In Young Hyun, Young Soo Kim, Ze Hong Woo
Journal: Clinical Nuclear Medicine (2002)

KIM, JEONG-HO M.D.†; YOUNG HYUN, IN M.D.*; SOO KIM, YOUNG M.D.‡; HONG WOO, ZE M.D.§ Author Information
Urinary Colloids in the Prevention of Kidney-Stone Formation
Authors: Arthur J. Butt, Ernst A. Hauser
Journal: New England Journal of Medicine (1952)

THE nature and process of kidney-stone formation has puzzled the medical profession for a long time. In the sixteenth century Paracelsus expressed the opinion that a material obtained from food constituted the basic cementing material essential to stone formation. In 1856 Meckel1 advanced the theory that the organic gluing or cementing matrix was a product of an inflammatory condition of the urinary tract. Fourcroy and Vauquelin2 considered the cementing substance to be albumin and gelatin. Ebstein,3 by dissection and analysis of stones, concluded that urinary calculi contain a framework of albuminous substances. He believed that this organic material resulted from . . .
VALIDITY OF CURRENT DEFINITION OF ACUTE KIDNEY INJURY IN CHRONIC KIDNEY DISEASE AFTER PERCUTANEOUS CORONARY INTERVENTION: A 10-YEAR RETROSPECTIVE STUDY
Authors: Elizabeth Hill, Amgad Mentias, Mohammad Raza, Rony Lahoud, E. Murat Tuzcu, Stephen Ellis, A. Lincoff, Samir Kapadia
Journal: Journal of the American College of Cardiology (2016)