tbuckley/cabot-search huggingface dataset:
Abstract 3720: Encouraging activity of bicalutamide and everolimus in castration-resistant prostate cancer (CRPC): Early results from a phase I/II clinical trial
Authors: Hongyong Zhang, Yu Wang, Paramita Ghosh, Primo N. Lara, Patricia Pasquinelli, Laurel Beckett, Ralph W. deVere White, Chong-Xian Pan
Journal: Cancer Research (2010)

Abstract Background: Multiple signaling pathways are involved in the development of CRPC. We previously showed that the mTOR pathway is activated in CRPC cell lines while inhibition of this pathway results in upregulation of androgen receptor (AR) signaling (Wang et al, Oncogene. 2008). Simultaneous blockade of the mTOR and AR pathways synergize in inducing PCa cell death and delaying tumor formation in mouse models. We hypothesize that simultaneous blockade of the AR and mTOR pathways in CRPC patients with bicalutamide and everolimus will result in improved efficacy compared to bicalutamide alone. Methods: A phase II clinical trial with a lead-in safety phase was designed to determine the efficacy and tolerability of the bicalutamide and everolimus combination in CRPC patients compared with bicalutamide alone. Patients must have histologically confirmed disease and demonstrated disease progression (either by PSA or radiographically) while on androgen deprivation therapy. At the lead-in phase, all patients receive both agents. At the phase II stage, patients are randomized to bicalutamide +/− everolimus. The primary endpoint is PSA response. The second endpoints include progression-free survival, time-to-treatment failure, overall survival and toxicity. Here, we report the results of the lead-in phase. Results: To-date, 13 patients have been screened and 8 have been enrolled with the age ranging XX-XX, and performance status of ECOG 0-1. In the lead-in phase, bicalutamide + everolimus has been well tolerated with no unexpected toxicities. One patient developed grade 3 interstitial pneumonitis (attributed to everolimus) that improved with dose reduction and steroid treatment. Seven of 8 patients have had either stable PSA or a PSA response after at least 8 weeks of therapy. Tumor and blood specimens are being collected for molecular correlative studies of mTOR pathway markers. Conclusions: Thus far, the rational combination of bicalutamide and everolimus appears to have promising anti-tumor activity and an acceptable toxicity profile. The randomized phase of the clinical trial is currently ongoing and will be reported. (Supported by Novartis) 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 3720.
P5-13-11: PTEN and Tau-Protein Expression: Predictive Value of Poor Response to Trastuzumab Plus Paclitaxel in Patients with HER2−Positive Breast Cancer.
Authors: DH Koo, J-H Ahn, DH Yoon, S-B Kim, HJ Lee, KY Kong, BH Son, SH Ahn, KH Jung
Journal: Cancer Research (2011)

Abstract Backgrounds: Trastuzumab-based chemotherapy has been an active treatment in patients (pts) with HER2−positive breast cancer; however, primary and secondary resistance has occurred in pts treated with trastuzumab (H) alone or in combination with chemotherapy. Material and Methods: Biomarkers were searched using tissue microarrays (TMA) in the HER2−positive breast cancer pts treated with H and paclitaxel (P) combination chemotherapy between October 2004 and August 2010. Tumor blocks of 101 pts were analyzed for VEGF, IGF-1R, p-Akt, beta-III tubulin, CD44, Tau-protein, p27 and PTEN by immunohistochemical (IHC) analysis. Eight biomarkers were assessed to investigate the correlation with the clinical outcomes, including response rate (RR), progression free survival (PFS), and overall survival (OS). Results: With a median follow-up duration of 21.7 months (range, 9.1−55.2 months), 101 pts received H+P chemotherapy in neoadjuvant setting (n=36, 35.6%) and recurrent or metastatic setting (n=65, 64.4%). Median age was 48 (range, 19–83 years), and the majority of pts (n=95, 94.1%) had good performance status. Premenopausal pts and hormone receptor-negative pts were 48 (47.5%) and 52 (51.5%), respectively. The median cycle of H+P chemotherapy was six (range, H 1–43; P 1–21). Overall RR was 68.3% (n=69) including complete response with 7 pts, and PFS and OS were significantly longer in pts responsive to H+P chemotherapy compared with non-responsive patients (PFS, p=0.001; OS, p=0.015). Although VEGF, IGF-1R, p-Akt, beta-III tubulin, CD44, p27 and PTEN status by IHC were not significantly associated with response to H+P chemotherapy, Tau-protein showed a trend of association without statistical significance (RR, 46.2% vs. 71.6%, p=0.066). Among 13 pts with high Tau protein expression, 9 pts with both high Tau-protein and low PTEN level showed statistically significant lower RR compared with other 92 pts (22.2% vs. 72.8%; p=0.002). None of the biomarkers was related to PFS and OS in pts with recurrent or metastatic disease, and to pathologic complete response in pts after H+P chemotherapy as neoadjuvant therapy. Conclusion: Our data showed that both low PTEN level and high Tauprotein expression were significantly associated with poor response to H+P chemotherapy in patients with HER2−positive breast cancer. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P5-13-11.
Abstract LB-106: Expression of stem cell biomarkers in benign breast tissue from patients with triple negative breast cancer
Authors: Rachel L. Atkinson, Wei T. Yang, Melissa D. Landis, Helen Wong, Chad Creighton, Susan G. Hilsenbeck, Michael T. Lewis, Wendy A. Woodward, Abenaa Brewster, Aysegul A. Sahin, Jenny C. Chang
Journal: Cancer Research (2011)

Abstract Numerous studies suggest that breast cancers contain a subpopulation of cancer stem cells that are thought to maintain the heterogeneity and self-renewing potential of the tumor. In our previously published data, we had described a breast cancer stem cell signature comprised of 493 statistically significant differentially expressed genes, which were present in a tumorigenic subpopulation of cells. Cells from patient samples with the cell surface markers CD44+CD49f+CD133/2+ have been shown to have self-renewal and tumorigenic properties – characteristics of breast cancer stem cells. In this study, we investigated the benign tissue from 42 patients with breast cancer treated with mastectomy to examine the incidence CD44+CD49f+CD133/2+ positive cells. Benign tissue was obtained at a distant site, at least 5 cm from the primary tumor, and examined with hematoxylin-eosin by a breast pathologist (AS), only samples containing normal breast tissue with at least 60% epithelial content were selected. A significant increase in expression of CD44+CD49f+CD133/2+ by immunofluorescence was identified in the benign tissue associated with patients with triple negative (ER negative/PR negative/Her2 negative) disease (8 out of 8), compared with ER positive and Her2 positive tumors combined (5 out of 36), P&amp;lt;0.001, Wilcoxon rank sum test. The definition of a positive score was more then 1% positive staining or negative for less then 1% triple positive cells, scoring approximately 1000 cells per sample. We further examined whether global RNA expression from these benign tissues correlated to our previously published tumorigenic microarray signature. We found that array data from benign tissue from patients with triple negative breast cancer was significantly correlated with our previously published tumorigenic signature (P=.01 two sided t test). Thus, these pathologically defined benign cells bearing cancer stem cell markers may be cells of origin for tumor development in triple negative breast cancer, and their presence in benign tissue (including tissue in some cases from the uninvolved contralateral breast) implies a systemic etiology to triple negative breast cancer. In conclusion, putative cancer stem cell markers are enriched in the benign breast tissue of women who have developed triple negative breast cancer, and their presence may represent a biomarker for increased breast cancer risk. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-106. doi:10.1158/1538-7445.AM2011-LB-106
1083 PROGNOSTIC SIGNIFICANCE OF HISTOLOGIC EXPRESSION OF HEPATOCYTE NUCLEAR FACTORS 4a AND 1a IN RESECTABLE HEPATOCELLULAR CARCINOMA
Authors: J.H. Shim, H.C. Lee, E. Yu, H.J. Kang, S. Han, Y.-J. Lee, S.-G. Lee, D. Lee, K.M. Kim, Y.-S. Lim, Y.-H. Chung, Y.S. Lee, D.J. Suh
Journal: Journal of Hepatology (2013)
THU0130 Assessment of transaminasitis with daily methotrexate therapy in patients with inflammatory rheumatic diseases. A long-term follow-up cohort study:
Authors: M.U. Martinez Martinez, A. Sánchez-Arriaga, C. Abud-Mendoza
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Methotrexate (MTX) is the most commonly used DMARD in the treatment of rheumatoid arthritis and other rheumatic diseases. MTX is often administered weekly (WMTX), because the drug has been considered more hepatototoxic when taking daily. A randomized clinical trial reported that nausea, vomiting, headache are less common side effects with daily MTX (DMTX).<sup>1</sup> We reported a comparative study of 180 patients which highlights the same or lower rate of transaminasitis in patients under DMTX than WMTX.<sup>2</sup> <h3>Objectives</h3> To determine the rate of hepatotoxicity of DMTX in a cohort with a large follow-up. <h3>Methods</h3> A retrospective study was performed of our patients treated with methotrexate in daily doses (DMTX) (our patients have been treated under DMTX for more than 20 years of medical practice). We describe the demographic factors including age, sex, diseases in which MTX is administrated, time of evolution of the disease; we compared patients with transaminasitis and patients without transaminasitis for describing factors associated with this event. ALT/AST levels were evaluated in our patients every 3 months. <h3>Results</h3> We included 875 patients with 2.6±3.6 years of treatment with methotrexate, 10 patients were under MTX treatment up to 20 years; 534 patients have rheumatoid arthritis (RA), 93 systemic lupus erythematosus (SLE), and 248 other rheumatic diseases. Sixty four patients were less than 18 year-old, and 91 over 65. Only 56/875 (6.4%) had transaminasitis (more than two-fold the normal level of ALT/AST), 18 patients had 2 or more episodes of transaminasitis, moreover, only 20 patients had 3-fold elevation of AST/ALT. Table 1 shows the main characteristics of the patients included in our study. Only alcoholism and higher body mass index (BMI) were statistically significant factors associated with transaminasitis. <h3>Conclusions</h3> Our study describes the security of daily dosage of MTX (liver toxicity) in a large follow-up. This study justifies a randomized clinical trial, to evaluate security and to confirm better profile of adverse events with DMTX than WMTX doses. The clinician must discard the association of alcohol and fatty liver disease in patients with transaminasitis and the use of MTX. <h3>References</h3> Radmanesh M, Rafiei B, Moosavi ZB, Sina N. Weekly vs. daily administration of oral methotrexate (MTX) for generalized plaque psoriasis: a randomized controlled clinical trial. Int J Dermatol. 2011;50:1291-3. Moreno-Valdes R, Martínez-Martínez MU, Cuevas-Orta E, et al. Methotrexate Every Day Is Safe and Effective As Weekly Dosage. Arthritis Rheum 2011; Suppl 63:S881 (abstract 2251). <h3>Disclosure of Interest</h3> None Declared
GAPDH enhances the aggressiveness and the vascularization of non-Hodgkin’s B lymphomas via NF-κB-dependent induction of HIF-1α
Authors: J Chiche, S Pommier, M Beneteau, L Mondragón, O Meynet, B Zunino, A Mouchotte, E Verhoeyen, M Guyot, G Pagès, N Mounier, V Imbert, P Colosetti, D Goncalvès, S Marchetti, J Brière, M Carles, C Thieblemont, J-E Ricci
Journal: Leukemia (2014)
Search for Serum Tumor Markers Continues
Authors: Hugh Mclntosh
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article Search for Serum Tumor Markers Continues Get access Hugh Mclntosh Hugh Mclntosh Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 6, 18 March 1992, Pages 387–389, https://doi.org/10.1093/jnci/84.6.387 Published: 18 March 1992
THE RISK OF THROMBOEMBOLIC COMPLICATIONS WITHOUT ANTICOAGULATION AFTER SURGICAL AORTIC VALVE REPLACEMENT WITH A BIOPROSTHESIS
Authors: Peter B. Berger, Deepak Vedamurthy, Alfred Casale, Haiyan Sun, Charles Benoit, Ashley Ferrari, Susan Trocciola, Ibrahim Ismail Sayed, Russell Carter
Journal: Journal of the American College of Cardiology (2015)
Prostate Cancer Meeting Confronts Controversies
Authors: L. Fintor, I. Hall
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article Prostate Cancer Meeting Confronts Controversies Get access Lou Fintor, Lou Fintor Search for other works by this author on: Oxford Academic PubMed Google Scholar Irene Hall Irene Hall Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 23, 6 December 1995, Pages 1743–1744, https://doi.org/10.1093/jnci/87.23.1743 Published: 06 December 1995
733 NEOEPITOPES DERIVED FROM EXTRACELLULAR MATRIX DEGRADATION REFLECT LIVER FUNCTION, FIBROSIS AND HVPG IN HIV-PATIENTS
Authors: D.J. Leeming, E. Anadol, A. Krag, K. Tack, M.J. Nielsen, B.A. Payer, S. Möller, F. Bendtsen, M.A. Karsdal, U. Spengler, C.P. Strassburg, M. Peck-Radosavljevic, T. Reiberger, T. Sauerbruch, J.K. Rockstroh, J. Trebicka
Journal: Journal of Hepatology (2013)
Abstract 1710: Epigenetic repression of regulator of G-protein signaling 2 promotes prostate cancer progression
Authors: Yaping Tu, Dennis W. Wolff, Zoran Gatalica, Yan Xie, Peter W. Abel
Journal: Cancer Research (2010)

Abstract Prostate cancer is the most common cancer in American men and acquisition of androgen independence by prostate cancer is the key problem causing prostate cancer progression to highly aggressive form of cancer, leaving limited modalities in its treatment. Recent studies suggest that G protein-coupled receptor (GPCR)-stimulated androgen-independent activation of androgen receptor (AR) contributes to development of androgen independence. We previously reported that RGS2, an inhibitor of GPCR signaling, inhibits androgen-independent AR activation in prostate cancer cells (Cao et al., (2006) Oncogene, 25: 3719-3734). Here, we report that RGS2 protein expression was significantly reduced in human prostate cancer specimens compared to adjacent normal prostate tissues. Interestingly, RGS2 repression in androgen-independent prostate cancer cells and human prostate cancer specimens is not simply due to the loss of the RGS2 gene. Instead, methylation-specific PCR analysis and bisulfite sequencing indicated that methylation of the RGS2 gene promoter correlates with RGS2 down-regulation in prostate cancer cells and human prostate cancer specimens. Hypermethylation of the RGS2 gene promoter abolished its promoter activity and suppressed RGS2 gene expression. Conversely, the DNA methyltransferase inhibitor, 5-aza-2’-deoxycytidine induced re-expression of RGS2 in androgen-independent prostate cancer cells via demethylation of the RGS2 promoter to inhibit androgen-independent prostate cancer growth. Furthermore, ectopic re-expression of RGS2 in androgen-independent prostate cancer cells by RGS2-adenovirus infection suppressed tumorigenicity and growth of xenografts in castrated nude mice. Taken together, our results suggest that RGS2 repression due to hypermethylation of its promoter could unmask a latent pathway for AR activation by various GPCRs, thus contributing to prostate cancer progression. 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 1710.
The Prevalence of Hepatitis C Virus Infection in the United States, 1988 through 1994
Authors: Miriam J. Alter, Deanna Kruszon-Moran, Omana V. Nainan, Geraldine M. McQuillan, Fengxiang Gao, Linda A. Moyer, Richard A. Kaslow, Harold S. Margolis
Journal: New England Journal of Medicine (1999)

Because many persons with chronic hepatitis C virus (HCV) infection are asymptomatic, population-based serologic studies are needed to estimate the prevalence of the infection and to develop and evaluate prevention efforts.We performed tests for antibody to HCV (anti-HCV) on serum samples from 21,241 persons six years old or older who participated in the third National Health and Nutrition Examination Survey, conducted during 1988 through 1994. We determined the prevalence of HCV RNA by means of nucleic acid amplification and the genotype by means of sequencing.The overall prevalence of anti-HCV was 1.8 percent, corresponding to an estimated 3.9 million persons nationwide (95 percent confidence interval, 3.1 million to 4.8 million) with HCV infection. Sixty-five percent of the persons with HCV infection were 30 to 49 years old. Seventy-four percent were positive for HCV RNA, indicating that an estimated 2.7 million persons in the United States (95 percent confidence interval, 2.4 million to 3.0 million) were chronically infected, of whom 73.7 percent were infected with genotype 1 (56.7 percent with genotype 1a, and 17.0 percent with genotype 1b). Among subjects 17 to 59 years of age, the strongest factors independently associated with HCV infection were illegal drug use and high-risk sexual behavior. Other factors independently associated with infection included poverty, having had 12 or fewer years of education, and having been divorced or separated. Neither sex nor racial-ethnic group was independently associated with HCV infection.In the United States, about 2.7 million persons are chronically infected with HCV. People who use illegal drugs or engage in high-risk sexual behavior account for most persons with HCV infection.
Abstract 1619: Discovering a new physiological substrate of Aurora-A kinase
Authors: Raheleh Toughiri, Achuth Padmanabhan, Xiang Li, Charles Bieberich
Journal: Cancer Research (2011)

Abstract Aurora-A is a serine/threonine kinase that has oncogenic properties in vivo. The expression and kinase activity of Aurora-A are up-regulated in many cancers including prostate cancer, which is the most frequently diagnosed malignancy in men and second leading cause of cancer death in the United States. Aurora-A is one of the key regulators of mitosis that localizes to the centrosome from G2 phase through mitotic exit, where it regulates mitotic spindle formation and centrosome separation. Although Aurora-A is known to be an oncogene, few Aurora-A substrates have been identified. It is essential to elucidate Aurora-A substrates to develop biomarkers for Aurora-A inhibitors, and to identify new targets downstream of Aurora-A for cancer therapy. To identify new Aurora-A substrates, an Aurora-A Reverse In-gel Kinase Assay was developed. The basis of this method is co-polymerization of a denatured protein kinase throughout a polyacrylamide gel followed by protein refolding. Subsequently, an in-gel kinase reaction in the presence of γ-32P-ATP allows phosphorylation of potential kinase substrates that can be located by autoradiography. Phosphorylated proteins can be extracted from the gel and identified by liquid chromatography mass spectrometry. Using this method, we were able to identify Nuclear Mitotic Apparatus (NuMA) as an Aurora-A kinase substrate. Preliminary in vitro kinase experiments verify phosphorylation of recombinant NuMA C-terminus by Aurora-A. The identification of Aurora-A phosphorylation site/s will permit a better understanding of Aurora-A function in normal and cancer cells. The location of Aurora-A phosphorylation of NuMA and consequences of their mutation will be discussed. 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 1619. doi:10.1158/1538-7445.AM2011-1619
H-PGD Synthase (H-PGDS) Gene Expression Increases in Eosinophils of Aspirin Exacerbated Respiratory Disease (AERD) Patients after Oral Graded Aspirin Challenge
Authors: Elina Jerschow, Ren Zhen, Victor Schuster, David L. Rosenstreich, Simon Spivack
Journal: Journal of Allergy and Clinical Immunology (2015)
Abstract 1478: The role of ERBIN in suppressing migration in colon cancer.
Authors: Payton D. Stevens, Mike Yang, Tianyan Gao
Journal: Cancer Research (2013)

Abstract The LAP (leucine-rich repeat (LRR) and PDZ domain) family protein, ERBIN, is basolaterally localized protein that has previously been identified as a regulator of epithelial cell polarity and an ERBB2/HER2 binding protein. In addition, ERBIN inhibits RAF activation by disrupting by the RAS/RAF interaction. However, the functional importance of ERBIN in cancer remains elusive. In this study, we examined the role of ERBIN in regulating colon cancer progression and metastasis. Stable colon cancer cell lines, including SW480, LIM2405, and Caco2, were generated using lentiviral shRNA to deplete endogenous ERBIN expression. Our results showed that knockdown of ERBIN induced epithelial-mesenchymal transition (EMT)-like phenotype as marked by spindle-like morphology, a decrease in E-cadherin and an increase in vimentin expression. Moreover, the overall rate of cell migration was significantly increased in ERBIN knockdown cells as determined using Transwell assays. When tracking the movement of individual cells using live cell imaging, we found that ERBIN knockdown cells were considerably more motile with faster migrating speed when compared to control cells. Mechanistically, knockdown of ERBIN expression resulted in an increase in both Akt and ERK signaling activation. Taken together, we have identified a novel role of ERBIN in suppressing EMT and cell motility in colon cancer cells. Citation Format: Payton D. Stevens, Mike Yang, Tianyan Gao. The role of ERBIN in suppressing migration in colon 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 1478. doi:10.1158/1538-7445.AM2013-1478
ETV6 and signaling gene mutations are associated with secondary transformation of myelodysplastic syndromes to chronic myelomonocytic leukemia
Authors: Eric Padron, Sean Yoder, Sateesh Kunigal, Tania Mesa, Jamie K. Teer, Najla Al Ali, Mikkael A. Sekeres, Jeffrey S. Painter, Ling Zhang, Jeffrey Lancet, Jaroslaw P. Maciejewski, Pearlie K. Epling-Burnette, Eduardo Sotomayor, Rami S. Komrokji, Alan F. List
Journal: Blood (2014)
Familial Occurrence of Congenital Hypothyroidism Due to Lingual Thyroid Gland
Authors: Mahmoud I. El-Desouki, Abdullah S. Al-Herbish, Nasir A. Al-Jurayyan
Journal: Clinical Nuclear Medicine (1999)

Two sisters who presented with midline neck masses proved to be biochemically hypothyroid. Thyroid scintigraphy supplemented with perchlorate discharge testing showed lingual thyroid glands and ruled out the expected autosomal recessive organification defect. The related literature is reviewed.