tbuckley/cabot-search huggingface dataset:
Abstract 514: Integrins dependent regulation of endothelial cell migration and tube formation by α6(IV)NC1
Authors: Sudhakar Akulapalli, Chandra S. Boosani
Journal: Cancer Research (2010)

Abstract Peptides or short protein domains derived from extracellular matrix were shown to possess anti-tumor properties. One such molecule, α6(IV)NC1 was derived from the carboxy terminal non-collagenous domain fragment of α6 chain, type (IV) collagen and was found to inhibit angiogenesis and tumor growth but the mechanism by which it inhibits the growth of solid tumors has not been reported yet. In the present study we demonstrate that the biological functions of α6(IV)NC1 are attributed to its binding to different integrins. In addition, we also demonstrate that α6(IV)NC1 binds to α3β1and α5β1 integrins and competes with the cells binding to α1β1 integrins on type IV collagen, and / with α5β1 integrins on fibronectin and inhibits migration and tube formation of human vascular and lymphatic endothelial cells. We further evaluated the role of α3β1 and α5β1 integrins in tube formation and regulation of cell migration by α6(IV)NC1. While both the integrins (α3β1 and α5β1) are required for the inhibition of tube formation by α6(IV)NC1 in human vascular and lymphatic endothelial cells, only α3β1 integrin was found to regulate lymphatic endothelial cells migration. In addition we also demonstrate that α6(IV)NC1 inhibits tumor growth, tumor lymphatic angiogenesis and circulating endothelial cells in-vivo. These in-vitro and in-vivo findings identify that α3β1 and α5β1 integrins are critical for α6(IV)NC1 mediated inhibition of angiogenic and lymph angiogenic signaling and inhibition of tumor progression. Collectively, our findings first time demonstrate that α6(IV)NC1 is a potent therapeutic candidate for targeting tumor angiogenesis and tumor lymphatic angiogenesis. 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 514.
Abstract 901: Specificities of CYFRA monoclonal antibodies KS 19.1 and BM 19.21 to cytokeratin 19
Authors: Ann-Jeanette Vasko, George D. Thorne, Timothy R. Kettlety, Zhong-Qian Li
Journal: Cancer Research (2011)

Abstract CYFRA 21-1 measures cytokeratin fragments of cytokeratin 19 with the aid of two specific monoclonal antibodies (mAb), BM 19.21 and KS 19.1. CYFRA 21-1 has been adopted in several immunoassays as a tumor marker for non-small-cell lung cancer (Sanchez-Carbayo et al. Clin Chem 1999; 45: 1944-1953). We evaluated the binding of these antibodies to cytokeratin 19 and three other types of cytokeratin. Potential cross-reactivity of these antibodies with six cancer biomarker antigens was also evaluated. METHODS: SDS-PAGE and Western blotting were used to observe the binding of KS 19.1 and BM 19.21 with recombinant cytokeratin 8, 14, 18 and 19. An ARCHITECT CYFRA 21-1 assay was used to investigate whether cancer biomarker antigens AFP, beta-HCG, CA 125, CA 15-3, CA 19-9 and CEA interfere with the binding of these two antibodies to cytokeratin 19. 10 – 100 fold of the normal reference levels (8 ng/mL AFP, 5 mIU/mL beta-HCG, 35 U/mL CA 125, 37 U/mL CA 19-9 and 5 ng/mL CEA) of these biomarker antigens were spiked into five (5) serum samples. The concentration of the biomarker antigen CA 15-3 used for this study was 10 and 17 fold of its normal reference levels (31.3 U/mL). RESULTS: SDS-PAGE and Western blotting showed that KS 19.1 and BM 19.21 antibodies bind specifically to cytokeratin 19. KS 19.1 and BM 19.21 antibodies exhibited no binding to cytokeratin 8, 14 and 18 even though the total amount of cytokeratin 19 loaded was less than that of the other three cytokeratin's. Cancer biomarker antigens AFP, beta-HCG, CA 125, CA 15-3, CA 19-9 and CEA did not interfere with the binding of these two antibodies to cytokeratin 19 significantly. Mean cross reactivity of each biomarker was 5% (1% – 11%) for AFP, 4% (0% – 7%) for beta-HCG, 4% (0% – 15%) for CA 125, 6% (0% – 15%) for CA 15-3, 3% (0% – 6%) for CA 19-9 and 2% (0% – 4%) for CEA. CONCLUSIONS: Monoclonal antibodies KS 19.1 and BM 19.21 bound to cytokeratin 19 specifically and showed no cross reactivity with cytokeratin 8, 14 and 18 in Western blotting. Also cytokeratin 19-binding specificity was not significantly interfered significantly by cancer biomarker antigens AFP, beta-HCG, CA 125, CA 15-3, CA 19-9 and CEA in an ARCHITECT CYFRA 21-1 assay. 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 901. doi:10.1158/1538-7445.AM2011-901
Case 33-2000
Authors: Eric Larsen, Laurence de Leval
Journal: New England Journal of Medicine (2000)

Presentation of CaseA seven-year-old girl was admitted to the hospital because of the superior vena cava syndrome.She had been in good health until the age of three years five months, when she had pain in her right upper arm of one week's duration. A physician found a mass in her right upper arm. Radiographic examination showed a soft-tissue mass without involvement of the adjacent bone. A magnetic resonance imaging (MRI) study (Figure 1) revealed that the mass arose in the region of the brachialis muscle and displaced the tendon of the biceps muscle; the radial nerve appeared to . . .
Development of a BRCA1-Like Signature in Triple Negative Breast Cancers Within the Rather (Rational Therapy for Breast Cancer) Consortium
Authors: I.M. Simon, J. Peeters, T. Severson, I. Majewski, A. Bosma, C. Caldas, S. Chin, R. Bernards, S. Linn
Journal: Annals of Oncology (2014)
Abstract 3554: The histone deacetylase inhibitor LBH589 augments anti-tumor immunity through direct effects on tumor and immune cells leading to impaired tumor progression <i>in vivo</i>
Authors: David M. Woods, Karrune V. Woan, Hongwei Wang, Fengdong Cheng, Zi Wang, Lianet Vazquez, Patricio Perez, Maritza Lienlaf, Jennifer Rock-Klotz, Eva Sahakian, John Powers, Susan Deng, Merino Oscar, Peter Atadja, Ed Seto, Javier Pinilla-Ibarz, Jeffrey S. Weber, Eduardo M. Sotomayor, Alejandro Villagra
Journal: Cancer Research (2012)

Abstract Overcoming immune tolerance is critical for the development of effective immunotherapy against cancer. Tumor cells induce tolerance through a variety of modalities including the secretion of IL-10 and TGF-β, the expression of inhibitory ligands, and the generation of cells with regulatory properties. Epigenetic modifiers have gained special attention due to their ability to modify immune regulatory pathways. In this context, a group of chemical compound collectively named histone deacetylase inhibitors (HDACi) have recently been shown to modulate tumor cell immunogenicity, adding a new property to their already well-documented cytotoxic effect against transformed cells. LBH589 is a potent, pan-HDACi that has been used in clinical trials for the treatment of several hematological malignancies. Here, we provide evidence of the anti-melanoma effect of LBH589 through its direct effects upon tumor cells as well as its modulatory effects upon immune cells. Indeed, treatment of human and murine melanoma cells in vitro with LBH589 resulted in inhibition of melanoma proliferation, characterized by cell cycle arrest in G1. Moreover, we found that LBH589 enhances the expression of MHC class I and II molecules on melanoma cells, which is critical for immune recognition. In addition, LBH589 treatment inhibits the production of IL-10, while enhancing the secretion of pro-inflammatory cytokines such as IL-12 and the expression of the costimulatory molecule B7.2 on antigen-presenting cells (APCs). LBH-treated APCs also displayed an enhanced capability to activate naïve antigen-specific T-cells as evidenced by their increased production of IL-2 and IFN-γ. More importantly, LBH589-treated APCs also restored the function of anergic T-cells isolated from tumor bearing mice. Finally, in vivo treatment of B16 melanoma bearing mice with LBH589 resulted in a substantial decrease in tumor growth when compared to vehicle-control treated mice (mean 602mm3 vs. 1316mm3, respectively). In conclusion, the dual ability of the pan-HDACi LBH589 to target both melanoma cells and to enhance anti-tumor immune responses provides the rationale for evaluating this compound either alone or in combination with immune enhancing therapeutic approaches (eg, CTLA4 blockade) for melanoma treatment. 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 3554. doi:1538-7445.AM2012-3554
House Marks Up 1993 NCI Budget
Authors: D. A. Tisevich
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article House Marks Up 1993 NCI Budget Get access Dorothy A. Tisevich Dorothy A. Tisevich Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 17, 2 September 1992, Page 1315, https://doi.org/10.1093/jnci/84.17.1315 Published: 02 September 1992
Abstract 854: Claudin-5 expression in tumor cells is a potential prognostic marker in pediatric ependymoma
Authors: József Virág, Gábor Baksa, Zsuzsa Schaff, József Tímár, Miklós Garami, Balázs Hegedũs
Journal: Cancer Research (2010)

Abstract Ependymomas are common pediatric brain tumors that originate from the ependymal cell layer and characterized by poor prognosis due to frequent recurrence. However, the current WHO grading system fails to accurately predict clinical behavior. In a retrospective study, we performed the immunohistochemical analysis of 35 pediatric ependymomas for critical components of the cell-cell junctions including cadherins, claudins and occludins. Surprisingly, we found that a number of supratentorial but not infratentorial ependymoma expressed high levels of the brain endothelial cell tight junction component claudin-5 in tumor cells. Interestingly, this region specific expression pattern was also found in the choroid plexus epithelium of the lateral ventricles from tumor free neonatal tissue samples. Ultrastructural studies of human ependyma from various brain regions confimed that the observed protein expression pattern results in distinct regional differences in cell-cell junction organization and thus in ependymal barrier function. Nevertheless, we observed a significant increase in overall survival in patients bearing claudin-5 expressing ependymoma cells. These findings might - at least in part - be explained by the high expression cell-cell junction proteins that can interfere with the invasive capacity of tumor cells. Our data indicates that the assessment of claudin-5 expression in ependymoma cells is a potentially useful prognostic marker in this pediatric CNS malignancy. 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 854.
26O Molecular epidemiology study of PD-L1 expression in patients (pts) with EGFR-mutant NSCLC
Authors: J. Cho, W. Zhou, Y.-L. Choi, J.-M. Sun, H. Choi, T.-E. Kim, M. Dolled-Filhart, K. Emancipator, M.A. Rutkowski, J. Kim
Journal: Annals of Oncology (2015)
NIMG-24HIGH SPATIOTEMPORAL DYNAMIC SUSCEPTIBILITY CONTRAST (DSC) PERFUSION MRI USING MULTIBAND ECHOPLANAR IMAGING (MB-EPI)
Authors: Benjamin Ellingson, Kevin Leu, Whitney Pope, Albert Lai, Phioanh Nghiemphu, Linda Liau, Timothy Cloughesy
Journal: Neuro-Oncology (2015)

NIMG-24. HIGH SPATIOTEMPORAL DYNAMIC SUSCEPTIBILITY CONTRAST (DSC) PERFUSION MRI USING MULTIBAND ECHOPLANAR IMAGING (MB-EPI) Benjamin Ellingson, Kevin Leu, Whitney Pope, Albert Lai, Phioanh Nghiemphu, Linda Liau, and Timothy Cloughesy; University of California Los Angeles, Los Angeles, CA, USA BACKGROUND: Dynamic susceptibility contrast (DSC)-MRI is a commonlyusedperfusion imaging techniqueused toassessbrain tumorvascularity and angiogenesis by estimation of relative cerebral blood volume (rCBV). Despite widespread use, technical limitations lead to compromises in terms of resolution, slice coverage, and temporal resolution when acquiring dynamic data using the current single-shot echoplanar (EPI) imaging approach. In the current study we demonstrate the use of a new “multiband” (MB)-EPI sequence for multislice excitation, originally developed for fMRI as part of the Human Connectome Project, to obtain DSC perfusion MRI with whole brain coverage, higher spatial resolution, and twice the temporal resolution of current strategies. METHODS: DSC data collected using standard EPI were compared with DSC obtained using MB-EPI in 20 prospective GBM patients. Standard DSC-MRI were collected on conventional 1.5T or 3T MR scanners using a temporal resolution of 1250-1900ms, matrix size 1⁄4 96x96–128x128, and 5-20 slices with 5mm slice thickness. High spatiotemporalDSC-MRI datawere collectedona3TSiemensPrismawith temporal resolution of 600-750ms, matrix size 1⁄4 100x100–200x200, and 30-32 slices with 4mm slice thickness. Both DSC-MRI datasets were post-processed using standard leakage correction and deconvolution techniques to calculate rCBV and rCBF. RESULTS: Data collected using standard and MB-EPI showed similar dynamic contrast-to-noise, although MB-EPI showed more T1-weighting and leakage effects. RCBV maps obtained using both techniques provided similar information regarding the extent of hypervascularity within the tumor after leakage correction; however, rCBV maps calculated from MB-EPI data had more brain coverage and higher spatial resolution. Parametric maps of blood flow differed slightly due to higher temporal resolution MB-EPI data. CONCLUSION: High spatiotemporal DSC perfusion MRI is desirable and clinically feasible using MB-EPI. DSC using MB-EPI provides comparablequantitativedataand dataqualitywith betteraccuracyandspatial resolution. Neuro-Oncology 17:v153–v171, 2015. doi:10.1093/neuonc/nov225.24 Published by Oxford University Press on behalf of the Society for Neuro-Oncology 2015.
Abstract 4120: UDP-Glucuronosyltransferase 1 (UGT1A1) down-regulation correlates to menopausal status and stage of disease in human breast cancer tissues
Authors: Athena Starlard-Davenport, Beverly R. Word, Beverly D. Lyn-Cook
Journal: Cancer Research (2012)

Abstract Estrogen metabolism, catalyzed by UGTs, is a major drug-metabolic pathway that results in the complete inactivation of estrogens and their hydroxylated metabolites. Alterations in UGTs, resulting in decreased UGT expression and glucuronidation activity towards estrogens and their metabolites, has been suggested to play a potential role in breast cancer risk. The purpose of this study was to: 1) compare the mRNA expression levels of UGTs responsible for conjugating estrogens in human breast cancers and normal breast tissues from women; 2) compare UGT1A1 mRNA expression to tumor stage, ER status, ethnicity, and menopausal status in a group of human breast tumors and normal breast tissues, and 3) investigate the association between variations in the number of TA repeats in the promoter region of UGT1A1 to gene expression. Quantification of UGT mRNA in breast tissues revealed that UGT1A4, UGT1A9, UGT1A10, and UGT2B7 mRNA levels were decreased in breast cancers as compared to normal breast tissues. UGT1A1 mRNA levels were also significantly decreased in breast cancers (N = 17) as compared to normal breast tissues (N = 30) (p = 0.02). UGT1A1 down-regulation strongly correlated with menopausal status (premenopausal vs. postmenopausal; p = 0.04) and stage of breast disease (p = 0.01). This may account for variations in response to chemotherapy used for the treatment of more aggressive breast cancers. UGT1A1 mRNA was also decreased in breast tumors as compared to normal breast tissues from both African American and European American women. We postulated that the decreased levels of UGT1A1 mRNA in breast cancers may be due to a genetic variant in the promoter of UGT1A1. In all UGT1A1 genotypes observed in our study, the mean UGT1A1 mRNA expression levels was significantly decreased among breast cancer cases as compared to controls (p = 0.04). Our research findings suggest that further investigations are necessary to determine the role of UGT1A1 in breast carcinogenesis. 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 4120. doi:1538-7445.AM2012-4120
Case 7-2009
Authors: Christopher J. Hartnick, William H. Barth, Charles J. Coté, Meredith A. Albrecht, P. Ellen Grant, Julia T. Geyer
Journal: New England Journal of Medicine (2009)

A 29-year-old woman was transferred to this hospital at 38 weeks 4 days of gestation because of a large cystic structure that had been detected by ultrasonography in the fetal oral cavity and appeared to obstruct the airway. The placenta was anterior, and a uterine fibroid was seen. A management decision was made.
Abstract 2644: No evidence for increased risk of cancers other than testicular cancer among first-degree relatives of testicular germ cell tumor (TGCT) patients from multiple-case TGCT families
Authors: Mary L. McMaster, Ketil R. Heimdal, Mark H. Greene
Journal: Cancer Research (2012)

Abstract Familial aggregation of testicular germ cell tumors (TGCT) has been reported, but it is unclear whether other cancers co-aggregate in multiple-case TGCT families. METHODS: We performed an observed-to-expected (O/E) analysis in a cohort of TGCT families with documented family cancer history assembled in Norway and the U.S. All bloodline first-degree relatives of TGCT cases were eligible. Relatives with missing vital status, gender, or dates of birth and/or death were excluded. We used population-based, age-adjusted cancer incidence rates from Norway and the Surveillance, Epidemiology and End Results (SEER) Program of the National Cancer Institute, respectively, to calculate expected numbers of cancer cases. Only non-TGCT cancers were analyzed. RESULTS: A total of 130 TGCT families with 84 reported cancers and 31,556 person-years at risk were included in the analysis. Overall, there was no excess cancer risk, all non-TGCT sites combined, observed among first-degree relatives of TGCT cases (O/E = 0.89; 95%CI 0.71 - 1.10), either collectively or stratified by center. Although numbers were small, site-specific increased risks were observed for soft tissue cancers (n=4; O/E=7.14; 95%CI 1.95 - 18.29) and leukemia (n=9; O/E=6.48; 95%CI 2.96 - 12.29), and site-specific decreased risk was observed for breast cancer (n=6; O/E=0.44; 95%CI 0.16 - 0.95). These risks were statistically significant overall and in Norway, but not in the U.S. CONCLUSION: In this, the largest study of site-specific cancer risk within multiple-case TGCT families yet performed, we found no excess risk of non-TGCT cancers overall among first-degree relatives of TGCT cases. There was limited evidence supporting altered site-specific risks for soft tissue cancer, leukemia and breast cancer; however, cancer numbers were small, and the results were not consistent between centers, suggesting that differences in cancer reporting among families, case validation methods, or other factors, rather than an etiologic association, explain these findings. Familial testicular cancer appears to be a site-specific syndrome. 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 2644. doi:1538-7445.AM2012-2644
You can't have your hypothesis and test it: The importance of utilities in theories of reasoning
Authors: Fenna H. Poletiek
Journal: Behavioral and Brain Sciences (2011)

Abstract Mercier and Sperber's (M&amp;S's) theory of reasoning cannot predict reasoning in the absence of an argumentative context. Applying the theory to hypothesis testing behavior, I propose that hypothesis testing is often motivated by determining the true inference and that reasoning models should account for utilities (affected by various motives, including the wish to convince) of reasoning outcomes.
NORMAL LIMITS OF HEART-TO-MEDIASTINUM RATIO (HMR) OF I-123 MIBG UPTAKE QUANTIFIED FROM HIGH-SENSITIVITY (HS) AND HIGH-RESOLUTION (HR) SPECT/CT
Authors: Yi-Hwa Liu, Taraneh Hashemi Zonouz, Veronica Sandoval, Rachel Lampert, Albert Sinusas
Journal: Journal of the American College of Cardiology (2016)
FRI0387 Sexual disorders in premenopausal women with systemic sclerosis
Authors: A. P. Cacheda, L. M. López Núñez, G. López Velandia, I. Padró, M. Sarbu, P. Rubio, A. Pros Simón
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Changes associated with systemic sclerosis (SSc)can have a negative impact on sexuality and sexual functioning (1). In women, common problems reported include vaginal dryness and discomfort, painful intercourse, and reduced frequency and intensity of orgasms (3). Prevalence of erectile dysfunction in men with SSc appears to be substantial, however literature on sexual function in women with SSc is scarce (2) and prevalenceof sexual disorders in premenopausal women with this disease has not been studied. <h3>Objectives</h3> To estimate the prevalence of female sexual disorders in premenopausal women with SSc, and to compare it with healthy controls. <h3>Methods</h3> Descriptive observational study of the premenopausal women with SSc of our department of Rheumatology who agreed to participate. The questionnaires Female Sexual Function Index (FSFI) and Female Sexual Function Test were distributed among patients and healthy controls of similar demographics characteristics. Data were analyzed using SPSS v.15. Statistical tests applied were Mann-Whitney U test and Fischer test. <h3>Results</h3> 7SSc premenopausal women agreed to participate in the study and were compared with seven healthy controls. The mean age was similar in both groups (p 0.38), being 40.4 years (SD 3.5) in the scleroderma group and 37.8 (SD 6.7) among women in the control group. 57% of women with SSc showed a moderate sexual dysfunction, while in the control group this percentage was 0, however no significant differences were found (p = 0.07). The Sexual Function Index was lower in patients with SSc, being of 16.78 [95% CI 5.47-28.1] in this group, and 33.87 [95% CI 32.54-35.19] in the control group (p = 0.001). <h3>Conclusions</h3> Inour study, more than half of premenopausal women with SSc showed moderate sexual dysfunction, and Sexual Function Index was significantly higher in the group of healthy women. However, further studies with larger numbers of patients are needed to confirm these findings. <h3>References</h3> Ann Julie Impens and James R. Seibold, "Vascular Alterations and Sexual Function in Systemic Sclerosis," International Journal of Rheumatology, vol. 2010, Article ID 139020, 5 pages, 2010. doi:10.1155/2010/139020 A. Schouffoer, J. van der Marel, M. M. Ter Kuile et al., "Impaired sexual function in women with systemic sclerosis: a cross-sectional study" Arthritis Care and Research, vol. 61, no. 11, pp. 1601–, 2009 Levis B, Burri A, Hudson M, Baron M, Thombs BD. "Rates and correlates of sexual activity and impairment among women with systemic sclerosis", Arthritis Care &amp; Research, Vol. 64, No. 3, March 2012, pp 340–350. DOI 10.1002/acr.20696 <h3>Acknowledgements</h3> We thankD.Osorio forthe statisticalanalysis. <b>Disclosure of Interest</b>: None Declared