tbuckley/cabot-search huggingface dataset:
Abstract 3014: Quantitative accuracy of Illumina HumanMethylation27 Infinium BeadChip data assessed by pyrosequencing
Authors: Zhiqing Huang, Ken Yamaguchi, Andrew Berchuck, Susan K. Murphy
Journal: Cancer Research (2011)

Abstract Purpose. Aberrant DNA methylation can lead to changes in gene expression, and this alteration is highly relevant in the context of cancer. The ability to accurately assess DNA methylation status is therefore of great importance in health and disease. The Illumina HumanMethylation27 Infinium BeadChip allows for analysis of whole genome DNA methylation by interrogating the methylation status of 27,578 CpG sites from the promoter regions of 14,475 annotated genes. However, one potential limitation of this platform as specified by the manufacturer is the inability to detect a β value difference between specimens of &amp;lt;0.2 (∼20% methylation). The present study assessed the quantitative nature of the Infinium platform through independent validation using a pyrosequencing approach. Procedures. Genomic DNA from 46 ovarian cell lines and 4 cultured normal cells, including ovarian surface epithelium and endometriotic cells, was modified with sodium bisulfite using the EZ DNA methylation kit from Zymo Research. Bisulfite conversion efficiency was confirmed by pyrosequencing at two chromosomal loci. Comparisons between normal and cancer cells identified differentially methylated genes using criteria of p0.3. Ten candidate differentially methylated genes (C14orf105, HNF1 β, HNF1α, KIF12, MIA2, PAX8, SERPINA6, SGK2, SRC, and TM4SF4) were selected for validation. Pyrosequencing assays were designed to allow for direct comparison of the same CpG site(s). The relationship between pyrosequencing and Infinium data was evaluated using correlation analyses. Results. Bisulfite conversion was &amp;gt;97% at BRCA1 (chr17) and IGF2 (chr11). Hypermethylation of 1,162 genes (1,452 CpG sites) and hypomethylation of 63 genes (74 CpG sites) was found in ovarian cancer cell lines as compared with cultured normal cells. The β values for 10 genes from Infinium analysis and percent methylation by pyrosequencing of the same CpG site(s) were highly correlated (R&amp;gt;0.98, p0.91, p&amp;lt;0.001). There was a significant positive correlation between platforms when data for all ten genes were grouped into 0-20%, 21-40%, 41-60% 61-80% and 81-100% bins (R value range, 0.32-0.73; p&amp;lt; 0.00002). Conclusions. Ovarian cancer cell lines exhibit significantly increased methylation as compared with normal cultured cells using the HumanMethylation27 Infinium BeadChip assay. The strong correlations between the Infinium and pyrosequencing data at the same CpG sites suggest that the Infinium platform is quantitative, lending support for use of this technology for assessment of methylation differences among specimens analyzed. 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 3014. doi:10.1158/1538-7445.AM2011-3014
1271 REDUCED DIETARY OMEGA-6:OMEGA-3 RATIO AND 12/15-LIPOXYGENASE DEFICIENCY PROTECT FROM HIGH FAT DIET-INDUCED STEATOHEPATITIS
Authors: M. Lazic, E. Inzaugarat, D. Povero, I. Chen, M. Chen, M. Nalbandyan, Y.I. Miller, A. Cherñavsky, A. Feldstein, D.D. Sears
Journal: Journal of Hepatology (2013)
Early Expression of Angiogenesis Factors in Acute Myocardial Ischemia and Infarction
Authors: Sang H. Lee, Paul L. Wolf, Ryan Escudero, Reena Deutsch, Stuart W. Jamieson, Patricia A. Thistlethwaite
Journal: New England Journal of Medicine (2000)

When the myocardium is deprived of blood, a process of ischemia, infarction, and myocardial remodeling is initiated. Hypoxia-inducible factor 1 (HIF-1) is a transcriptional activator of vascular endothelial growth factor (VEGF) and is critical for initiating early cellular responses to hypoxia. We investigated the temporal and spatial patterns of expression of the α subunit of HIF-1 (HIF-1α) and VEGF in specimens of human heart tissue to elucidate the early molecular responses to myocardial hypoxia.
Disability Income, Cocaine Use, and Repeated Hospitalization among Schizophrenic Cocaine Abusers — A Government-Sponsored Revolving Door?
Authors: Andrew Shaner, Thad A. Eckman, Lisa J. Roberts, Jeffery N. Wilkins, Douglas E. Tucker, John W. Tsuang, Jim Mintz
Journal: New England Journal of Medicine (1995)

Many patients with serious mental illness are addicted to drugs and alcohol. This comorbidity creates additional problems for the patients and for the clinicians, health care systems, and social-service agencies that provide services to this population. One problem is that disability income, which many people with serious mental illness receive to pay for basic needs, may facilitate drug abuse. In this study, we assessed the temporal patterns of cocaine use, psychiatric symptoms, and psychiatric hospitalization in a sample of schizophrenic patients receiving disability income.We evaluated 105 male patients with schizophrenia and cocaine dependence at the time of their admission to the hospital. They had severe mental illness and a long-term dependence on cocaine, with repeated admissions to psychiatric hospitals; many were homeless. The severity of psychiatric symptoms and urinary concentrations of the cocaine metabolite benzoylecgonine were evaluated weekly for 15 weeks.Cocaine use, psychiatric symptoms, and hospital admissions all peaked during the first week of the month, shortly after the arrival of the disability payment, on the first day. The average patient spent nearly half his total income on illegal drugs.Among cocaine-abusing schizophrenic persons, the cyclic pattern of drug use strongly suggests that it is influenced by the monthly receipt of disability payments. The consequences of this cycle include the depletion of funds needed for housing and food, exacerbation of psychiatric symptoms, more frequent psychiatric hospitalization, and a high rate of homelessness. The troubling irony is that income intended to compensate for the disabling effects of severe mental illness may have the opposite effect.
Ambient Particulate Matter Air Pollution Exposure and Mortality in the NIH-AARP Diet and Health Cohort
Authors: George D. Thurston, Jiyoung Ahn, Kevin R. Cromar, Yongzhao Shao, Harmony R. Reynolds, Michael Jerrett, Chris C. Lim, Ryan Shanley, Yikyung Park, Richard B. Hayes
Journal: Environmental Health Perspectives (2015)

Background:Outdoor fine particulate matter (≤ 2.5 μm; PM2.5) has been identified as a global health threat, but the number of large U.S. prospective cohort studies with individual participant data remains limited, especially at lower recent exposures.Objectives:We aimed to test the relationship between long-term exposure PM2.5 and death risk from all nonaccidental causes, cardiovascular (CVD), and respiratory diseases in 517,041 men and women enrolled in the National Institutes of Health-AARP cohort.Methods:Individual participant data were linked with residence PM2.5 exposure estimates across the continental United States for a 2000–2009 follow-up period when matching census tract–level PM2.5 exposure data were available. Participants enrolled ranged from 50 to 71 years of age, residing in six U.S. states and two cities. Cox proportional hazard models yielded hazard ratio (HR) estimates per 10 μg/m3 of PM2.5 exposure.Results:PM2.5 exposure was significantly associated with total mortality (HR = 1.03; 95% CI: 1.00, 1.05) and CVD mortality (HR = 1.10; 95% CI: 1.05, 1.15), but the association with respiratory mortality was not statistically significant (HR = 1.05; 95% CI: 0.98, 1.13). A significant association was found with respiratory mortality only among never smokers (HR = 1.27; 95% CI: 1.03, 1.56). Associations with 10-μg/m3 PM2.5 exposures in yearly participant residential annual mean, or in metropolitan area-wide mean, were consistent with baseline exposure model results. Associations with PM2.5 were similar when adjusted for ozone exposures. Analyses of California residents alone also yielded statistically significant PM2.5 mortality HRs for total and CVD mortality.Conclusions:Long-term exposure to PM2.5 air pollution was associated with an increased risk of total and CVD mortality, providing an independent test of the PM2.5–mortality relationship in a new large U.S. prospective cohort experiencing lower post-2000 PM2.5 exposure levels.Citation:Thurston GD, Ahn J, Cromar KR, Shao Y, Reynolds HR, Jerrett M, Lim CC, Shanley R, Park Y, Hayes RB. 2016. Ambient particulate matter air pollution exposure and mortality in the NIH-AARP Diet and Health cohort. Environ Health Perspect 124:484–490; http://dx.doi.org/10.1289/ehp.1509676
Hunt's team at the Department of Health includes doctor who left BMA over strike
Authors: N. Hawkes
Journal: BMJ (2012)

The new health secretary, Jeremy Hunt, will be backed by an almost new team of ministers. The only holdover from the Lansley era will be Earl Howe, who earned his place by a sterling parliamentary performance in marshalling the Health and Social Care Bill through the Lords.

The new minister of state, Norman Lamb, is already well known in health circles, having been the Liberal Democrat health spokesman between 2006 and the formation of the coalition government in 2010, when he was overlooked for a ministerial job. It went instead to Paul Burstow, whom he now replaces. Lamb was mollified by being appointed parliamentary private secretary to Nick Clegg, the deputy prime minister.

Lamb (54) is the son of climatologist Hubert Lamb, who started the Climate Research Unit at the University of East Anglia in 1972. In those days Lamb senior believed the world was heading for a new Ice Age, a view he soon reversed. Lamb junior also had a change of heart, albeit less extreme. He worked for …
Abstract 3066: Direct detection and enumeration of circulating tumor cells (CTCs) in blood by CastRT-qPCR
Authors: David X. Deng, Scott Sprout, Yun Bao, David Merrill, Pius Brzoska, Yu Wang, Caifu Chen
Journal: Cancer Research (2011)

Abstract Statistical data suggest that only approximately 25% of cancer patients will respond to the same treatment. Enumeration and molecular characterization of circulating tumor cells (CTCs) promise to be valuable for cancer cell diagnosis, survival prognosis, and treatment guidance. However, CTCs are very rare. There is no sensitive and specific assay available for analyzing CTCs from whole blood without extensive enrichment processes. Sample enrichment causes target cells loss, expensive and time-consuming. Here we report a highly specific competitive allele-specific TaqMan-based RT-qPCR (castRT-qPCR) for rare copies of DNA mutation detection. CastPCR can detect rare copies of mutant alleles for up to one in 10 million with a wide dynamic range of more than 6-log orders and &amp;lt;5 copy sensitivity. We have successfully designed and validated cast-PCR assays for more than 80 cancer-related SNPs of KRAS, EGFR, BRAF, KIT, pTEN, p53 and other oncogenes or tumor suppressor genes. CastRT-PCR was used to specifically detect and enumerate CTCs in blood samples with lung cancer cell lines spiking-in and lung cancer patient blood without prior biochemical enrichment processes. EGFR mutation (p.L858R) was detected in all 5 blood samples from late stage lung cancers. Approximately 50% of circulating lung tumor cells with positive EGFR p.L858R mutation had positive EGFR p.T790M mutation. In normal blood samples spiked in cell lines of known Kras and EGFR mutation at the level of 10 cells/mL of whole blood (close to actual patient samples), CastRT-PCR accurately detected the known mutations. Our data suggest that digital castRT-qPCR can be used to enumerate CTCs and detect cancer-related mutations in the blood, which paves the way for future individualized cancer treatment by monitoring CTC level and molecular characterization. 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 3066. doi:10.1158/1538-7445.AM2011-3066
Tc-99m- and Ga-68-Labeled Somatostatin Analogues in the Evaluation of Hurthle Cell Thyroid Cancer
Authors: Juan Pablo Gambini, Adriana Quagliata, Rosa Finozzi, Pilar Serra, Graciela Lago, Javier Gaudiano, Henry Engler, Omar Alonso
Journal: Clinical Nuclear Medicine (2011)

Tc-99m- and gallium-68-radiolabeled somatostatin analogues have been used to evaluate patients with neuroendocrine tumors as well as with thyroid cancer recurrences. We present a case of a patient with Hurthle cell thyroid cancer that had been previously treated with surgery and 5550 MBq of I-131. In the last year the patient noticed a palpable mass in the lower left neck. Tc-99m-HYNIC Octreotide scintigraphy and gallium-68-DOTA-TATE PET/CT scan confirmed 2 focal lesions located in the upper and lower left neck, being this information useful for surgery planning. Radioguided surgery was performed using Tc-99m-HYNIC Octreotide, confirming Hurthle cell cervical nodal recurrences.
PROGNOSTIC UTILITY OF CARDIAC INDEX MEASURED BY CMR IN PATIENTS WITH CORONARY ARTERY DISEASE
Authors: Ahmed Abdi Ali, Robert Miller, Danielle Southern, Mei Zhang, Yoko Mikami, Bobak Heydari, Carmen Lydell, Andrew Howarth, Matthew James, Stephen Wilton, Merril Knudtson, James White
Journal: Journal of the American College of Cardiology (2016)
Granulocyte Colony-Stimulating Factor (G-CSF) -Producing Metastatic Bone Tumors of the Unknown Primary Site
Authors: M. Yoneda, T. Kagoo, T. Hashimoto, J. Shiraishi, K. Ohashi, T. Hosoda, A. Yokoyama, S. Boku, H. Ueno, T. Yano
Journal: Annals of Oncology (2013)
Abstract B20: Acetaminophen enhances the cytotoxicity of cisplatin <i>in vitro</i> and in a subcutaneous tumor xenograft model of human ovarian carcinoma
Authors: Yingjen Jeffrey Wu, Alexander J. Neuwelt, Leslie L. Muldoon, Edward A. Neuwelt
Journal: Cancer Research (2009)

Abstract Background: High dose acetaminophen causes hepatotoxicity by depleting glutathione and increasing production of toxic metabolites. The objective of this study was to examine if these mechanisms of acetaminophen can enhance the cytotoxicity of cisplatin in human ovarian cancer cells both in vitro and in vivo. Methods: In vitro studies (glutathione concentration, cell viability and immunoblotting assays) were performed using SKOV3 human ovarian cancer cells cultured in combinations of acetaminophen and cisplatin. For the tumor model, female nude rats were pre-treated with cyclophosphamide (i.p. 100 mg/kg) one day prior to subcutaneous inoculation of SKOV3 cells with matrigel on the left flank. At 7 days after implantation, rats were randomly assigned into vehicle, cisplatin, and acetaminophen plus cisplatin treatment groups (n=3–5 per group). Subcutaneous tumor volume was measured by dial caliper. Acetaminophen pharmacology and the toxicity of treatments were monitored. Results: In vitro, acetaminophen decreased SKOV3 cellular glutathione level by approximately 30% over 2 hr time frame. Acetaminophen combined with cisplatin decreased cell growth and viability and enhanced apoptosis compared to cisplatin alone in vitro. In vivo, high dose acetaminophen showed uniform tissue distribution, but only decreased glutathione in the liver but not in the serum, brain, or subcutaneous tumor of nude rats. Acetaminophen pretreatment 2–4 hr prior to cisplatin enhanced cisplatin chemotherapeutic effect as determined by a reduction in subcutaneous tumor volume by 15–25% (55–85% vs 40–60%). Serum BUN and creatinine levels were elevated by the combination of acetaminophen with cisplatin treatment when compared to cisplatin alone (48.2±10.9 vs 24.4±4.1 mg/dL; 0.65±0.06 vs 0.30±0.04 mg/dL; p&amp;lt;0.01). Conclusions: Our results suggested that a chemotherapeutic regimen containing both high dose acetaminophen and cisplatin could be applied not only in hepatic tumors but also in ovarian or other tumor malignancies as a potentially promising approach for pre-clinical trial. Citation Information: Cancer Res 2009;69(23 Suppl):B20.
P494 LIVER AND SPLEEN STIFFNESS ASSESSED BY QUANTITATIVE REAL-TIME SUPERSONIC SHEAR WAVE ELASTOGRAPHY (SWE™) CORRELATE WITH CLINICAL STAGES AND PORTOHYPERTENSIVE COMPLICATIONS IN PATIENTS WITH LIVER CIRRHOSIS
Authors: I. Grgurevic, T. Bokun, D. Brnic, Z. Puljiz, R. Heinzl, M. Milosevic, B. Luksic, M. Kujundzic
Journal: Journal of Hepatology (2014)
Acute myeloblastic leukemia (AML) with inv (16)(p13;q22) and the rare I type CBFβ-MYH11 transcript: report of two new cases
Authors: N Grardel, C Roumier, V Soenen, JL Lai, I Plantier, C Gheveart, A Cosson, P Fenaux, C Preudhomme
Journal: Leukemia (2002)
P1284 FACTORS ASSOCIATED WITH RECENTLY ACQUIRED HEPATITIS C VIRUS INFECTION AMONG PEOPLE WHO INJECT DRUGS IN THE UNITED KINGDOM: NEW FINDINGS USING AN AVIDITY TESTING ALGORITHM
Authors: K.J. Cullen, V.D. Hope, S. Croxford, J. Shute, F. Ncube, J.V. Parry
Journal: Journal of Hepatology (2014)
Abstract 1257: Microarray analysis of BRONJ-like oral mucosal lesions in mice
Authors: Susan Bae, Drake Williams, Ju Eun Oh, Songtao Shi, Mo Kang, Ki-Hyuk Shin, No-Hee Park, Reuben H. Kim
Journal: Cancer Research (2012)

Abstract Bisphosphonates (BPs) are potent anti-resorptive agents that are widely used to treat bone-associated diseases including metastatic bone cancer. Many reports have indicated that long-term use of BPs can develop BP-related osteonecrosis of the jaw (BRONJ) that occurs largely at the site of tooth extraction; however, the pathophysiology of BRONJ is still poorly understood. Clinically, BRONJ is defined as exposed necrotic bone with unhealed and open oral mucosa, implying that the lack of wound closure may be caused either directly by BPs or indirectly via biological signals (i.e., cytokines) from the BP-affected surrounding structures. We hypothesize that oral mucosal tissues lose their capacity to close the wound properly at the affected sites and that the genes involved in wound healing processes are differentially expressed between BRONJ lesions and the normal counterparts. To test our hypothesis, we utilized the established BRONJ mice model. Zometa was administered via tail vein 1 week prior to tooth extraction. After extracting the upper first molar, the extracted socket was allowed to heal, and the overlaying oral mucosal tissues were harvested after 2 weeks from control and BRONJ groups (n=3). The fresh tissue samples were subjected to RNA isolation, cDNA sysnthesis, and cDNA hybridization onto microarray chip (Affymetrix MG 430 2.0). The data analysis by functions using IPA software revealed that the genes involved in skeletal and muscular disorders, dermatological diseases, cellular movement, cellular assembly and organization, and inflammatory disease were significantly associated with BRONJ. In particular, we found that growth factors (i.e., Igf2, Fgf7, Pdf2bp2), collagens (i.e., Col1a1, Col1a2, Col2a1, Col2a2, Col5a1, Col5a2, Col11a1, and Col11a2), and non-collagenous proteins (i.e., DMP-1, ITBP, and SPP1) were significantly down-regulated in BRONJ groups. Taken together, our study suggests that the diminution of growth factors as well as collagenous and non-collagenous structural proteins may be associated with the development of BRONJ. This study was supported by NIDCR/NIH (R03DE021114 and K08DE017121). 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 1257. doi:1538-7445.AM2012-1257
Abstract 1853: Monoclonal B-cell Lymphocytosis (MBL) has increased incidence in non-Hodgkin lymphoma (NHL) Families
Authors: Susan L. Slager, Kari G. Rabe, Sara J. Achenbach, Timothy G. Call, Celine M. Vachon, Thomas M. Habermann, Neil E. Kay, Stephen M. Ansell, Tait D. Shanafelt, James R. Cerhan, Curtis A. Hanson
Journal: Cancer Research (2010)

Abstract Background. MBL is defined as a monoclonal expansion of B lymphocytes (&amp;lt; 5 × 109/L) in the blood without associated lymphadenopathy or organomegaly; MBLs with a chronic lymphocytic leukemia (CLL) immunophenotype have been termed as CLL-like MBL. The prevalence of CLL-like MBL in the general population is 3.5-12% but increases with age; however, the frequency is even higher (∼13-18%) among unaffected relatives from CLL families (i.e., families with two or more CLL members). We and others have found that a small proportion of individuals with CLL-like MBL individuals and lymphocytosis will progress to CLL requiring treatment (∼1.1% per year). Because CLL and NHL have been shown to aggregate together within families, suggesting a shared pathogenesis, we evaluated the frequency of MBL in NHL families. Methods. Individuals were obtained from an ongoing study of NHL families (i.e., families with 2 or more NHL members). However, we limited to NHL families with at most 1 individual with CLL due to the known increased frequency of MBL in CLL families. Multi-color flow cytometry was performed on fresh peripheral blood samples. A CBC and differential count was simultaneously obtained using an automated blood cell counter. Five possible flow diagnoses were defined as: CLL-like MBL (CD5+CD20dim), atypical MBL (CD5+CD20bright), non-CLL like MBL (CD5−), and normal immunophenotype (NIPT). Medical records of NHL cases were reviewed to confirm disease. Results. A total of 30 individuals from 16 NHL families had available flow cytometry results. The mean age at flow analysis was 56 years (range 37− 83 years). We identified 5 individuals with MBL from 4 families: 3 of the 6 had CLL-like MBL, 1 had atypical MBL, and 1 had non-CLL like MBL. The remaining 25 individuals had a NIPT. Thus, the MBL rate in NHL families is 17% (5/30). Among the CD5+ MBL (both CLL-like and atypical MBL) individuals, all were female and the mean absolute lymphocyte count was 1.4 × 109/L. Of interest, 1 of the CLL-like MBL individuals is from a family where two members had monoclonal gammopathy of uncertain significance (MGUS). Conclusion: Our data show that MBLs of various phenotypes can be found at a higher prevalence in NHL families than that of the general population. Further, the frequency of MBL in NHL families is comparable to that of CLL families. Although more work is needed, our results suggest that MBL may be clustering within NHL families, and thus support a possible common inherited predisposition of NHL and CLL, with MBL signifying a shared early pathogenetic step. 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 1853.
P504 HEMODYNAMIC RESPONSE TO NON-SELECTIVE BETA BLOCKERS DESPITE LACK OF EFFECTS ON HEART RATE AND SYSTEMIC BLOOD PRESSURE
Authors: S. Bota, M. Mandorfer, P. Schwabl, P. Salzl, A. Ferlitsch, M. Peck-Radosavljevic, T. Reiberger
Journal: Journal of Hepatology (2014)