tbuckley/cabot-search huggingface dataset:
Abstract 3586: Benzopyrene diol epoxide attenuates p34cdc2 and inhibits cell growth: role of p53.
Authors: Jagat J. Mukherjee, Subodh Kumar
Journal: Cancer Research (2013)

Abstract Our previous findings demonstrated that DNA damage by polynuclear aromatic hydrocarbons (PAHs) triggers cellular protective response of cell growth inhibition (G1-S cell cycle arrest and inhibition of DNA synthesis) in human fibroblast associated with accumulation of p53 protein, a known cell growth inhibitory transcription factor. Here we report that in different cell lines BPDE treatment (ultimate carcinogenic metabolite of the PAH benzo[a]pyrene) triggers variable extent of cell growth inhibition which do not correspond to the extent of increased p53 accumulation as we observed. We also observed that BPDE treatment of cells significantly down-regulates expression of p34cdc2, a known cell cycle activating protein. Although the role of cdc2 down-regulation in inhibition of cell cycle progression is well known, to the best of our knowledge cdc2 down-regulation in response to cellular insult by PAHs has not been reported. Unlike p53 accumulation there is correspondence between extent of cell growth inhibition and the extent of cdc2 down-regulation by BPDE in different cell lines. Interestingly, BPDE-induced cdc2 down-regulation is observed to be p53 dependent although there is lack of correspondence between the extent of p53 accumulation and cdc2 down-regulation. However, extent of BPDE induced cdc2 down-regulation was observed to have correspondence with the extent of accumulation of cell cycle inhibitor protein p21 (transactivation product of p53) in different cell lines. These findings may have an implication that cell growth inhibition in response to DNA damaging PAHs may involve down-regulation of cdc2 protein mediated by p53 activation (transactivation ability), and the extent of p53 accumulation is not the determining factor in this regard. Citation Format: Jagat J. Mukherjee, Subodh Kumar. Benzopyrene diol epoxide attenuates p34cdc2 and inhibits cell growth: role of p53. [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 3586. doi:10.1158/1538-7445.AM2013-3586
PATIENT-REPORTED ANGINA AFTER BIORESORBABLE VASCULAR SCAFFOLDS VERSUS METALLIC EVEROLIMUS-ELUTING STENT FOR CORONARY ARTERY DISEASE: A SYSTEMATIC REVIEW AND META-ANALYSIS
Authors: Rodrigo Mendirichaga, Rhanderson Cardoso, Daniel Garcia, Gilson Fernandes, Mohammad Ansari
Journal: Journal of the American College of Cardiology (2016)
Abstract 1907: Heat shock protein 90 inhibition overcomes hepatocyte growth factor-triggering resistance to EGFR tyrosine kinase inhibitors in EGFR mutant lung cancer by decreasing client protein expression and angiogenesis
Authors: Tadaaki Yamada, Hitomi Koizumi, Shinji Takeuchi, Takayuki Nakagawa, Seiji Yano
Journal: Cancer Research (2012)

Abstract The three major, clinically relevant mechanisms of acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in EGFR mutant lung cancer are a second mutation in the EGFR gene (T790M), Met amplification, and increased expression of hepatocyte growth factor (HGF). Heat shock protein90 (Hsp90) is a 90kDa molecular chaperone for proteins that include EGFR, Met and EML4-ALK. Hsp90 inhibitors have been reported to reverse resistance to EGFR-TKIs caused by EGFR T790M mutation and Met amplification. Here, we determined whether inhibition of Hsp90 could overcome HGF-triggered EGFR-TKI resistance in EGFR mutant lung cancer cells. EGFR-TKI erlotinib inhibited the growth of PC-9, HCC827, and Ma-1 cells, with deletions in exon19 of EGFR, but not HGF-gene transfected Ma-1 (Ma-1/HGF) cells and H1975 cells, which contain the EGFR L858R and T790M mutations, respectively. Erlotinib also did not inhibit the growth of PC-9 and Ma-1 cells in the presence of HGF. However, an Hsp90 inhibitor, 17-DMAG, induced apoptosis and markedly inhibited the growth of these cell lines, even in the presence of HGF. This inhibition by 17-DMAG was associated with decreased expression of EGFR and Met, thereby decreasing Akt phosphorylation in tumor cells. In an in vivo model of HGF-triggered erlotinib-resistance, using Ma-1/HGF cells, 17-DMAG markedly suppressed tumor growth by decreasing angiogenesis and increasing apoptosis. These results indicate that Hsp90 inhibitors may overcome HGF-triggered resistance to EGFR-TKIs and that the use of Hsp90 inhibitors may result in more successful treatment of EGFR mutant lung cancers. 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 1907. doi:1538-7445.AM2012-1907
Retrograde Catheterization of the Left Ventricle and Angiography in the Diagnosis of Mitral-Valve Disease
Authors: Oscar E. Starobin, David Littmann, Charles A. Sanders, John D. Turner
Journal: New England Journal of Medicine (1961)

THE diagnosis of mitral regurgitation by conventional means is probably less satisfactory and more apt to be in error than the identification of any other valvular disturbance. For the best use of available therapeutic methods, the most precise diagnostic means are required. It is important, for example, to know whether or not mitral stenosis is accompanied by significant regurgitation before one decides first on the desirability and then on the method of surgical correction. Closed valvulotomy is commonly the procedure of choice in pure stenosis whereas "open" technics are required when significant regurgitation is also present. When mitral insufficiency is . . .
Hearing in an Aging Population
Authors: Robert E. Klotz, Marjorie Kilbane
Journal: New England Journal of Medicine (1962)

THIS paper represents the initial report of a study of presbycusis being carried out at the Age Center of New England, Incorporated. It was written with two purposes in mind: to acquaint the medical profession with the Age Center and the work being done there; and to add to the literature data gathered from an audiologic assessment of 170 older people.The Age Center of New England is a nonprofit organization devoted to intensive research into the problems of our aging population. There are approximately 800 older people registered with the Age Center, about half of whom are available for . . .
IMPORTANCIA DE ESCALAS VALIDADAS PARA EVALUACIÓN DE LIMPIEZA DEL COLON EN COLONOSCOPIA. EXPERIENCIA EN UN HOSPITAL DE TERCER NIVEL
Authors: VM Sastre, M Torregrosa, L Sevilla, S Morán
Journal: Endoscopy (2014)

Introducción: La decisión del endoscopista con respecto a la repetición de una colonoscopia debido a la preparación de limpieza insuficiente es un criterio actualmente no definido ni estandarizado en las guías de práctica clínica. Por lo tanto, es preciso unificar criterios para evitar la variabilidad interexplorador a la hora de evaluar este aspecto frecuente en la práctica endoscópica. Hay estudios que demandan un consenso internacional utilizando escalas validadas para tal efecto como la actual Escala de limpieza de colon de Boston (ELCB).
Abstract LB-432: Validation studies for Korean breast cancer prediction model
Authors: Boyoung Park, Ji Young Lee, Myung-Chul Chang, Dong-Young Noh, Sei-Hyun Ahn, Daehee Kang, Keun-Young Yoo, Sue K. Park
Journal: Cancer Research (2010)

Abstract Background: A model for predicting breast cancer risk has been developed in Korea. Associated risk factors included in the model were 1st degree relatives with breast cancer, age at menarche, menopausal status, number of children, age at first fullterm pregnancy, mammography, and exercise for patients less than 50 years of age and 1st degree relatives with breast cancer, age at menarche, age at menopause, number of children, BMI, mammography, and exercise for patients greater than 50 years of age. The area under the curve among over 50 year olds was 0.655 and 0.611 among under 50 year old. Objectives: The objective of the study was validation of an absolute risk prediction model for breast cancer in Korea by using a large, population cohort and patient registry. Method: The Korean Multi-center Cancer Cohort (KMCC) and registry data of breast cancer patients constructed by the Korean Breast Cancer Society were used to validate the model. 12221 women more than 30 years of age at baseline answered questions about demographic characteristics, reproductive factors, lifestyle, family history since 1993 and we identified 11 and 5 incident breast cancer patient more than 50 and less than 50 years of age, respectively. Age, resident area, and included year were matched to select controls; women aged less than 50 were matched 1:20 while women aged greater than 50 were matched 1:10. In the breast cancer registry, clinical, demographic characteristics and reproductive factors of breast cancer patients were collected since 1980. We selected 2727 patients under 50 years old and 2000 patients over 50 years old matched by age and diagnostic year and calculated their 10, 20, 30, and 40 year absolute risk. Result: In the KMCC data, 10 year absolute risk was 0.39 (95% CI 0.36-0.42) among cases and 0.36 (95% CI 0.35-0.37) among controls under 50 years old and 0.16 (95% CI 0.10-0.22) among cases and 0.08 (0.07-0.09) among controls over 50 years old and it was significantly different in the median test (P-value: 0.02 in both groups). Among breast cancer patient group over 50 years old, 10, 20, 30 and 40 year absolute risk were 0.22 (95% CI 0.21-0.23), 0.35 (95% CI 0.34-0.36), 0.43 (95% CI 0.42-0.45), 0.46 (95% CI 0.44-0.48) respectively and 0.56 (95% CI 0.55-0.57), 1.18 (95% CI 1.15-1.21), 1.53 (95% CI 1.50-1.57), 1.74 (95% CI 1.70-1.78). Conclusion: Due to the short follow up time and small number of cancer incidence in the KMCC cohort, although absolute risk was small, a significant difference was confirmed. Future validation study with a large number and enough follow up cohort time is needed. 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 LB-432.
Lack of evidence of an association between HHV-8 and multiple myeloma
Authors: D Bouscary, N Dupin, S Fichelson, M Grandadam, M Fontenay-Roupie, AG Marcelin, P Blanche, F Picard, JM Freyssinier, P Ravaud, F Dreyfus, V Calvez
Journal: Leukemia (1998)
Homozygous Familial Hypercholesterolemia
Authors: Jan L. Breslow, Duane R. Spaulding, Samuel E. Lux, Robert I. Levy, Robert S. Lees
Journal: New England Journal of Medicine (1975)

Patients with homozygous familial hypercholesterolemia fall into two groups: one responds to diet and drug therapy; the other does not. Fibroblasts from patients in each group were compared for low-density lipoprotein suppression of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and low-density lipoprotein binding. In fibroblasts from four therapy-responsive patients, low-density lipoprotein (100 mug per milliliter) suppressed 3-hydroxy-3-methylglutaryl coenzyme A reductase activity to 41 +/- 12 per cent of control (without low-density lipoprotein) whereas fibroblast enzyme activity from two therapy-unresponsive patients was not suppressed (P less than 0.001). Low-density lipoprotein binding to fibroblasts from both groups was defective as compared to normal controls. Fibroblasts from two therapy-responsive patients had specific binding of low-density lipoprotein of 27 +/- 4 per cent of normal -- greater than the 12 +/- 2 per cent (P less than 0.005) binding to fibroblasts from one therapy-unresponsive patient. These biochemical differences may help explain the variable response to therapy in homozygous familial hypercholesterolemia.
Preventing Asthma Epidemics Due to Soybeans by Dust-Control Measures
Authors: Josep M. Anto, Jordi Sunyer, Charles E. Reed, Josefina Sabria, Francesc Martinez, Ferran Morell, Rosa Codina, Robert Rodriguez-Roisin, Maria J. Rodrigo, Josep Roca, Marc Saez
Journal: New England Journal of Medicine (1993)

The inhalation of soybean dust released during the unloading of soybeans into a silo caused outbreaks of asthma in Barcelona, Spain. This study was designed to determine morbidity due to asthma and serum IgE reactivity before and after the installation of filters in the silo.We measured soybean-allergen concentrations in 136 samples of air collected for 9 months before and 24 months after the installation of filters. We compared the number of days on which there was an unexpected increase in emergency room visits for asthma, the number of days on which the number of emergency room visits for asthma in one four-hour period was so high that it was unlikely to be due to chance, and the mean daily number of emergency room and intensive care unit admissions for asthma for a total of 60 months before and after filter installation. Serum IgE antibodies against soybean allergens were measured in 38 patients before and after filter installation.The concentration of airborne soybean allergens on days when soybeans were unloaded decreased from 324 to 25 U per cubic meter after the installation of filters (P < 0.001). The number of days on which there was an unusually large number of visits to the hospital for asthma and the number of days on which asthma was epidemic both decreased significantly (both P < 0.001), from 29 to 6 and from 18 to 0, respectively. The mean daily number of emergency room and intensive care unit admissions for asthma on days when soybeans were unloaded decreased from 8.3 to 5.4 and from 0.26 to 0.01, respectively (both P < 0.001). The mean serum IgE antibody concentrations in the 38 patients studied decreased from 2 Pharmacia reference units per milliliter to 1 (P < 0.001).Installing filters on silos to prevent airborne dissemination of allergenic soybean dust eliminates outbreaks of asthma caused by inhalation of the dust, thus supporting the idea that the avoidance of allergens helps prevent asthma.
The β-Thalassemias
Authors: Nancy F. Olivieri
Journal: New England Journal of Medicine (1999)

In 1925, Thomas Cooley and Pearl Lee described a form of severe anemia, occurring in children of Italian origin and associated with splenomegaly and characteristic bone changes.1 Over the next decade, a milder form was described independently by several Italian investigators.24 Because all early cases were reported in children of Mediterranean origin, the disease was later termed thalassemia, from the Greek word for sea, thalassa.5 Over the next 20 years, it became apparent that Cooley and Lee had described the homozygous or compound heterozygous state for a recessive mendelian disorder not confined to the Mediterranean, but occurring widely . . .
Cellular Immune Response in Genital Herpes Simplex Virus Infection
Authors: Lawrence Corey, William C. Reeves, King K. Holmes
Journal: New England Journal of Medicine (1978)

We studied the relations between the cellular immune response, pre-existing complement-fixing antibody and virus type with duration of virus excretion in genital herpes simplex virus (HSV) infection. Thirty-six patients (seven with HSV-1 and 29 with HSV-2) with genital herpes underwent serologic testing, sequential viral cultures and weekly determination of lymphocyte-transformation stimulation index with inactivated HSV antic n. The duration of virus excretion was shortest in those with pre-existing complement-fixing antibody, was unrelated to virus type, and was inversely correlated with the magnitude of the mean peak stimulation index (r = -0.69, P less than 0.001). Prolonged virus excretion occurred in patients with a delayed and diminished peak index. Recurrent episodes had a higher peak index (29.4 compared to 14.5) (P less than 0.02), an earlier development of the peak during recurrences (9.1 vs. 25.8 days) (P less than 0.01) and a briefer duration of viral shedding than initial episodes. Thus, the temporal course and magnitude of the stimulation index correlate with and may determine the duration of genital HSV infection.
Abstract 3120: miR-489 function as tumor suppressor miRNA by targeting HER2 in HER2-positive breast cancer
Authors: Yogin Patel, Nirav Shah, Racheal Botbyl, Jishin Lee, Hexin Chen
Journal: Cancer Research (2015)

Abstract Human epidermal growth factor receptor 2 (HER2) is a receptor tyrosine kinase overexpressed in 20-30% of all breast cancer and associated with poor prognosis and outcome. Previous studies have shown that dysregulation of several micro RNAs (miRs), play a key role in breast cancer progression and metastasis. In this study, we evaluated ∼330 miRs, to find specific miRs dysregualted by HER2 signaling. After further screening we focused our study on miR-489, whose expression was ∼6-7 fold downregulated specifically by HER2 signaling. Restoration of miR-489 expression in several HER2-positive breast cancer cell lines resulted in increased cell death and cell cycle arrest. To investigate the molecular mechanism of action of miR-489, we studied effect of miR-489 on HER2 signaling pathway and found that higher expression of miR-489 led to the decreased levels of HER2 (both mRNA and protein) and decreased Akt activation. Furthermore, we for the first time demonstrated that HER2 is a direct target of miR-489 and therefore HER2 and miR-489 signaling pathways form a mutual regulatory loop. To further demonstrate clinical relevance of miR-489, we analyzed both normal and tumor human breast tissue samples using Fluorescent in situ hybridization technique (FISH). Our imaging data indicated that miR-489 is expressed at much lower level in tumor tissues compared to that of the normal breast tissue. Overall, our data indicates that miR-489 acts as a tumor suppressor miR at least partially by directly targeting HER2 in HER2 positive breast cancer cells. Citation Format: Yogin Patel, Nirav Shah, Racheal Botbyl, Jishin Lee, Hexin Chen. miR-489 function as tumor suppressor miRNA by targeting HER2 in HER2-positive breast cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3120. doi:10.1158/1538-7445.AM2015-3120
AB0887 Low dose computed tomography (low dose CT) for assessing sacroiliitis in patients with suspected axial spondyloarthritis and inconclusive radiographs
Authors: I.-H. Song, Z. Grozdanovic, J. Carrasco, K. Basic, J. Sieper, M. Rudwaleit
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Sensitivity and specificity of conventional radiographs of the sacroiliac joints (SI-joints) for assessing sacroiliitis is limited. Low dose CT may better visualise SI joints than plain radiographs and is associated with lower radiation exposure. <h3>Objectives</h3> Evaluation of the diagnostic role of low dose computed tomographies (CTs) of the SI-joints in assessing patients with chronic low back pain and low to moderate suscipition of axial SpA. <h3>Methods</h3> 51 Patients who presented to our clinic in a routine clinical setting for evaluation of chronic back pain of unknown origin and in whom x-rays of the SIJ were inconclusive underwent low dose CTs of the SI-joints. 7 patients also underwent magnetic resonance imaging (MRI) of the SIJ. We retrospectively analysed in how many patients low-dose CT helped to establish a diagnosis. <h3>Results</h3> 51 patients (47.1% male, 53.1% HLA-B27 positive, mean age 48.2 years (SD 10.3), mean disease duration 9.3 years (SD 7.9)) were retrospectively assessed. Only 36.4% presented with inflammatory back pain (IBP). Using low dose CTs of the SI-joints, finally: A) in 66.7% (34/51) of patients sacroiliitis was excluded, among them degenerative changes of SI-joints were found in 17.6% (9/51) of patients. In nearly all of these patients axial SpA was excluded. B) In 9.8% (5/51) a diagnosis of ankylosing spondylitis (AS) could be confirmed by CT. C) In 23.5% (12/51) of patients chronic sacroiliitis (mostly sacroiliitis unilaterally grade 2) was found however these findings were not sufficient to fulfil the modified New York criteria. Amongst others based on these findings in most of these patients a diagnosis of “undifferentiated axial spondyloarthritis” was made. In one of these patients MRI could not be performed because of claustrophobia. <h3>Conclusions</h3> In this group of slightly older chronic back pain with moderate suspicion of axial SpA only low-dose CT of the SI-joints helped to exclude axial SpA. Low dose CT which is associated with a lower radiation exposure may be used as an alternative to MRI in this population. <h3>Disclosure of Interest</h3> None Declared
Case 33-2006
Authors: Raymond T. Chung, Joseph Misdraji, Dushyant V. Sahani
Journal: New England Journal of Medicine (2006)

A 43-year-old man was evaluated as an outpatient for hypogonadism, new-onset diabetes, arthralgias, and fatigue. The patient was in his usual state of health until fatigue and decreased libido gradually developed 6 months before evaluation. An initial workup revealed hyperglycemia and elevated levels of liver enzymes and serum ferritin. A diagnostic procedure was performed.
Abstract 4230: The pro-inflammatory secretory phenotype and selection of stem-like cells in RAS-transformed ovarian epithelial cells
Authors: Weiwei Shan, Gong Yang, Imelda Mercado-Uribe, Jinsong Liu
Journal: Cancer Research (2010)

Abstract Epithelial ovarian cancer (EOC) is the deadliest gynecological cancer in the United States. Previously, our laboratory has successfully transformed human ovarian epithelial cells with oncogenic RAS carrying an activating mutation at valine12 (HRASV12) (T29H cells). By cDNA expression microarray we found that T29H cells exhibited marked activation of a wide spectrum of inflammatory genes and generated a pro-inflammatory phenotype. In this report, we identified a much more malignant phenotype in ovarian tumor explants derived from T29H (hereby denoted T29HT) cells, manifested by a significantly shorter latency of tumor onset after inoculation of T29HT cells back into nude mice than that of the parental T29H cells, suggesting that the T29H cells underwent a selective process in vivo that was favorable to the enhancement of tumorigenicity. By examining the ability of cells to form spheroids in suspension culture and staining spheroids with stem cell marker CD44, we showed that T29HT cells may contain a larger population of potential stem-like cells than do T29H cells. Western blot analysis confirmed higher expression levels of CD44 and genes involved in epithelial mesenchymal transition (EMT) in T29HT cells than in T29H cells. Our results suggest that T29H cells may acquire augmented malignancy in vivo by expanding the pool of potential cancer stem-like cells, and HRASV12-induced pro-inflammatory factors may play pivotal roles in mediating this effect. 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 4230.