tbuckley/cabot-search huggingface dataset:
Aberrations of HER2 and TOP2A Genes in Breast Cancer.
Authors: K. Nielsen, S. Müller, S. Møller, A. Schønau, E. Balslev, A. Knoop, B. Ejlertsen
Journal: Cancer Research (2009)

Abstract Copy number changes in TOP2A are frequently observed in HER2 amplified breast cancers, and amplification of a whole amplicon containing both genes has been suggested as the underling mechanism. Here, we describe copy number changes of HER2 and TOP2A in two cell lines; one characterized by having amplification of both genes and the other by having amplification of HER2 and deletion of TOP2A. The characteristics are compared to findings in patients with invasive breast cancer.Material and methods: Fluorescence in situ hybridization (FISH) with HER2, TOP2A and centromere 17 (CEN-17) probes was performed on metaphases, interphases and cut sections from breast cancer cell lines. Paired HER2/CEN-17 and TOP2A/CEN-17 data was available from 649 patients from a previously published biomarker study (Knoop et al. J Clin Oncol 2005;23:7483-90).Results: The physical localization of FISH signals in metaphase spreads from cell lines showed that simultaneous amplification is not a simple co-amplification of a whole amplicon containing both genes. HER2 and TOP2A aberrations seem to be due to different mechanisms of amplifications. Most gene signals are translocated to abnormal marker chromosomes. HER2 genes but not TOP2A genes are present in tandem amplicons, leading to a higher HER2 ratio. This observation was confirmed by patient FISH data: 373 tumors (57%) had normal status for both genes. Among the 276 abnormal tumors, 67% had different HER2 and TOP2A status. Simultaneous amplification of both genes was found in 28% of the abnormal tumors (12% of all patients) while deletion of both genes was observed in 5% of the cases (2% of all patients). The average gene/reference ratio was significantly different: 5.0 for TOP2A but 7.2 for HER2 in the amplified tumors (P&amp;lt;0.001; χ2-test). In the HER2 assay 398 (61%) of the 649 tumors had more than 4 gene signals per nucleus while only 96 (15%) of the tumors had more than 4 TOP2A signals per nucleus.Conclusion: In the majority of breast cancer patients, simultaneous aberration of HER2 and TOP2A is not explained by simple co-amplification. Amplification of the two genes may be caused by different mechanisms, leading to higher level of amplification for HER2 compared to TOP2A. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 2119.
TCT-841 ORAl iMmunosuppressive therapy to prevent in-Stent rEstenosiS (RAMSES) cooperation: a patient-level meta-analysis of randomized trials
Authors: Salvatore Cassese, Giuseppe De Luca, Flavio L. Ribichini, Carmelo Cernigliaro, Francesco Versaci, Igino Proietti, Goran Stankovic, Sinisa Stojkovic, Fabrizio Tomai, Corrado Vassanelli, David Antoniucci, Patrick W. Serruys, Adnan Kastrati, Alfredo Rodriguez
Journal: Journal of the American College of Cardiology (2013)
In-111-Labeled Leukocyte Infection Imaging: False-Positive Results Caused by Wound Dressing and Hematoma
Authors: JOSEPH G. RAJENDRAN, MICHAEL M. GRAHAM
Journal: Clinical Nuclear Medicine (1999)

In-111-labeled leukocyte imaging is associated with high sensitivity and specificity rates. False-positive studies with In-111-labeled leukocyte imaging and uptake in various noninfectious sites such as fistulas, colostomies, hematomas, recent surgical scars, and intravenous lines have been reported. The need to be aware of these possible findings is emphasized in this report of a patient with false-positive uptake in a hematoma and surgical dressing of an open wound. In-111 leukocyte imaging was done in a patient receiving renal dialysis who had an uninfected open surgical wound at the right knee stump and a superficial hematoma in the left medial thigh. Images must be repeated after the wound dressing is removed.
First Experience With Image-guided Resection of Paraganglioma
Authors: Ingo Einspieler, Alexander Novotny, Asli Okur, Markus Essler, Marc E Martignoni
Journal: Clinical Nuclear Medicine (2013)

A 32-year-old male patient showed 2 focal uptakes of I-MIBG next to the left renal vein in a diagnostic scan, corresponding to paragangliomas. An operation was indicated, and to guide resection during surgery we used the freehand SPECT system. In the operating room, using freehand SPECT, both lesions were found. The system was of additional value in planning the operative access to the region of interest and in determining the depth of 1 lesion for precise and more rapid extirpation. Furthermore, it confirmed no residues in the operating field after resection of the tumors.
Latest Developments in the Endoscopic Management of Gastroesophageal Reflux Disease and Barrett’s Esophagus: an Overview of the Year’s Literature
Authors: J J G H M Bergman
Journal: Endoscopy (2006)

The development of endoscopic techniques for the treatment of gastroesophageal reflux disease has come to an abrupt halt after some of the most widely disseminated and best evaluated techniques were withdrawn from the market. This underlines the importance of conducting high-quality endoscopic research before techniques are adopted in routine practice.The endoscopic surveillance of patients with Barrett’s esophagus needs to be improved in order to be cost-effective. Alternative techniques for tissue sampling are being explored (e. g., brush cytology, imaging cytometry), as well as the use of molecular markers, to select patients who are at risk and to improve compliance by patients. New endoscopic imaging techniques (such as autofluorescence endoscopy) may improve the detection of early neoplasia in those Barrett’s patients who are at risk for malignant degeneration. Subsequent endoscopic treatment should primarily consist of an endoscopic resection technique with restricted use of ablative therapies. Future studies should focus on the development of endoscopic resection techniques that allow en-bloc resection of Barrett’s lesions, stepwise complete resection of the whole Barrett’s segment, and/or easier and safer tissue ablation. Finally, histopathological studies are needed in order to detect risk factors for an adverse outcome after endoscopic treatment for early neoplasia in Barrett’s patients.
Daytime alertness in patients with primary insomnia
Authors: Q R Regestein, J Dambrosia, M Hallett, B Murawski, M Paine
Journal: American Journal of Psychiatry (1993)

In the absence of clear distinctions in alertness between patients with primary insomnia and normal subjects, the goal of this study was to identify psychometric and electrophysiological measures that would distinguish these two groups.The daytime alertness of 20 primary insomnia patients and 20 normal subjects was investigated through their scores on a 26-item hyperarousal scale and measurement of auditory evoked potentials and alpha and nonalpha band EEG activity. Statistical analysis of the data included correlation of the hyperarousal scores and the electrophysiological measures.The hyperarousal scores showed clearly higher daytime alertness in the insomnia patients compared with the normal subjects. In addition, during wakefulness, the insomnia patients showed greater amplitudes of P1N1, a durable, intrinsic, late (cortical) component of the auditory evoked potential, as well as greater EEG activity across the frequency spectrum. The hyperarousal scores correlated positively with the amplitude of P1N1 at each of three sound intensities.To the authors' knowledge, this is the first study to offer evidence that patients with primary insomnia have objectively definable features during wakefulness that clearly distinguish them from normal subjects. The measurement of hyperarousal might be used to refine descriptions of insomnia populations in experimental studies.
Endoscopic pyloromyotomy for postesophagectomy gastric outlet obstruction
Authors: Hyunsoo Chung, Bernard Dallemagne, Silvana Perretta, Sang Lee, Sung Shin, Jun Park, Jacques Marescaux, Yong Lee
Journal: Endoscopy (2014)

Postesophagectomy gastric outlet obstruction occurs in 20 % – 30 % of patients who undergo esophagectomy and is associated with significant morbidity and delayed recovery [1]. Recently, endoscopic pyloromyotomy, also called gastric peroral endoscopic myotomy (POEM), has been reported, in pigs and in a patient with refractory diabetic gastroparesis [2] [3]. We report a case of postesophagectomy delayed gastric emptying that was successfully treated with endoscopic pyloromyotomy.
Extravasation of Peripherally Administered Parenteral Nutrition
Authors: Benedetta Belloni, Christian Andres
Journal: New England Journal of Medicine (2011)

A 60-year-old woman with advanced Huntington's disease and a recent episode of aspiration pneumonia presented with erythema, edema, and blistering of the right forearm. An 18-gauge peripheral intravenous catheter had been partially displaced from the same site 10 hours earlier, resulting in infusion of an unknown quantity of parenteral-nutrition solution (80 g of dextrose per liter, 22 g of amino acids per liter, 200 kcal of lipids per liter, and 750 mOsm per liter) into the interstitial space. Peripherally delivered parenteral nutrition can act as a vesicant and cause blistering. Its potential to do so varies with the infusion site, . . .
FRI0141 Rheumatoid arthritis is a risk factor for atherosclerosis -the tomorrow study:
Authors: Y. Sugioka, T. Koike, K. Mamoto, T. Okano, M. Tada, S. Wakitani, H. Nakamura
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Cardiovascular diseases (CVD) have recently been recognized as important causes of mortality in patients with rheumatoid arthritis (RA). One aim of the prospective TOMORROW (TOtal Management Of Risk factors in Rheumatoid arthritis patients to lOWer morbidity and mortality; clinical trial registration number: UMIN000003876) study that started in 2010 was to determine associations between atherosclerosis and RA using carotid ultrasound. <h3>Methods</h3> Atherosclerosis was assessed using carotid ultrasound in 402 individuals (mean age 59.0) comprising 200 patients with RA and 202 healthy volunteers (HV). The presence of carotid atherosclerotic plaques and plaque scores defined as the sum of the thickness of carotid plaques were evaluated. <h3>Results</h3> The prevalence of carotid plaques and plaque scores was significantly greater in patients with RA than in controls (47% vs. 37%, p&lt;0.05 and 1.74 vs. 1.02, p&lt;0.01, respectively) Multivariate logistic regression analyses showed that a plaque score of &gt;2.0 was associated with RA after adjustment for atherosclerotic risk factors (age, gender, smoking, hypertension, diabetes mellitus and LDL-cholesterol) (OR 1.74, p&lt;0.05; Table 1). Steinbrocker class remained associated with plaque score (β = -0.148, P=0.03) in patients with RA after adjustment for risk factors. <h3>Conclusions</h3> Atherosclerosis is independently associated with RA. These observations might at least partly explain the high risk for atherosclerosis and cardiovascular disease among patients with RA. <h3>Disclosure of Interest</h3> Y. Sugioka: None Declared, T. Koike Grant/Research support from: Takeda Pharmaceutical, Mitsubishi Tanabe Pharma Corporation, Chugai Pharmaceutical, Eisai, Abbott Japan, Teijin Pharma, Banyu Pharmaceutical and Ono Pharmaceutical, K. Mamoto: None Declared, T. Okano: None Declared, M. Tada: None Declared, S. Wakitani: None Declared, H. Nakamura Grant/Research support from: Chugai Pharmaceutical, Astellas Pharma Inc.,Janssen Pharmaceutica, GlaxoSmithKline, Pfizer Inc. and Daiichi Sankyo, INC., Speakers Bureau: Ono Pharmaceutical
Associations between estrogen receptor (ER) Alpha expression levels and ER genotypes.
Authors: NL Henry, S Shak, M Banerjee, T Skaar, G Palmer, M Braman, V Stearns, DA Flockhart, C Kleer, DF Hayes, J Rae
Journal: Cancer Research (2009)

Abstract Abstract #3049 Background: Estrogen receptors (ER) and associated factors, including progesterone receptors (PgR), modulate estrogenic effects both in normal tissue and in hormone receptor (HR)-positive breast cancers. ERα expression occurs in the majority of breast cancers, although the level of overexpression varies between tumors. Multiple single nucleotide polymorphisms (SNPs) in the genes that encode ER, termed ESR1 (ERα) and ESR2 (ERβ), have been shown to affect phenotypic outcomes, including breast cancer risk, bone mineral density, hot flashes, and lipid levels. We hypothesized that SNPs in genes that encode ER may affect level of ER overexpression.&amp;#x2028; Methods: DNA was extracted from white blood cells from 100 subjects with HR-positive breast cancer enrolled in a tamoxifen observational study. SNPs in ESR1 (XbaI: rs#9340799, PvuII: rs#2234693) and ESR2 (01: rs#1256049; 02: rs#4986938) were determined from germline DNA using TaqMan. ER overexpression in paraffin-embedded formalin-fixed tumor specimens was quantified with immunohistochemistry (IHC) of tumor specimens on slides (Ventana Image Analysis System) and with RT-PCR using the Oncotype DX breast cancer assay (Genomic Health, Inc). Gene expression of other ER-associated genes (PgR, BCL2, and SCUBE2) was determined using RT-PCR (Oncotype DX). Expression of ER and associated genes across ER genotype was performed using the Kruskal-Wallis test. For all analyses, a p value of &amp;lt;0.05 was considered statistically significant.&amp;#x2028; Results: ER expression assessed using IHC and RT-PCR was statistically significantly correlated, with a Pearson correlation coefficient of 0.43 (p=0.0006). However, there was no association between the ESR1 or ESR2 genotypes and ER expression assessed by either method. A trend between ESR1 XbaI genotype and PgR expression by RT-PCR was noted (p=0.08 for gene-dose effect). No other associations between ER polymorphisms and expression of ER-related genes were identified.&amp;#x2028; Conclusions: SNPs in genes encoding for ER do not appear to be associated with level of ER expression in breast cancer. Differences in ER expression between individual tumors are likely due to mechanisms other than these inherited mutations in the ER genes. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 3049.
A novel disposable, transnasal esophagoscope: a pilot trial of feasibility, safety, and tolerance
Authors: J. Chung, S. Park, M. Chung, J. Park, S. Park, J. Chung, S. Song
Journal: Endoscopy (2012)

A novel disposable transnasal esophagoscope, the E.G. Scan (IntroMedic Co. Ltd., Seoul, Korea), was developed for the evaluation of esophageal diseases while eliminating the inconvenience associated with sterilization, portability, patient monitoring, complications, and the economic burden of sedation. The feasibility, safety, and tolerability of the first version of the E.G. Scan was evaluated in this pilot study. Nasal esophagoscopy was performed successfully in 46 patients with known or suspected esophageal diseases. At least 50 % of the Z-line was visualized by the E.G. Scan in 38 (82.6 %) of 46 patients. Abnormalities were identified in 27 patients: erosive esophagitis (n = 18), Barrett's esophagus (n = 1), esophageal varices (n = 7), and esophageal candidiasis (n = 1). Nasal pain was absent or mild in most patients, and adverse events were not observed. Further technical improvement of the E.G. Scan would increase the diagnostic usefulness in future clinical practice.
THORACIC AORTIC DILATATION IS A HEREDITARY DISEASE: A LARGE CROSS SECTIONAL IMAGING STUDY
Authors: Mirza Mujadil Ahmad, Khawaja Afzal Ammar, Mirza Nubair Ahmad, Rayan Yousefzai, Janardhan Krishnaswamy, Bijoy K. Khandheria, Renuka Jain, A. Jamil Tajik
Journal: Journal of the American College of Cardiology (2016)
Abstract 3923: Growth hormone activates ERK via EGFR, not IGF-IR, to potentiate estrogen-dependent breast cancer cell proliferation
Authors: Dana L. Felice, Terry G. Unterman, Steven M. Swanson, Jonna Frasor
Journal: Cancer Research (2012)

Abstract Estrogen receptor (ER) and insulin-like growth factor-I receptor (IGF-IR) interact and activate one another in breast cancer cells, and ER can up-regulate components of the IGF-I signaling pathway. Therapeutic strategies co-targeting ER and IGF-IR in ER-positive breast tumors have been developed, yet clinical trials of anti-IGF-IR therapies have not been as successful as had been hoped. Although growth hormone (GH) is implicated in having a role in breast cancer, its effects are often attributed to the actions of IGF-I. Since inhibition of IGF-IR can cause an increase in circulating levels of GH, we considered the possibility that GH may act directly on the tumor itself thus explaining the limited efficacy of anti-IGF-IR therapy in breast cancer. Therefore, we sought to determine whether GH has direct, IGF-I-independent effects on breast cancer. We demonstrate in T47D human breast cancer cells that while GH alone only weakly stimulates cell proliferation, it significantly enhances estradiol (E2)-stimulated proliferation. Inhibition of IGF-IR reduced E2-stimulated proliferation, confirming previous findings. Remarkably, GH+E2 overcame the IGF-IR blockade to promote proliferation. This indicates that GH not only acts in an IGF-I-independent manner, but can bypass IGF-IR inhibitors to restore E2 action on proliferation. Furthermore, we found that both epidermal growth factor receptor (EGFR) and ERK were required for proliferation stimulated by GH and E2, and that GH uses EGFR to activate ERK even in the presence of the IGF-IR inhibitor. Expression of proliferation genes up-regulated by GH+E2 treatment was abrogated by the EGFR and MEK inhibitors, but not by the IGF-IR inhibitor. Thus, we propose that while E2-stimulated proliferation requires IGF-IR, EGFR, and ERK, the presence of GH allows E2 to bypass the requirement for IGF-IR while remaining dependent on EGFR and ERK. Furthermore, we have found that GH can potentiate E2 stimulation of ER target gene transcription and this is dependent on ERK, but not on IGF-IR. Taken together, these findings indicate that GH not only can act directly on breast cancer cells independently of IGF-I, but can bypass IGF-IR blockade to stimulate ERK and potentiate E2 activity on proliferation and gene regulation. A better understanding of the interactions between GH and E2 will contribute to the development of novel drugs or improved combination therapies targeting the GH/IGF/E2 axis in breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3923. doi:1538-7445.AM2012-3923
Abstract 3024: FGFR1 amplification is linked to the squamous cell carcinoma subtype in esophageal carcinoma.
Authors: Katharina von Loga, Jule Kohlhaussen, Andreas H. Marx, Guido Sauter, Tobias Grob, Alexander Quaas
Journal: Cancer Research (2013)

Abstract Introduction Stimulation of Fibroblast-growth-factor-receptor-1 (FGFR1) plays an important role in cell differentiation and cell growth. Amplification of the FGFR1 gene was described in various cancer types. Clinical phase I trials are currently performed to address the potential applicability of anti-FGFR1-drugs in squamous cell carcinoma of the lung. Prevalence and clinical significance of FGFR1 amplification are unknown in esophageal carcinoma. Material and Methods In this study, six hundred formalin-fixed paraffin-embedded tissue samples from patients with esophageal carcinoma were analysed, including 346 patients with adenocarcinoma and 254 patients with squamous cell carcinoma. Dual-labeling Fluorescence in situ hybridization (FISH) was applied using probes for FGFR1 and centromere 8. The initial analysis was in a tissue microarray (TMA) format. All available tumor blocks from amplified tumors were subsequently analysed for heterogeneity on large sections. When available, lymph node metastases and tumor-adjacent dysplasia were also analysed on large sections from these tumors, Results FGFR1 amplification was more frequently seen in squamous cell carcinoma (9.4% of 202 interpretable cases) than in adenocarcinoma (1.6% of 308). High polysomy was found in an additional 5.9% of squamous cell carcinoma and 0.6% of adenocarcinoma. FGFR1 amplification was significantly associated with histologic grade (p=0.02) but was unrelated to tumor type, pT, pN, pM, UICC stage and survival. FGFR1 amplification was homogeneous across the tumor in most cases. FGFR1 heterogeneity was observed in only 3 of 24 cases. FGFR1 amplification was similarly observed in the primary tumor and in 6 cases each of lymph node metastases and dysplasia. Summary In conclusion, FGFR1 amplification in squamous cell carcinoma of the esophagus occurs at similar frequencies as in squamous cell carcinoma of the lung. The high homogeneity of FGFR1 in the primary tumor and the lack of discordant results in dysplasia argue for FGFR1 amplification, representing an early alteration in a subgroup of esophageal cancers. The high homogeneity of FGFR1 amplification provides further arguments for FGFR1 representing an interesting drug target in these cancers. Citation Format: Katharina von Loga, Jule Kohlhaussen, Andreas H. Marx, Guido Sauter, Tobias Grob, Alexander Quaas. FGFR1 amplification is linked to the squamous cell carcinoma subtype in esophageal carcinoma. [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 3024. doi:10.1158/1538-7445.AM2013-3024