tbuckley/cabot-search huggingface dataset:
CC-011 Case report: colocutaneous fistula – a rare complication of PEG tube insertion
Authors: A M Verma, J A D Stewart
Journal: Gut (2010)

<h3>Introduction</h3> A 69-year-old man with myotonia and history of partial gastrectomy for ulcer presented in Apr 09 with 2-wk history of diarrhoea and PEG site infection, it was noted that the discharge from the PEG tube and site was offensive. The PEG tube had been placed in 05 for swallowing difficulties with no apparent complications. <h3>Methods</h3> OGD revealed a small “hole” visible in the anterior gastric wall, surrounded by inflamed tissue. A abdominal CT showed the internal bumper and tube sited within the transverse colon. When the PEG was sited, it was placed through the transverse colon into the stomach, forming a tract. The internal bumper had eventually eroded through the stomach in 09, passing through the tract and finished in the transverse colon. This caused a faecalent discharge from the PEG. The remnant gastrocolic fistula caused the diarrhoea. <h3>Results</h3> The PEG tube was cut externally and allowed to pass through defecation. Patient was fed with a NG tube. Colocutaneous fistula remained patent. Diarrhoea had stopped, indicating closure of gastrocolic fistula. Radiological feeding tube insertion was attempted and abandoned as the transverse colon was adherent to the stomach. A PEG insertion was abandoned as trans-illumination was unsuccessful. The patient was not suitable for a surgical feeding tube insertion and he was discharged with long-term NG tube feeding. <h3>Conclusion</h3> PEG tube placement was first described in 1980.1 It is a safe technique to allow long-term feeding in patients with swallowing difficulties of various aetiologies. However, placement of PEG tubes are not without risk. Approximately 4% of patients experience major complications, such as gastric perforation, gastric bleeding, haematoma, aspiration and death. Another 13% may experience relatively minor complications, such as wound infection, tube dislodgment, aspiration, stomal leak, fever, or ileus.2 Colocutaneous fistulas are a rare complication of PEG tube insertion with only a small number of case reports cited in a Medline literature search.34 This appears to be a higher risk in patients who have undergone a partial gastrectomy, possibly due to the colon migrating into the space around the remnant stomach and/or adhesions.5
Abstract 3406: Enhancer of zeste homolog 2 (EZH2) expression and proliferation index (Ki-67) in neuroendocrine tumors of the gastrointestinal tract and pancreas
Authors: Jia Qin, Raag Agrawal, Miguel G. Echevarria, LAura A. Martello, M.A Haseeb, Raavi Gupta
Journal: Cancer Research (2015)

Abstract EZH2 is a polycomb group protein that is involved in the progression of multiple human cancers including prostatic, endometrial, and colonic adenocarcinomas. Its expression has been shown to increase from typical carcinoid to atypical carcinoid and further to small cell/large cell neuroendocrine carcinomas of the lung. Here we examine the EZH2 expression and the proliferation index (PI) by Ki-67 expression in neuroendocrine tumors of the gastrointestinal tract (GI) and pancreas. We retrieved 72 cases of GI and pancreatic neuroendocrine tumors of grades G1 (n = 56), G2 (n = 6) and G3 (n = 10) which were graded according to the WHO classification. Expression of EZH2 and Ki-67 was analyzed by immunohistochemistry using monoclonal antibodies (EZH2 at 1:200; Ki-67 at 1:70). Expression of EZH2 was determined to be low (10%), and was compared with the respective PI. All G1 tumors had low EZH2 expression and a low PI (20%). In G2 tumors, EZH2 expression was intermediate (1-10%) and PI was between 0-8%. One of the G2 tumors had a low PI of 0, however, the EZH2 expression was intermediate (3%). There was increased EZH2 expression relative to increasing tumor grade from G1 to G3 (p &amp;lt;0.05). EZH2 expression increases incrementally from G1 neuroendocrine tumors to G2 and further to G3 tumors, suggesting an association or a role in progression of neuroendocrine tumors. There is strong correlation between the expression of EZH2 and PI in G1, G2 and G3 tumors. EZH2 appears to be a better predictor of tumor grade in G2 tumors as compared to PI. Thus, EZH2 could be used as an additional diagnostic marker in examining atypical GI neuroendocrine tumors. Citation Format: Jia Qin, Raag Agrawal, Miguel G. Echevarria, LAura A. Martello, M.A Haseeb, Raavi Gupta. Enhancer of zeste homolog 2 (EZH2) expression and proliferation index (Ki-67) in neuroendocrine tumors of the gastrointestinal tract and pancreas. [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 3406. doi:10.1158/1538-7445.AM2015-3406
Abstract 4830: The correlation between CXCR7 expression and EGFR mutation in non-small cell lung cancer
Authors: Yiping Han
Journal: Cancer Research (2015)

Abstract Objective: To explore the correlation between CXCR7 expression and EGFR mutation in NSCLC. Materials and Methods: Forty-nine paired cases of NSCLC carcinoma and para-carcinoma tissues were analyzed for the expression of CXCR7 mRNA by RT-PCR and CXCR7 protein by IHC. EGFR mutations were detected in carcinoma tissues by ARMS. T-test, one-way ANOVA and correlation analysis were used to analyze the data with SPSS software version 18.0. Results: In NSCLC, CXCR7 protein expression in carcinoma tissues was higher than in para-carcinoma tissues (14450±2049 vs 5206±1066, p&amp;lt;0.0001), while CXCR7 mRNA was not. In NSCLC, CXCR7 mRNA and CXCR7 protein expression levels were both related to the TNM stage (p = 0.007, p = 0.008) and metastatic status (p&amp;lt;0.0001; p&amp;lt;0.0001), but not to gender, age, smoking index and pathology. EGFR and CXCR7 protein were positively correlated (r = 0.289,p = 0.044) Conclusion: Like EGFR, CXCR7 can be used as a marker to predict the prognosis and guide clinical therapy in NSCLC. Keywords: CXCR7 RDC1 EGFR NSCLC Note: This abstract was not presented at the meeting. Citation Format: Yiping Han. The correlation between CXCR7 expression and EGFR mutation in non-small cell lung 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 4830. doi:10.1158/1538-7445.AM2015-4830
Interpreting Periodic and Rhythmic Electroencephalographic Patterns in Critically Ill Patients
Authors: Sonia Krish, Carl W. Bazil
Journal: JAMA Neurology (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Neurology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Neurology journal
CECA Results in Improved Response Rates and Ability to Proceed to Stem Cell Transplantation in Adult Refractory or Relapsed Acute Myeloid Leukemia
Authors: Sukanthini Subbiah, Randy A. Brown, Myron N Chang, Christopher R Cogle, John W. Hiemenz, W. Stratford May, Jan Moreb, Maxim Norkin, John R. Wingard, Baldeep Wirk, Jack W Hsu
Journal: Blood (2011)
To Dose or Not to Dose: Are IL-10 and IL-6 Accurate Biomarkers to Detect Leptomeningeal Involvement in Small B-Cell Lymphoproliferation?
Authors: Rathana Kim, Myrto Costopoulos, Sylvain Choquet, Karim Maloum, Caroline Algrin, Khe Hoang-Xuan, Catherine Settegrana, Juliette Villemonteix, Martine Brissard, Frederic Davi, Veronique Leblond, Helene Merle-Beral, Magali Le Garff-Tavernier
Journal: Blood (2015)
Abstract 2148: Ras-mediated evasion of detachment-induced cell death involves differential signaling pathways for metabolism and anoikis
Authors: Joshua A. Mason, Calli Versagli, Amy Leliaert, Sienna Durbin, Cassandra Buchheit, Zachary Schafer
Journal: Cancer Research (2015)

Abstract In order for successful metastasis to occur, cells must overcome anoikis, a caspase-dependent cell death process triggered by detachment from the extracellular matrix (ECM). In addition, recent studies have revealed that ECM-detached cells must also rectify detachment-induced metabolic defects that compromise cell survival. However, the precise signals involved in the inhibition of anoikis and the restoration of proper cell metabolism during ECM-detachment are poorly understood. Of particular interest to our studies is the oncogene Ras, which is constitutively active in approximately 30% of all cancers and is well known to be regulate cell death pathways and metabolism. We have discovered that Ras facilitates the survival of ECM-detached cancer cells by utilizing distinct signaling pathways to block anoikis and regulate metabolism. Using MCF-10A cells engineered to overexpress oncogenic Ras and HCT116 cells (which contain an activating Ras mutation), we investigated the signaling pathways downstream of Ras that facilitate the survival of ECM-detached cells. Interestingly, we discovered that while Ras-mediated PI(3)K signaling is critical for rectifying metabolic defects during ECM-detachment, the downstream effector is not Akt, but rather SGK-1. SGK-1 stimulates glucose uptake, enhances ATP generation, promotes luminal filling in 3-dimensional cell culture, and drives anchorage-independent growth in soft agar. Interestingly, our data also indicate that oncogenic Ras utilizes an entirely distinct signaling pathway to block anoikis. We discovered that Ras diminishes the expression of the phosphatase PHLPP1. This inhibits the dephosphorylation-induced activation of a signaling cascade that culminates in the activation of pro-apoptotic p38 MAPK. In aggregate, these data unveil a novel survival strategy utilized by ECM-detached cancer cells and implicate both SGK-1 and PHLPP1 function downstream of Ras during ECM-detachment. The molecular mechanisms unveiled here could be utilized for the design of novel therapies that eliminate ECM-detached, metastatic cancer cells with Ras mutations through simultaneous modulation of SGK-1 and PHLPP1. Citation Format: Joshua A. Mason, Calli Versagli, Amy Leliaert, Sienna Durbin, Cassandra Buchheit, Zachary Schafer. Ras-mediated evasion of detachment-induced cell death involves differential signaling pathways for metabolism and anoikis. [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 2148. doi:10.1158/1538-7445.AM2015-2148
Risk Factors and Clinical Outcome of Thrombotic and Bleeding Complications in 527 Patients Following Hematopoietic Stem-Cell Transplantation (HSCT)
Authors: Yue Han, Wu Depei, Luping Hu, Yongya Ren, Aining Sun, Huiying Qiu, Xiaohui Hu, Ying Wang, Xiaojin Wu, Wei Zhang, Zhaoyue Wang, Changgeng Ruan
Journal: Blood (2011)
Abstract 5282: A 3q amplification gene signature associated with triple negative breast cancer lung-specific metastasis
Authors: Jun Qian, Heidi Chen, Pierre P. Massion
Journal: Cancer Research (2015)

Abstract Triple negative breast cancers (TNBC), devoid of expression of the estrogen, progesterone and HER2 receptors, are among the most aggressive and deadly breast cancers, with high rates of tumor recurrence and metastatic spread. New prognostic markers are needed to identify patients who are at the highest risk for developing metastases, which might assist in tailoring treatment strategies. We previously identified 20 candidate driver genes in Chromosome 3q26-29, a critical amplified region in many human cancers including breast and lung cancer. The aim of this study was to assess the prognostic power of this 20-gene signature in TNBC patients. 855 breast tumors combined from four breast cancer cohorts (GSE12276, GSE2603, GSE2034 and NKI295) were used to evaluate the signature for prediction of organ-specific distant metastasis free survival (DMFS). The predictive ability of the 20-gene signature was evaluated by Cox proportional hazards model and was compared against other published breast cancer gene signatures including MammaPrint (70-gene), Veridex (76-gene), PAM50, 54 lung metastasis signature genes, HIF1 hypoxia pathway (8-gene), TGF β pathway (153-gene), BACH1 pathway metastasis gene signature (25-gene) and Gene Expression Prognostic Index Using Subtypes (GENIUS). The 20-gene signature was strongly associated with worse lung-specific metastasis-free survival (HR, 2.0, 95%CI, 1.4 to 2.87, P=0.00014) in TNBC patients (n = 131), independently of intrinsic subtype or published gene signatures and less so in non-TNBC patients (n = 724, HR, 1.3, 95%CI, 1.01 to 1.69, P=0.04). In conclusion, we discovered an amplified 20-gene signature in 3q26-29 that are associated with lung metastasis in patients with TNBC, suggesting on a potential role of 3q genes in the mechanism of lung-specific metastasis and incriminating cancer driver genes in this location as potential attractive novel therapeutic targets in this disease. The work is supported by the NIH Grant R01 CA102353 to PPM. Citation Format: Jun Qian, Heidi Chen, Pierre P. Massion. A 3q amplification gene signature associated with triple negative breast cancer lung-specific metastasis. [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 5282. doi:10.1158/1538-7445.AM2015-5282
The role of integrated treatments for patients with cancer with bone metastases: The quarterback study.
Authors: M. Ali, A. Todaro, R. A. Aiello, A. D'agostino, G. Scandurra, E. Taibi, C. Costa, M. Caruso, A. Girlando
Journal: Journal of Clinical Oncology (2011)

e19655 Background: Palliative radiotherapy has been shown to improve quality of life in some patients affected by advanced incurable cancers, being also able to reduce major skeletal events and prolonge overall survivall. The integration of radiotherapy and palliative care, such as bisphosphonates and opioid drugs, may lead to further clinical benefit. Our study aimed at evaluating the pain relief score on day 3 and 14 in cancer patients with bone metastases, with particular emphasis to backbone localization. Methods: Sixty patients were evaluated, M/F ratio 22/38, median age 68 years (range 40-78), median ECOG PS 3. The metastases involved bone (100% of cases), backbone (50%), liver (33.3%), lung (30%), lymph nodes (30%), brain (10%), peritoneum (10%), and pleura (3.33%). The primary tumor was breast (40% of cases), lung (NSCLC 23.3%; SCLC 3.33%), prostate (10%), unknown primitive origin (6.72%), colon (6.66%), sarcoma (3.33%), ovary (3.33%), non-Hodgkin’s lymphoma (3.33%). Radiotherapy was administered in 5 fractions with total dose of 20 Gy. The patients were treated with opioids (70%) and bisphosphonates too. Results: The median pain intensity measured by Numerical Rating Scale (NRS) was 6 (range 3-9) before the treatment start. The median Oral Morphine Equivalent Doses consumption was 80 mg (range 30-240). The integrated treatment tested in the study led to quick and considerable pain relief. In fact, the median NRS pain intensity was 4 (± 1.5) on day 3 and 2 (± 1) on day 14. Conclusions: The present data confirm the high prevalence of breast, lung and prostate cancer in patients with bone metastases and support the synergistic use of radiotherapy and palliative care in order to improve the quality of life in our setting of patients.
Capture-Based Targeted Ultradeep Sequencing in Paired Tissue and Plasma Samples Demonstrates Differential Subclonal ctDNA-Releasing Capability in Advanced Lung Cancer
Authors: Xiaowei Mao, Zhou Zhang, Xiaoxuan Zheng, Fangfang Xie, Feidie Duan, Liyan Jiang, Shannon Chuai, Han Han-Zhang, Baohui Han, Jiayuan Sun
Journal: Journal of Thoracic Oncology (2016)
PWE-012 Outcomes of endoscopic mucosal resection of large (≥20 mm) sessile colorectal polyps in ysbyty gwynedd, north wales performed between january 2010 and may 2014: Abstract PWE-012 Table 1
Authors: J Ishtiaq, J gasem
Journal: Gut (2015)

<h3>Introduction</h3> Endoscopic mucosal resection (EMR) is an effective therapeutic technique for removal of large colorectal sessile polyps, and provides an alternative to surgery. To minimise the risks of serious complications only experienced and appropriately trained endoscopists should perform EMR. We aimed to evaluate the outcomes, major complications and recurrence rate for large (20 mm–39 mm) and giant (≥ 40 mm) sessile colorectal polyps. <h3>Method</h3> All EMRs for large ((≥ 20mm) sessile polyps performed between January 2010 and May 2014 were evaluated. The post-EMR major complications, recurrence rate and the technique (en bloc versus piecemeal resection) were analysed. This retrospective study was performed during two separate time periods. The initial study was performed for the polyps managed from January 2010 to December 2012. Post-analysis, specific recommendations were made, particularly to restrict the EMR to the experienced and appropriately trained endoscopists. The subsequent study was performed on the data collected between January 2013 and May 2014, and the comparison of the two studies confirmed better outcomes of the management of the polyps due to the recommendations made in the initial study. <h3>Results</h3> A total of 121 polyps were resected in 117 patients. There were 76 (64.95%) males and 41 females. Mean (± SD) age of the patients was 71.15 (± 10.13) years. There were 92 large polyps (76%) with a mean size of 26.93 (± 4.80) mm (range 20 – 39 mm), and 29 giant polyps (24%) with a mean size of 50.68 (± 12.79) mm (range 40 – 90 mm). The most frequent location was the sigmoid colon (24.79%). 42.14% of the total polyps were on the right side of colon. Enbloc resection was performed in 35 (29.91%) and piecemeal in 82 (70.08%). No immediate or delayed major bleeding occurred. One patient had bowel perforation. Two patients had intramucosal cancer, two had adenocarcinoma, and one patient had a rare finding of MALT lymphoma. Recurrence occurred in 6 polyps. <h3>Conclusion</h3> In our experience EMR- related major complications are low and comply with international standards. The technique requires an individualised approach by the experienced endoscopist, taking into consideration a thorough assessment of a particular patient and their polyp. <h3>Disclosure of interest</h3> None Declared. <h3>References</h3> British Society of Gastroenterology Guidelines American Society of Gastroenterology Guidelines
Abstract A90: Mesothelin confers tumor cell vulnerabilities for gefitinib treatment
Authors: Ethan Poteet, Zhengdong Liang, Youwen Wang, Changyi Chen, Qizhi Yao
Journal: Cancer Research (2016)

Abstract Combination therapy for pancreatic adenocarcinoma (PDAC) has recently had two successful stage III trials with FOLFIRINOX (combination folinic acid, fluorouracil, irinotecan, and oxalplatin) and combination gemcitabine and paclitaxel. Because of the heterogeneity of PDAC, the benefits of combination therapy are immediately apparent since it targets multiple facets of cancer simultaneously. However, FOLFIRINOX and gemcitabine + paclitaxel are highly toxic and affect all dividing cells, making apparent the need for better understanding of the cell profiles in PDAC. The epidermal growth factor receptor (EGFR) is involved in the pathogenesis and progression of many cancers, with EGFR or its ligands often overexpressed or mutated. Recently we have found that EGFR expression is correlated to mesothelin (MSLN) expression in PDAC. MSLN, a cell surface glycoprotein, has been shown by us and other labs to be overexpressed in 80 to 90% of all PDAC cases. To examine the relationship between MSLN and EGFR, we modulated MSLN expression by generating a MSLN overexpressing cell line from MIA-PaCa2 cells, and a MSLN knockdown cell line from CAPAN-2 cells. The change in EGFR signaling mimicked that of MSLN, with MSLN overexpression significantly increasing EGFR expression and MSLN knockdown significantly decreasing EGFR expression. Furthermore, high MSLN (and therefore high EGFR expression) showed increased sensitivity to gefitinib, an EGFR ATP binding site inhibitor, at concentrations as low as 100 nM, while MSLN low expressing cells did not exhibit any effect from gefitinib at concentrations below 10 µM. Cell Cycle analysis demonstrated that gefitinib increased the number of cells in G1 phase after 24 hours in MSLN high expressing cells, but had no effect on MSLN low expressing cells. In addition, western blot analysis of EGFR downstream pathways showed an increase in phosphorylated phospholipase C-Υ (PLC-Υ) in MSLN high expressing cells, which could be mitigated by treatment with gefitinib. Finally, combination therapy with gemcitabine and 100 nM gefitinib showed an additive effect in MSLN high expressing cells, while in MSLN low expressing cells combination gemcitabine and gefitinib had no additional effect over gemcitabine alone. This study demonstrates the correlation between MSLN expression and EGFR expression and indicates that gefitinib could be a potential addition to combination therapy for PDAC in patients with high MSLN expression. Citation Format: Ethan Poteet, Zhengdong Liang, Youwen Wang, Changyi Chen, Qizhi Yao.{Authors}. Mesothelin confers tumor cell vulnerabilities for gefitinib treatment. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; 2016 May 12-15; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2016;76(24 Suppl):Abstract nr A90.