tbuckley/cabot-search huggingface dataset:
Colovesical Fistula in a Patient With Recurrent Cervical Cancer Detected by FDG PET/CT
Authors: Kuan-Yung Chen, Chih-Hung Hsu, Chia-Hung Kao, Guang-Uei Hung, Jainn-Shiun Chiu, Kuo-Wei Ho
Journal: Clinical Nuclear Medicine (2010)

We report the case of a 57-year-old woman with the history of stage IB cervical cancer. She was found to have a metastatic squamous cell carcinoma in sigmoid colon. FDG PET/CT was then performed for whole-body cancer work-up. Intense FDG activity accumulated in the sigmoid tumor, with an unusually high SUVmax of 72.42, and was seen downwardly connected with the activity of urinary bladder on PET images. On the coregistered CT images, irregular wall thickening was noted for both sigmoid colon and urinary bladder with a hypodensity tract communicating with each other. It was concluded that recurrent cervical cancer involving urinary bladder and sigmoid colon resulted in colovesical fistula.
Abstract LB-20: Serum antioxidant levels and survival time in advanced non-small cell lung cancer patients.
Authors: Kosin Wirasorn, Pranithi Hongprabhas, Veeradej Pisprasert, Kulthida Klarod, Patcharee Boonsiri
Journal: Cancer Research (2013)

Abstract Background: Oxidative stress is involved with carcinogenesis of lung cancer and promotes tumor growth. Antioxidants play roles in inhibition of oxidative stress; consequently slow progression of tumor growth. This study aimed to show the correlation between median survival in advanced-stage non-small cell lung cancer (NSCLC) patients and antioxidant levels. Methods: Newly diagnosed advanced-stage NSCLC patient in Khonkaen University Hospital during June 2006 and June 2008 were enrolled. Participants who had history of taking dietary supplements were excluded. Tumor data and nutritional status were evaluated in all patients. Serum from each participant was taken since the date of diagnosis to determine non-enzymatic antioxidants, trace element antioxidants, and peroxidase levels. Each antioxidant level was categorized into quartiles to analyze the correlation with survival time. Both univariate analysis and COX regression model which included nutritional status were used in the analysis. Results: Thirty patients with mean age of 59.8 (range, 35-82) were enrolled. The majority of patients was male (76%), malnourished (90%), had a history of smoking (80%), and received chemotherapy for treatment of NSCLC (73%). Patients with the highest quartile of zinc had significantly longer survival time than with the lowest quartile (14.7 Vs 5.6 months) in both univariate and multivariate analysis (P = 0.01 and 0.007, respectively); while the significance of manganese was proven in only univariate model. Other antioxidants levels including retinol, α-tocopherol, β-carotene, lycopene, β-cryptoxanthin, selenium, copper, and peroxidase did not demonstrate relationship with survival time. Conclusion: The low level of some antioxidants, particularly zinc, produced a significantly poor prognosis in advanced-stage non-small cell lung cancer patients. Citation Format: Kosin Wirasorn, Pranithi Hongprabhas, Veeradej Pisprasert, Kulthida Klarod, Patcharee Boonsiri. Serum antioxidant levels and survival time in advanced non-small cell lung cancer patients. [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 LB-20. doi:10.1158/1538-7445.AM2013-LB-20
Abstract 1287: Epigenetic deregulation of breast cancer is associated with DNA Repair Capacity.
Authors: Jaime Matta, Tal Hadar, Luisa Morales, Kim Ostrow, David Sidransky, Rafael E. Guerrero-Preston
Journal: Cancer Research (2013)

Abstract Introduction 226,870 women are estimated to be diagnosed with breast cancer in 2012. Search for accurate methods for screening, diagnosis and treatment follow up, that will be minimally invasive are ongoing. Hypermethylation of gene promoters occurs frequently in the pathogenesis of breast cancer, and causes silencing of tumor suppressor genes. Hypermethylation of Mal, Kif1a and OGDHL in breast cancer cell lines and tissue samples was previously reported. Aberrant DNA repair capacity (DRC) has been studied and shown to elevate the risk for breast cancer. However, information on the association between the epigenetic promoter hypermethylation and DRC is lacking in the literature. Objective The aim of this study is to assess the association between breast cancer and promoter hypermethylation of Mal, Kif1a and OGDHL in serum of breast cancer patients and controls in association with the DRC. Methods 240 serum samples from breast cancer patients and controls from Puerto Rico were collected. DNA was extracted and methylation levels were measured after bisulfite treatment, by QMSP. DRC was assessed by host reactivation assay of blood samples. The overall risk for breast cancer was calculated and adjusted for patient characteristics including DRC. Results Methylation of at least one of the genes was found in 49% of breast cancer samples compared to 20% of controls. ROC curves for individual genes showed values of 0.64 for MAL, 0.51 for Kif1a and 0.53 for OGDHL. In the linear regression unadjusted analysis, mean methylation levels (what are the values?) of the three genes and odds ratio (OR) were higher in breast cancer cases compared to controls, with Kif1a and OGDHL values being statistically significant. These values became non significant after adjusting for DRC. Hypermethylation of Kif1a, but not MAL or OGDHL was found to be significantly associated with DRC. Conclusion Correlation between promoter hypermethylation of the genes Mal, Kif1a and OGDHL and breast cancer was non significant when adjusted for DRC. A significant association between hypermethylation of Kif1a and DRC was shown. The association between promoter hypermethylation and DRC needs to be further studied. Citation Format: Jaime Matta, Tal Hadar, Luisa Morales, Kim Ostrow, David Sidransky, Rafael E. Guerrero-Preston. Epigenetic deregulation of breast cancer is associated with DNA Repair Capacity. [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 1287. doi:10.1158/1538-7445.AM2013-1287
SC-15 * ISOLATING GLIOBLASTOMA TUMOR INITIATING PROGENITOR CELLS FROM THE SUBVENTRICULAR ZONE USING A NOVEL MINIMALLY INVASIVE APPROACH
Authors: R. Kumar, A. Gont, J. Hanson, A. Cheung, G. Nicholas, J. Woulfe, V. Da Silva, I. Lorimer, A. Kassam
Journal: Neuro-Oncology (2014)

Over 50% of brain tumor patients do not have effective therapeutic options, partly due to the delicate location of the brain tumor in the brain, suggesting the need for improved neurosurgical approaches. Furthermore, for those patients who do receive standard care, although tumor shrinkage is often observed, 90% of patients with Glioblastoma Multiforme (GBM) exhibit tumor relapse. Mechanistically, this could be attributed to residual GBM tumor initiating cells (GTICs). One important variable in the isolation of GTICs from patients may be the anatomic site from where they are harvested. We report a novel minimally invasive corridor-based approach to resect the primary GBM, but also move beyond the Magnetic Resonance Image (MRI)-visible GBM in a more accurate, efficient, and targeted manner towards the subventricular zone (SVZ). Most importantly, the reported approach preserves the sample biology and integrity while respecting surrounding healthy tissues. Through this approach, we harvested samples from four consented GBM patients from two locations, the MRI-visible GBM and the SVZ. We demonstrate that GTICs can be isolated with a 100% success rate from the SVZ as oppose to 50% from the MRI-visible GBM. SVZ-GTICs were tumorigenic in xenografts and contained GBM-associated mutations EGFR and PTEN confirming that they were not endogenous neural stem cells residing in the SVZ. The high harvest rate of GTICs can be attributed to the closed-loop system that we employed which allowed the harvested samples to be kept in physiologic conditions, preserving sample biology and integrity. Furthermore, it could also be attributed to our ability to isolate GTICs directly from their niche in the SVZ. In conclusion, we demonstrate here the directed and targeted isolation of GTICs from their SVZ niche in human GBM patients intraoperatively.
P2-04-02: Identification of a Novel Glycosyltransferase-Like Gene as an Autophagic Inducer in Human Mammary Carcinoma Cells Via Down Regulation of BCL-2.
Authors: BG Shastri, Y Jung, M Steiner, JK Perry, PE Lobie, D-X Liu
Journal: Cancer Research (2011)

Abstract Here we report the identification of a previously undescribed glycosyltransferase-like gene, GLTx, and its cellular effect on mammary carcinoma cells. GLTx codes for a novel human protein which is highly conserved in primates. Data obtained from the mRNA expression database Oncomine, demonstrate that GLTx is differentially expressed in a variety of cancers including breast cancer. Western blot analysis of a multiple human tissue blot using a rabbit polyclonal antibody against GLTx demonstrated that GLTx was highly expressed in liver, moderately in kidney, intestine and stomach and undetectable in any other tissues. To functionally characterize GLTx, we attempted to establish stable cell lines with forced expression. However, forced expression of GLTx was completely lethal and resulted in severe cell death in the mammary carcinoma cell lines, MCF-7 and BT549, as well as in any other cell lines tested. Staining of MCF-7 cells transiently transfected with a GLTx expression plasmid by either Hoechst 33258 or fluorescein isothiocyanate-conjugated annexin V and propidium iodide confirmed that the observed cell death was not caused by apoptosis. Further investigation confirmed that GLTx expressing cells exhibited cytoplasmic accumulation of autophagosomes, consistent with the induction of autophagy, as measured by the fluorescently labelled autophagosome marker LC3. In addition we have shown that GLTx downregulated BCL-2, an inhibitor of autophagy, as measured by BCL-2 gene promoter luciferase activity assay and western blot assay following transient transfection of a GLTx expressing plasmid. Thus, we have demonstrated that GLTx is a novel autophagic inducer that causes cell death by down regulating BCL-2. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P2-04-02.
AB0494 Early Clinical Experiences with Belimumab in Polish Patients with Systemic Lupus Erythematosus
Authors: M. Majdan, E.J. Kucharz, S. Jeka, S. Sierakowski, P. Leszczyński, W. Tł ustochowicz, M. Olesińska, P. Gł uszko, M. Krężelok, D. Suszek, M. Kopeć-Mędrek, K. Kolossa, I. Domysławska, K. Pawlak-Buś, J. Kur-Zalewska, A. Felis-Giemza, A. Zielińska, S. Brużewicz, K. Skoczylas
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Belimumab is a monoclonal antibody, inhibitor of soluble B-cell activating factor, that is used in the adjuvant treatment of adult patients with active seropositive systemic lupus erythematosus (SLE) [1]. Belimumab was approved in Poland in 2011. <h3>Objectives</h3> To analyze the influence of belimumab therapy on the severity of SLE (expressed as SLEDAI score) and glucocorticoid (GC) use in Polish patients qualified to Early Access Program (EAP). <h3>Methods</h3> Recruitment to EAP was started in April 2012 in 8 Polish tertiary rheumatology centers. A total of 23 subjects were enrolled. The data of 22 patients (mean age 38.5±8.7 years, 18 women) with at least 3-month follow-up were analyzed. Median time elapsed between the diagnosis of SLE and the enrollment was 7 years (range: 1-39 years). Median SLEDAI score at baseline equaled 13.5 points (range: 6-32 points), and median baseline prednisone equivalent amounted to 11 mg (range: 5-35 mg). <h3>Results</h3> Median SLEDAI score at 3 months (7 points, range: 3-14 points) was significantly lower than the respective baseline value (p&lt;0.001). Moreover, a significant decrease in the median GC use was documented after 3 months of the treatment (down to 8 mg, range: 2-35 mg; p=0.033). The dose of GCs was reduced in 12/22 patients (median reduction: 33%, range: 17-67%). 13/22 patients continued therapy with belimumab for at least 12 months after the enrollment. Both median SLEDAI score (4 points, range: 0-13 points) and median GCs dose (7.5 mg, range: 0-40 mg) at 12 months were significantly lower than the respective baseline values (p=0.002 and p=0.033, respectively). The treatment was stopped in 4 cases due to remission (n=2) or other causes (surgery, pregnancy plans, n=2), or withdrawn due to its inefficacy (n=3), IgA deficit/leukopenia and infection (n=2). <h3>Conclusions</h3> The obtained results point to the efficacy of belimumab in the management of SLE. Our findings are similar to those documented in the BLISS trial [2]. <h3>References</h3> Ginzler EM, Wallace DJ, Merrill JT, et al. Disease control and safety of belimumab plus standard therapy over 7 years in patients with systemic lupus erythematosus. J Rheumatol. 2013 [Epub ahead of print]. van Vollenhoven RF, Petri MA, Cervera R, et al. Belimumab in the treatment of systemic lupus erythematosus: high disease activity predictors of response. Ann Rheum Dis. 2012 Aug;71(8):1343-9. <h3>Acknowledgements</h3> GlaxoSmithKline provided support for data analysis. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.2880
Spontaneous dislodgement of a biliary tumor in a patient with hepatocellular carcinoma
Authors: H. Kogure, K. Miyabayashi, T. Tsujino, H. Isayama, R. Tateishi, K. Koike
Journal: Endoscopy (2011)

A 72-year-old woman with Child–Pugh B cirrhosis was hospitalized in our department for transarterial chemoembolization (TACE) for the recurrence of hepatocellular carcinoma with biliary invasion. She had undergone radiofrequency ablation (RFA) therapy 1 year earlier. Contrast-enhanced computed tomography (CT) showed a 15-mm hypervascular tumor in the common hepatic duct adjacent to the area previously treated with RFA ([Fig. 1]).
THU0025 Complement Deficiencies in A Cohort of Pediatric Onset Lupus: A Preliminary Study from A Tertiary Care Centre in North India:
Authors: S. Bhattad, A. Rawat, S. Singh, A. Gupta, D. Suri, R. Garg, M. de Boer, T. Kuijpers
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Deficiency of the early components of the classical complement pathway (C1q, C1r, C1s, C4 and C2) is the strongest single genetic predisposing risk factor for the development of Systemic lupus erythematosus<sup>1</sup>. However data regarding complement deficiencies from developing countries is sparse, especially for pediatric onset systemic lupus erythematosus. <h3>Objectives</h3> To assess complement levels C1q, C2, C3 and C4 in children with pediatric onset lupus during quiescent stage of disease. <h3>Methods</h3> A cross sectional descriptive study was conducted between January and December 2012. 34 consecutive children with pediatric onset SLE (onset below 12 years), in quiescent stage (SLEDAI score zero) being followed at pediatric rheumatology clinic were enrolled. 29 age and sex matched healthy children were enrolled as controls. Clinical and immunological profile of patients was obtained from hospital records. C1q, C2, C3 were estimated by enzyme linked immunosorbent assay and C4 by end-point nephelometry. Genetic analysis was carried out in children with depressed levels of these complements. <h3>Results</h3> Mean age at onset of lupus in study cohort was 9±2.1 yrs (range 1.5 – 12 years) and M: F ratio was 1:3. Mean duration of disease was 5.4 years (range 6 months – 11 years). ANA was positive in all, whereas anti dsDNA was positive in 19/34. Mean complement C1q, C2, C3 and C4 levels were 50.32, 17.28, 1320 and 236 mg/L respectively. Levels of complements were low in 7/34 children with SLE (features in table). Children with complement deficiency had distinct clinical and immunological profile. A very young age at onset and predominant skin manifestations were noted in C1q deficient children. Anti dsDNA titres were characteristically low in these patients and a speckled pattern was noted on ANA-IF. Mutation analysis revealed homozygous nonsense mutation in C1QA gene in two children with characteristic early onset disease at 1.5 and 2.5 years respectively. <h3>Conclusions</h3> Clinical and immunological profiles were distinct among complement deficient lupus children, who had early and more severe disease. Inherited C1q deficiency (mutation in C1QA gene) was noted in two children in the cohort. <h3>References</h3> Manderson AP, Botto M, Walport MJ. The role of complement in the development of systemic lupus erythematosus. Annu Rev Immunol. 2004;22:431-56. <h3>Acknowledgements</h3> This study was carried out as a MD Thesis, with support from the institute (PGIMER, Chandigarh, India). <h3>Disclosure of Interest</h3> : None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.1608
Surgical Resection of a Tuberculous Aneurysm of the Ascending Aorta
Authors: John L. Kline, John Durant
Journal: New England Journal of Medicine (1961)

IN 1885 Sir William Osler1 coined the term "mycotic aneurysm." Although the phrase may have become antiquated by modern-day terminology, it is one that seems to have become firmly established in medical literature owing to long usage and perhaps in deference to its originator. Numerous case reports dealing with "mycotic" aneurysms of bacterial origin have been reported; however, those due to tuberculosis are few, and, if one limits the survey to the aorta, they are exceedingly rare. In 1945 Revell2 made an exhaustive review of the literature in which he located 23 primary mycotic aneurysms, none of which were tuberculous . . .
P1-05-02: Epigenetic Regulation by Alcohol Reactivates Estrogen Receptor alpha in Estrogen Receptor alpha-Negative Cells.
Authors: AW Wong, N Nunez
Journal: Cancer Research (2011)

Abstract Introduction: Alcohol consumption is an established risk factor for breast cancer development and contributes to mammary tumorigenesis through the regulation of estrogen receptor alpha (ERα) expression. Previously, we reported that alcohol consumption in the MMTV-neu ERα-negative mouse model of human breast cancer resulted in significantly increased ERα expression compared to non-alcohol consuming mice. Thus, our results indicated that alcohol consumption led to reexpression of ERα in an ERα-negative mouse model. Several lines of evidence suggest that ERα expression in ERα-negative cancer cells is inhibited through epigenetic mechanisms. In this study, we examine the role of alcohol on ERα reactivation through changes in histone modifications, DNA methylation, and recruitment of transcriptional regulation complexes on the ERα promoter, in vitro. Methods: ERα-negative MDA-MB-231 human breast cancer cells were treated with 0.1%, 0.2% and 0.5% v/v ethanol in culture media for 24 h. Chromatin immunoprecipitation (ChIP) assays were used to examine the enrichment of active and inactive markers of chromatin on the ERα promoter following alcohol treatment. DNA methylation at three ERα promoter CpG dinucleotide sites was assessed following alcohol treatment using methyl-sensitive restriction enzyme (MSRE)-qPCR. ChIP assays are used to determine the binding of the transcriptional regulation complexes, pRb2/p130-E2F4/5-HDAC1-SUV39H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1, to the ERa promoter following alcohol treatment. MCF-7 human breast cancer cells served as an ERα-positive control. Results: We report that histone modifications were affected by alcohol treatment in a dose-dependent manner. Enrichment levels of all five chromatin markers tested, which includes markers of active and inactive transcription, were significantly altered as a result of alcohol treatment (p&amp;lt;0.05). We also found significantly decreased DNA methylation at three ERα promoter CpG sites as a result of alcohol treatment (p&amp;lt;0.05). Experiments testing the recruitment of the transcriptional regulation complexes, pRb2/p130-E2F4/5-HDAC1-SUV39H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1, are currently ongoing. Discussion: ERα expression has been linked to mammary carcinogenesis and clinical outcome in breast cancer patients. However, approximately one out of three breast cancers lack ERα expression at the time of diagnosis and many breast cancers lose ERα expression during the course of tumor progression. Thus, understanding the regulation of ERα expression in breast cancer cells is critical and results from this study will facilitate the development of novel therapeutic strategies and treatment options for hormone-resistant breast cancer. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P1-05-02.
AB0932 Sapho syndrome - comparison of different methods of imaging of sterno-clavicular joints
Authors: H. Przepiera-Bedzak, L. Cyrylowski, I. Brzosko, M. Brzosko
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> SAPHO syndrome is an uncommon but recognized subgroup of psoriatic arthritis and is characterized by dermatological symptoms such as palmo-plantar pulstulosis and acne and osteoarticular symptoms. Radiographic assessment belongs to the diagnostic procedures of SAPHO syndrome although the present of them doesn’t belong to diagnostic criteria. <h3>Objectives</h3> To compare usefulness different methods of imaging of sterno-clavicular joints in SAPHO syndrome <h3>Methods</h3> We studied 15 patients (14 female, 1 male) with confirmed diagnosis of SAPHO syndrome. 14 patients had palmo-plantar pustulosis, 1 patient had severe acne. All of patients had pain and swelling of sterno-clavicular joints. Mean age of patients was 50,4±12,1 years, mean disease duration was 2,9 ± years. All of patients underwent bone scintigraphy, routine x-ray and computed tomography (CT) of sterno-clavicular joints. <h3>Results</h3> Increased tracer uptake on bone scintigraphy was found in 13(86,7%) of patients. In 9 of them in sterno-clavicular joints, in 4 – in sacroiliac joints and in 2 – in peripheral joints. Routine x-ray assessment of sterno-clavicular joints presented abnormalities in 4(26,7%) patients. These were: clavicle enlargement (1 patient), erosions with hyperostosis (1 patient), irregular calcifications (1 patient), irregular surface of clavicles (1 patient). Computed tomography of sterno-clavicular joints presented abnormalities in 6(40%) patients. These were: erosions (4 patients), hyperostosis (3 patients) and geodes (1 patients). All of patients with abnormal result in CT had increased tracer uptake on bone scintigraphy. Four of them had abnormal result on routine x-ray. Two of them had no changes on routine x-ray. <h3>Conclusions</h3> In patients with SAPHO syndrome routine x-ray in not sensitive and seems not necessary in diagnostic procedures. CT assessment is more sensitive in this group of patients. Bone scintigraphy is very sensitive but it could be nonspecific. <h3>References</h3> Przepiera-Bedzak H, Brzosko I, Flicinski J, Samborski W, Brzosko M: SAPHO syndrome – Clinical features. Pol Arch Med Wewn2006 116(6): 1172-7. Colina M, Govoni M, Orzincolo C, Trotta F: Clinical and radiological evolution of synovitis, acne, pulstulosis, hyperostosis and osteitis syndrome: a single center study of a cohort of 71 subjects. Arthritis Rheum 2009; 61(6): 813-21. Salles M, Olive A, Perez-Andres R, Holgado S, Mateo L, Riera E, Tena X: The SAPHO syndrome: a clinical and imaging study. Clin Rheumatol 2011; 30: 245-9. <h3>Disclosure of Interest</h3> None Declared
HBcrAg predicts hepatocellular carcinoma development: An analysis using time-dependent receiver operating characteristics
Authors: Toshifumi Tada, Takashi Kumada, Hidenori Toyoda, Seiki Kiriyama, Makoto Tanikawa, Yasuhiro Hisanaga, Akira Kanamori, Shusuke Kitabatake, Tsuyoki Yama, Junko Tanaka
Journal: Journal of Hepatology (2016)