tbuckley/cabot-search huggingface dataset:
Incidental Detection of Gastrointestinal Bleeding From an Aortoenteric Fistula on 99mTc Leukocyte Scintigraphy
Authors: Julia Cortés, Javier Villaverde, Miguel Garrido, María Pombo, Alvaro Ruibal
Journal: Clinical Nuclear Medicine (2012)

A 50-year-old-man with abdominal pain, who had undergone aortic aneurysm reconstructive surgery (aortic graft) 3 years before, was admitted to the hospital. A CT scan showed findings suggestive of perigraft infection. Scintigraphy with 99mTc-hexamethylpropylene amine oxime (HMPAO)-labeled leukocytes confirmed the diagnosis of aortic graft infection and documented an active concurrent bleeding in the gastrointestinal tract from a secondary aortoenteric fistula. This case illustrates the diagnosis of the precise location of the source of bleeding from aortoenteric fistula by leukocyte scintigraphy. The images aided the surgical team by revealing the aortic site of bleeding and the severity of the problem.
COLLAGEN BIOMARKERS IN RELATION TO NON-CARDIOVASCULAR, NON-CANCER INFLAMMATORY-RELATED EVENTS, CANCER EVENTS AND TOTAL DEATH VERSUS INCIDENT CARDIOVASCULAR DISEASE EVENTS: THE MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS
Authors: Daniel A. Duprez, Myron Gross, Otto Sanchez, Jorge Kizer, Joachim H. Ix, Joao Lima, Russell Tracy, David Jacobs
Journal: Journal of the American College of Cardiology (2016)
Dutch Trial Casts Doubt on Colorectal Adjuvant Therapy
Authors: T. Reynolds
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article Dutch Trial Casts Doubt on Colorectal Adjuvant Therapy Get access Tom Reynolds Tom Reynolds Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 7, 5 April 1995, Pages 476–479, https://doi.org/10.1093/jnci/87.7.476 Published: 05 April 1995
Abstract 2541: A prospective study of medical diagnostic x-rays and risk of thyroid cancer.
Authors: Gila I. Neta, Preetha Rajaraman, Amy Berrington de Gonzalez, Michele Doody, Bruce Alexander, Steve Simon, D. Michal Freedman, Martha Linet, Alice Sigurdson
Journal: Cancer Research (2013)

Abstract While diagnostic x-rays provide important medical benefits, cancer risks associated with their exposure are also possible. The thyroid gland is the most radiosensitive organ, and radiotherapy to the head and neck is associated with an increased risk of thyroid cancer. However, it is not known whether diagnostic x-rays, which yield a lower dose of ionizing radiation to the thyroid gland than radiotherapy, also increase the risk. The United States Radiological Technologists study (1983-2006) is a nationwide, prospective cohort with extensive questionnaire data on history of personal diagnostic imaging procedures collected prior to cancer diagnosis. Cox proportional hazards were used to estimate thyroid cancer (TC) risks related to the number and type of selected procedures. Potential modifying effects of age and calendar year of the first x-ray in each category of procedures were assessed. Incident thyroid cancers (n=251) were diagnosed among 75,494 technologists (1.3 million person-years, mean follow-up=17 years). Overall, there was no clear evidence of TC risks associated with diagnostic x-rays, except for dental x-rays. The authors observed a 13% increase in TC risk for every 10 reported dental x-rays (95%CI: 1.01-1.26), driven by dental x-rays first received before 1970, but no evidence that the relationship between dental x-rays and TC was associated with childhood or adolescent exposures as would have been anticipated. The lack of association of TC with x-rays which expose the thyroid to higher radiation doses than dental x-rays underscores the need to conduct a detailed radiation exposure assessment to enable quantitative evaluation of risk. Citation Format: Gila I. Neta, Preetha Rajaraman, Amy Berrington de Gonzalez, Michele Doody, Bruce Alexander, Steve Simon, D. Michal Freedman, Martha Linet, Alice Sigurdson. A prospective study of medical diagnostic x-rays and risk of thyroid cancer. [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 2541. doi:10.1158/1538-7445.AM2013-2541 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
P646The adult murine heart is protected against ischemia-reperfusion injury in the absence of both mitofusin (Mfn) proteins
Authors: N Burke
Journal: Cardiovascular Research (2014)

Background: Cardiac-specific ablation of both Mfn1 and Mfn2 in the adult heart results in mitochondrial fragmentation and a lethal cardiomyopathy after about 6 weeks. The effect of combined Mfn1 and Mfn2 deletion on the susceptibility to acute ischemia-reperfusion injury (IRI) and subsequent calcium overload is not known, and is investigated in this study. Methods and Results: Cardiac-specific ablation of both Mfn1 and Mfn2 (DKO) was initiated in mice aged 5 weeks using 5 days administration of tamoxifen (MerCreMer), resulting in total knockout of both these proteins at the age of 10 weeks. These mice were subjected to in vivo myocardial ischemia (30 mins) followed by 24 hrs reperfusion before myocardial infarct size was determined. The sustained MI size in the DKO mice was 50% smaller than that in the WT control mice. These findings were associated with decreased MPTP opening susceptibility (assessed by calcium-induced mitochondrial swelling), reduced mitochondrial calcium overload after simulated IR (assessed by Rhod2 staining) and impaired mitochondrial respiration in the DKO hearts when compared to WT control. Conclusions: We have shown that the adult murine heart deficient in both Mfn1 and Mfn2 was protected against acute IRI, a finding which was associated with defects in mitochondrial function and reduced mitochondrial calcium overload. This data suggests that the Mitofusins may be therapeutic targets for cardioprotection.
AB0608 Bone mineral density and body composition by dual energy x-ray absorptiometry in men with rheumatoid arthritis
Authors: A. Muradyants, N. Shostak, A. Kondrashov, V. Shemenkova
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Loss of bone mineral density (BMD) and muscle mass are common symptoms in patients with rheumatoid arthritis (RA). Changes in body composition in men with RA have been little studied. <h3>Objectives</h3> To evaluate the bone mineral density (BMD) and changes of body composition in men with RA. <h3>Methods</h3> 49 men with RA (median disease duration 6.4 yrs) were enrolled in the study. The mean age was 60.1 + 1.02 years. A control group included 20apparently healthy men matched for age. Clinical risk factors for osteoporosis and osteoporotic fracture were evaluated by a specific questionnaire, include FRAX. Whole body composition (total and regional lean mass, fat mass) and BMD of the lumbar spine (L1–L4), total hip, femoral neck and total body were measured by DXA using theStratos dR densitometer (DMS, France). The weight in kg divided by height in meters<sup>2</sup> was used to calculate BMI. Data are presented as means ± standard deviations (SD). P values less than 0.05 are considered statistically significant. <h3>Results</h3> The prevalence of osteoporosis in men with RA was 26.5% (13 patients), of osteopenia 34.7% (17 patients) while 38.8% were normal (19 patients). The RA group had a femoral neck BMD of 858.16 + 26.32 g/cm2, which is equal to -1.85 ± 0.52 SD, while the control group had this index of 1098.76 ± 14.54 g/cm2, which is equal to -0.4 ± 0.23 SD as shown by the T-test. Also there were significant differences inthe lumbar spine BMD among the groups (944.87 ± 17.89 g/cm2, which is equal to -1.15 ± 0.12 SD vs 1257.43 ± 21.38 g/cm2, which is equal to -0.35 ± 0.10 SD). The highest risk of osteoporosis was noted with high RA activity and X-ray stages III—IV. Total lean mass in patients with RA is reduced in comparison to the control group (62.26±1.63%vs 79.31±1.5), but total fat mass was significant higher compared to the healthy men (28.18±1.76% vs 15.98±1.82%). <h3>Conclusions</h3> The BMD values in both the femoral neck and lumbar spine were significantly lower in the men with RA than those in the control group<i>.</i> The men with RA had lower total lean mass and higher total body fat mass than matched controls. <h3>Disclosure of Interest</h3> None Declared
Abstract 5061: Roles for matrix metalloproteinase-3 (MMP-3) in the prostate tumor-bone microenvironment.
Authors: Jeremy S. Frieling, Lizzie Atomi Pamen, Leah M. Cook, Shengyu Yang, Conor C. Lynch
Journal: Cancer Research (2013)

Abstract Prostate cancer commonly metastasizes to bone, resulting in lesions hallmarked by a mixture of osteolysis and osteogenesis. The “vicious cycle” is the paradigm describing tumor-bone interaction, and MMPs have been implicated in regulating the bioavailability and activity of growth factors that control the cycle. We have found that MMP-3, also known as stromelysin-1 and typically generated by host/stromal cells, is differentially expressed in the prostate tumor-bone microenvironment. Based on our initial observations, we hypothesize that host derived MMP-3 expression contributes to prostate tumor growth in bone. Using an in vivo intratibial model of prostate to bone metastases (PaIII), we found that that tumor growth and tumor induced bone remodeling were significantly mitigated (p&amp;lt;0.05) in MMP-3 null animals compared to wild type controls. Using a candidate approach to examine potential mechanisms, we focused on parathyroid hormone related protein (PTHrP), a powerful regulator of osteoblast behavior in the vicious cycle. We identified that MMP-3 processes mature PTHrP1-36 to yield PTHrP1-16, PTHrP17-26, and PTHrP27-36 fragments in vitro. The fragments did not impact osteoblast proliferation (MTT assay) or differentiation (Alizarin red staining), however, we observed a significant increase in migration of osteoblasts and osteoblast precursors in response to 10nM PTHrP1-16. The stimulation of migration by PTHrP1-16 was significantly greater than that induced by mature PTHrP1-36. Further analysis via confocal microscopy revealed a reduction in actin stress fibers as well as variations in lamellipodia and vinculin organization of osteoblasts treated with PTHrP1-16. In addition, western blots show a reduction of myosin light chain phosphorylation suggesting that PTHrP1-16 may mediate osteoblast migration by modulating Rho-associated protein kinase (ROCK) activity. Our data demonstrate that host MMP-3 contributes to prostate tumor growth and tumor induced changes in bone remodeling in vivo. Further, we have identified that mature PTHrP1-36 is subject to cleavage by MMP-3 resulting in PTHrP1-16, PTHrP17-26, and PTHrP27-36 fragments of which PTHrP1-16 significantly stimulates migration of osteoblasts and osteoblast precursors. Collectively, these data indicate that specific inhibition of MMP-3 and/or targeting MMP generated neo-epitopes would be efficacious for the treatment of prostate to bone metastases. Citation Format: Jeremy S. Frieling, Lizzie Atomi Pamen, Leah M. Cook, Shengyu Yang, Conor C. Lynch. Roles for matrix metalloproteinase-3 (MMP-3) in the prostate tumor-bone microenvironment. [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 5061. doi:10.1158/1538-7445.AM2013-5061
Abstract 1967: UvrABC excision of interstrand crosslink mitomycin C-DNA lesion induces double-stranded DNA breaks
Authors: Mao Wen Weng, Yi Zheng, Vijay P. Jasti, Elise Champeil, Maria Tomasz, Yin sheng Wang, Ashis K. Basu, Moon Shong Tang
Journal: Cancer Research (2010)

Abstract Mitomycin C (MC) forms at least nine different covalent DNA adducts including an N2-2’-deoxyguanosine monoadduct (MC-mono-dG) and inter- and intrastrand bis-adducts with 2’-deoxyguanosine (dG) in vivo. Inter-strand cross-linked (ICL) dG-MC-dG-DNA adducts can prevent strand separation, and therefore, the MC antitumor activity is most likely derived from formation of ICL-MC adducts. In Escherichia coli cells, UvrABC, the nucleotide excision repair (NER) enzyme complex can repair ICL psoralen lesions that cause DNA bending. The mechanism and the consequence of NER of ICL dG-MC-dG lesions that do not induce DNA bending remain unclear. In order to compare the NER of MC-mono-dG with an ICL dG-MC-dG adduct, we constructed DNA fragments containing the adducts in the same DNA sequence context. We determined that UvrABC incises only at the strand containing MC-mono-dG adduct. In contrast, UvrABC makes three types of incisions on a site specific ICL dG-MC-dG adduct: type 1 (40 %), a single 5’ incision on one strand and 3’ incision on the other; type 2 (21 %), dual incisions on one strand and a single incision on the other strand; and type 3 (39%), dual incisions on both strand of both 5’ and 3’ sides of the ICL dG-MC-dG adduct. These three types of incisions occur with similar kinetics. An important consequence of these incisions is formation of DNA double-stranded breaks (DSB). Contrary to conventional model, we also found that UvrA, UvrA+UvrB and UvrA+UvrB+UvrC bind to MC-modified DNA specifically and form complexes that include UvrA. No UvrB- and UvrB+UvrCDNA complexes were observed. Our findings challenge the current UvrABC incision model of ICLs. We propose that NER of ICL dG-MC-dG adduct produces DSB, a lethal event that contributes to MC antitumor activity, and causes a non-homologous end-to-end joining that leads to DNA translocation and deletion mutations. 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 1967.
Abstract 2626: Thiazole antibiotic/proteasome inhibitor thiostrepton against cancer
Authors: Bulbul Pandit, Ming Wang, Marianna Halasi, Andrei L. Gartel
Journal: Cancer Research (2011)

Abstract Thiazole antibiotic, thiostrepton was identified as an inhibitor of oncogenic transcription factor FoxM1, later demonstrated to exhibit proteasome inhibitory activity. We found that polymeric micelle-encapsulated thiostrepton reduced tumor growth rate in MDA-MB-231-luc breast cancer xenografts. Encapsulation of thiostrepton into polymeric micelles can aid its solubilization and increase its accumulation into tumor sites. Furthermore, its anti-cancer effects on breast cancer xenografts were found to be through reducing cell proliferation and inducing cell death. Thiostrepton is sulfur containing highly modified macrocyclic antibiotic with a central pyridine/tetrapyridine/dehydropiperidine ring with up to three thiazole substituents on positions 2, 3 and 6, which has macrocyclic loop connecting thiazole rings at position 2 and 3 described as ring A. In addition, it has a quinaldic acid macrocycle also connected to thiazole on position 2 described as ring B. Structural modification of thiostrepton to thiostrepton methyl ester (with open B ring) did not demonstrate proteasome inhibitory activity. These data suggest that B ring of thiostrepton and similar thiazole antibiotic Siomycin A that is absent in other thiazole antibiotics determines the proteasome inhibitory activity of these drugs. We investigated the therapeutic potential of the combination of thiostrepton and proteasome inhibitor bortezomib (Velcade) on various human tumor cell lines. Combination of sublethal concentrations of thiostrepton and bortezomib induced potent apoptosis and inhibition of long-term colony formation in a wide variety of human cancer cell lines. The synergistic realtionship between thiostrepton and bortezomib combination was also quantitatively demonstrated by low combination index between 0.1 and 0.8. The synergy between these drugs was based on their proteasome inhibitory activities of both drugs, because structurally similar thiostrepton modification, thiostrepton methyl ester that did not have proteasome inhibitory activity failed to increase apoptosis in combination with bortezomib Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2626. doi:10.1158/1538-7445.AM2011-2626
Phase Ii Study with Immunotherapy with Dendritic Cells (Dc) Combined with Intratumoral Hiltonol in Patients with Advanced Cancer
Authors: A. Gurpide, J.M. Lopez-Picazo, C. Alfaro, M.E. RodrÍguez-Ruiz, J.L. Perez Gracia, M. Fernandez de Sanmamed, A. Benito, D. Cano, A. Gonzalez, I. Rodriguez Lopez, J.P. Fusco, J. Rodriguez, S. Martin Algarra, R. Martínez-Monge, I. Melero
Journal: Annals of Oncology (2014)
Abstract 1991: Integrated analysis of copy number alteration and RNA expression profile in pediatric diffuse intrinsic pontine glioma
Authors: Maryam Zarghooni, Ute Bartels, Eric Bouffet, Cynthia Hawkins
Journal: Cancer Research (2010)

Abstract DIPG is one of the most devastating of pediatric malignancies and one for which no effective therapy exists. A major contributor to the failure of therapeutic trials is the assumption that biologic properties of childhood brainstem tumors are identical to adult high-grade gliomas. A better understanding of the biology of DIPG itself is needed in order to develop agents targeted more specifically to these children's disease. Here we address this lack of knowledge by performing the first high-resolution, DNA- and RNA-microarray analysis of pediatric DIPG. Nine DIPGs were prospectively collected at post-mortem following consent for research purposes. Four pre-treatment surgical samples were also retrieved from our pathology archives. All samples were hybridized to Affymetrix SNP-arrays (250k or 6.0). Nine samples were also hybridized to the HumanRef-8 v3.0 (DASL) or HumanWG-6 v3.0 expression beadchip from Illumina. Data were analyzed using the Copy Number Analysis Tool (Affymetrix) and Partek Genomics Suite using HMM and segmentation algorithm for copy number and clustering algorithm for gene expression. DASL and Whole genome beadchip from Illumina have 18,404 probes in common. Those common probes were selected in the two data sets and the gene intensities related to those probes were pulled out for each sample separately. The differentially expressed genes were then identified using one-way ANOVA. For each sample, a gene list was created containing genes having a fold change between 2 and −2. The intersection of the seven gene lists was found using a Venn diagram. In total 234 genes were found that are differentially expressed in all seven samples. The gene expression and gene copy number data were then integrated. In total 5 genes show correlation between copy number and gene expression in all seven samples. Among the 234 differentially expressed genes, Ingenuity pathway analysis identified 63 genes associated with different aspect of cancer including proliferation, metastasis, polyploidization, neoplasia, adhesion, migration, survival, acidification, attachment, cell cycle progression, differentiation, growth and invasion. Our data provides the first, comprehensive, genomic analysis of pediatric DIPG. A thorough understanding of the genetic abnormalities in DIPG is a crucial first step in the development of targeted therapies for this devastating group of tumors. This is of particular importance for DIPG given the lack of efficacy of current treatment regimens and the dismal prognosis for these patients. 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 1991.
Cryptogenic multifocal ulcerous stenosing enteritis (CMUSE), and neuromuscular and vascular hamartoma (NMVH): two sides of the same coin?
Authors: Lisa Setaffy, María Osuna, Wolfgang Plieschnegger, María del Pino Florez Rial, Karel Geboes, Cord Langner
Journal: Endoscopy (2014)

Multifocal stenosing enteritis, not related to Crohn’s disease or drug intake, has been described under two different terms: “cryptogenic multifocal ulcerous stenosing enteritis” (CMUSE) and “neuromuscular and vascular hamartoma” (NMVH). We present three new cases of this condition and argue that the two terms reflect the same disease entity. Although etiology and pathogenesis of the disease remain largely unclear, obliterative vascular changes may play an important role.
Interactive Technology Enters Realm of Cancer Education
Authors: E. Taylor
Journal: JNCI Journal of the National Cancer Institute (1994)

Journal Article Interactive Technology Enters Realm of Cancer Education Get access Ellen Taylor Ellen Taylor Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 86, Issue 17, 7 September 1994, Pages 1272–1274, https://doi.org/10.1093/jnci/86.17.1272-a Published: 07 September 1994
Bilateral Periventricular Nodular Heterotopia
Authors: CLAUS GERT HAASE, HARALD MASUR, PETER MATHEJA, TORSTEN KUWERT, OTMAR SCHOBER
Journal: Clinical Nuclear Medicine (1997)

A 29-year-old right-handed female nurse presented with complex, focal epilepsy and secondary MRI generalized seizures. Magnetic resonance imaging showed symmetrical bilateral periventricular nodular heterotopia, caused by an ontogenic migration disorder. Glucose consumption of these aberrant gray-matter structures measured using PET with F-18 (FDG) was of the same magnitude as that of the cortical gray matter. This further illustrates that PET-FDG may detect cortical heterotopia, which supplements differential diagnostic work-up of migration disorders.