tbuckley/cabot-search huggingface dataset:
Abstract 5199: Promotion of prostate cancer cell migration and invasion via CXCR3 signaling
Authors: Qian Wu, Alan Wells
Journal: Cancer Research (2010)

Abstract Tumor cells exist within, and cross-communicate with their local milieu that includes non-neoplastic cells using a variety of soluble chemokines. CXCR3-binding chemokines have recently been implicated in breast cancer metastasis, though inversely correlated with prostate tumor growth. There are two CXCR3 isoforms differing by a 5′ splice variant, that vary in their distribution, with CXCR3A found mainly on cells of the hematopoietic lineage and CXCR3B the predominant species on adherent cells. These isoforms vary in their predilection for the four common ligands, and the consequences of signaling through these different isoforms can be divergent. How these two isoforms inform tumorigenesis and invasion still remains unclear. Here, we examined the expression and function of the two different variants of CXCR3 in prostate cancer cells. In contrast to normal prostate epithelial cells (RWPE-1), in which CXCR3B was the primary splice variant, CXCR3A was highly expressed in two tested prostate cancer cell lines (DU-145 and PC-3). Two known ligands of CXCR3, CXCL10/IP10 and CXCL11/IP9/I-TAC, were down-regulated in these two prostate cancer cell lines, while the CXCR3B-selective ligand CXCL4/PF4 was overexpressed, allowing for autocrine stimulation. Instead of inhibiting cell migration as in RWPE-1 cells, CXCL4/PF4 and CXCL10/IP10 promoted cell motility and invasiveness in both DU-145 and PC-3 cells in vitro, which might be a result of PLCβ3 activation. Overexpression of CXCR3B in DU-145 cells slightly decreased cell chemoattractant movement and invasion. These data suggest that the aberrant expression of CXCR3A and down-regulation of CXCR3B may promote prostate tumor metastasis via stimulating cell migration. (Funded by a VA Merit Award) 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 5199.
Evaluating the Differential Effect of Diet on Rat Carcinogenesis
Authors: L. A. COHEN, M. E. KENDALL, E. ZANG
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Evaluating the Differential Effect of Diet on Rat Carcinogenesis Get access L. A. COHEN, L. A. COHEN Search for other works by this author on: Oxford Academic PubMed Google Scholar M. E. KENDALL, M. E. KENDALL Search for other works by this author on: Oxford Academic PubMed Google Scholar E. ZANG E. ZANG Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 17, 4 September 1991, Page 1262, https://doi.org/10.1093/jnci/83.17.1262 Published: 04 September 1991
Kyphoscoliosis Preventing Gallbladder Assessment
Authors: SANJAY M. GANDHI, BORYS KRYNYCKYI, DAVID M. MILSTEIN
Journal: Clinical Nuclear Medicine (1998)

A 92-year-old woman reported nonspecific epigastric abdominal pain and had mild elevation of the serum SGOT (177) and significantly elevated levels of alkaline phosphatase. Abdominal ultrasound showed a distended, thickened gallbladder containing stones and surrounded by pericystic fluid. Hepatobiliary imaging demonstrated an unusual configuration of the liver, almost a mirror image of its expected appearance on the anterior view. Intense activity was noted in the intrahepatic biliary radicals, but these drained promptly. Gastrointestinal activity appeared by 55 minutes after injection. No definite gallbladder activity could be identified. CT showed significant scoliosis with marked distortion and displacement of the liver and other abdominal viscera.
DRENAJE ENDOSCÓPICO DE PSEUDOQUISTES PANCREÁTICOS SINTOMÁTICOS. EXPERIENCIA EN NUESTRO CENTRO
Authors: B Merino Rodríguez, C González Asanza, O Nogales Rincón, A Huerta Madrigal, A Cruz Moratinos, E Cos Arregui, P Menchén Fernández Pacheco
Journal: Endoscopy (2010)

Introducción: La cirugía es el enfoque tradicional de los pseudoquistes pancreáticos sintomáticos, sin embargo, la morbilidad asociada es alta. El drenaje endoscópico mínimamente invasivo es una técnica segura y eficaz.
Diffuse Intrasinusoidal Liver Metastasis of Pancreatic Carcinoma Causing Fulminant Hepatic Failure
Authors: Y. Kamihara, A. Fujimi, Y. Kanisawa, T. Okuda, N. Uemura, S. Minami, T. Doi, A. Hashimoto, K. Ishikawa, T. Matsuno
Journal: Annals of Oncology (2013)
Abstract 3351: Cancer stem cell marker CD133 effects on invasion and self-renewing in malignant brain tumors
Authors: Dong-Ok Kim, Jeong-Hoon Kim, Young-Shin Ra
Journal: Cancer Research (2010)

Abstract Background and Purpose: Patients with malignant brain tumors have been suffering from its recurrence or short median survival with only a few years, despite advanced medical development. Present studies have shown that cancer stem cell marker CD133 is correlated with invasiveness and metastasis in malignant brain tumors. Some researchers have reported that CD133 in brain tumors influenced on survival regardless of grades. Hence, we analyzed the invasion and self-renewal abilities in a variety of brain tumors having the different WHO grades and compared the differences between low and high malignant brain tumors expressing CD133. Methods and Results: CD133+ cells were stained by immunocytochemistry and followed by counting under fluorescence microscope. We identified cell invasion ability using Matrigel invasion chamber and capacity for self-renew by colony-forming assay, respectively, following CD133 isolation by MACS column. As a result, we found that although the number of CD133+ cells in high malignant brain tumors(HMBTs) was less than those in low malignant brain tumors(LMBTs), the CD133+ cells in HMBTs showed powerful invasion abilities recording the differences of three to six times than in the CD133- cells. In contrast, in LMBTs, the CD133+ cells hardly effected on invasion. We also observed stronger self-renewal potential in CD133+ cells generated from HMBTs than in LMBTs. Conclusions: Taken together, even though various brain tumors expressed CD133 as a cancer stem cell marker, the CD133+ cells functioned as a useful tool in terms of evaluating invasion and self-renewal properties in just HMBTs, but not in LMBTs. Therefore, CD133 will be powerful marker as a poor prognostic factor in brain tumors and this may provide us some strategies to treat HMBTs. 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 3351.
EUS-FNA: Comparing the Learning Curve of Two New Endosonographers With a High Volume Center
Authors: MA Abadia, J Dot Bach, JR Armengol-Miro, M Al-Haddad, S Gross, M Raimondo, T Woodward, MB Wallace
Journal: Endoscopy (2006)

Background: Endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) is established as an effective technique for tissue diagnosis in patients with suspected gastrointestinal and mediastinal malignancies. The objective of this study is compare the learning curve of a two “self-taught“ operators from two different institutions compared to a centre with more experience in EUS-FNA.
Efficacy of treatment with AM3 (inmunoferon) in the prevention of proctitis in patients with prostate carcinoma treated with radiotherapy
Authors: M. Santos, S. Rodriguez, N. Carballo, A. Ruiz, G. Vazquez, E. Reyes, M. Alvarez-Mon
Journal: Journal of Clinical Oncology (2004)

4741 Background: Proctitis and cystitis are known complications of radiotherapy of pelvic malignancies. Radiation-induced mucosal lesions increase the risk of infectious complications and reduce patient quality of life. Furthermore, cystitis and/or proctitis often interfere with therapeutic radiation schedule reducing its potential benefits. AM3 (Inmunoferon) is a protein-associated polysaccharide with proven immunomodularoty effects. Oral AM3 treatment promotes: (a) enhancement of the innate and acquired immune responses against infectious agents (b) reduced production of proinflamatory cytokines, and (c) increased secretion of regulatory cytokines such as granulocyte-monocyte colony stimulation factor. Herein, we have investigated the potential effects of AM3 on the prevention of radiotherapy-induced proctitis and cystitis. Methods: 24 consecutive patients with histologically-proven diagnosis of prostate carcinoma were treated with prostate tridimensional radiation. 15 patients received adjuvant treatment with oral AM3 at a dose of 3 g per day from the first day of radiation treatment (180 cGy/fraction, total dose 7032±284 cGy). Daily AM3 was mainteined for 30 days after completion of radiotherapy. 9 patients did not receive AM3 (control group, total dose 6702 ± 391 cGy). Patients follow-up was performed for 90 days after radiotherpy. Results: The incidence of radiation induced proctitis was significantly lower in the AM3 arm (40%) than in controls (89% ) (p=0.033). The mean time for the appearance of proctitis was significantly delayed in AM3 arm (44 days) with respect to control group (22 days) (p=0.005). The clinical intensity of cystitis was lower in the AM3 arm than in controls(47% and 67% of grade II, respectively). Serum levels of proinflammatory cytokines (TNFalpha, IL-1 and 6) remained stable along the follow up in the AM3 arm. Conclusions: In this prospective controlled pilot study, treatment with the AM3 immunomodulator significantly reduces the incidence of radiation-induced proctitis in prostate carcinoma patients. No significant financial relationships to disclose.
Primary malignant melanoma of the esophagus
Authors: Gabriel Wallis, Vinay Sehgal, Aiman Haider, John Bridgewater, Marco Novelli, Khaled Dawas, Rehan Haidry
Journal: Endoscopy (2015)

A 75-year-old Caucasian man was referred to his local hospital complaining of a 2-month history of dysphagia. Esophagogastroduodenoscopy (EGD) demonstrated widespread mucosal hyperpigmented plaques throughout the esophagus. An exophytic esophageal lesion was also visualized in the mid to distal esophagus ([Fig. 1]). Biopsies of the exophytic lesion revealed findings consistent with primary malignant melanoma of the esophagus.
Abstract 4477: Progesterone (P4) and testosterone (T) concentrations in random fine needle aspirates of the breast in pre- and postmenopausal women
Authors: Richard E. Heinz, Kara Kenney, Oukseub Lee, Sivaraman Iyer, Seema A. Khan, Robert T. Chatterton
Journal: Cancer Research (2012)

Abstract Background: The availability of steroid hormones in the breast may be an important measure of the potential for proliferation of hormone-dependent breast cancer, and because retention of hormones may be influenced by serum levels, in situ formation, and the presence of binding proteins and lipids in the tissue, measurements of tissue concentrations are more informative than serum concentrations alone. Methods: Subjects were normal women, aged 36-65 yr, without breast cancer and not taking hormones. Tissue was obtained by fine needle aspiration of the breast. The cellular pellet was saved for analysis of DNA, and lipids were extracted from the supernatant including the fatty layer. Previous work had shown the cellular pellet contained a very little of the total steroids of the sample. Triglycerides were precipitated from 90% methanol at –20 °C and the remaining lipids were applied to a C18 HPLC column for purification in a gradient of methanol and acetonitrile in phosphate buffer. Fractions containing P4 and T were analyzed by immunoassays. The total DNA in the cellular pellet was isolated and quantified by UV absorbance. The steroid content was expressed as either per mg of purified lipid or per microgram of DNA. The data, when expressed as the natural log of the concentrations, followed a normal distribution. Differences in pre- and postmenopausal concentrations were analyzed by group t-tests. Results: The geometric means of the hormone concentrations are shown in the table. Comment: Despite the almost complete loss of progesterone in serum of postmenopausal women, the concentrations in the tissue are reduced but remain, on average, at more than 25% of the premenopausal level, somewhat more than the previously reported percentage in NAF of 5%. Relationships within individual women to other risk factors will be explored. Testosterone is also maintained at a relatively high level in the tissue of postmenopausal women, and may serve as a substrate for aromatase. 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 4477. doi:1538-7445.AM2012-4477
Homocystinuria and Megaloblastic Anemia Responsive to Vitamin B<sub>12</sub>Therapy
Authors: Suzanne Schuh, David S. Rosenblatt, Bernard A. Cooper, Maria-Louise Schroeder, Agnes J. Bishop, Lorne E. Seargeant, James C. Haworth
Journal: New England Journal of Medicine (1984)

Original Article from The New England Journal of Medicine — Homocystinuria and Megaloblastic Anemia Responsive to Vitamin B12 Therapy — An Inborn Error of Metabolism Due to a Defect in Cobalamin Metabolism
OP0157 Disease activity as an important treatment target for rheumatoid arthritis: Direct and indirect effects on functional disability over the disease course and the influence of intensity of treatment
Authors: S. Nair, J. Bijlsma, J.H.V.D. Werf, M.J.V.D. Veen, S.P. Linn-Rasker, S. Vreugdenhil, F.P.J.G. Lafeber, P. Welsing
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Disease activity influences functional disability [1,2]. This influence constitutes a direct effect (through signs and symptoms) and an indirect effect through the effect on joint damage over time. It has been found that the direct relation between disease activity and functional disability weakens with longer disease duration [2], but it has been questioned whether this still is the case with current intensive treatment strategies. The indirect effect has not been studied. <h3>Objectives</h3> To explore the relationship between disease activity and functional disability over time considering indirect and direct associations and the influence of treatment strategy. <h3>Methods</h3> Data from 3 consecutive randomized clinical trials studying increasing intensive (tight control) treatment strategies were used. Functional capacity (HAQ) and disease activity (DAS28) were measured every 12 months. Linear mixed modeling was used to study the relation of DAS28 (current and lagged DAS28), other variables on HAQ. Interaction terms were introduced to study the influence of lagged DAS28 on HAQ was constant over time and differed with treatment strategy. <h3>Results</h3> Current DAS28 was positively associated with HAQ over time. Also, independently lagged DAS28 was positively associated with HAQ. When specifically looking at the longitudinal relation, the association of a change in DAS28 with a change in HAQ decreased over disease duration, whereas the influence of a change in the lagged DAS28 with a change in HAQ increased with duration of the disease. HAQ progression was less in the more intensively treated patients, but did not modify the relation between (lagged) DAS28 and HAQ. <h3>Conclusions</h3> Although the influence of current DAS28 on HAQ decreases with disease duration, the influence of preceding disease activity on progression of functional disability actually increases. This further underpins the importance of disease activity over time as an important treatment target to prevent long term functional decline in RA patients over the complete course of the disease. These relationships should also be taken into account in health economic modeling studies simulating the progression of RA. <h3>References</h3> van der Kooi E, et.al. Ann Rheum Dis 2010;70:168-71. Welsing PM, et al. Arthritis Rheum 2001;44:2009-17. <h3>Disclosure of Interest</h3> None Declared
428 BONE MARROW MONONUCLEAR CELLS THERAPY IMPROVES LIVER PERFUSION IN CIRRHOTIC PATIENTS
Authors: R. Bica, C. Resende, A. Alves, A. Torres, B. Couto, F. Azevedo, D. Mercante, J. Dias, T. Kasai-Brunswick, H.S. Coelho, A.C. Campos-de-Carvalho, R. Goldenberg, G. Rezende
Journal: Journal of Hepatology (2012)
Abstract 3385: Increased eIF4E phosphorylation prevents response of prostate cancer cells to mTOR inhibitors.
Authors: Leandro S. D'Abronzo, Ryan Beggs, Swagata Bose, Paramita Ghosh
Journal: Cancer Research (2013)

Abstract Inhibitors of the mammalian target of rapamycin (mTOR) had been used in various clinical trials, but with limited efficacy. The overall goal of the present studies was to identify predictive markers of response to mTOR inhibitors in prostate cancer (PCa) cells. We previously showed that the mTOR pathway is activated in castration resistant PCa (CRPC), while its inhibition upregulates androgen receptor (AR) signaling, resulting in resistance to mTOR inhibitors (Wang et al, Oncogene, 2008). mTOR forms two complexes, mTORC1 and mTORC2: in this study we compared the effects of RAD001, an mTORC1 inhibitor, BEZ235, a dual mTOR/PI3K inhibitor, and Torin1, which inhibits both mTORC1 and mTORC2. Comparison of the effects of RAD001, alone, or in combination with the AR inhibitor bicalutamide in various CRPC cell lines showed that although C4-2 cells responded well to the combination, other cell lines, such as LNCaP-AI, PC-346C and CWR-R1, did not. The resistance of LNCaP-AI and CWR-R1 was partially overcome by treatment with BEZ-235 or Torin1, alone or in combination with bicalutamide; however, PC-346C cells were resistant to all three drugs. In an effort to identify the mechanism of resistance to mTOR inhibitors, therefore, the molecular effects of the drugs in downstream targets p70S6 kinase, 4E-BP1, eIF4G, Akt and eIF4E were compared in C4-2 (least resistant) and PC-346C (most resistant) cell lines. Western blots revealed that p70S6 kinase was downregulated by all the drugs whereas 4E-BP1 phosphorylation was effectively downregulated by BEZ235, but not Torin1, or RAD001. Phosphorylation of both p70S6K and 4E-BP1 results in activation of the translation initiation complex: a complex of eIF4E and eIF4G, therefore, inactivation of the translation initiation complex requires inhibition of eIF4E phosphorylation, which is independent of mTOR activation. In C4-2 cells, eIF4E phosphorylation was increased by RAD001 but suppressed by the other two drugs. However, in PC-346C cells, despite inhibition of 4E-BP1 phosphorylation, eIF4E phosphorylation was increased by all 3 drugs. Our data indicate eIF4E phosphorylation as a likely cause of resistance to mTOR inhibitors in PCa. Citation Format: Leandro S. D'Abronzo, Ryan Beggs, Swagata Bose, Paramita Ghosh. Increased eIF4E phosphorylation prevents response of prostate cancer cells to mTOR inhibitors. [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 3385. doi:10.1158/1538-7445.AM2013-3385
Abstract 1897: <i>RAS signaling pathway gene mutations and acquired resistance to EGFR tyrosine-kinase inhibitors in EGFR mutant lung cancer</i>
Authors: Kadoaki Ohashi, Juliann Chmielecki, Ya-Lun Lin, Helen Pan, Cindy Vnencak-Jones, Maria Arcila, Lu Wang, Lynnette Fernandez, Aoe Keisuke, Kazuhiko Shien, Hiromasa Yamamoto, Shinichi Toyooka, Katsuyuki Kiura, Roman Thomas, James Chih-Hsin Yang, Vincent Miller, Marc Ladanyi, Katerina Politi, William Pao
Journal: Cancer Research (2012)

Abstract EGFR mutant lung cancers are highly sensitive to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), but in the metastatic setting, acquired drug resistance is inevitable. Second-site EGFR mutations, MET amplification, PIK3CA mutations, and histologic changes (transformation to small cell lung cancer, epithelial-mesenchymal transition (EMT)) have been reported as resistance mechanisms. Up to 40% of cases are still mechanistically unexplained. Surprisingly, despite the importance of the RAS signaling pathway downstream of EGFR, no RAS pathway signaling gene mutations have been reported to occur in acquired resistance. Here, we investigated further the significance of this pathway in preclinical models and tumor specimens. First, we screened 21 lung tumors from 11 mice with acquired resistance to erlotinib (Politi et al. Dis Model Mech. 2010; 3(1-2): 111-9) and found one tumor with a KrasG12V mutation. Next, we established 6 new cell-line based models of acquired erlotinib resistance in 5 different drug-sensitive EGFR mutant cell lines. While 5 lines developed known mechanisms of resistance (i.e. EGFR T790M, MET amplification, EMT), 1 (11-18 cells) developed de novo a NRASQ61K mutation. Single cell cloning suggested that both the EGFR mutation (L858R) and NRASQ61K mutations were in the same cell. Consistent with these findings, NRAS activity was higher in 11-18 resistant cells (11-18R) compared to parental cells. In growth inhibition assays, 11-18R were sensitive only to combined EGFR inhibition with siRNA knockdown of NRAS or with MEK inhibitors. Expression of NRASQ61K in drug-sensitive PC-9 cells conferred resistance to erlotinib. Finally, we screened 127 tumor samples from patients with acquired resistance patients to EGFR-TKIs. No NRAS or KRAS mutations were found, but one patient's tumor harbored in addition to EGFR L858R both EGFRT790M and BRAFV600E mutations. BRAFV600E expression also conferred resistance to EGFR inhibition, both in PC-9 (EGFR exon 19 deletion) and PC-9R cells (EGFR exon 19 deletion plus T790M). Collectively, these data shown that mutations in RAS pathway signaling genes may be infrequent but occur and could influence therapeutic outcomes in trials for patients with acquired resistance to EGFR TKIs. 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 1897. doi:1538-7445.AM2012-1897
MID-TERM OUTCOMES OF PACLITAXEL-COATING NITINOL STENT PLACEMENT FOR CHRONIC TOTAL OCCLUSION IN THE FEMOROPOPLITEAL ARTEY
Authors: Naotaka Murata, Yoshimitsu Soga, Tomoi Yusuke, Yohei Kobayashi, Seiichi Hiramori, Kei Ichihashi, Tanaka Nobuhiro
Journal: Journal of the American College of Cardiology (2015)
Animal Research at Stanford University
Authors: James A. Thomas, Thomas E. Hamm, Pamela L. Perkins, Thomas A. Raffin
Journal: New England Journal of Medicine (1988)

Ever since biomedical scientists began using animals as subjects for investigation, they have encountered opposition to the practice.1 As research on animals and opposition to it have evolved, many of the terms and tactics of confrontation have changed. The current battle has been pitched on four fronts: in the popular media, in legislatures, in burglarized and vandalized laboratories, and in philosophical forums. The charges and denials exchanged by the parties to the dispute, however, have often obscured both facts and common sense in discussions of animal research. The confusion engendered by this controversy led the Stanford University Medical Center Committee . . .