tbuckley/cabot-search huggingface dataset:
Abstract 5198: Different functions of the chemokine receptor CXCR3 in normal and malignant mammary epithelial cells
Authors: Yanchun Li, Xinrong Ma, Namita Kundu, Olga Goloubeva, Dawn Holt, Amy M. Fulton
Journal: Cancer Research (2010)

Abstract Our previous studies detected chemokine receptor CXCR3 in malignant epithelium of early stage breast cancers by immunohistochemistry and the expression levels were positively correlated with significantly poorer survival. We also showed that CXCR3 contributes to metastatic potential in a murine model of metastatic breast cancer. Interestingly, although immortalized normal murine and human mammary epithelial cells (EpH4 and MCF-10A) also express CXCR3, they respond to CXCR3 ligands differently than malignant cells. Migration of tumor cells was enhanced by stimulation with CXCR3 ligands, but a negligible chemotactic response to these ligands was observed in normal cells. Signal transduction activation patterns also differ between malignant and normal cells. In tumor cells, ERK1/2 is robustly activated after CXCR3 ligand stimulation, whereas the same pathway is inhibited in normal cells. Likewise the p38 pathway is activated in tumor cells and decreased in normal cells. Thus, CXCR3 activation alters the behavior of both malignant and normal cells, but in different ways. One possible mechanism to explain different functions of CXCR3 between normal and malignant mammary epithelial cells is the expression of different CXCR3 isoforms. It has been shown that the “classical” CXCR3 receptor (CXCR3-A) mediates proliferation and migration of various cell lines, while CXCR3-B, a splice variant of CXCR3-A, has opposing functions. To determine the expression pattern of these two CXCR3 isoforms in a panel of human breast cancer cell lines, we conducted real-time quantitative PCR and showed that the CXCR3-B/CXCR3-A mRNA expression ratio is decreased (0.16-0.63) compared with normal epithelial cell line MCF-10A (2.16). CXCR3-B expression dominates in MCF-10A cells, while CXCR3-A expression dominates in tumor cells, with the most metastatic cell line (MDA-MB-231) exhibiting the lowest CXCR3-B/CXCR3-A ratio (0.16). Taken together, these data indicate that the level of CXCR3 receptor expression is not the only determinant of function; the relative amounts of CXCR3-A and CXCR3-B may also be important. Further studies will elucidate how the balance between CXCR3-A and CXCR3-B contributes to the behavior of cells and allow us to optimize therapeutic strategies targeting CXCR3. 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 5198.
THU0112 Myeloid-Derived Suppressor Cells have Regulatory Roles in Mouse Collagen-Induced Arthritis
Authors: W. Fujii, E. Ashihara, H. Hirai, H. Nagahara, K. Fujioka, K. Murakami, T. Seno, A. Yamamoto, H. Ishino, M. Kohno, T. Maekawa, Y. Kawahito
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Myeloid-derived suppressor cells (MDSCs) are of myeloid origin and are able to suppress T cell responses. MDSCs are characterized by the co-expression of the myeloid differentiation antigens Gr-1 and CD11b in mice (1). MDSCs in cancer have been studied in detail and are known to play roles in tumor associated immune suppression. However, the roles of MDSCs in autoimmune disease remain controversial and little is known about MDSCs in autoimmune arthritis. <h3>Objectives</h3> We investigate the roles of MDSCs in autoimmune arthritis using collagen-induced arthritis (CIA) mouse models. <h3>Methods</h3> We determined the number of Gr-1<sup>+</sup> CD11b<sup>+</sup> MDSCs in the spleens of CIA mice by flow cytometry. Next, we isolated MDSCs from CIA mice by magnetic cell sorting and cultured with CD4<sup>+</sup> T cells to analyze the functions of MDSCs. We investigated the proliferation of CD4<sup>+</sup> T cells by CFSE dye dilution assay and estimated cytokine levels produced by CD4<sup>+</sup> T cells using ELISA. Furthermore, we investigated CD4<sup>+</sup> T cell differentiation into Th17 cells by flow cytometry. Finally, we performed adoptive transfer of MDSCs into CIA mice and investigated the severity of arthritis. <h3>Results</h3> MDSCs significantly accumulated in the spleens of mice with CIA when arthritis severity peaked. These MDSCs inhibited CD4<sup>+</sup> T cell proliferation and differentiation into Th17 cells. Moreover, MDSCs inhibited the production of IFNγ, IL-2, TNFα, and IL-6 by CD4<sup>+</sup> T cells <i>in vitro</i>, whereas they promoted the production of IL-10. Adoptive transfer of MDSCs reduced both clinical (Image A) and histological arthritis scores (Image B) <i>in vivo</i>, which was accompanied by a decrease in the number of CD4<sup>+</sup> T cells and Th17 cells in the draining lymph nodes. <h3>Image/graph</h3> <h3>Conclusions</h3> MDSCs in CIA suppress the progression of CIA by inhibiting the pro-inflammatory immune response of CD4<sup>+</sup> T cells. These observations suggest that MDSCs play crucial roles in the regulation of autoimmune arthritis, which could be exploited in new cell-based therapies for human rheumatoid arthritis (RA). <h3>References</h3> Gabrilovich, D. I., and S. Nagaraj. 2009. Myeloid-derived suppressor cells as regulators of the immune system. <i>Nat. Rev. Immunol.</i> 9: 162-174. <h3>Disclosure of Interest</h3> None Declared
Case 84-1962
Authors: Gordon S. Myers, Benjamin Castleman
Journal: New England Journal of Medicine (1962)

Presentation of Case A seventy-two-year-old woman was admitted to the hospital because of marked weakness and abdominal pain.Five months before entry the patient was admitted to another hospital because of the sudden onset of steady substernal pain that radiated through to the back, was accompanied by weakness and sweating and was not exacerbated by breathing. The pain gradually subsided a few days later. While she was in the hospital dull, aching pain began in the left side of the chest and persisted until two weeks before entry to this hospital. A Grade 2 apical systolic murmur and a Grade . . .
Presence of Diabetic Glomerulosclerosis in Patients with Hemochromatosis
Authors: Donald Becker, Max Miller
Journal: New England Journal of Medicine (1960)

SOME authors have stated that patients with diabetes mellitus due to hemochromatosis are not prone to the vascular complications seen in ordinary diabetes mellitus. Lonergan and Robbins1 examined the kidney sections of 62 patients with hemochromatosis and diabetes and reported the absence of the Kimmelstiel-Wilson nodular glomerular lesion. Sheldon,2 who collected 311 authentic cases of hemochromatosis, stated that in only 8 subjects could atherosclerosis have been present. Bell3 noted only 1 serious vascular lesion, a myocardial infarction, in 29 cases of hemochromatosis with diabetes, and Warren4 stated that renal glomerular lesions have not been reported in hemochromatosis with diabetes.However, . . .
“Stupid people deserve what they get”: The effects of personality assessment on judgments of intentional action
Authors: Berit Brogaard
Journal: Behavioral and Brain Sciences (2010)

Abstract Knobe argues that people's judgments of the moral status of a side-effect of action influence their assessment of whether the side-effect is intentional. I tested this hypothesis using vignettes akin to Knobe's but involving economically or eudaimonistically (wellness-related) negative side-effects. My results show that it is people's sense of what agents deserve, and not the moral status of side-effects, that drives intuition.
A8.7 Hydrogen sulfide treatment reduces joint degradation in autoimmune arthritis
Authors: D Sieghart, V Saferding, E Goncalves-Alves, MI Koenders, S Blüml, G Steiner
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Background and objectives</h3> The gasotransmitter hydrogen sulfide (H<sub>2</sub>S) has been demonstrated to exert anti-inflammatory effects on different types of cells important in the pathogenesis of rheumatoid arthritis (RA) and osteoarthritis such as monocytes/macrophages, synovial fibroblasts or chondrocytes. It was the aim of this study to investigate whether treatment with the H<sub>2</sub>S donor sodium hydrogen sulfide (NaHS) may influence disease development and outcome of experimental RA. <h3>Materials and methods</h3> In a first series of experiments NaHS was applied three times a week to healthy mice. Two hours before the end of the experiment, mice were challenged with LPS or PBS as negative control. Collagen-induced arthritis (CIA) was induced by a dual injection of bovine collagen type II. NaHS was applied two times before the first collagen injection and six times between the first collagen injection and the boost. On day 57 the experiment was terminated and blood, spleen, lymph nodes and paws were analysed in detail. Serum transfer arthritis was induced in C57BL/6 mice by two i.p. injections (day 0 and 2) of arthritogenic serum from K/BxN mice and NaHS was applied on days -1, 1, 3, 6 and 8. The experiment was terminated on day 9 and blood, spleen and paws were collected. <h3>Results</h3> LPS challenged mice treated with 0.4 mM NaHS had reduced serum levels of TNF-α, IL-4 and IL-23 compared to placebo treated animals without showing clinical symptoms of intoxication. In both disease models NaHS treatment did not influence clinical signs of arthritis such as paw swelling and grip strength. However, histological evaluation of affected paws revealed significant reduction of joint degradation in mice with serum transfer arthritis with reduced inflammation and cartilage loss and almost complete absence of bone erosion and osteoclasts. In contrast, NaHS treatment during the preclinical phase did not influence histological parameters in mice with CIA. <h3>Conclusions</h3> Our investigations in the serum transfer arthritis model which largely reflects the effector phase of arthritis involving mainly the innate immune system showed highly reduced joint degradation and almost complete inhibition of bone erosion in NaHS treated mice. This is in line with recently published data demonstrating that NaHS inhibits osteoclastogenesis, both in murine bone marrow cells<sup>1</sup> and human CD11b+ cells.<sup>2</sup> <h3>References</h3> Lee <i>et al</i> . <i> J Cell Biochem </i> 2013; <b> 114 </b>:1183–93. Gambari L, Lisignoli G, Cattini L, <i>et al</i> . <i> Pharmacol Res </i> 2014; <b> 87 </b>:99–112.
Abstract 5409: Ron silencing by shRNA inhibits growth, induces apoptosis and sensitizes tumor response to c-Met inhibitor treatment through down-regulating MAPK signaling in B-Raf mutant colon carcinomas
Authors: Helen Y. Zou, Qiuhua Li, Ming Qiu, Keith Tatsukawa, Karen Wu, Douglas Fang, Jean Cui, Steve Bender, Neil W. Gibson, Tod Smeal
Journal: Cancer Research (2010)

Abstract RON, the receptor for macrophage-stimulating protein, belongs to the MET receptor tyrosine kinase family and shares many common features with MET. Inappropriate activation of RON signaling plays an important roll in colon carcinoma cell proliferation, survival, migration and invasive growth. Ron and Met are overexpressed in patient colon tumors, where co-overexpression of both Ron and Met correlates with the worst patient survival compared to the overexpression of Ron or Met alone. BRaf-activating mutations occur in about 10% of colorectal carcinomas. Mutant BRaf has constitutive kinase activity and causes hyperactivation of the mitogen-activated protein kinase (MAPK) pathway, and BRaf mutant cancers are generally resistant to standard therapies. Here we report that knockdown of the Ron gene by Ron shRNA in BRafV600E mutant HT29 colon carcinoma cells induced HT29 tumor apoptosis and resulted in significant tumor growth inhibition (TGI) by 59%, which is comparable to that observed with the selective EGFR inhibitor-Erlotinib treatment (57% TGI), but more potent than that of the selective Met inhibitor-PF-04217903 treatment (38% TGI). When Ron shRNA knockdown and treatment with the selective Met inhibitor were combined, enhanced tumor growth inhibition (76%) was observed. Comparable experiments using the BRaf mutant Colo205 model yielded similar results. Western Blot analysis showed that combination of Ron shRNA and Met inhibition in HT29 cells decreased phosho-ERK, elevated cleaved caspase-3 and, surprisingly, increased total Ras protein levels. No significant changes in total and phospho-AKT levels were observed. In vitro, the stable HT29-shRon cells initially grew more slowly compared to HT29-vector cells, but the growth rate gradually increased, approaching that observed in normal cell culture conditions. Interestingly, when co-culturing stable HT29-shRon or HT29-vector cells with bone marrow derived mesenchymal stem cells, the selective Met inhibitor-PF-04217903 induced significant cell death only in the HT29-shRon cells under hypoxic conditions (1% oxygen). No cell death was observed with either HT29-shRon cells under normoxia or HT29-vector cells under hypoxia or normoxia conditions, indicating the collaborative roll of Ron and Met in colon cancer cell survival during hypoxia. In summary, inhibiting both Ron and Met pathways in BRaf mutant colon cancer cells down- regulated ERK activity, induced apoptosis and led to enhanced antitumor efficacy in vivo. 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 5409.
Breast Cancer Screening: Benefit or Harm?
Authors: Karsten Juhl Jørgensen, Peter C. Gøtzsche
Journal: JAMA (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 HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Abstract LB-294: Transforming growth factor beta 3 (TGF-ß3) contributes to epithelial-mesenchymal transitions (EMT) in human prostate cancer
Authors: Qiang Zhang, Xiao Lin, Brian Helfand, Lin Chen, James Kozlowski, Ximing J Yang, Lihua J Zhu, Chung Lee
Journal: Cancer Research (2012)

Abstract Introduction and Objective: TGF-ß3 is considered as an important endogenous mediator of normal developmental and cellular repair, but its role in cancer is not well characterized. We recently reported that over-production of TGF-ß1 by tumor cells is involved in the epithelial-mesenchymal transition (EMT) in cancer cells. Based upon our prior findings, we hypothesized that, in addition to TGF-ß1, TGF-ß3 may also be involved in the EMT and contribute to prostate cancer (PCa) progression. In the present study, we explored the relationship between TGF-ß3 and TGF-ß1 induced EMT pathway in PCa. Methods: We studied 287 prostatectomy specimens obtained from the Northwestern University Prostate SPORE tissue bank. 165 specimens had low Gleason score (≤6, LGS), 55 had intermediate Gleason score (7, IGS), and 67 had high Gleason score (8-10, HGS). The median follow-up was 60 months (range 22-82). Levels of TGF-ß 1, TGF-ß 3, NF-kB and vimentin were analyzed using a high-throughput tissue microarray analysis and immunohistochemistry staining. Clinical correlation was performed based on patient follow-up information from the Prostate SPORE clinical-linked database which includes pre- and post-operative serum PSA levels. Results: High levels of TGF-ß3 expression were identified in 33.8%, 2.8% and 1.1% of HGS, IGS and LGS tumors, respectively, while high levels of vimentin expression occurred in 23.9%, 3.6% and 1.8% of HGS, IGS and LGS tumors, respectively. Expression of vimentin was significantly associated with high levels of TGF- ß3 (P=3.22E-06). Furthermore, TGF- ß3 overexpression was significantly associated with more aggressive tumors with high Gleason score (P=9.76E-09). Furthermore, there was a positive and significant correlation between expression of TGF- ß 3 and TGF-ß1 (P=2.29E-07), and between the expression levels of TGF- ß3 and NF-kB (P=7.52E-12), which were previously reported to be important mediators of the EMT in PCa. Conclusion: Our results firstly demonstrate that TGF-ß3 has a close correlation with TGF-ß 1 mediated overexpression of vimentin in PCa, which highly suggests that TGF-ß3 may play a critical role in the TGF- ß1 induced NF-kB mediated EMT signaling pathway. This pathway was reported to play a dramatic effect on the progression of human PCa and disease recurrence after prostatectomy. Consideration of TGF- ß3 tissue immunohistochemistry should be considered as a novel potential biomarker for EMT of PCa in clinic. 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 LB-294. doi:1538-7445.AM2012-LB-294
Effect of Exercise on Coronary Endothelial Function in Patients with Coronary Artery Disease
Authors: Rainer Hambrecht, Anamaria Wolf, Stephan Gielen, Axel Linke, Jürgen Hofer, Sandra Erbs, Nina Schoene, Gerhard Schuler
Journal: New England Journal of Medicine (2000)

Studies of the cardioprotective effects of exercise training in patients with coronary artery disease have yielded contradictory results. Exercise training has been associated with improvement in myocardial perfusion even in patients who have progression of coronary atherosclerosis. We therefore conducted a prospective study of the effect of exercise training on endothelial function in patients with coronary artery disease.
Drug Designers Target Ras for Cancer Treatment
Authors: E. Blume
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Drug Designers Target Ras for Cancer Treatment Get access Elaine Blume Elaine Blume Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 19, 6 October 1993, Pages 1542–1544, https://doi.org/10.1093/jnci/85.19.1542 Published: 06 October 1993
Other Possible Mechanisms of AIDS Retrovirus Pathenogenicity
Authors: S. RAAM
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article Other Possible Mechanisms of AIDS Retrovirus Pathenogenicity Get access SHANTHI RAAM SHANTHI RAAM Oncology Laboratory Division, Tufts University Medical Cancer Unit, Lemuel Shattuck Hospital12 North, 170 Morton St. Boston, MA 02130 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 1, January 1989, Pages 70–71, https://doi.org/10.1093/jnci/81.1.70-a Published: 01 January 1989
Abstract 2008: Effect of histone deacetylase inhibitor in combination with 5-fluorouracil on pancreas cancer and cholangiocarcinoma cell line
Authors: Shinichiro Yamada, Mitsuo Shimada, Tohru Utsunomiya, Yuji Morine, Satoru Imura, Tetsuya Ikemoto, Jun Hanaoka, Hiroki Mori, Mami Kanamoto, Shuichi Iwahashi, Yu Saito, Michihito Asanoma
Journal: Cancer Research (2011)

Abstract Background: Histone deacetylase (HDAC) is well known to be associated with epigenetic regulation and carcinogenesis, and its inhibitors (HDACIs) induce the differentiation or apoptosis of cancer cells. Valproic acid (VPA) is one of the HDACIs, and it is clinically available as an oral antiepilepsy drug. We have reported that VPA augmented the anti-tumor effects of gemcitabine (GEM) in pancreas cancer cell lines and a cholangiocarcinoma cell line (2010 ASCO-GI), and we plan the clinical trial of combination therapy, S-1, that is a novel oral fluoropyrimidine derivative consisting of 5-fluorouracil (5-FU) prodrug tegafur, and VPA. We examined the augment effects of VPA with a combination of 5-FU in vitro. Methods: A human pancreas cancer cell line (SUIT-2) and a cholangiocarcinoma cell line (HuCCT1) were used. The anticancer effects of VPA combined with 5-FU in SUIT-2 and HuCCT1. The cell viability was evaluated by MTT assay. Results: Pancreas cancer cell line (SUIT-2): In 5-FU alone group, no effect of 5-FU was observed in dose of 1.0μM, and 17% and 30% of proliferation-inhibitory effects were observed in dose of 2.5 and 5.0μM, respectively. VPA (0.5mM) weakly suppressed cell viability by 13%. In combination of 5-FU and VPA, 19% of inhibitory effect was observed in dose of 5-FU 1.0μM/VPA 0.5mM, respectively. Cholangiocarcinoma cell line: 5-FU (1.0μM) did not suppress the cell viability, 5-FU (2.5μM) suppressed by 23%. VPA (0.5mM) did not suppress the cell viability, while VPA (1.0mM) weakly decreased it by 11%. 5-FU (1.0μM) and VPA (0.5mM) reduced by 30%, which significantly augmented the anticancer effect of 5-FU alone or VPA alone (P&amp;lt;0.01). Conclusion: VPA augmented the anti-tumor effect of 5-FU in both a pancreas cancer cell line and a cholangiocarcinoma cell line. Therefore, 5-FU plus VPA is suggested to be a promising therapeutic option for both pancreas cancer and cholangiocarcinoma. 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 2008. doi:10.1158/1538-7445.AM2011-2008
Videodisks Help Patients Choose Therapy
Authors: C. Vanchieri
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Videodisks Help Patients Choose Therapy Get access Cori Vanchieri Cori Vanchieri Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 23, 4 December 1991, Pages 1711–1712, https://doi.org/10.1093/jnci/83.23.1711 Published: 04 December 1991
P424 NOVEL BIOMARKER FOR HEPATOCELLULAR CARCINOMA: THE ANTIOXIDANT RESPONSE IN THE CARCINOGENESIS
Authors: R. Sánchez-Rodríguez, J.E. Torres-Mena, V. Quintanar-Jurado, S. Villa-Treviño, V. Chagoya-Hazas, E. Rojas del Castillo, G. Velasco-Loyden, L. Pozo-Yauner, K. Carrillo-Sánchez, J.I. Pérez-Carreón
Journal: Journal of Hepatology (2014)