tbuckley/cabot-search huggingface dataset:
Abstract 5182: Sialofucosylated glycosphingolipids expressed on head and neck cancer cells mediate adhesion to endothelial cells
Authors: Steven M. Wood, Jocelyn Marshall, Courtney Abram, Monica M. Burdick
Journal: Cancer Research (2010)

Abstract The development of innovative strategies can be used to detect and prevent cancer metastasis once the molecular mediators are known. Cancer metastasis is the spread of cancer from a primary site, from which cancer cells break away and travel to a new organ via the bloodstream or the lymphatic system. However, the molecular signals responsible for the cancer cells to travel from the primary site to a new location are largely unknown. It has been hypothesized that cancer invasion is similar to leukocyte migration during response of vascular tissue to harmful stimuli. In this process, leukocytes travel through the bloodstream, attach to the vessel endothelium, and migrate through the endothelium to the site of injury. Using leukocyte migration as a model for cancer metastasis it is hypothesized that E-selectin is a major molecular mediator for head and neck squamous cell carcinoma (HNSCC) metastasis. E-selectin is expressed on the surface of vascular endothelial cells and initiates cell-cell interactions by binding to proteins and lipids on the surface of cancer cells that have sialofucosylated carbohydrate epitopes. We have previously shown that HNSCCs bind to E-selectin expressed on stimulated human umbilical vein endothelial cells (HUVECs) under physiological shear stress. Also, it has been shown that glycosphingolipids isolated from HNSCCs support adhesive interactions with E-selectin-transfected Chinese hamster ovary cells. To further reveal the role of sialofucosylated glycosphingolipids in cell-cell interactions, polystyrene microsphere beads were utilized, in an in vitro model of cell adhesion under fluid flow conditions. Polystyrene beads were coated with sialyated non-fucosylated gangliosides (GM1) or sialofucosylated glycosphingolipids from HNSCCs. The expression of glycosphingolipids on the newly coated microspheres was checked by flow cytometry to ensure that the lipids adsorbed to the beads. When coated microspheres were perfused over cytokine-stimulated HUVECs, the microspheres with sialofucosylated glycosphingolipids tethered and rolled on the endothelium similar to HNSCCs, while the microspheres coated with GM1 did not bind to the endothelium. Treatment of the sialofucosylated glycosphingolipid coated microspheres with sialidase or fucosidase also eliminated adhesion of the beads to the endothelium. Our study signifies the importance of the role that glycosphingolipids play in adhesion to endothelial E-selectin under physiological shear stress. Further studies are needed to determine if sialofucosylated glycosphingolipids should be targeted for patients with HNSCCs. 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 5182.
Abstract 2568: Genetic association of POU5F1B at 8q24 with prostate cancer.
Authors: Joan P. Breyer, Jeffrey R. Smith
Journal: Cancer Research (2013)

Abstract Numerous genetic variants at 8q24 have been associated with risk for multiple common cancers, most prominently for prostate cancer. POU5F1B is a retrotransposed copy of the master stem cell factor OCT4, and one of few known genes within the 8q24 interval. While OCT4 is expressed selectively in embryonic stem cells, POU5F1B retains its open reading frame and has been shown to be expressed in cancers. Ectopic expression of OCT4 blocks progenitor cell differentiation and causes dysplasia, raising the possibility that aberrant expression of POU5F1B might have analogous effects. Because POU5F1B sequence is non-unique, a potential contribution of POU5F1B genetic variation to cancer risk has not been investigated in prior GWAS. We evaluated genetic variants of POU5F1B for association with prostate cancer within a case-control study of familial prostate cancer at Vanderbilt University that included 830 familial prostate cancer probands, and 830 age-matched control probands without a personal or family history of prostate cancer. Our study identified four missense variants within POU5F1B, and eight haplotypes of &amp;gt; 1% frequency. G176E was associated with prostate cancer (P = 3.1 x 10−4) and was in LD with GWAS SNP rs6983267 (r2 = 0.69). The minor allele (encoding glutamate) uniquely marked a single haplotype (the most common) with an inverse association with prostate cancer (P = 5.7 x 10−4, OR = 0.78 (95%CI 0.7-0.9)). As expected, the haplotype association was correlated with that of GWAS SNP rs6983267. A second haplotype differing from the first only at G176E (encoding glycine) was independently associated with risk of prostate cancer (P = 5.5 x 10−7, OR = 1.91 (95%CI 1.5-2.5)). However, glycine would also be encoded at this position by all other haplotypes, none carrying a risk effect. The risk haplotype was tagged by the pair of missense variants, G176E (glycine) and E238Q (glutamine). In a single allele analysis, the latter variant had no apparent association with prostate cancer. The risk effect of the former adjusted for the latter was OR = 2.12 (95%CI 1.6-2.7), P = 1.7 x 10−8; the risk effect of the latter adjusted for the former was OR = 1.79 (95%CI 1.4-2.3), P = 9.4 x 10−6. The two missense variants would alter each of the DNA-binding domains: one altering a highly conserved site with a non-conservative substitution, and the other abrogating a kinase site known to physiologically regulate other POU transcription factors. Our data suggest that combinations of these variants may be associated with risk of prostate cancer and warrant further investigation of the potential role of POU5F1B in the 8q24 cancer associations. Citation Format: Joan P. Breyer, Jeffrey R. Smith. Genetic association of POU5F1B at 8q24 with prostate 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 2568. doi:10.1158/1538-7445.AM2013-2568
PREVALENCE AND CLINICAL CORRELATES OF RIGHT VENTRICULAR DYSFUNCTION IN PATIENTS WITH HYPERTROPHIC CARDIOMYOPATHY
Authors: Gherardo Finocchiaro, Aleksandra Pavlovic, Yael Shmargad, Gianfranco Sinagra, Francois Haddad, Euan Ashley
Journal: Journal of the American College of Cardiology (2013)
Allogeneic Bone Marrow Transplantation after Hyperfractionated Total-Body Irradiation and Cyclophosphamide in Children with Acute Leukemia
Authors: Joel A. Brochstein, Nancy A. Kernan, Susan Groshen, Constance Cirrincione, Brenda Shank, David Emanuel, Joseph Laver, Richard J. O'Reilly
Journal: New England Journal of Medicine (1987)

Ninety-seven children with either acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML) received HLA-identical bone marrow transplants from sibling donors, after preparation with 1320 cGy of hyperfractionated total-body irradiation and high-dose cyclophosphamide. Kaplan–Meier product–limit estimates (means ±SE) of disease-free survival at five years among patients with ALL in second remission, third remission, and fourth remission or relapse were 64±9, 42±14, and 23±11 percent, respectively, with probabilities of relapse of 13±7, 25±13, and 64±16 percent. Among patients with AML in first remission, second remission, and third remission or relapse, five-year disease-free survival estimates were 66±10, 75±15, and 33±19 percent, with respective relapse probabilities of 0, 13±12, and 67±19 percent. The most frequent cause of death in patients in early remission (ALL in second or third remission or AML in first or second remission) was bacterial sepsis, fungal sepsis, or both, most often in the presence of acute or chronic graft-versus-host disease. Among patients with ALL who received transplants while in second remission, the duration of the initial remission had no effect on the probability of relapse after transplantation. The only pretransplantation factor that significantly affected outcome was the disease status at the time of transplantation; patients in early remission had better disease-free survival. We conclude that transplantation after preparation with hyperfractionated total-body irradiation and cyclophosphamide is an effective mode of therapy in children with refractory forms of acute leukemia. (N Engl J Med 1987; 317:1618–24.)
Abstract 788: Effects of ATF3 on the gain-of-function of mutant p53.
Authors: Saisai Wei, Sarah Malmut, Hongbo Wang, Chunhong Yan
Journal: Cancer Research (2013)

Abstract Activating Transcription Factor 3 (ATF3) is a member of the ATF/CREB family of transcription factors and can be rapidly induced by DNA damage and other cellular stresses. We previously found that ATF3 activates p53 by binding to the C-terminus of the tumor suppressor and blocking its ubiquitination, and consequently inhibits cellular transformation. Since TP53 is mutated in half of human cancers and mutant p53 proteins (mutp53) acquire oncogenic activities including promoting drug resistance and driving cancer cell invasion and metastasis, we were interested to explore effects of ATF3 on the mutp53 gain-of-functions (GOF). One major mechanism by which mutp53 promotes tumorigenesis is through binding another p53 family member p63 and inhibiting its tumor suppressor functions. We found that ATF3, but not a mutated ATF3 protein (▵102-139) devoid of its p53-binding region, bind the p53R175H mutant and disrupted the interactions between mutp53 and p63. As a consequence, while mutp53 inhibited the p63 transcriptional activity, ATF3 but not the ▵102-139 protein counteracted mutp53 and resumed p63 activity. Consistent with these results, ATF3 expression inhibited mutp53-promoted cell migration and invasion. In addition to effects on the mutp53-p63 interaction, we also found that ATF3 repressed mutp53-induced NFκB activity, thereby sensitizing mutp53-expressing cells to treatments with etoposide and cisplatin. We conclude that ATF3 suppresses the GOF of mutant p53 and thus may also contribute to tumor suppression in p53-mutated cancer cells. Citation Format: Saisai Wei, Sarah Malmut, Hongbo Wang, Chunhong Yan. Effects of ATF3 on the gain-of-function of mutant p53. [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 788. doi:10.1158/1538-7445.AM2013-788
Abstract 1172: Prodigiosin and its structural analogue rescue deficient p53 pathway signaling and anti-tumor effects via p73 upregulation in p53 mutant and null colorectal cancer cells
Authors: Bo Hong, David T. Dicker, Levy Kopelovich, Wafik S. El-Deiry
Journal: Cancer Research (2012)

Abstract The tumor suppressor p53 gene is mutated in over 50% of human cancers, and this is associated with resistance to radiotherapy and chemotherapy as well as tumor progression. Therefore, p53 pathway functional reactivation in p53-deficient cancers is an attractive strategy for cancer therapy and may address an unmet need in the clinic for progressive therapy-refractory human tumors. We previously showed that Prodigiosin and its structure analogue can reactivate the p53 pathway in p53 mutant and null colorectal cancer cells (Hong et al. AACR 2011, abstract 607). Here, we examined the mechanism of p53 pathway reactivation by Prodigiosin and its structural analogue in colorectal cancer cells. p73, a p53 family protein, shares a high degree of sequence homology with p53 and regulates the expression of similar genes by binding to p53 responsive elements within gene promoters and performs similar functions to p53. However, unlike p53, p73 is not a target for mutational inactivation in human cancer. In the study, we hypothesized that Prodigiosin and its structural analogue induce p73 expression to activate the p53 pathway and further induce cellular apoptosis in p53-deficient cancer cells. We showed that Prodigiosin and its structural analogue induced p73 expression in p53 mutant SW480 and p53−/− HCT116 cells. We also showed that the induction of p53-responsive transcriptional activities by Prodigiosin and its structural analogue was reduced in SW480 cells with p73 stable knockdown, as compared with parental SW480 cells. Western blot analysis indicated that the induction of a p53 target protein DR5 by Prodigiosin and its structural analogue was decreased in SW480 cells with p73 stable knockdown, as compared with parental SW480 cells. The sub-G1 analysis demonstrated that Prodigiosin and its structural analogue induced less apoptosis in SW480 cells with p73 stable knockdown than parental SW480 cells. Together, these findings indicate that p73 upregulation is involved in the mechanism of p53 pathway activation and apoptotic induction by Prodigiosin and its structural analogue. The study suggests that p73 induction may be a useful alternative way to reactivate p53 pathway in p53 mutant and null cancer cells and provides important mechanistic insights into the activity of a potent p53 pathway function restoring small molecule that is a candidate therapeutic for human cancer. This work was supported by the NCI Developmental Therapeutics Program through NCI Contract N01-CN-43302. 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 1172. doi:1538-7445.AM2012-1172
Actions of the Symptom Control Research Group (SCORE-G) in the Palliative Care Field in Japan: Report 3
Authors: S. Tanda, T. Yoshimoto, T. Hashizume, S. Tomiyasu, T. Tamaki, K. Yomiya, E. Ryu, H. Kagaya, T. Suzuki, M. Matoba
Journal: Annals of Oncology (2013)
AB0368 Epidemiology and therapeutic option of bacterial pneumonia in RA patients treated with biologics from multi-center registry in japan
Authors: D. Kato, T. Kojima, N. Takahashi, K. Funahashi, H. Matsubara, Y. Hattori, N. Ishiguro
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Bacterial pneumonia is most common respiratory complication in rheumatoid arthritis (RA) patients treated with biologics. There are few reports about detail of pathogenic bacteria or guideline to make a decision on the treatment. <h3>Objectives</h3> To investigate the outline of bacterial pneumonia in RA patients treated with biologics focusing on pathogens and therapeutic intervention. <h3>Methods</h3> 1575 RA patients were registered in multi-center registry for the treatment of RA with biologics in Japan (Tsurumai Biologics Communication registry; TBCR) till 2011. 57 cases were interrupted or discontinued the biologics administration due to respiratory infectious complication. We reviewed medical records of those patients and assessed about the pathogens and therapeutic intervention especially in antimicrobial agents retrospectively. <h3>Results</h3> Excluded the cases of tuberculosis, non tuberculous mycobacteriosis and pneumocystis pneumonia, 31 cases (2.0%) of biologics related bacterial pneumonia (BRP) were investigated. BRP group showed significantly higher age, baseline DAS and longer disease duration (Table 1). The character of BRP was biphasic. 6cases with mild symptoms were successfully treated with oral fluoroquinolones or macrolides without detecting the pathogens in ambulatory care. But 13cases with severe symptoms that's pathogens were isolated, all patients needed parenteral antimicrobial therapy under hospitalization. Isolated pathogens were higher pathogenic as presented in Table 2. Resistant bacterium such as BLNAR or MRSA were isolated in one case (7.7%) respectively. yogenic or atypical isolates tend to be more often from Community-acquired pneumonia (CAP) to Hospital-acquired pneumonia (HAP) as reported in previous reports, and BRP showed the profile among CAP and Healthcare-associated pneumonia (HCAP) as showed in Table 3. <h3>Conclusions</h3> The BRP profile of pathogens corresponded with that of HCAP or HAP rather than that of CAP. Classifying criteria for BRP should be established, and if the patient needs intensive care for severe symptoms, therapeutic decision should be made under consideration about resistant bacteria or atypical pathogens as recommended in HCAP or HAP guideline. <h3>Disclosure of Interest</h3> D. Kato: None Declared, T. Kojima Speakers Bureau: Abbott Japan, Chugai Pharmaceutical, Bristol-Myers Squibb, Eisai, Mitsubishi Tanabe, Pharma, Pfizer Japan, Takeda Pharmaceutical, N. Takahashi: None Declared, K. Funahashi: None Declared, H. Matsubara: None Declared, Y. Hattori: None Declared, N. Ishiguro Speakers Bureau: Abbott Japan, Chugai Pharmaceutical, Bristol-Myers Squibb, Eisai, Mitsubishi Tanabe, Pharma, Pfizer Japan, Takeda Pharmaceutical
Differentiation of colonic polyps by confocal laser endomicroscopy
Authors: X. Xie, C. Li, X. Zuo, T. Yu, X. Gu, Z. Li, R. Ji, Q. Wang, Y. Li
Journal: Endoscopy (2010)

See also: Commentaire de travail de X. J. Xie et al., pp. 87Endoscopy 2011; 43(02): 172-173DOI: 10.1055/s-0031-1291812
Metastatic Behavior of the RIF-1 Murine Fibrosarcoma: Inhibited by Hypophysectomy and Partially Restored by Growth Hormone Replacement
Authors: A. Sekyi-Otu, R. Bell, I. Andrulis, M. Pollak
Journal: JNCI Journal of the National Cancer Institute (1994)

Journal Article Metastatic Behavior of the RIF-1 Murine Fibrosarcoma: Inhibited by Hypophysectomy and Partially Restored by Growth Hormone Replacement Get access Ato Sekyi-Otu, Ato Sekyi-Otu Samuel Lunenfeld Research Institute, and Division of Orthopaedic Surgery, Mount Sinai Hospital and University of TorontoToronto, Ontario, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar Robert Bell, Robert Bell Robert S Bell, M D., Department of Orthopaedic Surgery, Mount Sinai Hospital, 600 University Ave, Rm 476, Toronto, ON M5G 1X5, Canada. Search for other works by this author on: Oxford Academic PubMed Google Scholar Irene Andrulis, Irene Andrulis Samuel Lunenfeld Research Institute, and Departments of Molecular and Medical Genetics and Pathology, Mount Sinai Hospital and University of TorontoQuebec, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar Michael Pollak Michael Pollak Lady Davis Research Institute of the Jewish General Hospital, McGill University, MontrealQuebec, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 86, Issue 8, 20 April 1994, Pages 628–632, https://doi.org/10.1093/jnci/86.8.628 Published: 20 April 1994 Article history Received: 01 September 1993 Revision received: 05 January 1994 Accepted: 31 January 1994 Published: 20 April 1994
Commentary: Some Critical Issues and Concerns Related to Research Advances on the Toxicology of Chemical Mixtures
Authors: Raymond S. H. Yang
Journal: Environmental Health Perspectives (1998)

This paper addresses some of the issues and concerns on research advances on the toxicology of chemical mixtures.Emphases will be selectively given to the following questions and answers: Can mechanistic studies be conducted on chemical mixtures?The fact that any studies, including mechanistic studies, of single chemicals are really the study of the parent chemical plus its metabolites underscores the relevance of mechanistic studies on chemical mixtures.Can predictions be made on the health effects of chemical mixtures?Some successes are already evident in the literature on simpler chemical mixtures.For more complex mixtures, it is possible and we propose an approach here.What can we learn from other disciplines (the importance of interdisciplinary collaboration)?Two aspects, the knowledge and methodologies available in clinical pharmacology and the latest advances in structure-oriented lumping in chemical engineering, are discussed in detail.Unrepeatable results: The possibility of magnification of biologic variability because of low-level exposures to chemical mixtures is suggested with special reference to some known examples, including the controversial study on synergistic interactions of endocrine disruptors.Is the driving force for scientific investigations on chemical mixtures the legislative and regulatory atmosphere?Two laws with chemical mixtures specifically in the language are quoted and discussed.Their implications regarding research funding and activities are described.What are the pitfalls of applying for research funding on investigating chemical mixtures?The dilemma at least one investigator faces in pursuing research funding is elaborated.The questions and issues listed above are not all inclusive, but they represent some of the aspects that need to be brought into the open in the scientific community for discussion and/or debate.Thus, the primary objective of this paper is to provide some momentum for the beginning of a fruitful and stimulating discussion.
Ceftriaxone-Resistant Salmonella Infection Acquired by a Child from Cattle
Authors: Paul D. Fey, Thomas J. Safranek, Mark E. Rupp, Eileen F. Dunne, Efrain Ribot, Peter C. Iwen, Patricia A. Bradford, Frederick J. Angulo, Steven H. Hinrichs
Journal: New England Journal of Medicine (2000)

The emergence of resistance to antimicrobial agents within the salmonellae is a worldwide problem that has been associated with the use of antibiotics in livestock. Resistance to ceftriaxone and the fluoroquinolones, which are used to treat invasive salmonella infections, is rare in the United States. We analyzed the molecular characteristics of a ceftriaxone-resistant strain of Salmonella enterica serotype typhimurium isolated from a 12-year-old boy with fever, abdominal pain, and diarrhea.
Emotional Effects of Lower-Limb Amputation in the Aged
Authors: Lloyd M. Caplan, Thomas P. Hackett
Journal: New England Journal of Medicine (1963)

THE emotional responses of people to the loss of an extremity have been dealt with by a number of investigators. In most of these studies the subjects have been young, and attention has been chiefly focused on the curious phenomenon of the phantom limb.1 In the last few years we have examined a number of elderly patients with amputations. From this group 12 were selected for intensive study. Ten of these 12 patients complained of phantom sensations, but far more troubling was another postoperative manifestation that has not been thoroughly discussed in the literature: in each case a serious reactive . . .