tbuckley/cabot-search huggingface dataset:
Dietary effect on ileocolitis in a mouse model of inflammatory bowel disease with genetic disruption of genes encoding two intracellular glutathione peroxidases
Authors: Fong-Fong Chu, Qiang Gao, Byung-Wook Kim, Marucha Sanchez, R. Steven Esworthy
Journal: Cancer Research (2007)

3066  Mice deficient in two glutathione peroxidases, Gpx1 and Gpx2, (Gpx1/2-DKO mice) on a mixed C57BL/6 and 129S1/SvJ (B6.129) genetic background are prone to ileocolitis and later develop ileal and colonic cancer by 8 months of age. It is well appreciated that multiple factors are involved in inflammation and cancer; these include genetical susceptibility, environmental factors (luminal microflora, diet, smoking, etc.), and immune deregulations. We reported previously that nearly 25% of B6.129 Gpx1/2-DKO mice develop ileocolonic tumors by 6-9 months of age, when their non-DKO littermates (having at least one wildtype Gpx1 or Gpx2 allele) rarely have inflammation and none have tumors. B6 Gpx1/2-DKO mice are more resistant to inflammation and they only have 2.5% tumor rate. In the current study, we are investigating dietary factors such as yeast and fat content affecting inflammation and cancer in these DKO mice.  We have observed that DKO mice appear to be highly sensitive to dietary contents. When B6.129 DKO mice were placed on a Torula-yeast diet (Harlan Teklad), they had more severe symptoms including weight loss, diarrhea, and ileocolitis than those on a regular Purina 5001 chow (which contains brewers yeast and 5% fat) or those on Purina 5020 (also has yeast and 9% fat). DKO mice on Purina 5020 had better health than those on 5001. When B6 DKO mice were placed on Newmark’s purified diet (AIN76A with 20% corn oil and low in Vit.D and calcium), there was almost no symptoms or inflammation. Those B6 DKO mice on Newmark diet were much healthier than B6 DKO mice on a diet containing AIN76A with 5% corn oil (and normal vit. D and calcium), and those B6 DKO mice on Purina 5001 diet had the worst symptoms and pathology among those on the three diets. Taken together, we propose that higher fat content can protect DKO mice from inflammation, and dietary yeast may promote inflammation in the DKO mice.  Our result support the notion that yeast components, phosphopeptidomannans, which often induce immune response by generating anti-Saccharomyces cerevisiae antibodies (ASCA) in patients suffering inflammatory bowel disease (IBD), may contribute to IBD pathogenesis.
Anti-angiogenic and anti-tumor activity of 2-methoxyestradiol sulfamate analogs in the MCF-7 breast cancer xenograft nude mouse model
Authors: Takeshi Kitazaki, Mikio Oka, Hiroshi Soda, Yoichi Nakamura, Junji Tsurutani, Seiji Doi, Shigeru Kohno
Journal: Cancer Research (2004)

4544  A better understanding of the tumorigenic process has led to the realization that to effectively treat cancers requires the development of drugs that are multi-targeting in their action. Our group has synthesized and evaluated 2-methoxyestradiol-3,17-bis-sulfamate (STX 140) and a novel 2-methoxy D-ring modified estradiol sulfamate analog (STX 641). In vitro studies have shown them to target and inhibit steroid sulfatase enzyme activity, microtubule polymerization, and angiogenesis. These compounds were evaluated in vivo for their multi-targeting effects by measuring anti-angiogenic and anti-tumor activity in the MCF-7 breast cancer xenograft nude mouse model. Adult female ICRF nude (nu/nu) mice were injected with 10x106 MCF-7 cells/0.1ml Matrigel subcutaneously and tumor growth was monitored weekly. When tumors reached 100-150mm3 in volume, mice were divided into control, STX 140 and STX 641 groups. Compounds were given 5 times per week (20mg/kg/day, p.o.) for a 3 week period; controls received vehicle only. Mice were injected intravenously with 0.1ml of 25mg/ml FITC-Dextran solution 20 minutes prior to killing to allow the visualization and quantification of tumor angiogenesis. Liver and tumor steroid sulfatase activities were also determined. Imaging showed that tumors in the control group had a well defined and structured vasculature, whereas in STX 140 and STX 641 treated animals the tumor vasculature was disrupted and ill defined. FITC quantification of tumor angiogenesis revealed that levels were significantly lower in STX 140 and STX 641 treated animals (40% and 60% respectively, ANOVA p
hnRNP B1, an early detection marker for lung cancer, impairs DNA repair mediated through inhibition of DNA-dependent protein kinase activity
Authors: Naoko Sueoka, Kentaro Iwanaga, Akemi Sato, Shinichiro Hayashi, Eisaburo Sueoka
Journal: Cancer Research (2005)

3059  Dibenzo[a,l]pyrene (DB[a,l]P), a very potent carcinogenic polycyclic aromatic hydrocarbon (PAH), adaptively induces base excision repair (BER) genes, including DNA polymerase β (Polβ) in mouse skin (Chakravarti et al., Proc Am Assoc Cancer Res, 2004). This response is correlated with mutagenesis from the rapidly formed apurinic sites generated by DB[a,l]P-induced depurinating DNA adducts. Therefore, Polβ may be a candidate for inducing mutations by erroneous BER. Polβ also modulates abasic site-induced cytotoxicity by removing dRP residues generated during BER. We investigated the cytotoxic and mutagenic roles of Polβ in response to apurinic sites induced by DB[a,l]P in mouse fibroblasts with an isogenic defect in Polβ (Mβ16 tsA, Polβ+, and Mβ19 tsA, Polβ-). DB[a,l]P, which rapidly generates apurinic sites, induced significantly more cytotoxicity in the Polβ+ cells than Polβ- cells. Low doses of DB[a,l]P did not show an adaptive resistance to cytotoxicity to a second (challenge) dose of DB[a,l]P. Although the adaptive response was not observed, we obtained evidence for the role of DB[a,l]P-induced abasic sites in mediating cytotoxicity in Polβ+ cells. Specifically, the cytotoxic response of DB[a,l]P could be potentiated by methoxyamine, which reacts with abasic sites to form conjugates that interfere with BER. DB[a,l]P treatment resulted in the induction of abundant amounts of A.T to G.C mutations in Polβ+ cells, but not in Polβ- cells. The induction of the A.T to G.C mutations in Polβ+ cells could be blocked by methoxyamine. These results strongly suggest that apurinic sites induced by DB[a,l]P are involved in inducing cytotoxicity and mutations in a Polβ-dependent manner (Supported by NIH grants P20-RR017675 and PO1 CA 49210).
Inhibition of human prostate cancer growth and osteolysis in a bone metastasis model by a mechanism-based specific gelatinase inhibitor (SB-3CT)
Authors: R. Daniel Bonfil, Aaron Sabbota, Sanaa Nabha, Zhong Dong, J. Carlos Trindade Filho, Sreenivasa R. Chinni, Wan-Ming Zhang, Margarida Bernardo, Int Taek Lim, Mayland Chang, Shahriar Mobashery, Michael L. Cher, Rafael Fridman
Journal: Cancer Research (2005)

4348  Using a model of prostate cancer (PC) skeletal metastases, where human cancer cells are injected into the marrow of human bone xenografts previously implanted in SCID mice, we previously demonstrated that systemic administration of the broad spectrum MMP inhibitor BB-94 reduced intraosseous PC cell proliferation, decreased osteoclast recruitment, and prevented degradation of trabeculae (J. Natl. Cancer Inst. 94: 17, 2002). Recently, in the same in vivo model, we demonstrated specific upregulation of net tissue MMP-9 activity two weeks after intraosseous injection of PC cells, most likely due to an influx of osteoclasts induced by the presence of cancer cells (In press, Am J of Path, 2005). Herein, we investigated the effect of the first irreversible mechanism-based MMP inhibitor, designated SB-3CT. Biochemical studies have demonstrated that SB-3CT is a selective gelatinase inhibitor (J. Am. Chem. Soc. 122: 6799, 2000). In this study, 1x105 PC3 cells were injected into the marrow of human fetal femur fragments previously implanted in SCID mice. Beginning one day later, mice in the experimental arm received 50 mg/kg SB-3CT i.p. every other day. Mice in the control arm received vehicle alone (10% DMSO). Five weeks later, the bone xenografts (bone tumors) were harvested, imaged, and processed for histological and histomorphometric analysis. Bone tumors obtained from mice treated with SB-3CT demonstrated significantly reduced intraosseous tumor area compared to bone tumors from control mice (38.1±10.0 % vs. 68.3±8.9 %, respectively, p
Clinical and pathologic characteristics of patients with breast cancer and a second non-breast primary tumor.
Authors: Gul Atalay Basaran, Aziz Yazar, Cihan Uras, Evrim Tezcanli, Devrim Cabuk, Banu Atalar, Enis Ozyar
Journal: Journal of Clinical Oncology (2013)

e11539 Background: We aimed to investigate the clinical and pathologic characteristics of patients with breast cancer (BC) who had a non-breast primary tumor and treated in our hospital. Methods: We identified BC patients with a second non-breast primary tumor retrospectively in our database. The tumors arising in a sequence by less than 2 months are accepted as synchronous malignancies. We noted clinical and pathological characteristics of breast tumors and analyzed the relapse patterns, the frequency and type of second non-breast primary tumors. Results: A total of 48 patients were identified. Median age was 59 years old. Thirty-four patients were postmenopausal, 41 tumors were IDC, 2 were DCIS only, eight were multiffocal. Two patients had metastatic BC at the time of diagnosis. Ninety-three (n: 26) % patients had breast conserving surgery, 2 had bilateral BC. Twenty-eight patients had node negative disease, 12 had node positive disease and 2 had micrometatatic nodal involvement. Fifty-four % were T1, 31% were T2 tumors. Histological grade was 3 for 14, 2 for 15 and 1 for 7 breast tumors. Forty patients had ER positive disease, 4 had ER/ PR negative disease, 2 tumors were triple negative and 6 tumors were Her-2 positive. Among non-breast second primary tumors; 29 arose after, 11 arose before the diagnosis of BC and 8 arose synchronously with BC. The most common non-breast second primary tumors were as follows: 15% lung cancer, 20% colorectal cancers, 13% ovarian cancer, 10% thyroid cancer, and 8% lymphoma/leukemia. With a median follow up of 76 months, there were 6 relapses; 4 of them were BC relapses. Among these 4 BC relapses, 3 patients had brain metastases and one patient had bone metastasis. There were 4 deaths; 2 were due to BC metastases, one was due to rectal cancer metastasis and the other was due to relapse of sarcoma. Conclusions: Most breast tumors were at early stage and were hormone sensitive. The most common second non-breast primary tumors arising after diagnosis of BC were colorectal, thyroid and lung cancers. The most common second non-breast tumor arising synchronously with BC was lung cancer and the most common second non-breast tumor arising before diagnosis of BC was lymphoma/leukemia.
Abstract #2865: The role of tumor-derived MFG-E8 in triggering chemoresistance and immune suppression in patients with various solid tumors
Authors: Masahisa Jinushi, Marimo Sato, Akira Kanamoto, Akihiko Itoh, Martin Mihm, Glenn Dranoff, Hideaki Tahara
Journal: Cancer Research (2009)

Identification of the molecular target would be important for treating malignant tumors especially at recurrent or metastatic stage. Within the tumor microenvironment, a secreted protein milk fat globule EGF-8 (MFG-E8) stimulates melanoma progression through coordinated \#945;v\#946;3 integrin signaling in tumor and host cells (Jinushi,M., J. Clin. Invest., 2007 & Cancer Res., 2008). The MFG-E8 enhances tumor cell survival, invasion, and angiogenesis, and contributes to local immune suppression in murine tumor models, but it remains unclear whether MFG-E8 may contribute to disease progression in patients with various malignant tumors. We found in this study that MFG-E8 is expressed in tumors at much higher levels in the invasive phase than intraepithelial phase in patients with various solid tumors. The MFG-E8 is constitutively produced from most of the human tumor cells, and might trigger resistance to chemo- and targeted therapy induced apoptosis through the coordinated activation of integrin-mediated Src/MAPK and Akt/mTOR signaling pathways. Tumor-derived MFG-E8 might also induce tolerogenic dendritic cells upon the stimulation with MFG-E8-producing tumor cells, and compromise specific antitumor responses in part through the transcriptional activities of EMT master regulator twist-1. The therapeutic strategies of MFG-E8 knockdown with specific small interference RNA or integrin \#945;v\#946;3 neutralizing antibodies against tumor cells attenuated integrin-mediated oncogenic signaling and thereby compromised tumor cell survival, increased sensitivity to apoptosis with various targeted therapies, such as novel MEK-1 kinase inhibitor for melanoma. Tumor-associated tolerogenic dendritic cells produced large amounts of Il-12 in stimulation with MFG-E8 siRNA-transfected melanoma cells, and triggered antitumor Th1 immune recognition against autologous human tumor cells. These results collectively suggest that MFG-E8 is a master regulator of human tumor progression through coordinated \#945;v\#946;3 integrin signaling in the tumor microenvironment, and raise the possibility that the therapeutic interference of MFG-E8 may be a promising strategy to overcome intrinsic resistance to current therapeutic regimens and immune suppression within tumor microenvironments.  Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 2865.
Reconsidering the Association Between Infection-Related Health Care Use and Occurrence of Eating Disorders
Authors: Katrin E. Giel, Florian Junne, Stephan Zipfel
Journal: JAMA Psychiatry (2019)

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 Psychiatry HomeNew OnlineCurrent IssueFor Authors Podcast 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 Psychiatry journal
Analysis of the Effect of Mesenchymal Stem Cells Culture with Interleukin 2 Overexpression on Human Mononuclear Cells Activation in Vitro
Authors: Daria Chulpanova, Valeriya Soloveva, Leisan G Tazetdinova, Marina O. Gomzikova, Svetlana Khaiboullina, Albert Rizvanov
Journal: Blood (2018)
Asymmetric conflict: Structures, strategies, and settlement
Authors: Carsten K. W. De Dreu, Jörg Gross
Journal: Behavioral and Brain Sciences (2019)

Abstract Our target article modeled conflict within and between groups as an asymmetric game of strategy and developed a framework to explain the evolved neurobiological, psychological, and sociocultural mechanisms underlying attack and defense. Twenty-seven commentaries add insights from diverse disciplines, such as animal biology, evolutionary game theory, human neuroscience, psychology, anthropology, and political science, that collectively extend and supplement this model in three ways. Here we draw attention to the superordinate structure of attack and defense, and its subordinate means to meet the end of status quo maintenance versus change, and we discuss (1) how variations in conflict structure and power disparities between antagonists can impact strategy selection and behavior during attack and defense; (2) how the positions of attack and defense emerge endogenously and are subject to rhetoric and propaganda; and (3) how psychological and economic interventions can transform attacker-defender conflicts into coordination games that allow mutual gains and dispute resolution.
Ultrasound-mediated cavitation enhances the delivery of an EGFR-targeting liposomal formulation designed for chemo-radionuclide therapy
Authors: Eloise Thomas, Jyothi U. Menon, Joshua Owen, Irini Skaripa-Koukelli, Sheena Wallington, Michael Gray, Christophoros Mannaris, Veerle Kersemans, Danny Allen, Paul Kinchesh, Sean Smart, Robert Carlisle, Katherine A. Vallis
Journal: Theranostics (2019)

Nanomedicines allow active targeting of cancer for diagnostic and therapeutic applications through incorporation of multiple functional components. Frequently, however, clinical translation is hindered by poor intratumoural delivery and distribution. The application of physical stimuli to promote tumour uptake is a viable route to overcome this limitation. In this study, ultrasound-mediated cavitation of microbubbles was investigated as a mean of enhancing the delivery of a liposome designed for chemo-radionuclide therapy targeted to EGFR overexpressing cancer.
Evaluation of a mouse gallbladder cancer cell line for tumorigenicity and preclinical therapeutic efficacy studies
Authors: Takuya Kitamura, Mikiro Takaishi, Kevin Connolly, John DiGiovanni, Kaoru Kiguchi
Journal: Cancer Research (2008)

2949  The prognosis of patients with biliary tract cancer is poor despite recent advances in diagnostic and therapeutic techniques. The establishment of a mouse biliary tract cancer cell line could be an important tool for investigating the mechanisms of the development of these tumors and for exploring novel therapeutic strategies. We previously reported that overexpression of erbB2 in gallbladder epithelial cells in BK5.erbB2 transgenic mice leads to development of gallbladder adenocarcinoma in homozygous transgenic mice. Recently, we established a cell line (A2), derived from a gallbladder carcinoma taken from a BK5.erbB2 mouse. This is the first mouse gallbladder cancer cell line reported. The tumor cells, cultured in DMEM supplemented with 10% FBS, grew as monolayers showing epithelial-like morphology with a population doubling time of 26.4 hr during exponential growth. Western blot analyses showed that both total and phosphorylated forms of EGFR and Akt and total erbB2 were upregulated in these cells compared to and control mouse gallbladder tissue. The upregulation and activation of these molecules have been frequently reported in human biliary tract cancer including gallbladder carcinomas. A2 cells were tumorigenic when transplanted into the kidney capsule of SCID mice. Immunohistochemical analysis of these xenografted tumors showed that the lesions formed ductal structures, with cytokeratin-positive staining. These lesions included highly proliferating cells as determined by Ki67 staining. In addition, our preliminary data indicate that the growth of A2 cells was inhibited by rapamycin (an inhibitor of mTOR) and by GW2974 (an inhibitor of both EGFR and ErbB2) both at concentrations of 10 nM. The effect of small molecule inhibitors, including rapamycin and GW2974, on xenograft and orthograft implantation of A2 cells in the gallbladder of SCID mice is currently being investigated. This new gallbladder cancer cell line will provide serve a valuable resource to explore novel therapeutic strategies for treating GBCa.
Activity and tolerability of mitomycin-C (MMC) and chronomodulated capecitabine (C) in advanced colorecatal cancer (ACC) patients
Authors: C. Campanella, B. Vanni, C. Garufi, A. Torsello, L. Di Lauro, M. Pellicciotta, E. Terzoli
Journal: Journal of Clinical Oncology (2006)

13563 Background: MMC plus continuous infusion (CI) 5-fluorouracil (5-FU) showed activity with acceptable toxicity profile in ACC patients (pts). Nocturnal infusion of 5-FU was shown to reduce hematological and gastrointestinal toxicity. Capecitabine (C) is an oral pro-drug converted to 5-FU which mimics 5-FU CI activity. C is effective as single drug and in combination, providing equivalent activity and efficacy. Aim of the study was to evaluate activity and tolerability of MMC plus C in ACC patients. Methods: fifty-one pts received MMC 7 mg/mq i.v on day 1 followed by C 2000 mg/mq /die for 14 days out of 21 days; 20% of C dose was given at 8:00 while 80% was given at 20:00; each course (c)was repeated q 6 weeks. Pts data: M/F 33/18; median age: 64 (41–88); WHO PS0: 36, 1: 11, ≥2 :2; metastatic sites: liver (35), lung (17), lymphonodes (9), peritoneum (8), other (14); no measurable disease 1; site: colon/rectum 40/11; previuos lines: 0 (17), 1(18), ≥2(16); 43% and 29% of patients had been previously treated by 5-FU with oxaliplatin or irinotecan. Results: Toxicity was evaluated in 45 out of 51 pts and in 94 courses. Grade 2–3 neutropenia occurred in 5 pts/8 c (10/6%), G2-G3 thrombocitopenia in 4 pts/8 c (8/6%). One pt (2%) experienced G3 anemia. G2–3 nausea and vomiting occurred in 5 pts/5 (10/5%), G2–3 diarrhea in 8 pts/12 c (15/13%) and only 1 pt experienced G4 diarrehea. Mucositis of grade 2 was observed in 3 pts/ (6%). G2–3 hand foot syndrome and G2–3 asthenia both occurred in 5 pts (10%). No differences in toxicity were observed between pre-treated and untreated pts. At this time of the study 45 out of 51 pts were evaluated for response: stable disease was observed in 16 pts (31%), partial response in 5, untreated, patients (10%), progression in 23 (45%). Median time to progression (TTP) was 6,0 months (3,0- 8,5 mo) for both groups. Conclusions: Chronomodulated administration of C plus MMC seems to have an excellent toxicity profile even in pre-treated population, with a TTP similar to more expensive treatments. No significant financial relationships to disclose.
GP app service Livi expands to cover 1.85 million patients in England
Authors: Elisabeth Mahase
Journal: BMJ (2019)

The digital GP service provider Livi will now cover 1.85 million patients in Birmingham, Northamptonshire, Shropshire, and Surrey, after agreeing new partnerships with local GP federations.

The Swedish private company launched its video consultations app in the UK last October with 40 NHS general practices in the North West Surrey clinical commissioning group (CCG) area, covering 360 000 patients.1

It has now announced new deals with several more federations, including …
Evidence-Based Treatment Paradigms for Management of Invasive Cervical Carcinoma
Authors: Krishnansu S. Tewari, Bradley J. Monk
Journal: Journal of Clinical Oncology (2019)

Article Tools REVIEW ARTICLES Gynecologic Cancer Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES Erratum. October 18, 2019 ARTICLE CITATION DOI: 10.1200/JCO.18.02303 Journal of Clinical Oncology - published online before print August 12, 2019 PMID: 31403858 Evidence-Based Treatment Paradigms for Management of Invasive Cervical Carcinoma Krishnansu S. Tewari, MD1xKrishnansu S. TewariSearch for articles by this author and Bradley J. Monk, MD2,3xBradley J. MonkSearch for articles by this author Show More 1University of California, Irvine, CA2University of Arizona, Phoenix, AZ3Creighton University, Phoenix, AZ https://doi.org/10.1200/JCO.18.02303 First Page Full Text PDF Figures and Tables Supplements © 2019 by American Society of Clinical Oncology Errata Erratum
Twist of Fate for Acute Promyelocytic Leukemia: TRIB3–TWIST1 Interaction Promotes Resistance
Authors: Stephen Z. Peeke, Kira Gritsman
Journal: Clinical Cancer Research (2019)

While acute promyelocytic leukemia has a good prognosis with all-trans retinoic acid (ATRA) treatment, ATRA resistance is a major obstacle. It is now demonstrated that TRIBBLES 3 (TRIB3) stabilizes TWIST1, leading to ATRA resistance. Peptides that disrupt this interaction lead to the degradation of TWIST1 and overcome ATRA resistance.See related article by Lin et al., p. 6228.