tbuckley/cabot-search huggingface dataset:
Abstract 2861: ACKR3 promotes cell metastasis via activating TGF-beta 1/Smad signaling in head and neck squamous cell carcinoma
Authors: Nayoung Kim, Solbi Kim, Mina Joo, Heung Jin Jeon, Myung-Won Lee, Hyewon Ryu, Hyo Jin Lee
Journal: Cancer Research (2019)

Abstract Background: The atypical chemokine receptor, ACKR3, has been shown to play as a tumor promoter, which is upregulated in various types of cancer. However, the biological role of ACKR3 and its underlying mechanism in head and neck squamous cell carcinoma (HNSCC) is still unknown. In this study, we investigated the functional role of ACKR3 and the underlying molecular mechanism of tumor progression in HNSCC. Methods: We examined the ACKR3 expression and its association with clinicopathological characteristics in 103 cases of HNSCC by immunohistochemical staining. The biological roles of ACKR3- and ACKR3-induced downstream signaling were investigated in HNSCC cell through ACKR3 overexpression and knockdown of ACKR3 in vitro and in vivo. Results: We detected differential expression of ACKR3 in HNSCC cells and tissues. High ACKR3 expression was significantly associated with invasion depth of tumor (T status; P = 0.007), lymph node involvement (N status; P = 0.004), and higher stage III/IV (P = 0.02). Overexpression of ACKR3 dramatically enhanced cell migration and invasion in HNSCC cells in vitro, and promoted lymph node metastasis in vivo. ACKR3 overexpression also induced the epithelial-mesenchymal transition. Vimentin, Slug, and Twist were increased but E-cadherin and Ep-CAM were decreased by ACKR3 expression. Upregulation of TGF-β1 was observed in ACKR3 overexpression, and TGF-β1/Smad signaling activation and Akt phosphorylation were induced in HNSCC cells with ACKR3 overexpression. Treatment with a PI3K inhibitor reduced Slug and Twist levels while suppression of Smad2/3 signaling by siRNA reduced Akt phosphorylation, as well as Slug and Twist. Furthermore, inhibition of Smad2/3 decreased tumor cell migration and invasion in HNSCC. ACKR3 knockdown using siRNA in HNSCC cells reduced the secretion of TGF-β1 and also recovered the cell migratory and invasive behavior of HNSCC cells. Conclusions: ACKR3 expression was associated with an aggressive tumor behavior in HNSCC. ACKR3 contributed to migration and invasion of HNSCC cell through the TGF-β1/Smad signaling axis and epithelial-mesenchymal transition in vitro, and was involved in lymph node metastasis in vivo, suggesting that ACKR3 plays an important role during HNSCC progression and metastasis. Citation Format: Nayoung Kim, Solbi Kim, Mina Joo, Heung Jin Jeon, Myung-Won Lee, Hyewon Ryu, Hyo Jin Lee. ACKR3 promotes cell metastasis via activating TGF-beta 1/Smad signaling in head and neck squamous cell carcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2861.
Cabozantinib (C) versus placebo (P) in patients (pts) with advanced hepatocellular carcinoma (HCC) who have received prior sorafenib: Results from the randomized phase 3 CELESTIAL trial.
Authors: Ghassan K. Abou-Alfa, Tim Meyer, Ann-Lii Cheng, Anthony El-Khoueiry, Lorenza Rimassa, Baek-Yeol Ryoo, Irfan Cicin, Philippe Merle, Yen-Hsun Chen, Joong-Won Park, Jean-Frédéric Blanc, Luigi Bolondi, Heinz Josef Klümpen, Stephen Lam Chan, Vincenzo Dadduzio, Colin Hessel, Anne E. Borgman-Hagey, Gisela Schwab, Robin Kate Kelley
Journal: Journal of Clinical Oncology (2018)

4019 Background: C, an inhibitor of MET, VEGFR, and AXL, has previously shown clinical activity in pts with advanced HCC. This phase 3 trial (NCT01908426) evaluated C vs P in previously treated pts with advanced HCC. Methods: In this double-blind, global, phase 3 trial, pts were randomized 2:1 to C (60 mg qd) or matched P stratified by etiology, geographic region, and presence of extrahepatic spread and/or macrovascular invasion (EHS/MVI). Eligible pts had pathologic diagnosis of HCC, Child-Pugh score A, and ECOG PS ≤1. Pts must have received prior sorafenib, were allowed to receive up to 2 lines of prior systemic therapy for HCC, and must have progressed following at least one. The primary endpoint was overall survival (OS). Secondary endpoints were investigator-assessed progression-free survival (PFS) and objective response rate (ORR) per RECIST 1.1. The study was designed to detect a hazard ratio (HR) for OS of 0.76 (90% power, 2-sided α = 0.05) at the final analysis with 2 prespecified interim analyses at 50% and 75% of the planned 621 events. Results: As of 1 Jun 2017, 707 pts were randomized, and 484 deaths had occurred (317 out of 470 for C; 167 out of 237 for P). Baseline characteristics were balanced between the arms: median age was 64 years, 82% were male, 38% had HBV, 24% had HCV, 25% enrolled in Asia, 85% had EHS/MVI, and 27% had received 2 prior systemic regimens for advanced HCC. The study met the primary endpoint at the second planned interim analysis with median OS 10.2 mo for C vs 8.0 mo for P (HR 0.76, 95% CI 0.63–0.92; p = 0.0049). Median PFS was 5.2 mo for C vs 1.9 mo for P (HR 0.44, 95% CI 0.36–0.52; p < 0.0001), and ORR was 4% vs 0.4% (p = 0.0086). The most common grade 3/4 adverse events (predominantly grade 3) with higher incidence in the C vs P arm included hand-foot skin reaction (17% vs 0%), hypertension (16% vs 2%), increased aspartate aminotransferase (12% vs 7%), fatigue (10% vs 4%), and diarrhea (10% vs 2%). Subgroup analyses of OS and PFS by baseline characteristics will also be presented. Conclusions: C significantly improved OS and PFS vs P in previously treated pts with advanced HCC. Adverse events were consistent with the known safety profile of C. Clinical trial information: NCT01908426.
This Week in &lt;EMPH TYPE="ITAL"&gt;JAMA&lt;/EMPH&gt;
Journal: JAMA (2003)

A Piece of My Mindno one to oversee the appropriate treatment, no one to emphasize to the family the paramount importance of adherence to treatment, and no one to confirm that the bacterium was indeed sensitive to the prescribed formula, it was destined to be a recipe for disaster." SEE PAGE 998 Contempo UpdatesDiagnosis and treatment of genital lesions.
Science and Politics
Journal: JAMA (2002)

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
Congenital hypothyroidism control programs. A cost-benefit analysis
Authors: P. M. Layde
Journal: JAMA (1979)

Comprehensive screening programs to control congenital hypothyroidism (CH), a preventable form of mental retardation, are being considered by some public health agencies. The proposed programs would test neonates' blood for thyroxine and, if warranted, provide follow-up testing and therapy. The estimated cost of detecting a single case of CH is $9,300, which includes specimen collection, laboratory analysis, and retesting of border-line cases. The present value of the treatment costs for CH adds $2,500 per case, a total cost of $11,800 per case detected and child treated. The economic benefits (averted costs of institutionalization and special education and increased productivity of the affected person) are estimated to have a present value of $105,000 per case, yielding a cost-benefit ratio of 1:8.9. (<i>JAMA</i>241:2290-2292, 1979)
TREATMENT OF PHTHISIS.
Journal: JAMA (1891)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
New IUDR Uses Tested
Journal: JAMA (1966)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
DOCTORS' DOLLARS FOR BONDS
Journal: JAMA (1942)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Effect of Sacubitril/Valsartan on Biomarkers of Extracellular Matrix Regulation in Patients With HFpEF
Authors: Jonathan W. Cunningham, Brian L. Claggett, Eileen O’Meara, Margaret F. Prescott, Marc A. Pfeffer, Sanjiv J. Shah, Margaret M. Redfield, Faiez Zannad, Lu-May Chiang, Adel R. Rizkala, Victor C. Shi, Martin P. Lefkowitz, Jean Rouleau, John J.V. McMurray, Scott D. Solomon, Michael R. Zile
Journal: Journal of the American College of Cardiology (2020)

Myocardial fibrosis may contribute to the pathophysiology of heart failure with preserved ejection fraction. Given the biochemical targets of sacubitril/valsartan, this study hypothesized that circulating biomarkers reflecting the mechanisms that determine extracellular matrix homeostasis are altered by sacubitril/valsartan compared with valsartan alone. This study investigated the effects of sacubitril/valsartan on biomarkers of extracellular matrix homeostasis and the association between biomarkers and the primary endpoint (total heart failure hospitalizations and cardiovascular death). N-terminal propeptide of collagen I and III, tissue inhibitor of matrix metalloproteinase 1, carboxyl-terminal telopeptide of collagen type I, and soluble ST2 were measured at baseline (n = 1,135) and 16 (n = 1,113) and 48 weeks (n = 1,016) after randomization. The effects of sacubitril/valsartan on these biomarkers were compared with those of valsartan alone. Baseline biomarker values and changes from baseline to 16 weeks were related to primary endpoint. At baseline, all 5 biomarkers were higher than published referent control values. Sixteen weeks after randomization, sacubitril/valsartan decreased tissue inhibitor of matrix metalloproteinase 1 by 8% (95% confidence interval [CI]: 6% to 10%; p < 0.001), soluble ST2 by 4% (95% CI: 1% to 7%; p = 0.002), and N-terminal propeptide of collagen III by 3% (95% CI: 0% to 6%; p = 0.04) and increased carboxyl-terminal telopeptide of collagen type I by 4% (95% CI: 1% to 8%; p = 0.02) compared with valsartan alone, consistently in men and women and patients with left ventricular ejection fraction above or below the median of 57%. Higher levels of tissue inhibitor of matrix metalloproteinase 1 and soluble ST2 at baseline and increases in these markers at 16 weeks were associated with higher primary endpoint event rates. Biomarkers reflecting extracellular matrix homeostasis are elevated in heart failure with preserved ejection fraction, favorably altered by sacubitril/valsartan, and have important prognostic value. (Prospective Comparison of ARNI With ARB Global Outcomes in HF With Preserved Ejection Fraction [PARAGON-HF]; NCT01920711)
Science and clinical medicine
Authors: J. A. Barondess
Journal: JAMA (1976)

Modification of antigens does improve immunity to ragweed and other allergens. Heating tumor antigen could modify it in a way which stimulates immunity. Immunization of mice with heated Ehrlich carcinoma cells induced greater protection to implantation with viable cells than did immunization with radiation-killed cells.<sup>1</sup>The present work suggests that heated antigen may be a better stimulus in humans.
References and Reviews
Journal: JAMA (1969)

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
Human Experimentation
Authors: Hugh H. Hussey
Journal: JAMA (1973)

In 1971<i>JAMA</i>published "Covert Drug Abuse Among Voluntary Hospitalized Psychiatric Patients" by Blumberg et al (217:1659-1661, 1971). In the following year, Szasz wrote a letter to the editor—not the editor of<i>JAMA</i>but of the<i>New England Journal of Medicine</i>(286:111, 1972)—and impugned the moral responsibility of Blumberg and his associates because they did not inform the patients of the true purpose of the urine testing, thereby abusing their trust in their physicians. Szasz also implied that the editors of<i>JAMA</i>were ethically at fault for accepting and publishing the article in question. In due time, Blumberg and his colleagues ably responded (<i>New Engl J Med</i>286:547, 1972): Obviously, the treatment of the patients involved was not affected at all by our study. On the other hand, the study would have been invalid if patients were aware of the purpose of collection since they could alter the data by
Abstract 1418: Brother of regulator of imprinted sites (BORIS) inhibits cisplatin induced DNA damage in non-small-cell lung cancer
Authors: Yongfei Song, Chao Li, Mengdie Fang, Juan Ren, Jianfei Fang, Xiaoju Wang, Yanmei Zhang
Journal: Cancer Research (2019)

Abstract Cisplatin (DDP) treatment is primary modality for non-small-cell lung cancer (NSCLC) chemotherapy. However, patients benefited from DDP treatment limitedly due to the DDP resistance. Brother of Regulator of Imprinted Sites (BORIS, CTCFL) is the paralogue of CCCTC-binding factor (CTCF) and expressed abnormally in most type of cancers and is potential tumor target for breast, cervical carcinoma and lung cancer. However, the funciton of BORIS on carcinoma is unrevealed. In our previous study, we found that BORIS suppressed apoptosis and resisted 5-FU (Fluorouracil) treatment in colorectal cancer. As either 5-FU or DDP induces DNA damage and apoptosis of carcinoma cells, BORIS perhaps resists DDP treatment too. Based on the prevalent expression of BORIS and the high incidence of DDP resistance in NSCLC, we proposed that BORIS contributed to DDP resistance by suppressing DNA damage in NSCLC. We collected RNA sequencing data of 156 NSCLC patients who received DDP chemotherapy from The Cancer Genome Atlas and analyzed the expressions of BORIS. We found high BORIS expression correlated with short survival in NSCLC patients who received DDP chemotherapy. BORIS expression declined from prospective to retrospective collected tissue which responded to DDP chemotherapy. It suggested the probability function of BORIS on DNA damage repair. In cell cultured lung cancer cell lines, BORIS was silenced or over-expressed including DDP resistant cell line. It indicated that A549/DDP (DDP resistant A549 cell line) expressed relative higher BORIS than A549 parental cells and BORISexpression levels correlated with cell viability. H1299 and A549/DDP expressed comparative BORIS and growed comparativly. H460 and A549 expressed relative lower BORIS levels and grew slower than H1299 and A549/DDP. BORIS knockdown inhibited the proliferation of NSCLC cells, enhanced the sensitivity of A549/DDP and H1299 to DDP treatment and induced DNA damage. Reversely DDP induced DNA damage was suppressed by BORIS over-expression. The excision repairing gene ERCC1, which is regulated by BORIS, might be the assistant for DDP resistance. Either high expression of BORIS or ERCC1 indicated short survival rates of NSCLC patients. Our data suggested that BORIS suppressed DNA damage and promoted the progression of NSCLC and DDP resistance, which indicated its potential in NSCLC prognosis and therapy. Citation Format: Yongfei Song, Chao Li, Mengdie Fang, Juan Ren, Jianfei Fang, Xiaoju Wang, Yanmei Zhang. Brother of regulator of imprinted sites (BORIS) inhibits cisplatin induced DNA damage in non-small-cell lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1418.
Anthracosilico-Tuberculosis as Seen in a General Hospital
Journal: JAMA (1963)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Development of Bioassays and Approaches for the Risk Assessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin and Related Compounds
Authors: Stephen Safe
Journal: Environmental Health Perspectives (1993)

Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related haloge- nated aromatic hydrocarbons (HAHs) are industrial compounds or by-products that have been identified as contaminants in almost every component ofthe global ecosystem.2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is the most toxic HAH, and studies in rodents have shown that this compound is a carcinogen.Analysis of environmental samples for HAHs has shown that these extracts contain complex mixtures of isomers and congeners, and this greatly complicates risk assessment due to the paucity of data available for most of the individual compounds.Extensive research has demonstrated a common receptor-mediated mechanism of action for TCDD and related toxic HAHs, and this has led to the development of a mechanism-based risk assessment approach for HAHs.Toxic equivalency factors (TEFs; relative potency compared to TCDD) have been developed for selected HAH congeners, and the TEF values can be used to determine "toxic equivalents" (TEQs) for HAH mixtures.In addition, several bioassays that use receptor-mediated end points have been developed and can be used directly to determine the TEQs for HAH mixtures.The applications ofthe TEF/TEQ approach for the risk assessment of HAHs are considerable, particularly with the conversion of complex analytical data into TEQs.However, there appear to be several limitations to this approach, particularly with PCBs because their potential nonadditive (antagonistic), interactive effects with "2,3,7,8-TCDD-like" com- pounds may invalidate the use of the risk assessment procedure for some environmental matrices.