tbuckley/cabot-search huggingface dataset:
Abstract B20: miR-211 Functions as a metabolic switch in human melanoma cells
Authors: Joseph Mazar, Feng Qi, Bongyong Lee, John Marchica, Subramaniam Govindarajan, John Shelley, Jian-Liang Li, Animesh Ray, Ranjan J. Perera
Journal: Cancer Research (2016)

Abstract The microRNA (miRNA) miR-211 negatively regulates genes that drive invasion of metastatic melanoma. Compared to normal human melanocytes, miR-211 expression is significantly reduced or absent in non-pigmented melanoma cells and lost during human melanoma progression. To investigate mechanisms of its tumor suppressor function, miR-211 was ectopically expressed in non-pigmented melanoma cells. Ectopic miR-211 expression destabilized hypoxia-inducible factor 1α (HIF-1α) and caused increased cell death during hypoxia. HIF-1α destabilization was correlated with down-regulation of a novel miR-211 target gene, pyruvate dehydrogenase kinase 4 (PDK4). We present evidence that resumption of miR-211 mediated down-regulation of PDK4 in melanoma cells caused hypoxia-induced cell death via HIF-1α destabilization. Thus the tumor suppressor miR-211 acts as a metabolic switch, and its loss is expected to promote cancer hallmarks in human melanomas. Citation Format: Joseph Mazar, Feng Qi, Bongyong Lee, John Marchica, Subramaniam Govindarajan, John Shelley, Jian-Liang Li, Animesh Ray, Ranjan J. Perera. miR-211 Functions as a metabolic switch in human melanoma cells. [abstract]. In: Proceedings of the AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines ; 2015 Dec 4-7; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2016;76(6 Suppl):Abstract nr B20.
In vivo production of interleukin-5, granulocyte-macrophage colony- stimulating factor, macrophages colony-stimulating factor, and interleukin-6 during intravenous administration of high-dose interleukin-2 in cancer patients [see comments]
Authors: MR Schaafsma, JH Falkenburg, JE Landegent, N Duinkerken, S Osanto, P Ralph, K Kaushansky, G Wagemaker, J Van Damme, R Willemze
Journal: Blood (1991)
Mind MELD or Ignore It at Your Peril
Authors: Ali Zarrinpar
Journal: JAMA Surgery (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 Surgery 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 Surgery journal
Damage Induced in Sarcoma 37 with Chemical Agents. II. Trivalent and Pentavalent Arsenicals&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/xref&gt;&lt;xref ref-type="fn" rid="fn2"&gt;&lt;sup&gt;3&lt;/sup&gt;&lt;/xref&gt;
Authors: J. Leiter, V. Downing, J. L. Hartwell, M. J. Shear
Journal: JNCI Journal of the National Cancer Institute (1952)

Damage Induced in Sarcoma 37 with Chemical Agents. II. Trivalent and Pentavalent Arsenicals J. Leiter, J. Leiter Laboratory of Chemical Pharmacology, National Cancer Institute4Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar V. Downing, V. Downing Laboratory of Chemical Pharmacology, National Cancer Institute4Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar J. L. Hartwell, J. L. Hartwell Laboratory of Chemical Pharmacology, National Cancer Institute4Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar M. J. Shear M. J. Shear Laboratory of Chemical Pharmacology, National Cancer Institute4Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 13, Issue 2, October 1952, Pages 365–378, https://doi.org/10.1093/jnci/13.2.365 Published: 01 October 1952 Article history Received: 12 May 1952 Published: 01 October 1952
&lt;emph type="ital"&gt;Spoiled Child&lt;/emph&gt;
Authors: Janet M. Torpy
Journal: JAMA (2009)

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
Anaphylactoid Reaction to Sodium Dehydrocholate
Authors: Robert P. Coggins, James M. Skinner, Zeb L. Burrell
Journal: New England Journal of Medicine (1953)

BECAUSE few reactions to the administration of sodium dehydrocholate (Decholin) in the determination of the circulation time have been reported, only 1 of which was of an anaphylactoid nature, the following case is considered worthy of report.Case ReportA 64-year-old Negress was admitted to the hospital on July 22, 1952, with complaints of pain, swelling and ulceration of the left leg of 4 days' duration, shortness of breath for some months and dizziness for many years. She had been treated with radium insertion in this hospital for cancer of the cervix on several previous admissions, having received a total . . .
Case report of a toxic reaction from a combination of tryptophan and phenelzine
Authors: J M Thomas, E H Rubin
Journal: American Journal of Psychiatry (1984)

The addition of tryptophan to a monoamine oxidase inhibitor (MAOI) has been recommended for patients failing to respond to an MAOI alone. The authors report acute behavioral and neurologic toxicity immediately after tryptophan administration in a patient taking phenelzine.
Recombinant erythropoietin therapy in cancer patients.
Authors: H F Bunn
Journal: Journal of Clinical Oncology (1990)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1990.8.6.949 Journal of Clinical Oncology - published online before print September 22, 2016 PMID: 2189955 Recombinant erythropoietin therapy in cancer patients. H F BunnxH F BunnSearch for articles by this author https://doi.org/10.1200/JCO.1990.8.6.949 First Page PDF © 1990 by American Society of Clinical Oncology
Abstract P2-06-05: LINC00478: A novel tumor suppressor in breast cancer
Authors: Y Gökmen-Polar, M Zavodszky, X Chen, X Gu, C Kodira, S Badve
Journal: Cancer Research (2016)

Abstract Background: LncRNAs may play a role in cancer and serve as new potential targets for improving cancer diagnosis, prognosis or treatment. Long intergenic non-protein coding RNA 478 (LINC00478), the miR99a-let-7c cluster host gene, has been shown to be downregulated in estrogen-independent ER-positive (ER+) breast cancer cells. However, its expression in breast tumors and its significance in recurrence has not been well characterized. Methods: The clinical relevance of LINC00478 in ER+ breast tumors was first determined by analysis of the expression levels in MiTranscriptome database (RNAseq-based), which contains ∼8000 most differentially expressed lncRNAs for each cancer and/or tissue type. Additionally, the expression of LINC00478 mRNA was determined in a) a cohort of matched pairs of primary and (nodal) metastatic tumors (n=18) (RNA-seq) and b) a cohort of 60 paraffin-embedded ER-positive, node-negative breast carcinomas with Oncotype DX recurrence scores (QRT-PCR). Results: LINC00478 was significantly downregulated in patients with ER-positive tumors compared to uninvolved normal breast tissue. In RNA-seq analysis, metastatic tumors had significant low expression as compared to matched primary tumors (FC: -2.2 fold-down; P=0.0027). Quantitative RT-PCR analysis showed that LINC00478 expression was significantly lower in ER+ node-negative patients with Oncotype DX high recurrence score when compared with low recurrence score patients (FC: -4.14-fold down; P=0.02). Conclusion: We document for the first time that LINC00478 functions as a tumor suppressor in ER-positive breast cancer. Its loss is associated with tumor progression and recurrence/metastasis. Novel strategies that focus on re-expression of LINC00478 might be useful for targeting breast cancer and preventing the metastases. Citation Format: Gökmen-Polar Y, Zavodszky M, Chen X, Gu X, Kodira C, Badve S. LINC00478: A novel tumor suppressor in breast cancer. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P2-06-05.
Lead in the Water: A Tale of Social and Environmental Injustice
Authors: Lawrence O. Gostin
Journal: JAMA (2016)

In 1854, British physician John Snow famously wrote, “The most terrible outbreak of cholera which ever occurred in this kingdom, is probably that which took place in Broad Street, Golden Square, and the adjoining streets, a few weeks ago.” (http://bit.ly/1TUQnje). Snow linked cholera to polluted water flowing from the Broad Street pump. City officials removed the pump handle and the cholera epidemic suddenly ended. Cholera is one of many gastrointestinal illnesses caused by drinking water carrying disease-causing microbes. In 2000, for example, hundreds of Milwaukee residents became ill when they drank city water contaminated with cryptosporidium (http://bit.ly/1OPvioB).
Neonatal Hemolytic Anemia and (δβ)0-Thalassemia Caused By Novel Deletions Involving The β-Globin Gene Cluster
Authors: Morrison Tasha, Hong-yuan Luo, Lance Davis, Roger Theberge, Mark E McComb, Catherine E. Costello, Jeanne Boudreaux, Zeqiu Han, Martin H. Steinberg, Bernard G. Forget, David H.K. Chui
Journal: Blood (2013)
Spontaneous Leukemia at High Altitude in C58 Mice&lt;xref ref-type="fn" rid="FN1"&gt;2&lt;/xref&gt;
Authors: Pablo Mori-Chavez, M.D.
Journal: JNCI Journal of the National Cancer Institute (1958)

A lower incidence of spontaneous leukemia was found in 329 C58 mice kept at high altitude than in 448 mice of the same strain kept at sea level. The difference was statistically significant. The amount of infiltration by leukemic cells and the weights of the localized tumors were greater in mice kept at sea level than in mice kept at high altitude. No difference in histology or cytology of the neoplasms could be detected. Leukemia occurred more often in female than in male mice, irrespective of altitude. A lower incidence was found in males kept at high altitude than in males kept at sea level, and the difference was statistically significant. The difference in the females was not so great but also was higher at sea level.
GPs reject cap on locum GP fees
Authors: Abi Rimmer
Journal: BMJ (2016)

GPs have rejected a cap on fees charged by locum doctors and said that locums and general practices should be able to agree terms and conditions mutually.

GPs attending the BMA’s conference of local medical committees (LMCs), the bodies that represent GPs at a local level, in London on Friday 20 May voted in favour of a motion that “affirms that locum GPs are an essential part of the GP workforce.” The motion …
Abstract B1-38: PARADIGM-SHIFT: Predicts the functional impact of ‘driver modules’ in multiple cancers using pathway impact analysis
Authors: Sam Ng, Christopher Benz, David Haussler, Joshua M. Stuart
Journal: Cancer Research (2015)

Abstract The major mechanism by which cancer arises is through genomic alterations. These alterations can lead to changes in gene regulation, protein structure, and function. Individual tumors can contain hundreds to thousands of alterations. It is critical to distinguish alterations that have an important role defining the cancer – drivers – from alterations that are unimportant to the tumor – passengers. Driver genes can lead to significant changes in their pathways; however, alterations in a single gene may not be sufficient to explain all the pathway perturbations across patients. Additional alterations could range from DNA copy number changes, gene-fusions, or even lesser understood non-coding mutations. Identifying these ‘driver modules’ is essential for understanding cancer disease mechanisms, which can help guide treatment decisions as well as identify novel targets for treatment. We have developed a functional impact prediction method called PARADIGM-SHIFT based on integrated pathway analysis to discriminate loss-of-function, neutral, and gain-of-function alterations. Utilizing the set of regulatory interactions annotated for a given gene, we can detect a shift in the downstream effects of an altered gene compared to what is expected from its upstream influences. Additionally, since these shifts in pathway signal can be detected for all samples, PARADIGM-SHIFT can be used to identify additional genomic alterations that lead to similar changes to the altered pathway to form ‘driver modules.’ Application of our method to the TCGA Pan-Cancer cohort identifies many genes with significant alterations that lead to loss- and gain- of function. PARADIGM-SHIFT then identifies several additional genomic alterations, including non-coding mutations variants, which are significantly implicated in these pathway changes. This analysis offers insight into the mechanism of non-coding mutations orthogonal to sequence-based methods by interpreting the pathway consequences of these variants. Citation Format: Sam Ng, Christopher Benz, David Haussler, Joshua M. Stuart. PARADIGM-SHIFT: Predicts the functional impact of ‘driver modules’ in multiple cancers using pathway impact analysis. [abstract]. In: Proceedings of the AACR Special Conference on Computational and Systems Biology of Cancer; Feb 8-11 2015; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(22 Suppl 2):Abstract nr B1-38.
Differential Effects of Temperature on the Growth of Certain Transplanted Tumors in Strain DBA Mice
Authors: J C HUNTER
Journal: JNCI Journal of the National Cancer Institute (1955)

Differential Effects of Temperature on the Growth of Certain Transplanted Tumors in Strain DBA Mice Get access Jehu C. Hunter Jehu C. Hunter Cytochemistry Section, Laboratory of Biochemistry, National Cancer Institute,3Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 16, Issue 2, October 1955, Pages 405–414, https://doi.org/10.1093/jnci/16.2.405 Published: 01 October 1955 Article history Received: 07 February 1955 Published: 01 October 1955
Abstract MP21: No Significant Association of n-3 polyunsaturated Fatty Acids (PUFAs) with T-helper Type 1 (Th1) Cells: Results From the Multi-Ethnic Study of Atherosclerosis (MESA)
Authors: Naoko Sagawa, Nels C Olson, Abhishek Vishnu, Vasudha Ahuja, Margaret F Doyle, Bruce M Psaty, Nancy S Jenny, David S Siscovick, Rozenn N Lemaitre, Lyn M Steffen, Michael Y Tsai, Akira Sekikawa
Journal: Circulation (2016)

Introduction: T-helper type 1 (Th1) cells provide important stimulatory and regulatory signals to immune cells and are positively associated with subclinical atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA). Fish and fish oils are a major source of n-3 polyunsaturated fatty acids (PUFAs), and several studies in Japanese populations with high fish consumption reported inverse associations with subclinical atherosclerosis. Animal studies have suggested an inverse relationship of n-3 PUFAs with Th1 cells; however, this has not been investigated in humans. We hypothesized that n-3 PUFAs would have an inverse association with Th1 cells in MESA. Methods: We included 895 MESA participants with data on n-3 PUFAs at exam 1 (2000-02) and Th1 cells at exam 4 (2005-07) (age 61±10 years, 467 women, 396 Caucasians, 219 Hispanics, 185 African-Americans, 95 Chinese-Americans). Th1 cells were measured by flow cytometry as a percentage of CD4+ lymphocytes that were interferon-γ+ (%Th1). Phospholipid n-3 PUFAs (% of total fatty acids), defined as the sum of eicosapentaenoic and docosahexaenoic acids, were measured by gas chromatography. Dietary intake of n-3 PUFAs was evaluated by food frequency questionnaire (n=847). General linear models were used to analyze cross-sectional associations of n-3 PUFA quartiles with %Th1 adjusting for covariates. Results: Mean n-3 PUFA and %Th1 levels were 4.8±2.1% and 15.9±8.3%. n-3 PUFAs were not significantly associated with %Th1 (P for trend=.58). The association remained non-significant after adjusting for covariates. Dietary intake of n-3 PUFAs also showed no significant association with %Th1 (Table). Conclusion: Circulating levels and dietary intake of n-3 PUFAs were not significantly associated with %Th1 in this multi-ethnic U.S. population. n-3 PUFA levels in this cohort may be too low to have an effect on Th1 levels. Further research is needed to assess potential benefits of n-3 PUFA supplementation and dietary consumption of fish on T helper cell profiles and atherogenesis.
Photothermal Therapy: Highly Selective Photothermal Therapy by a Phenoxylated-Dextran-Functionalized Smart Carbon Nanotube Platform (Adv. Healthcare Mater. 10/2016)
Authors: Seungmin Han, Taeyun Kwon, Jo-Eun Um, Seungjoo Haam, Woo-Jae Kim
Journal: Advanced Healthcare Materials (2016)

Phenoxylated dextran-coated single-walled carbon nanotubes (pD-SWNT) as photothermal agents that selectively target inflammatory macrophages over normal cells by a specific antibody interaction with the dextran are presented by S. Haam, W.-J. Kim, and co-workers on page 1147. This solution to the nonspecific SWNT-targeting problem shows promise for therapeutic applications since it allows destroying inflammatory macrophages upon NIR irradiation, while leaving normal cells unaffected.
Alteration of platelet benzodiazepine receptors by stress of war
Authors: R Weizman, N Laor, L Karp, E Dagan, A Reiss, D E Dar, L Wolmer, M Gavish
Journal: American Journal of Psychiatry (1994)

Mitochondrial benzodiazepine receptors play a major role in steroidogenesis. The authors determined plasma cortisol levels, platelet levels of mitochondrial benzodiazepine receptors, and anxiety and depression scores in 11 civilians exposed to the Persian Gulf war. The density of mitochondrial benzodiazepine receptors was 22% and 15% lower before and during the war, respectively, than 4 weeks after the end of the war. Relief of stress led to an increase in receptors, which correlated with the improvement in anxiety but not mood.
Abstract A05: BRCA1 promoter hypermethylation loss in recurrent high-grade serous carcinoma.
Authors: Maria Bisogna, Fanny Dao, Narciso Olvera, Ruben Bacares, Liying Zhang, Douglas A. Levine
Journal: Clinical Cancer Research (2016)

Abstract Objective: BRCA1 germline mutations are associated with improved ovarian cancer survival, yet secondary revertant mutations that impair chemo-sensitivity can develop after platinum-based therapy. BRCA1 promoter hypermethylation, present in ~10% of all high-grade serous carcinomas (HGSCs), is associated with reduced gene and protein expression. We hypothesize that BRCA1 promoter hypermethylation decreases in recurrent HGSCs compared with matched primary samples. Methods: Primary, untreated HGSCs with known BRCA1 promoter methylation status and matched recurrent samples were macrodissected from archival slides. After DNA was extracted and bisulfite treated, pyrosequencing was performed across 11 CpG sites within the BRCA1 promoter to quantify methylation using a CLIA-approved assay. The methylation percentage was calculated from allele frequencies and 10% or greater is considered hypermethylated. Validation data were obtained from The Cancer Genome Atlas (TCGA) substudy of paired primary and recurrent HGSCs. Results: Eleven patients with matched primary and recurrent tumors were evaluated. Six patients had hypermethylated primary tumors, with methylation percentages ranging from 35-69%. We found that BRCA1 promoter methylation decreased 16-95% in five recurrent samples compared to their primary tumors. One patient with a demethylated recurrent tumor had platinum refractory disease clinically and died 12 months after diagnosis. In contrast, the only patient with an increase (74%) in promoter methylation between primary and recurrent specimens is a long-term survivor alive with disease 14 years after diagnosis. There was negligible change in promoter methylation between primary and recurrent cases for the five unmethylated samples. Three of 17 paired samples from the ovarian TCGA substudy had BRCA1 promoter hypermethylation and showed a 20-50% decrease between primary and recurrent samples with a corresponding increase in BRCA1 gene expression. Conclusion: BRCA1 promoter hypermethylation generally decreases between primary and recurrent HGSCs and can be associated with remarkable clinical outcomes. BRCA1 promoter methylation may be a marker of platinum response in the recurrent disease setting and can be assessed in prospective clinical trials. In addition to BRCA1 somatic revertant mutations, loss of BRCA1 promoter methylation may be another mechanism to restore BRCA1 function in recurrent disease. Citation Format: Maria Bisogna, Fanny Dao, Narciso Olvera, Ruben Bacares, Liying Zhang, Douglas A. Levine. BRCA1 promoter hypermethylation loss in recurrent high-grade serous carcinoma. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; Oct 17-20, 2015; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(2 Suppl):Abstract nr A05.