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Institution

Case Western Reserve University

EducationCleveland, Ohio, United States
About: Case Western Reserve University is a education organization based out in Cleveland, Ohio, United States. It is known for research contribution in the topics: Population & Health care. The organization has 54617 authors who have published 106568 publications receiving 5071613 citations. The organization is also known as: Case & Case Western.


Papers
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Journal ArticleDOI
TL;DR: A “state of the science” review of current research into causes and risk factors for gliomas in adults is provided.
Abstract: Gliomas are the most common primary intracranial tumor, representing 81% of malignant brain tumors Although relatively rare, they cause significant mortality and morbidity Glioblastoma, the most common glioma histology (∼45% of all gliomas), has a 5-year relative survival of ∼5% A small portion of these tumors are caused by Mendelian disorders, including neurofibromatosis, tuberous sclerosis, and Li-Fraumeni syndrome Genomic analyses of glioma have also produced new evidence about risk and prognosis Recently discovered biomarkers that indicate improved survival include O⁶-methylguanine-DNA methyltransferase methylation, isocitrate dehydrogenase mutation, and a glioma cytosine-phosphate-guanine island methylator phenotype Genome-wide association studies have identified heritable risk alleles within 7 genes that are associated with increased risk of glioma Many risk factors have been examined as potential contributors to glioma risk Most significantly, these include an increase in risk by exposure to ionizing radiation and a decrease in risk by history of allergies or atopic disease(s) The potential influence of occupational exposures and cellular phones has also been examined, with inconclusive results We provide a “state of the science” review of current research into causes and risk factors for gliomas in adults

1,536 citations

Journal ArticleDOI
TL;DR: Credibility is increased if subgroup effects are based on a small number of a priori hypotheses with a specified direction; subgroup comparisons come from within rather than between studies; tests of interaction generate low P-values; and have a biological rationale.

1,535 citations

Journal ArticleDOI
28 Jan 2016-Cell
TL;DR: The complete set of genes associated with 1,122 diffuse grade II-III-IV gliomas were defined from The Cancer Genome Atlas and molecular profiles were used to improve disease classification, identify molecular correlations, and provide insights into the progression from low- to high-grade disease.

1,535 citations

Journal ArticleDOI
Nicholas J Kassebaum1, Megha Arora1, Ryan M Barber1, Zulfiqar A Bhutta2  +679 moreInstitutions (268)
TL;DR: In this paper, the authors used the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015) for all-cause mortality, cause-specific mortality, and non-fatal disease burden to derive HALE and DALYs by sex for 195 countries and territories from 1990 to 2015.

1,533 citations

Journal ArticleDOI
19 Mar 1998-Nature
TL;DR: It is shown that CIN is consistently associated with the loss of function of a mitotic checkpoint in cancers displaying CIN, and in some cancersThe loss of this checkpoint wasassociated with the mutational inactivation of a human homologue of the yeast BUB1 gene; BUB 1 controls mitotic checkpoints and chromosome segregation in yeast.
Abstract: Genetic instability was one of the first characteristics to be postulated to underlie neoplasia1,2,3. Such genetic instability occurs in two different forms. In a small fraction of colorectal and some other cancers, defective repair of mismatched bases results in an increased mutation rate at the nucleotide level and consequent widespread microsatellite instability4,5,6,7. In most colorectal cancers, and probably in many other cancer types, a chromosomal instability (CIN) leading to an abnormal chromosome number (aneuploidy) is observed8. The physiological and molecular bases of this pervasive abnormality are unknown. Here we show that CIN is consistently associated with the loss of function of a mitotic checkpoint. Moreover, in some cancers displaying CIN the loss of this checkpoint was associated with the mutational inactivation of a human homologue of the yeast BUB1 gene; BUB1 controls mitotic checkpoints and chromosome segregation in yeast. The normal mitotic checkpoints of cells displaying microsatellite instability become defective upon transfer of mutant hBUB1 alleles from either of two CIN cancers.

1,529 citations


Authors

Showing all 54953 results

NameH-indexPapersCitations
Robert Langer2812324326306
Bert Vogelstein247757332094
Zhong Lin Wang2452529259003
John Q. Trojanowski2261467213948
Kenneth W. Kinzler215640243944
Peter Libby211932182724
David Baltimore203876162955
Carlo M. Croce1981135189007
Ronald Klein1941305149140
Eric J. Topol1931373151025
Paul M. Thompson1832271146736
Yusuke Nakamura1792076160313
Dennis J. Selkoe177607145825
David L. Kaplan1771944146082
Evan E. Eichler170567150409
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023142
2022411
20214,337
20204,141
20193,978
20183,663