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Joseph R. Nevins

Researcher at Duke University

Publications -  261
Citations -  44398

Joseph R. Nevins is an academic researcher from Duke University. The author has contributed to research in topics: E2F & Transcription factor. The author has an hindex of 105, co-authored 261 publications receiving 42988 citations. Previous affiliations of Joseph R. Nevins include Thomas Jefferson University & Durham University.

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Activation of a preexisting cellular factor as a basis for adenovirus E1A-mediated transcription control.

TL;DR: It is concluded that activation of E2F, as a posttranslational event, is responsible for the stimulation of E 2 transcription by E1A.
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Age- and sex-specific genomic profiles in non-small cell lung cancer.

TL;DR: Among a cohort of patients with NSCLC, subgroups defined by oncogenic pathway activation profiles were associated with recurrence-free survival, and these findings require validation in independent patient data sets.
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Characterizing the developmental pathways TTF-1, NKX2–8, and PAX9 in lung cancer

TL;DR: It is suggested that the cohort of patients with coactivation of TTF-1 and NKX2–8 pathways appears to be resistant to standard cisplatin therapy, suggesting the need for alternative therapies in this cohort of high-risk patients.
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Alternative poly(A) site utilization during adenovirus infection coincides with a decrease in the activity of a poly(A) site processing factor.

TL;DR: It is found that there is a substantial decrease in the level of CF1 activity when an adenovirus infection proceeds to the late phase, and it is suggested that this reduction inCF1 activity contributes to the reduced use of the L1 poly(A) site during the late stage of anAdenov virus infection.
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Gene-expression patterns predict phenotypes of immune-mediated thrombosis

TL;DR: The ability to predict APS, but more importantly, those patients at risk for venous thrombosis, represents a paradigm for a genomic approach that can be applied to other populations of patients with venousThromBosis, providing for more effective clinical management of disease, while also reflecting the possible underlying biologic processes.