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Andrei Thomas-Tikhonenko

Researcher at Children's Hospital of Philadelphia

Publications -  105
Citations -  10265

Andrei Thomas-Tikhonenko is an academic researcher from Children's Hospital of Philadelphia. The author has contributed to research in topics: microRNA & Exon. The author has an hindex of 37, co-authored 91 publications receiving 9374 citations. Previous affiliations of Andrei Thomas-Tikhonenko include University of Pennsylvania.

Papers
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Journal ArticleDOI

Widespread microRNA repression by Myc contributes to tumorigenesis.

Tsung Cheng Chang, +8 more
- 01 Jan 2008 - 
TL;DR: In this paper, the c-Myc oncogenic transcription factor (Myc) is pathologically activated in many human malignancies and the predominant consequence of activation of Myc is widespread repression of miRNA expression.
Journal Article

Widespread microRNA repression by Myc contributes to tumorigenesis

Tsung Cheng Chang, +8 more
- 01 Jan 2008 - 
TL;DR: It is shown here that Myc regulates a much broader set of miRNAs than previously anticipated, and extensive reprogramming of the miRNA transcriptome by Myc contributes to tumorigenesis.
Journal ArticleDOI

Autophagy inhibition enhances therapy-induced apoptosis in a Myc-induced model of lymphoma

Ravi K. Amaravadi, +7 more
- 01 Feb 2007 - 
TL;DR: Evidence that autophagy serves as a survival pathway in tumor cells treated with apoptosis activators and a rationale for the use of autophagic inhibitors such as chloroquine in combination with therapies designed to induce apoptosis in human cancers are provided.
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Augmentation of tumor angiogenesis by a Myc-activated microRNA cluster

Michael Dews, +10 more
- 30 Jul 2006 - 
TL;DR: Findings establish a role for microRNAs in non–cell-autonomous Myc-induced tumor phenotypes and suggest that Ras-only cells with a miR-17-92–encoding retrovirus reduced Tsp1 and CTGF levels and formed larger, better-perfused tumors.
Journal ArticleDOI

Convergence of Acquired Mutations and Alternative Splicing of CD19 Enables Resistance to CART-19 Immunotherapy

Elena Sotillo, +29 more
- 01 Dec 2015 - 
TL;DR: It is discovered that the underlying mechanism is the selection for preexisting alternatively spliced CD19 isoforms with the compromised CART-19 epitope, which suggests a possibility of targeting alternative CD19 ectodomains, which could improve survival of patients with B-cell neoplasms.