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Lianbo Yu

Researcher at Ohio State University

Publications -  136
Citations -  7609

Lianbo Yu is an academic researcher from Ohio State University. The author has contributed to research in topics: microRNA & Medicine. The author has an hindex of 33, co-authored 113 publications receiving 5975 citations. Previous affiliations of Lianbo Yu include The Ohio State University Wexner Medical Center.

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Journal ArticleDOI

Loss of miR-1469 expression mediates melanoma cell migration and invasion.

TL;DR: In this paper, the miR-1469 was found to contribute to altered tumor cell functions mediating disease progression in primary cutaneous melanoma, which can contribute to the differences in disease progression associated with tumor ulceration.
Proceedings ArticleDOI

Abstract B01: Ets-2 acts as a novel oncogene in cancer associated fibroblasts and promotes pancreatic tumor initiation and development

TL;DR: This report shows that deleting a gene in pancreatic fibro Blasts causes a change in tumor-stroma co-evolution and that Ets-2 is able to act as a novel oncogene in cancer associated fibroblasts to promote pancreatic carcinogenesis.
Journal ArticleDOI

Variants in LRRC34 reveal distinct mechanisms for predisposition to papillary thyroid carcinoma

TL;DR: Two separate mechanisms, one in G protein signalling and the other in transcriptional control, dictating PTC risk at 3q26 are demonstrated using both biochemical and genetic techniques.
Journal ArticleDOI

Expression patterns of microRNAs and associated target genes in ulcerated primary cutaneous melanoma.

TL;DR: In this article , a unique miR profile exists in ulcerated relative to nonulcerated melanoma and that miR expression inversely correlates with target genes of biologic importance.
Posted ContentDOI

HDAC1 regulates the chromatin landscape to establish transcriptional dependencies in chronic lymphocytic leukemia

TL;DR: This work definitively establishes the composition of the regulatory chromatin that enables HDAC1 to function as an activator and repressor at distinct target genes within the same tumor to drive transcriptional dysregulation and allow the expression of B cell specific signaling and survival networks that are critical for survival.