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Cheng Li

Researcher at Peking University

Publications -  238
Citations -  49764

Cheng Li is an academic researcher from Peking University. The author has contributed to research in topics: Gene & Medicine. The author has an hindex of 63, co-authored 200 publications receiving 42539 citations. Previous affiliations of Cheng Li include University of California, Los Angeles & Tongji University.

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Growth arrest, apoptosis, and telomere shortening of Barrett’s-associated adenocarcinoma cells by a telomerase inhibitor

TL;DR: It is concluded that telomerase inhibition by PPA induces cell growth arrest in BEAC cells and demonstrates the potential of telomersase inhibitors in chemoprevention and treatment of Barrett's-associated esophageal adenocarcinoma.
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Nuclear actin regulates inducible transcription by enhancing RNA polymerase II clustering

TL;DR: This work unveils that nuclear actin promotes the formation of transcription factory on inducible genes, acting as a general mechanism underlying the rapid response to environmental cues.
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Two-round coamplification at lower denaturation temperature-PCR (COLD-PCR)-based sanger sequencing identifies a novel spectrum of low-level mutations in lung adenocarcinoma.

TL;DR: The ability to identify and sequence low‐level mutations in the absence of elaborate microdissection, via COLD‐PCR‐based Sanger sequencing, provides a platform for accurate mutation profiling in clinical specimens and the use of TP53 as a prognostic/predictive biomarker, evaluation of cancer risk, recurrence, and further understanding of cancer biology.
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NF1 Inactivation in Adult Acute Myelogenous Leukemia

TL;DR: NF1 null states are present in 7 of 95 (7%) of adult AML and delineate a disease subset that could be preferentially targeted by Ras or mammalian target of rapamycin–directed therapeutics.
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YAP suppresses lung squamous cell carcinoma progression via deregulation of the DNP63-GPX2 axis and ros accumulation

TL;DR: In patient-derived xenograft models, digitoxin treatment efficiently inhibited lung SCC progression in correlation with reduced expression of YAP, highlighting a novel tumor-suppressor function of Y AP via downregulation of GPX2 and ROS accumulation.