scispace - formally typeset
X

Xiaojun Zhao

Researcher at Harvard University

Publications -  18
Citations -  10338

Xiaojun Zhao is an academic researcher from Harvard University. The author has contributed to research in topics: Loss of heterozygosity & Lung cancer. The author has an hindex of 16, co-authored 18 publications receiving 9852 citations. Previous affiliations of Xiaojun Zhao include Broad Institute & Novartis.

Papers
More filters
Journal ArticleDOI

MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling

TL;DR: It is proposed that MET amplification may promote drug resistance in other ERBB-driven cancers as well after it was found that amplification of MET causes gefitinib resistance by driving ERBB3 (HER3)–dependent activation of PI3K, a pathway thought to be specific to EGFR/ERBB family receptors.
Journal ArticleDOI

Somatic mutations affect key pathways in lung adenocarcinoma

Li Ding, +96 more
- 23 Oct 2008 - 
TL;DR: Somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B are found.
Journal ArticleDOI

An Integrated View of Copy Number and Allelic Alterations in the Cancer Genome Using Single Nucleotide Polymorphism Arrays

TL;DR: The simultaneous measurement of DNA copy number changes and loss of heterozygosity events by SNP arrays should strengthen the ability to discover cancer-causing genes and to refine cancer diagnosis.
Journal ArticleDOI

High-resolution mapping of copy-number alterations with massively parallel sequencing

TL;DR: A collection of ∼14 million aligned sequence reads from human cell lines has comparable power to detect events as the current generation of DNA microarrays and has over twofold better precision for localizing breakpoints (typically, to within ∼1 kilobase).
Journal ArticleDOI

Allelic dilution obscures detection of a biologically significant resistance mutation in EGFR-amplified lung cancer

TL;DR: It is suggested that allelic dilution of biologically significant resistance mutations may go undetected by direct sequencing in cancers with amplified oncogenes and that restoration of PI3K activation via either a T790M mutation or other mechanisms can provide resistance to gefitinib.