Lei Song

National Cancer Institute

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Document Type

Co-Authors

Stephen J. Chanock

National Cancer Institute

Jianxin Shi

National Cancer Institute

Bin Zhu

National Cancer Institute

Nilanjan Chatterjee

Johns Hopkins University

Tongwu Zhang

National Cancer Institute

Belynda Hicks

National Cancer Institute

Xing Hua

National Cancer Institute

Amy Hutchinson

Leidos (United States)

Alisa M. Goldstein

National Cancer Institute

Ghislaine Scélo

Observational & Pragmatic Research Institute

Cooperative Institutions

National Cancer Institute

434

National Institutes of Health

381

Division of Cancer Epidemiology and Genetics

259

Harvard University

244

Cancer Genetics (United States)

177

The University of Texas MD Anderson Cancer Center

172

Broad Institute

166

Dana-Farber Cancer Institute

149

University of Cambridge

145

Heidelberg University

143

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Identification of Molecular Pathway Aberrations in Uterine Serous Carcinoma by Genome-wide Analyses

JNCI Journal of the National Cancer Institute (2012)

Elisabetta Kuhn Ren‐Chin Wu Bin Guan Gang Wu Jinghui Zhang

BackgroundUterine cancer is the fourth most common malignancy in women, and uterine serous carcinoma is the most aggressive subtype. However, the molecular pathogenesis of uterine serous carcinoma is largely unknown. We analyzed the genomes of uterine serous carcinoma samples to better understand the molecular genetic characteristics of this cancer.

Serous carcinoma

Sanger sequencing

Uterine cancer

10.1093/jnci/djs345

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Citations (243)

Frequency of Pathogenic Germline Variants in Cancer-Susceptibility Genes in the Childhood Cancer Survivor Study

JNCI Cancer Spectrum (2021)

Jung Kim Matthew Gianferante Danielle M. Karyadi Stephen W. Hartley Megan N. Frone

Pediatric cancers are the leading cause of death by disease in children despite improved survival rates overall. The contribution of germline genetic susceptibility to pediatric cancer survivors has not been extensively characterized. We assessed the frequency of pathogenic or likely pathogenic (P/LP) variants in 5451 long-term pediatric cancer survivors from the Childhood Cancer Survivor Study.

Childhood Cancer

Pediatric cancer

10.1093/jncics/pkab007

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Citations (28)

Integrative molecular characterisation of gallbladder cancer reveals micro-environment-associated subtypes

Journal of Hepatology (2020)

Chirag Nepal Bin Zhu Colm J. O’Rourke Deepak Kumar Bhatt Donghyuk Lee

Gallbladder Cancer

Exome

10.1016/j.jhep.2020.11.033

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Citations (50)

Correction: Distinct germline genetic susceptibility profiles identified for common non-Hodgkin lymphoma subtypes

Leukemia (2023)

Sonja I. Berndt Joseph Vijai Yolanda Benavente Nicola J. Camp Alexandra Nieters

10.1038/s41375-023-01978-x

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Citations (0)

Detection and quantification of viral RNA in human tumors using open source pipeline: viGEN

bioRxiv (Cold Spring Harbor Laboratory) (2017)

Krithika Bhuvaneshwar Lei Song Subha Madhavan Yuriy Gusev

An estimated 17% of cancers worldwide are associated with infectious causes. The extent and biological significance of viral presence/infection in actual tumor samples is generally unknown but could be measured using human transcriptome (RNA-seq) data from tumor samples. We present an open source bioinformatics pipeline viGEN that combines existing well-known and novel RNA-seq tools for not only detection and quantification of viral RNA, but also variants in the viral transcripts. The pipeline includes 4 major modules: The first module allows to align and filter out human RNA sequences; second module maps and count (remaining un-aligned) reads against reference genomes of all known and sequenced human viruses; the third module quantifies read counts at the individual viral genes level thus allowing for downstream differential expression analysis of viral genes between experimental and controls groups. The fourth module calls variants in these viruses. To the best of our knowledge, there are no publicly available pipelines or packages that would provide this type of complete analysis in one open source package. In this paper, we use this pipeline in a case study to examine viruses present in RNA-seq data from 75 TCGA liver cancer patients. We were able to quantify viral transcriptomes at a viral-gene/CDS level, find differentially expressed viral transcripts between the groups of patients, extract variants, and connect them to clinical outcome. The results presented corresponded with published literature in terms of rate of detection, viral gene expression patterns and impact of several known variants of HBV genome. Results also show novel information about distinct patterns of expression and co-expression in Hepatitis B, Hepatitis C, Human Endogenous Retrovirus (HERV) K113 viruses.

RNA-Seq

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Supplementary fig 5 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Jiwei Bai Jianxin Shi Yazhuo Zhang Chuzhong Li Yujia Xiong

Figure S5. SNAI1, SNAI3, and TWIST expression in CC1 and CC2 tumors.

Profiling (computer programming)

Chordoma

10.1158/1078-0432.22489379.v1

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Supplementary Legend 1 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Jiwei Bai Jianxin Shi Yazhuo Zhang Chuzhong Li Yujia Xiong

Supplementary Legend

Legend

Profiling (computer programming)

Chordoma

10.1158/1078-0432.22489397

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Table S1-S5 from Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes

Jiwei Bai Jianxin Shi Yazhuo Zhang Chuzhong Li Yujia Xiong

Table S1. Genes included in the targeted DNA panel sequencing. Table S2. Differences in clinical characteristics by molecular subtype. Table S3. Distributions of mutation status in PBRM1 and SETD2 by molecular subtype in RNASeq and Nanostring datasets. Table S4. Differentially expressed genes among molecular subtypes. Table S5. GSEA results for up- and down-regulated gene sets comparing CC2 to CC1.

Table (database)

10.1158/1078-0432.22489376.v1

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Shared and distinct genetic etiologies for different types of clonal hematopoiesis

Nature Communications (2023)

Derek W. Brown Liam D. Cato Yajie Zhao Satish K. Nandakumar Erik L. Bao

Abstract Clonal hematopoiesis (CH)—age-related expansion of mutated hematopoietic clones—can differ in frequency and cellular fitness by CH type (e.g., mutations in driver genes (CHIP), gains/losses and copy-neutral loss of chromosomal segments (mCAs), and loss of sex chromosomes). Co-occurring CH raises questions as to their origin, selection, and impact. We integrate sequence and genotype array data in up to 482,378 UK Biobank participants to demonstrate shared genetic architecture across CH types. Our analysis suggests a cellular evolutionary trade-off between different types of CH, with LOY occurring at lower rates in individuals carrying mutations in established CHIP genes. We observed co-occurrence of CHIP and mCAs with overlap at TET2 , DNMT3A , and JAK2 , in which CHIP precedes mCA acquisition. Furthermore, individuals carrying overlapping CH had high risk of future lymphoid and myeloid malignancies. Finally, we leverage shared genetic architecture of CH traits to identify 15 novel loci associated with leukemia risk.

Genetic architecture

10.1038/s41467-023-41315-5

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Citations (16)

Abstract 18021: Overexpression of microRNA-221 Cause Heart Failure by Inhibiting Autophagy

Circulation (2012)

Ming‐Jai Su Yilu Wang Jizheng Wang Wang Chang-xin Xiaojian Wang

Background MicroRNAs serve as crucial intracellular regulators of cardiac function in health and disease, through negatively regulating target gene expression. We have previously identified that mi...

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Citations (1)