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Article ; Online: VCF2CNA: A tool for efficiently detecting copy-number alterations in VCF genotype data and tumor purity.

Putnam, Daniel K / Ma, Xiaotu / Rice, Stephen V / Liu, Yu / Newman, Scott / Zhang, Jinghui / Chen, Xiang

2019 Volume 9, Issue 1, Page(s) 10357

Abstract: VCF2CNA is a tool (Linux commandline or web-interface) for copy-number alteration (CNA) analysis and tumor purity estimation of paired tumor-normal VCF variant file formats. It operates on whole genome and whole exome datasets. To benchmark its ... ...

Abstract	VCF2CNA is a tool (Linux commandline or web-interface) for copy-number alteration (CNA) analysis and tumor purity estimation of paired tumor-normal VCF variant file formats. It operates on whole genome and whole exome datasets. To benchmark its performance, we applied it to 46 adult glioblastoma and 146 pediatric neuroblastoma samples sequenced by Illumina and Complete Genomics (CGI) platforms respectively. VCF2CNA was highly consistent with a state-of-the-art algorithm using raw sequencing data (mean F1-score = 0.994) in high-quality whole genome glioblastoma samples and was robust to uneven coverage introduced by library artifacts. In the whole genome neuroblastoma set, VCF2CNA identified MYCN high-level amplifications in 31 of 32 clinically validated samples compared to 15 found by CGI's HMM-based CNA model. Moreover, VCF2CNA achieved highly consistent CNA profiles between WGS and WXS platforms (mean F1 score 0.97 on a set of 15 rhabdomyosarcoma samples). In addition, VCF2CNA provides accurate tumor purity estimates for samples with sufficient CNAs. These results suggest that VCF2CNA is an accurate, efficient and platform-independent tool for CNA and tumor purity analyses without accessing raw sequence data.
MeSH term(s)	Adult ; Algorithms ; Artifacts ; Child ; Clone Cells ; DNA Copy Number Variations ; DNA, Neoplasm/genetics ; Datasets as Topic ; Gene Amplification ; Genes, Neoplasm ; Glioblastoma/genetics ; Humans ; Internet ; Neoplasms/genetics ; Neuroblastoma/genetics ; Polymorphism, Single Nucleotide ; Rhabdomyosarcoma/genetics ; Software ; User-Computer Interface ; Whole Exome Sequencing ; Whole Genome Sequencing
Chemical Substances	DNA, Neoplasm
Language	English
Publishing date	2019-07-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-45938-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: RNAIndel: discovering somatic coding indels from tumor RNA-Seq data.

Hagiwara, Kohei / Ding, Liang / Edmonson, Michael N / Rice, Stephen V / Newman, Scott / Easton, John / Dai, Juncheng / Meshinchi, Soheil / Ries, Rhonda E / Rusch, Michael / Zhang, Jinghui

Bioinformatics (Oxford, England)

2020 Volume 36, Issue 14, Page(s) 4231

Language	English
Publishing date	2020-03-06
Publishing country	England
Document type	Journal Article ; Published Erratum
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btaa247
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Article ; Online: SequencErr: measuring and suppressing sequencer errors in next-generation sequencing data.

Davis, Eric M / Sun, Yu / Liu, Yanling / Kolekar, Pandurang / Shao, Ying / Szlachta, Karol / Mulder, Heather L / Ren, Dongren / Rice, Stephen V / Wang, Zhaoming / Nakitandwe, Joy / Gout, Alexander M / Shaner, Bridget / Hall, Salina / Robison, Leslie L / Pounds, Stanley / Klco, Jeffery M / Easton, John / Ma, Xiaotu

Genome biology

2021 Volume 22, Issue 1, Page(s) 37

Abstract: Background: There is currently no method to precisely measure the errors that occur in the sequencing instrument/sequencer, which is critical for next-generation sequencing applications aimed at discovering the genetic makeup of heterogeneous cellular ... ...

Abstract	Background: There is currently no method to precisely measure the errors that occur in the sequencing instrument/sequencer, which is critical for next-generation sequencing applications aimed at discovering the genetic makeup of heterogeneous cellular populations. Results: We propose a novel computational method, SequencErr, to address this challenge by measuring the base correspondence between overlapping regions in forward and reverse reads. An analysis of 3777 public datasets from 75 research institutions in 18 countries revealed the sequencer error rate to be ~ 10 per million (pm) and 1.4% of sequencers and 2.7% of flow cells have error rates > 100 pm. At the flow cell level, error rates are elevated in the bottom surfaces and > 90% of HiSeq and NovaSeq flow cells have at least one outlier error-prone tile. By sequencing a common DNA library on different sequencers, we demonstrate that sequencers with high error rates have reduced overall sequencing accuracy, and removal of outlier error-prone tiles improves sequencing accuracy. We demonstrate that SequencErr can reveal novel insights relative to the popular quality control method FastQC and achieve a 10-fold lower error rate than popular error correction methods including Lighter and Musket. Conclusions: Our study reveals novel insights into the nature of DNA sequencing errors incurred on DNA sequencers. Our method can be used to assess, calibrate, and monitor sequencer accuracy, and to computationally suppress sequencer errors in existing datasets.
MeSH term(s)	Algorithms ; Calibration ; Gene Library ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Models, Genetic ; SARS-CoV-2 ; Sequence Analysis, DNA/methods
Language	English
Publishing date	2021-01-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-020-02254-2
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Article ; Online: Defining the condensate landscape of fusion oncoproteins.

Tripathi, Swarnendu / Shirnekhi, Hazheen K / Gorman, Scott D / Chandra, Bappaditya / Baggett, David W / Park, Cheon-Gil / Somjee, Ramiz / Lang, Benjamin / Hosseini, Seyed Mohammad Hadi / Pioso, Brittany J / Li, Yongsheng / Iacobucci, Ilaria / Gao, Qingsong / Edmonson, Michael N / Rice, Stephen V / Zhou, Xin / Bollinger, John / Mitrea, Diana M / White, Michael R /

McGrail, Daniel J / Jarosz, Daniel F / Yi, S Stephen / Babu, M Madan / Mullighan, Charles G / Zhang, Jinghui / Sahni, Nidhi / Kriwacki, Richard W

Nature communications

2023 Volume 14, Issue 1, Page(s) 6008

Abstract: Fusion oncoproteins (FOs) arise from chromosomal translocations in ~17% of cancers and are often oncogenic drivers. Although some FOs can promote oncogenesis by undergoing liquid-liquid phase separation (LLPS) to form aberrant biomolecular condensates, ... ...

Abstract	Fusion oncoproteins (FOs) arise from chromosomal translocations in ~17% of cancers and are often oncogenic drivers. Although some FOs can promote oncogenesis by undergoing liquid-liquid phase separation (LLPS) to form aberrant biomolecular condensates, the generality of this phenomenon is unknown. We explored this question by testing 166 FOs in HeLa cells and found that 58% formed condensates. The condensate-forming FOs displayed physicochemical features distinct from those of condensate-negative FOs and segregated into distinct feature-based groups that aligned with their sub-cellular localization and biological function. Using Machine Learning, we developed a predictor of FO condensation behavior, and discovered that 67% of ~3000 additional FOs likely form condensates, with 35% of those predicted to function by altering gene expression. 47% of the predicted condensate-negative FOs were associated with cell signaling functions, suggesting a functional dichotomy between condensate-positive and -negative FOs. Our Datasets and reagents are rich resources to interrogate FO condensation in the future.
MeSH term(s)	Humans ; HeLa Cells ; Oncogene Proteins, Fusion ; Biomolecular Condensates ; Carcinogenesis ; Cell Transformation, Neoplastic
Chemical Substances	Oncogene Proteins, Fusion
Language	English
Publishing date	2023-09-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-41655-2
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Article ; Online: RNAIndel: discovering somatic coding indels from tumor RNA-Seq data.

Hagiwara, Kohei / Ding, Liang / Edmonson, Michael N / Rice, Stephen V / Newman, Scott / Easton, John / Dai, Juncheng / Meshinchi, Soheil / Ries, Rhonda E / Rusch, Michael / Zhang, Jinghui

Bioinformatics (Oxford, England)

2019 Volume 36, Issue 5, Page(s) 1382–1390

Abstract: Motivation: Reliable identification of expressed somatic insertions/deletions (indels) is an unmet need due to artifacts generated in PCR-based RNA-Seq library preparation and the lack of normal RNA-Seq data, presenting analytical challenges for ... ...

Abstract	Motivation: Reliable identification of expressed somatic insertions/deletions (indels) is an unmet need due to artifacts generated in PCR-based RNA-Seq library preparation and the lack of normal RNA-Seq data, presenting analytical challenges for discovery of somatic indels in tumor transcriptome. Results: We present RNAIndel, a tool for predicting somatic, germline and artifact indels from tumor RNA-Seq data. RNAIndel leverages features derived from indel sequence context and biological effect in a machine-learning framework. Except for tumor samples with microsatellite instability, RNAIndel robustly predicts 88-100% of somatic indels in five diverse test datasets of pediatric and adult cancers, even recovering subclonal (VAF range 0.01-0.15) driver indels missed by targeted deep-sequencing, outperforming the current best-practice for RNA-Seq variant calling which had 57% sensitivity but with 14 times more false positives. Availability and implementation: RNAIndel is freely available at https://github.com/stjude/RNAIndel. Supplementary information: Supplementary data are available at Bioinformatics online.
MeSH term(s)	Child ; High-Throughput Nucleotide Sequencing ; Humans ; INDEL Mutation ; Neoplasms/genetics ; RNA-Seq ; Software ; Exome Sequencing
Language	English
Publishing date	2019-10-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btz753
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Article: SequencErr: measuring and suppressing sequencer errors in next-generation sequencing data

Genome biology. 2021 Dec., v. 22, no. 1

2021

Abstract: BACKGROUND: There is currently no method to precisely measure the errors that occur in the sequencing instrument/sequencer, which is critical for next-generation sequencing applications aimed at discovering the genetic makeup of heterogeneous cellular ... ...

Abstract	BACKGROUND: There is currently no method to precisely measure the errors that occur in the sequencing instrument/sequencer, which is critical for next-generation sequencing applications aimed at discovering the genetic makeup of heterogeneous cellular populations. RESULTS: We propose a novel computational method, SequencErr, to address this challenge by measuring the base correspondence between overlapping regions in forward and reverse reads. An analysis of 3777 public datasets from 75 research institutions in 18 countries revealed the sequencer error rate to be ~ 10 per million (pm) and 1.4% of sequencers and 2.7% of flow cells have error rates > 100 pm. At the flow cell level, error rates are elevated in the bottom surfaces and > 90% of HiSeq and NovaSeq flow cells have at least one outlier error-prone tile. By sequencing a common DNA library on different sequencers, we demonstrate that sequencers with high error rates have reduced overall sequencing accuracy, and removal of outlier error-prone tiles improves sequencing accuracy. We demonstrate that SequencErr can reveal novel insights relative to the popular quality control method FastQC and achieve a 10-fold lower error rate than popular error correction methods including Lighter and Musket. CONCLUSIONS: Our study reveals novel insights into the nature of DNA sequencing errors incurred on DNA sequencers. Our method can be used to assess, calibrate, and monitor sequencer accuracy, and to computationally suppress sequencer errors in existing datasets.
Keywords	DNA ; DNA libraries ; accuracy ; cells ; data collection ; flow ; genome ; high-throughput nucleotide sequencing ; population ; quality control ; research institutions ; surfaces ; tiles
Language	English
Dates of publication	2021-12
Size	p. 37.
Publishing place	BioMed Central
Document type	Article
ZDB-ID	2040529-7
ISSN	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-020-02254-2
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Clinical genome sequencing uncovers potentially targetable truncations and fusions of MAP3K8 in spitzoid and other melanomas.

Nature medicine

2019 Volume 25, Issue 4, Page(s) 597–602

Abstract: Spitzoid melanoma is a specific morphologic variant of melanoma that most commonly affects children and adolescents, and ranges on the spectrum of malignancy from low grade to overtly malignant. These tumors are generally driven by fusions of ALK, RET, ... ...

Abstract	Spitzoid melanoma is a specific morphologic variant of melanoma that most commonly affects children and adolescents, and ranges on the spectrum of malignancy from low grade to overtly malignant. These tumors are generally driven by fusions of ALK, RET, NTRK1/3, MET, ROS1 and BRAF
MeSH term(s)	Animals ; Child ; Exons/genetics ; Genome, Human ; Humans ; MAP Kinase Kinase Kinases/genetics ; Male ; Melanoma/genetics ; Mice ; Mutation/genetics ; NIH 3T3 Cells ; Oncogene Proteins, Fusion/genetics ; Proto-Oncogene Proteins/genetics ; Sequence Analysis, DNA
Chemical Substances	Oncogene Proteins, Fusion ; Proto-Oncogene Proteins ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP3K8 protein, human (EC 2.7.11.25)
Language	English
Publishing date	2019-03-04
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-019-0373-y
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Article ; Online: Pediatric Cancer Variant Pathogenicity Information Exchange (PeCanPIE): a cloud-based platform for curating and classifying germline variants.

Genome research

2019 Volume 29, Issue 9, Page(s) 1555–1565

Abstract: Variant interpretation in the era of massively parallel sequencing is challenging. Although many resources and guidelines are available to assist with this task, few integrated end-to-end tools exist. Here, we present ... ...

Abstract	Variant interpretation in the era of massively parallel sequencing is challenging. Although many resources and guidelines are available to assist with this task, few integrated end-to-end tools exist. Here, we present the
MeSH term(s)	Child ; Cloud Computing ; Computational Biology/methods ; Databases, Genetic ; Genetic Predisposition to Disease ; Germ-Line Mutation ; High-Throughput Nucleotide Sequencing ; Humans ; Neoplasms/genetics ; User-Computer Interface
Language	English
Publishing date	2019-08-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1284872-4
ISSN	1549-5469 ; 1088-9051 ; 1054-9803
ISSN (online)	1549-5469
ISSN	1088-9051 ; 1054-9803
DOI	10.1101/gr.250357.119
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Article ; Online: Molecular Mechanism of Telomere Length Dynamics and Its Prognostic Value in Pediatric Cancers.

Journal of the National Cancer Institute

2019 Volume 112, Issue 7, Page(s) 756–764

Abstract: Background: We aimed to systematically evaluate telomere dynamics across a spectrum of pediatric cancers, search for underlying molecular mechanisms, and assess potential prognostic value.: Methods: The fraction of telomeric reads was determined from ...

Abstract	Background: We aimed to systematically evaluate telomere dynamics across a spectrum of pediatric cancers, search for underlying molecular mechanisms, and assess potential prognostic value. Methods: The fraction of telomeric reads was determined from whole-genome sequencing data for paired tumor and normal samples from 653 patients with 23 cancer types from the Pediatric Cancer Genome Project. Telomere dynamics were characterized as the ratio of telomere fractions between tumor and normal samples. Somatic mutations were gathered, RNA sequencing data for 330 patients were analyzed for gene expression, and Cox regression was used to assess the telomere dynamics on patient survival. Results: Telomere lengthening was observed in 28.7% of solid tumors, 10.5% of brain tumors, and 4.3% of hematological cancers. Among 81 samples with telomere lengthening, 26 had somatic mutations in alpha thalassemia/mental retardation syndrome X-linked gene, corroborated by a low level of the gene expression in the subset of tumors with RNA sequencing. Telomerase reverse transcriptase gene amplification and/or activation was observed in 10 tumors with telomere lengthening, including two leukemias of the E2A-PBX1 subtype. Among hematological cancers, pathway analysis for genes with expressions most negatively correlated with telomere fractions suggests the implication of a gene ontology process of antigen presentation by Major histocompatibility complex class II. A higher ratio of telomere fractions was statistically significantly associated with poorer survival for patients with brain tumors (hazard ratio = 2.18, 95% confidence interval = 1.37 to 3.46). Conclusion: Because telomerase inhibitors are currently being explored as potential agents to treat pediatric cancer, these data are valuable because they identify a subpopulation of patients with reactivation of telomerase who are most likely to benefit from this novel therapeutic option.
MeSH term(s)	Adolescent ; Child ; Child, Preschool ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Mutation ; Neoplasms/genetics ; Telomerase/genetics ; Telomere/genetics ; Telomere Homeostasis ; Telomere Shortening ; Whole Genome Sequencing
Chemical Substances	TERT protein, human (EC 2.7.7.49) ; Telomerase (EC 2.7.7.49)
Language	English
Publishing date	2019-10-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2992-0
ISSN	1460-2105 ; 0027-8874 ; 0198-0157
ISSN (online)	1460-2105
ISSN	0027-8874 ; 0198-0157
DOI	10.1093/jnci/djz210
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Article ; Online: Polygenic Determinants for Subsequent Breast Cancer Risk in Survivors of Childhood Cancer: The St Jude Lifetime Cohort Study (SJLIFE).

Wang, Zhaoming / Liu, Qi / Wilson, Carmen L / Easton, John / Mulder, Heather / Chang, Ti-Cheng / Rusch, Michael C / Edmonson, Michael N / Rice, Stephen V / Ehrhardt, Matthew J / Howell, Rebecca M / Kesserwan, Chimene A / Wu, Gang / Nichols, Kim E / Downing, James R / Hudson, Melissa M / Zhang, Jinghui / Yasui, Yutaka / Robison, Leslie L

Clinical cancer research : an official journal of the American Association for Cancer Research

2018 Volume 24, Issue 24, Page(s) 6230–6235

Abstract: Purpose: The risk of subsequent breast cancer among female childhood cancer survivors is markedly elevated. We aimed to determine genetic contributions to this risk, focusing on polygenic determinants implicated in breast cancer susceptibility in the ... ...

Abstract	Purpose: The risk of subsequent breast cancer among female childhood cancer survivors is markedly elevated. We aimed to determine genetic contributions to this risk, focusing on polygenic determinants implicated in breast cancer susceptibility in the general population. Experimental design: Whole-genome sequencing (30×) was performed on survivors in the St Jude Lifetime Cohort, and germline mutations in breast cancer predisposition genes were classified for pathogenicity. A polygenic risk score (PRS) was constructed for each survivor using 170 established common risk variants. Relative rate (RR) and 95% confidence interval (95% CI) of subsequent breast cancer incidence were estimated using multivariable piecewise exponential regression. Results: The analysis included 1,133 female survivors of European ancestry (median age at last follow-up = 35.4 years; range, 8.4-67.4), of whom 47 were diagnosed with one or more subsequent breast cancers (median age at subsequent breast cancer = 40.3 years; range, 24.5-53.0). Adjusting for attained age, age at primary diagnosis, chest irradiation, doses of alkylating agents and anthracyclines, and genotype eigenvectors, RRs for survivors with PRS in the highest versus lowest quintiles were 2.7 (95% CI, 1.0-7.3), 3.0 (95% CI, 1.1-8.1), and 2.4 (95% CI, 0.1-81.1) for all survivors and survivors with and without chest irradiation, respectively. Similar associations were observed after excluding carriers of pathogenic/likely pathogenic mutations in breast cancer predisposition genes. Notably, the PRS was associated with the subsequent breast cancer rate under the age of 45 years (RR = 3.2; 95% CI, 1.2-8.3). Conclusions: Genetic profiles comprised of small-effect common variants and large-effect predisposing mutations can inform personalized breast cancer risk and surveillance/intervention in female childhood cancer survivors.
MeSH term(s)	Age Factors ; Breast Neoplasms/epidemiology ; Breast Neoplasms/etiology ; Cancer Survivors/statistics & numerical data ; Child ; Child, Preschool ; Cohort Studies ; Female ; Follow-Up Studies ; Genetic Predisposition to Disease ; Genetic Variation ; Germ-Line Mutation ; Humans ; Incidence ; Neoplasms, Second Primary/epidemiology ; Neoplasms, Second Primary/etiology ; Odds Ratio ; Population Surveillance ; Risk Assessment ; Risk Factors ; Sex Factors
Language	English
Publishing date	2018-10-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-18-1775
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