Pieter Faber
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View article: Supplementary Table S5 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S5 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Copy number variation segments.
View article: Supplementary Table S6 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S6 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Core amplifications and deletions.
View article: Data from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Data from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Accumulating evidence has supported the fallopian tube rather than the ovary as the origin for high-grade serous ovarian cancer (HGSOC). To understand the relationship between putative precursor lesions and metastatic tumors, we performed …
View article: Supplementary Table S4 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S4 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
TP53 mutations in the patient cohort.
View article: Supplementary Table S7 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S7 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Newick trees and cophenetic correlation coefficients.
View article: Supplementary Table S1 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S1 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Clinicopathologic features of high grade serous ovarian cancer (HGSOC) cohort.
View article: Supplementary Table S2 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S2 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Exome sequencing quality metrics.
View article: Supplementary Table Legends, Figures S1 - S6 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table Legends, Figures S1 - S6 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Supplementary Figure S1. Sequencing of HGSOC reveals conserved mutational signatures and TP53 mutations. Supplementary Figure S2. Distribution of mutations and mutational signatures in HGSOC. Supplementary Figure S3. Genomic instability is…
View article: Supplementary Table S3 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S3 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Single nucleotide variants and indels.
View article: Supplementary Table S3 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S3 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Single nucleotide variants and indels.
View article: Supplementary Table S7 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S7 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Newick trees and cophenetic correlation coefficients.
View article: Supplementary Table S5 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S5 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Copy number variation segments.
View article: Supplementary Table S6 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S6 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Core amplifications and deletions.
View article: Supplementary Table Legends, Figures S1 - S6 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table Legends, Figures S1 - S6 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Supplementary Figure S1. Sequencing of HGSOC reveals conserved mutational signatures and TP53 mutations. Supplementary Figure S2. Distribution of mutations and mutational signatures in HGSOC. Supplementary Figure S3. Genomic instability is…
View article: Data from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Data from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Accumulating evidence has supported the fallopian tube rather than the ovary as the origin for high-grade serous ovarian cancer (HGSOC). To understand the relationship between putative precursor lesions and metastatic tumors, we performed …
View article: Supplementary Table S1 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S1 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Clinicopathologic features of high grade serous ovarian cancer (HGSOC) cohort.
View article: Supplementary Table S4 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S4 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
TP53 mutations in the patient cohort.
View article: Supplementary Table S2 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube
Supplementary Table S2 from Genomics of Ovarian Cancer Progression Reveals Diverse Metastatic Trajectories Including Intraepithelial Metastasis to the Fallopian Tube Open
Exome sequencing quality metrics.
View article: Data from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis
Data from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis Open
Viral oncogene expression is insufficient for neoplastic transformation of human cells, so human papillomavirus (HPV)–associated cancers will also rely upon mutations in cellular oncogenes and tumor suppressors. However, it has been diffic…
View article: Data from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis
Data from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis Open
Viral oncogene expression is insufficient for neoplastic transformation of human cells, so human papillomavirus (HPV)–associated cancers will also rely upon mutations in cellular oncogenes and tumor suppressors. However, it has been diffic…
View article: Supplemental Methods, Tables 1-9, and Figures 1-9 from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis
Supplemental Methods, Tables 1-9, and Figures 1-9 from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis Open
Supplemental Methods, Tables 1-9 and Figures 1-9. Supplemental Methods: Animals; Sleeping Beauty transposon mapping; Reagents and antibodies; HPV recombination, T2/Onc excision and Hras mutation specific PCRs. Supplemental Table 1: Mouse s…
View article: Supplemental Methods, Tables 1-9, and Figures 1-9 from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis
Supplemental Methods, Tables 1-9, and Figures 1-9 from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis Open
Supplemental Methods, Tables 1-9 and Figures 1-9. Supplemental Methods: Animals; Sleeping Beauty transposon mapping; Reagents and antibodies; HPV recombination, T2/Onc excision and Hras mutation specific PCRs. Supplemental Table 1: Mouse s…
View article: A functional genomics pipeline to identify high-value asthma and allergy CpGs in the human methylome
A functional genomics pipeline to identify high-value asthma and allergy CpGs in the human methylome Open
This study revealed signature features of high-value CpGs and evidence for epigenetic regulation of genes at AS EWAS loci that are robust to race/ethnicity, ascertainment, age, and geography.
View article: A Functional Genomics Pipeline to Identify High-Value Asthma and Allergy CpGs in the Human Methylome
A Functional Genomics Pipeline to Identify High-Value Asthma and Allergy CpGs in the Human Methylome Open
Background DNA methylation of cytosines at CpG dinucleotides is a widespread epigenetic mark; but genome-wide variation has been relatively unexplored due to the limited representation of variable CpGs on commercial high-throughput arrays.…
View article: Transcriptome clarifies mechanisms of lesion genesis versus progression in models of Ccm3 cerebral cavernous malformations
Transcriptome clarifies mechanisms of lesion genesis versus progression in models of Ccm3 cerebral cavernous malformations Open
Cerebral cavernous malformations (CCMs) are dilated capillaries causing epilepsy and stroke. Inheritance of a heterozygous mutation in CCM3/PDCD10 is responsible for the most aggressive familial form of the disease. Here we studied the dif…
View article: Comprehensive transcriptome analysis of cerebral cavernous malformation across multiple species and genotypes
Comprehensive transcriptome analysis of cerebral cavernous malformation across multiple species and genotypes Open
The purpose of this study was to determine important genes, functions, and networks contributing to the pathobiology of cerebral cavernous malformation (CCM) from transcriptomic analyses across 3 species and 2 disease genotypes. Sequencing…
View article: Additional file 7: of Transcriptome clarifies mechanisms of lesion genesis versus progression in models of Ccm3 cerebral cavernous malformations
Additional file 7: of Transcriptome clarifies mechanisms of lesion genesis versus progression in models of Ccm3 cerebral cavernous malformations Open
Table S6. 1876 gene ontology (GO) terms used for generating the heatmap. (XLSX 157 kb)
View article: Additional file 3: of Transcriptome clarifies mechanisms of lesion genesis versus progression in models of Ccm3 cerebral cavernous malformations
Additional file 3: of Transcriptome clarifies mechanisms of lesion genesis versus progression in models of Ccm3 cerebral cavernous malformations Open
Table S2. Top 20 genes by fold change for acute in vivo neurovascular units (NVUs), chronic in vivo NVUs and in vitro brain microvascular endothelial cells models (fold change |FC| ≥ 2; p < 0.05, false discovery rate corrected). (XLSX 18 k…
View article: Additional file 5: of Transcriptome clarifies mechanisms of lesion genesis versus progression in models of Ccm3 cerebral cavernous malformations
Additional file 5: of Transcriptome clarifies mechanisms of lesion genesis versus progression in models of Ccm3 cerebral cavernous malformations Open
Table S4. List of unique differentially expressed genes for all models according to the Venn diagram of the models (fold change |FC| ≥ 2.0; p < 0.05, false discovery rate corrected). (XLSX 745 kb)
View article: Additional file 9: of Transcriptome clarifies mechanisms of lesion genesis versus progression in models of Ccm3 cerebral cavernous malformations
Additional file 9: of Transcriptome clarifies mechanisms of lesion genesis versus progression in models of Ccm3 cerebral cavernous malformations Open
Table S8. List of 105 putative targets of mmu-miR-3472a within the differentially expressed genes common between acute and chronic in vivo neurovascular units. (XLSX 34 kb)