A5065400947- Cancer Genomics and Diagnostics
- Prostate Cancer Treatment and Research
- RNA Research and Splicing
- RNA modifications and cancer
- Circular RNAs in diseases
- Genetics, Bioinformatics, and Biomedical Research
- Renal and related cancers
- Tissue Engineering and Regenerative Medicine
- Genetic factors in colorectal cancer
- Genomics and Chromatin Dynamics
- RNA Interference and Gene Delivery
- CRISPR and Genetic Engineering
- Prostate Cancer Diagnosis and Treatment
- FOXO transcription factor regulation
- Molecular Biology Techniques and Applications
- Bioinformatics and Genomic Networks
- Advanced Proteomics Techniques and Applications
- Science, Research, and Medicine
- Mechanisms of cancer metastasis
- Renal cell carcinoma treatment
- Animal Genetics and Reproduction
- Cancer, Lipids, and Metabolism
- Cancer therapeutics and mechanisms
- Extracellular vesicles in disease
- Epigenetics and DNA Methylation
Princess Margaret Cancer Centre
2019-2024
University Health Network
2019-2024
University of Toronto
2019-2024
Ontario Institute for Cancer Research
2015
University of Washington
1984
Massachusetts Institute of Technology
1984
University of Zurich
1984
University of California, San Diego
1984
University of California, Davis
1984
Columbia University
1984
Abstract Prostate cancer is the second most commonly diagnosed malignancy among men worldwide. Recurrently mutated in primary and metastatic prostate tumors, FOXA1 encodes a pioneer transcription factor involved disease onset progression through both androgen receptor-dependent receptor-independent mechanisms. Despite its oncogenic properties however, regulation of expression remains unknown. Here, we identify set six cis -regulatory elements regulatory plexus harboring somatic...
Abstract Predicting and treating recurrence in intermediate-risk prostate cancer patients remains a challenge despite having identified genomic instability [1] hypoxia [2, 3] as risk factors. This underlies challenges assigning the functional impact of these factors to mechanisms promoting progression. Here we show chronic (CH), observed tumours [4], leads adoption an androgen-independent state cells. Specifically, CH results cells adopting transcriptional metabolic alterations typical...
Abstract Transposable elements hold regulatory functions that impact cell fate determination by controlling gene expression. However, little is known about the transcriptional machinery engaged at transposable in pluripotent and mature versus oncogenic states. Through positional analysis over repetitive DNA sequences of H3K27ac chromatin immunoprecipitation sequencing data from 32 normal states, we report pluripotent/stem state–specific “regulatory elements.” Pluripotent/stem are binding...
Abstract The impact of variations in the three-dimensional structure genome has been recognized, but solid cancer tissue studies are limited. Here, we performed integrated deep Hi-C sequencing with matched whole-genome sequencing, bisulfite 5-hydroxymethylcytosine (5hmC) and RNA across a cohort 80 biopsy samples from patients metastatic castration-resistant prostate cancer. Dramatic differences were present gene expression, 5-methylcytosine/5hmC methylation structural variation versus...
Prostate cancer is a heterogeneous disease whose progression linked to genome instability. However, the impact of this instability on noncoding and its three-dimensional organization aid unclear. Using primary benign tumor tissue, we find high concordance in higher-order organization. This argues for constraints topology prostate genomes. Nonetheless, identified changes focal chromatin interactions, typical loops bridging cis-regulatory elements, showed how structural variants can induce...
Whole-genome sequencing of primary breast tumors enabled the identification cancer driver genes and noncoding plexuses from somatic mutations. However, differentiating passenger events among genetic variants remains a challenge. Herein, we reveal cancer-driver cis-regulatory elements linked to transcription factors previously shown be involved in development luminal cancers by defining tumor-enriched catalogue approximately 100,000 unique 26 estrogen receptor (ER)+ progesterone (PR)+ tumors....
Abstract Prostate cancer is a heterogeneous disease whose progression linked to genome instability. However the impact of this instability on three-dimensional chromatin organization and how drives unclear. Using primary benign tumour tissue, we find high concordance in higher-order across normal prostate cells. This argues for constraints topology genomes. Nonetheless, identify changes focal interactions show structural variants can induce these guide cis -regulatory element hijacking. Such...
<div>Abstract<p>Prostate cancer is a heterogeneous disease whose progression linked to genome instability. However, the impact of this instability on noncoding and its three-dimensional organization aid unclear. Using primary benign tumor tissue, we find high concordance in higher-order organization. This argues for constraints topology prostate genomes. Nonetheless, identified changes focal chromatin interactions, typical loops bridging <i>cis</i>-regulatory...
<p>Supplementary Figures and descriptions for Supplementary Tables</p>
<p>Compartmentalization changes in tumours is not associated with widespread differential gene expression.</p>
<p>Characterization of chromatin interactions in benign and tumour tissue.</p>
<p>Assembly of structural variants involving enhancer-hijacking events.</p>
<p>Structural variant detection from Hi-C data.</p>
<p>Relationship between inter-chromosomal rearrangements and differential gene expression.</p>
<p>Sample processing and TAD similarity between samples.</p>