Aller au contenu principal
En cours de chargement...

Fil d'Ariane

Accueil / Publications Canadiennes /

Voici une liste de publications scientifiques évaluées par les pairs sur l'épigénétique et l'épigénomique dont le premier auteur ou le chercheur principal est canadien. Manque-t-il une publication canadienne sur l'épigénétique dans cette liste ? Vous êtes un scientifique canadien et vous aimeriez que vos travaux sur l'épigénétique soient présentés sur notre site web ou mis en valeur dans un article de fond? Envoyez la citation à info@epigenomes.ca.

Science, 2022

Authors:
Yanchus, C., Drucker, K.L., et. al.
Publication Abstract:

Establishing causal links between inherited polymorphisms and cancer risk is challenging. Here, we focus on the single-nucleotide polymorphism rs55705857, which confers a sixfold greater risk of isocitrate dehydrogenase (IDH)–mutant low-grade glioma (LGG). We reveal that rs55705857 itself is the causal variant and is associated with molecular pathways that drive LGG. Mechanistically, we show that rs55705857 resides within a brain-specific enhancer, where the risk allele disrupts OCT2/4 binding, allowing increased interaction with the Myc promoter and increased Myc expression.

Cancer Discovery, 2022

Authors:
Langille, E., Al-Zahrani, K.N., et. al.
Publication Abstract:

Systematically investigating the scores of genes mutated in cancer and discerning disease drivers from inconsequential bystanders is a prerequisite for Precision Medicine but remains challenging. Here, we developed a somatic CRISPR/Cas9 mutagenesis screen to study 215 recurrent ‘long-tail’ breast cancer genes, which revealed epigenetic regulation as a major tumor suppressive mechanism.

Leukemia, 2022

Authors:
Héléna Boutzen, Seyed Ali Madani Tonekaboni, Michelle Chan-Seng-Yue, Alex Murison, Naoya Takayama, Nathan Mbong, Elvin Wagenblast, Elias Orouji, Andrea Arruda, Amanda Mitchell, Faiyaz Notta, Mark Minden, Mathieu Lupien, Kerstin Kaufmann & John Di
Publication Abstract:

Many cancers are organized as cellular hierarchies sustained by cancer stem cells (CSC), whose eradication is crucial for achieving long-term remission. Difficulties to isolate and undertake in vitro and in vivo experimental studies of rare CSC under conditions that preserve their original properties currently constitute a bottleneck for identifying molecular mechanisms involving coding and non-coding genomic regions that govern stemness.

eLife, 2022

Authors:
Ramirez, M., Badayeva, Y., Yeung, J., Wu, J., Abdalla-Wyse, A., Yang, E., Trost, B., Scherer, S.W., Goldowitz, D.
Publication Abstract:

We have identified active enhancers in the mouse cerebellum at embryonic and postnatal stages which provides a view of novel enhancers active during cerebellar development. The majority of cerebellar enhancers have dynamic activity between embryonic and postnatal development. Cerebellar enhancers were enriched for neural transcription factor binding sites with temporally specific expression. Putative gene targets displayed spatially restricted expression patterns, indicating cell-type specific expression regulation.

Genome Biol., 2022

Authors:
Mehran Karimzadeh & Michael M. Hoffman
Publication Abstract:

Existing methods for computational prediction of transcription factor (TF) binding sites evaluate genomic regions with similarity to known TF sequence preferences. Most TF binding sites, however, do not resemble known TF sequence motifs, and many TFs are not sequence-specific. We developed Virtual ChIP-seq, which predicts binding of individual TFs in new cell types, integrating learned associations with gene expression and binding, TF binding sites from other cell types, and chromatin accessibility data in the new cell type.

Proc Natl Acad Sci U S A., 2022

Authors:
Lebeau B, Jangal M, Zhao T, Wong CK, Wong N, Cañedo EC, Hébert S, Aguilar-Mahecha A, Chabot C, Buchanan M, Catterall R, McCaffrey L, Deblois G, Kleinman C, Park M, Basik M, Witcher M.
Publication Abstract:

The contribution of deregulated chromatin architecture, including topologically associated domains (TADs), to cancer progression remains ambiguous. CCCTC-binding factor (CTCF) is a central regulator of higher-order chromatin structure that undergoes copy number loss in over half of all breast cancers, but the impact of this defect on epigenetic programming and chromatin architecture remains unclear. We find that under physiological conditions, CTCF organizes subTADs to limit the expression of oncogenic pathways, including phosphatidylinositol 3-kinase (PI3K) and cell adhesion networks.

Cell Reports Methods, 2022

Authors:
Samantha L. Wilson, Shu Yi Shen, Lauren Harmon, Justin M. Burgener, Tim Triche Jr., Scott V. Bratman, Daniel D. De Carvalho, Michael M. Hoffman
Publication Abstract:

Cell-free methylated DNA immunoprecipitation sequencing (cfMeDIP-seq) identifies genomic regions with DNA methylation, using a protocol adapted to work with low-input DNA samples and with cell-free DNA (cfDNA). We developed a set of synthetic spike-in DNA controls for cfMeDIP-seq to provide a simple and inexpensive reference for quantitative normalization.

, 2022

Authors:
Shalini Bahl, Jason S Carroll, Mathieu Lupien
Publication Abstract:

Breast cancer presents as multiple distinct disease entities. Each tumor harbors diverse cell populations defining a phenotypic heterogeneity that impinges on our ability to treat patients. To date, efforts mainly focused on genetic variants to find drivers of inter- and intratumor phenotypic heterogeneity. However, these efforts have failed to fully capture the genetic basis of breast cancer. Through recent technological and analytical approaches, the genetic basis of phenotypes can now be decoded by characterizing chromatin variants.

, 2022

Authors:
Anne-Sophie Pépin, Patrycja A. Jazwiec, Vanessa Dumeaux, Deborah M. Sloboda, Sarah Kimmins
Publication Abstract:

Paternal obesity has been implicated in adult-onset metabolic disease in offspring. However, the molecular mechanisms driving these paternal effects and the developmental processes involved remain poorly understood. One underexplored possibility is the role of paternally driven gene expression in placenta function. To address this, we investigated paternal high-fat diet-induced obesity in relation to sperm epigenetic signatures, the placenta transcriptome and cellular composition. C57BL6/J males were fed either a control or high-fat diet for 10 weeks beginning at 6 weeks of age.

, 2022

Authors:
Kiran Nakka, Sarah Hachmer, Zeinab Mokhtari, Radmila Kovac, Hina Bandukwala, Clara Bernard, Yuefeng Li, Guojia Xie, Chengyu Liu, Magid Fallahi, Lynn A Megeney, Julien Gondin, Bénédicte Chazaud, Marjorie Brand, Xiaohui Zha, Kai Ge, F Jeffrey Dilworth
Publication Abstract:

Muscle stem cells (MuSCs) reside in a specialized niche that ensures their regenerative capacity. Although we know that innate immune cells infiltrate the niche in response to injury, it remains unclear how MuSCs adapt to this altered environment for initiating repair. Here, we demonstrate that inflammatory cytokine signaling from the regenerative niche impairs the ability of quiescent MuSCs to reenter the cell cycle.