Our group aims at addressing the following questions:
- Adjust methodology for studying genetic and epigenetic changes in cancer
- Determine the role of epigenetic remodeling in oncogenic transformation for tumors with recurrent copy number changes
- Investigate the consequences of somatic genomic alterations on the epigenetic landscape in cancer.
We are currently interested in understanding the oncogenic processes related to two cancer types: neuroblastoma and adrenocortical carcinoma.
Our methodological research is centered on data integration and the development of high throughput data analysis methods to study regulation in cancer with a special focus on epigenetic regulation.
Methods we are specialists in include:
- ChIP-seq data analysis: transcription factors, histone modifications in normal and cancer cells
- Analysis of whole genome / whole exome / target sequencing data: detection of copy number alterations and structural variants
- Analysis of cancer RNA-seq: detection of abnormal transcripts expressed in cancer cells
The team is a laureate of ATIP-Avenir Young group leader Program 2016.
Official Lab openning: January, 2016
- HMCan-diff: a method to detect changes in histone modifications in cells with different genetic characteristics. Ashoor H, Louis-Brennetot C, Janoueix-Lerosey I, Bajic VB, Boeva V.
Nucleic Acids Res. 2017 Jan 3.[Epub ahead of print]
- SV-Bay: structural variant detection in cancer genomes using a Bayesian approach with correction for GC-content and read mappability. D. Iakovishina, I. Janoueix-Lerosey, E. Barillot, M. Regnier and V. Boeva. Bioinformatics. 2016. 32 (7): 984-92
- RNF: a general framework to evaluate NGS read mappers. K. Brinda, V. Boeva, and G. Kucherov. Bioinformatics. 2016. 32(1):136-9.
- HMCan: a method for detecting chromatin modifications in cancer samples using ChIP-seq data. H. Ashoor, A. Hérault, A. Kamoun, F. Radvanyi, V.B. Bajic, E. Barillot and V. Boeva. Bioinformatics, 2013, 29 (23): 2979-2986.
PI's Postdoctoral & graduate work :
- Analysis of genomic sequence motifs for deciphering transcription factor binding and transcriptional regulation in eukaryotic cells. V. Boeva. Frontiers in Genetics. 2016 7:24
- Chimeric oncogene regulates the EGR2 sarcoma susceptibility gene via a GGAA-microsatellite. T.G.P. Grünewald, V. Bernard, P. Gilardi-Hebenstreit, V. Raynal, D. Surdez, M.-M. Aynaud, O. Mirabeau, F. Cidre-Aranaz, F. Tirode, S. Zaidi, G. Perot, A.H. Jonker, C. Lucchesi, M.-C. Le Deley, O. Oberlin, P. Marec-Bérard, A.S. Véron, S. Reynaud, E. Lapouble, V. Boeva, T. Rio Frio, J. Alonso, S. Bhatia, G. Pierron, G. Cancel-Tassin, O. Cussenot, D.G. Cox, L.M. Morton, M.J. Machiela, S.J.Chanock, P. Charnay and O. Delattre. Nature Genetics. 2015 Sep;47(9):1073-8.
- Jarid2 is implicated in the initial Xist-induced targeting of PRC2 to the inactive X chromosome. S.T. da Rocha, V. Boeva, M. Escamilla-Del-Arenal, K. Ancelin, C. Granier, N. Reis Matias, S. Sanulli, J. Chow, E. Schulz, C. Picard, S. Kaneko, K. Helin, D. Reinberg, A. F. Stewart, A. Wutz, R. Margueron and E. Heard. Molecular Cell, 2014, 53 (2): 301-316.