- Other groups
- Chromatin and Cell Fate
- Disease Genomics
- Epigenetic Mechanisms of Cancer and Cell Differentiation
- Cancer Genetics and Epigenetics
- Cancer and Iron
- ICO-IMPPC Joint Program - Genetic Diagnostics
- Genetic Variation and Cancer
- Genomics and Bioinformatics
- Regulatory Genomics
- ABO Histo-Blood Groups and Cancer
- Cancer Genome Biology
Our long-term goal is to understand how gene expression and genome packaging is affected by genetic and epigenetic changes that happen during evolution, development and in disease, in particular cancer. Our research approach is to computationally analyse global datasets in order to understand general mechanisms, test existing (but previously untested) ideas or propose novel hypotheses. We believe that this is a very complementary research approach to the traditional way of experimentally dissecting the parts of the cell.
In the past we have analysed data from yeast to human to understand why some genes are harmful when they are overexpressed. Increased gene dosage, as for example by gene amplification, is associated with diverse human pathologies, including cancer. We have also studied the origins and stability of genetic redundancy, the phenomenon whereby mutations in many genes have little effect on an organism. A better understanding of genetic redundancy, or buffering, may offer insight into how to target cancer cells where this redundancy is failing.
More recently we have shown that sequence composition determines the packaging of the human genome in the male germline. GC-rich sequences remain packaged in nucleosomes in the male gametes. This raises the possibility that at these GC-rich sites epigenetic information can be transmitted from one generation to the next. Understanding how and to what extent epigenetic information can be transmitted between generations is important because in the long term it may help us predict better disease risk in individuals.
We are currently studying how the promoter type of human genes affects their chromatin organization. We recently showed that genes with CpG-island promoters have distinct chromatin from genes with other types of promoter. Cancer cells often have very different epigenetic marks from normal cells. Our aim is to understand how global epigenetic changes, associated with cancer or induced by anti-cancer therapeutic drugs, affect the regulation of different types of human genes.
Previous Members of Lab:
Tanya Vavouri (email@example.com)
Office 1- 5 (first floor)
Tel: (+34) 93 554 3078
Castillo J, Amaral A, Azpiazu R, Vavouri T, Estanyol JM, Ballescà JL, Oliva R. Genomic and proteomic dissection and characterisation of the human sperm chromatin. Mol. Hum. Reprod. 2014 Sep;
Doglio L, Goode DK, Pelleri MC, Pauls S, Frabetti F, Shimeld SM, Vavouri T, Elgar G. Parallel evolution of chordate cis-regulatory code for development. PLoS Genet. 2013 Nov; 9(11): e1003904
Vavouri T, Lehner B. Human genes with CpG island promoters have a distinct transcription-associated chromatin organization. Genome Biol. 2012 Nov; 13(11): R110
Vavouri T, Lehner B. Chromatin organization in sperm may be the major functional consequence of base composition variation in the human genome. PLoS Genet. 2011 Apr; 7(4): e1002036
Vavouri T, Semple JI, Garcia-Verdugo R, Lehner B. Intrinsic protein disorder and interaction promiscuity are widely associated with dosage sensitivity. Cell 2009 Jul; 138(1): 198-208
Vavouri T, Lehner B. Conserved noncoding elements and the evolution of animal body plans. Bioessays 2009 Jul; 31(7): 727-35
Vavouri T, Semple JI, Lehner B. Widespread conservation of genetic redundancy during a billion years of eukaryotic evolution. Trends Genet. 2008 Oct; 24(10): 485-8
Vavouri T, Walter K, Gilks WR, Lehner B, Elgar G. Parallel evolution of conserved non-coding elements that target a common set of developmental regulatory genes from worms to humans. Genome Biol. 2007; 8(2): R15
Vavouri T, McEwen GK, Woolfe A, Gilks WR, Elgar G. Defining a genomic radius for long-range enhancer action: duplicated conserved non-coding elements hold the key. Trends Genet. 2006 Jan; 22(1): 5-10