Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 4th International Congress on Epigenetics & Chromatin London, UK.

Day 3 :

Keynote Forum

Charles De Smet

De Duve Institute–University of Louvain, Belgium

Keynote: Transcriptional overlap links DNA hypo-methylation and hyper-methylation of contiguous promoters in cancer
OMICS International Epigenetics 2018 International Conference Keynote Speaker Charles De Smet photo

Charles De Smet is a Professor of Molecular Biology and Embryology at the School of Medicine and Biomedical Sciences of the University of Louvain, Belgium. He is
leading the Group of Epigenetics at the de Duve Institute in Brussels. His research has led to the demonstration, that DNA hypomethylation in tumors causes the aberrant
activation of a group of germline-specific genes, the so-called cancer-germline genes. Due to their highly restricted expression, these genes are being exploited as targets
of anti-cancer vaccinations.


DNA methylation is an epigenetic mark associated with gene repression. It is now well established that alterations in DNA
methylation patterns contribute to tumor development. Both gains (hyper-methylation) and losses (hypo-methylation) of
DNA methylation marks are frequently observed in tumors. The mechanisms underlying these two are opposite, yet co-existing,
alterations in tumors remain, however unclear. Our recent work reveals an unsuspected connection between DNA hypo- and hypermethylation
in tumors. We show indeed that DNA hypo-methylation in tumors can lead to the activation of long non-coding
transcripts that overlap downstream promoters and trigger their hyper-methylation. Promoters that have gone through this process
of hyper-methylation are characterized by an enrichment of H3K36me3, a histone mark known to be deposited during progression
of the transcription machinery and to attract DNMT3A/B DNA methyltransferases. Finally, we show that this process of inter
dependent epigenetic alteration contributes to the repression of a tumor suppressor gene, RERG, in non-small cell lung carcinomas.

Keynote Forum

Alvaro Macieira Coelho

French National Institute of Health, France

Keynote: The decline of the prevalence of cancers during organism senescence
OMICS International Epigenetics 2018 International Conference Keynote Speaker Alvaro Macieira Coelho photo

Dr. Alvaro Macieira-Coelho is a Research Director at the French National Institute of Health. He received an MD from the University of Lisbon, Portugal, and a PhD from the
University of Uppsala Sweden. He made an internship at the University Hospital in Lisbon and was a research associate at the Wistar Institute in Philadelphia (USA) and
at the Department of Cell Biology of the University of Uppsala (Sweden). He became Head of the Department of Cell Pathology at the Cancer Institute in Villejuif (France)
and was a visiting Professor at the University of Linkoping (Sweden). He published 150 papers in professional Journals and 9 books on cancer and aging. He received
the following awards: Fritz Verzar Prize (University of Vienna, Austria), “Seeds of Science” Career Prize (Lisbon, Portugal), Dr. Honoris Causa (University of Linkoping,
Sweden), Johananof International Visiting Professor (Institute Mario Negri, Milano, Italy).


In general the scientific literature reports that aging favors the development of cancers. Each type of cancer however, initiates and
evolves differently and their natural history can start way back at earlier ages before their clinical manifestations. The incidence
of cancers is spread through the human life span, it is the result of pre- and post-natal aggressions, individual susceptibility, and
developmental changes that evolve continuously from the beginning to the end. Finally during human senescence the incidence
declines for all cancers. Frequently the progression of cancers is also slower in the old. There are several possible explanations for
this decline at the tissue, cellular, and molecular levels. It is time to ask why some tumors are characteristic of the young, others of
maturity, others of the time of the decline of the reproductive period, and finally why the incidence of cancers declines late during
senescence of the human organism. These questions should be answered before the origin of cancers can be understood.