Arturo Falaschi Conference Series 2016: At the intersection of DNA Replication and Genome Maintenance


The international meeting “At the Intersection of DNA Replication and Genome Maintenance: from Mechanisms to Therapy” is part of the “Arturo Falaschi Conference Series” organized by the International Centre for Genetic Engineering and Biotechnology to honor the memory of the late Professor Arturo Falaschi.

The Conference will be held from 27 June to 1 July 2016 at the historical “Stazione Marittima” Congress Centre in Trieste, Italy and will bring together world leaders working in the fields of DNA damage and replication to achieve a full understanding of how these mechanisms impact upon cancer and aging.

Our genome is under constant attack 
by agents that arise from our normal metabolic activities as well as from exposure to environmental factors. DNA lesions can occur as often as 100,000 times per cell per day. Scientists are still discovering additional causes of replication stress and the pathways that the cellular replication machinery uses to respond to the enormous load of DNA damages. The meeting will represent a unique forum to learn how our cells faithfully replicate our genome and cope with DNA lesions.

An outstanding and diverse group of invited speakers will discuss recent discoveries on the strategies cells use when they face DNA damage and replication stress. Plenary sessions will include selected oral communications and poster presentations by meeting participants to foster opportunities for interaction. The organizing committee comprises Alessandro Vindigni, Saint Louis University, Saint Louis MO, USA, Massimo Lopes, University of Zurich, Switzerland, and Johannes Walter, Harvard Medical School, Boston MA, USA. 

Maintaining the stability and
 the correct sequence composition
 of the three million bases that
 form our genome is critical for a correct transmission of genomic information. Our genome is under constant attack 
by agents that arise from our normal metabolic activities, like free radicals, as well as from exposure to environmental factors such as UV radiation, X-rays and chemical compounds. DNA lesions can occur as often as 100,000 times per cell per day. Our cells have evolved several tactics that can help them overcome DNA lesions or other obstacles during replication in order to ensure faithful transmission of their genetic information. These tactics all give cells a chance to fix the obstacles in their paths and avoid passing along genetic mistakes to their daughter cells. If these tactics fail to work, aberrant DNA replication and improper repair of DNA lesions can lead to mutations, abnormal chromosome structures, or loss of genetic information that in turn can cause premature aging, cancer and genetic abnormalities. This is why understanding the molecular pathways that help maintain genome stability is integral to the diagnosis and treatment of several human diseases.

Understanding more about how cells react to replication stress is key to designing future therapies, particularly for cancer. While it is beneficial for healthy cells to fix these DNA roadblocks, researchers are also considering the flip side of the coin when it comes to cancer cells, which use these same mechanisms to survive DNA-damaging chemotherapy. Many chemotherapeutic agents act by creating DNA damages and perturbing DNA replication in actively proliferating cancer cells. The problem is that cancer cells have these same mechanisms that our healthy cells have to repair these damages. Researchers will discuss recent discoveries about drugs that specifically block these mechanisms in cancer cells, thereby sensitizing cancer cells to chemotherapeutics that are already in use and improving their potency.



Further reading:

Link to the Meeting Website

Link to the Meeting Programme

Link to Arturo Falaschi


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