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The silence of the genes - Françoise Stutz’s team elaborates a new scenario to explain this natural biological phenomenon, endowed with immense therapeutic potential.
The DNA, guardian of our genetic patrimony, contains all necessary information (genes) to synthesize the different proteins of the organism.
It also possesses many sequences that do not code for any protein. This fraction of the genome, the major part of which has been considered for a long time as a genetic waste, comprises in fact essential elements to modulate gene expression.
It is within this context that Françoise Stutz, leader of project at the NCCR Frontiers in Genetics, has unveiled a hitherto unknown process used by the cell to silence some of its genes.
This resounding discovery has been published in the 16th November issue of Cell magazine.
• Details on UNIGE website (In French)
• Publication in Cell
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Stunning doublet - Ariel Ruiz i Altaba receives two prizes in one month for his research on a groundbreaking treatment against cancer.
The professor, leader of project at the NCCR Frontiers in Genetics, wins the top prize of the Swiss Bridge Award 2007.
The foundation awarded him in October 350’000 francs for his pioneer’s studies on the role of stem cells in tumour growth. His group has succeeded in blocking the development of human brain cancers transplanted in mice, by targeting the resident stem cells.
This is the first time a potential drug aims at inhibiting the multiplication of these cells, thought to play a key role in tumour growth and metastasis formation.
Ariel Ruiz i Altaba is currently developing a specific treatment for humans.
The Swiss Bridge Award will be used to detail the molecular mechanisms targeted by candidate therapies and involved in the regulation of cancer stem cell behaviour.
The creation of the scientists’ start-up Phistem will provide the frame for the development of this promising therapy.
By becoming one of the eight laureates of the Venture Kick Award, which comprises three stages, he just received encouraging signals for his project.
This private initiative backs up the implementation of innovative commercial ideas emerging from academic surroundings.
Ariel Ruiz i Altaba received the amount of 10’000 francs, which represents the first step. He is now taking place on the starting blocks for the next two races.
The winners will be awarded 20’000 and 100’000 francs, respectively.
• See Swiss Bridge website
• See Venture Kick website
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Telomeres - The tiny cellular biological clocks reveal new facets. These discoveries could lead to new therapeutic targets against cancer.
Introduction
Telomeres, small fragments of DNA named from the Greek telos (extremity) and meros (part), are located at the end of the chromosomes.
They namely act as “caps” by preventing DNA strands to aggregate with one another.
These genetic elements, which contain a predefined number of repeat sequences, also play the role of nanoscopic clocks.
Each time a cell divides, the telomeres loose part of their content until they become too short.
This in turn triggers a signal to stop the division process. Each cell has thus its own “quality control” label, with the length of the telomeres providing a use-by date.
Embryonic cells, however, are not submitted to this control, because they need to proliferate without being hampered.
This relative immortality is mainly due to the activity of telomerase, an enzyme capable of elongating the extremities of DNA strands.
Studies of Joachim Lingner’s group
Cancer cells, which are able to bypass proliferation control check points, also possess an active telomerase.
Yet little is known about the mechanisms involved in telomere elongation.
Joachim Lingner, leader of project at the NCCR Frontiers in Genetics, whose work was published in Science magazine in October, provides today a crucial piece of the puzzle, in human tumor cells.
His team has demonstrated that, in contrast to what was hitherto believed, telomeres are not “silent”.
Certain fragments are indeed transcribed into RNA molecules that integrate within the telomeric caps, probably in order to modulate their structure.
Another key discovery is the fact that telomeric RNA interacts with the telomerase.
There are several possibilities to explain this phenomenon. These molecules may control the activity of the enzyme.
The RNAs could also favor telomerase recruitment towards DNA extremities or, on the contrary, keep the enzyme apart from them.
If the ongoing studies reveal a link with the immortalization process, telomeric RNA could become a new therapeutic target to stop anarchic tumor proliferation.
• Publication in Science
Studies of David Shore’s group
In the majority of cells, chromosome ends undergo controlled erosion resulting from the competition between enzymes that elongate them and those that shorten them.
Thus, the tiny caps have to be continuously maintained in order to function with precision.
David Shore, leader of project at the NCCR Frontiers in Genetics, discovers new mechanisms involved in the functioning and protection of telomeres, in yeast.
In Genes & Development of February, his team disclosed that a protein named Rap1 associates specifically with long telomeres, in order to prevent their interaction with telomerase.
Moreover, Rap1 protects the mini caps from being targeted by other enzymes that, on the contrary, would shorten them drastically.
The telomeres are therefore able to degrade slowly, in a programmed fashion, while benefiting from maintenance adapted to each cell division.
Very short telomeres, however, are submitted to a specific treatment. The study published last March in Cell reveals that these chromosome extremities are tended to much earlier than the other ones during cell division.
They replicate precociously and the telomerase’s activity increases.
The scientist also points out that this derives from an epigenetic process (that is not provoked by genes): “It is the shortened telomere’s structure itself that sets in motion the replication mechanism and triggers enzyme activity”.
How is the length of the telomeres evaluated, at the level of the cell ? There is a group of proteins, named the telomeric complex, which seems to play the role of “molecular dimmer”.
The researcher’s group proposes a model describing how those different actors influence the recruitment of the telomerase, in the Genes & Development edition of June.
The identification of the forces involved in this fragile equilibrium should allow a better understanding of how the clockwork can break down and lead to tumor formation.
• Details on UNIGE website: February 2007 - April 2007 (In French)
• Publications: Genes & Development - Cell
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ENCODE - The UNIGE and UNIL, Swiss partners of ENCODE. The pilot project of encyclopedia for functional elements in the human genome releases its first results.
• Details on UNIGE website (In French)
• Publication in Nature
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Tumours - Group of Ariel Ruiz i Altaba, Project Leader Member of the NCCR, report that they have found a way of killing brain tumour cells that could eventually be applied to other types of incurable cancer.
The researchers at Geneva University Medical School say the results from tests on mice and in vitro are encouraging but caution that human trials have yet to start.
Speaking at a news conference in Geneva on Wednesday, January 24, Prof Ariel Ruiz i Altaba said he was “very confident” that a way had been found for stopping glioma, an aggressive form of brain tumour.
• Details on UNIGE website (In French)
• Publication in Current Biology
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