New insight into genomic alterations associated with telomere maintenance mechanisms in cancer

To gain an infinite lifespan, cancer cells need to maintain the ends of their chromosomes, known as telomeres. They achieve this in various different ways. Scientists from the German Cancer Research Center systematically investigated more than 2,500 tumor genomes of 36 types of cancer to find out how these mechanisms are manifest in changes in the DNA. Active lengthening of the telomeres is one of the hallmarks of all cancer cells and hence an important focus in developing targeted treatments. The study is part of the Pan-Cancer Analysis of Whole Genomes (PCAWG).

Healthy body cells have a natural expiry date defined by the length of their telomeres. Telomeres are part of DNA and protect the end of the chromosomes. They become shorter each time the cell divides, however, until a minimum length is reached - the telomere has then been used up so to speak. Stem cells are the only type of cells to produce the 'immortality enzyme' telomerase, which can lengthen the telomeres again. All other cells stop dividing after around 50 cycles.

Cancer cells depend on intact telomeres for unlimited cell division. Earlier studies showed that around 85 percent of all tumors upregulate telomerase via different mechanisms. The remaining tumors use alternative mechanisms to lengthen telomeres.

A team of researchers led by Lars Feuerbach from the German Cancer Research Center (DKFZ) studied more than 2,500 tumor samples to gain a better understanding of these mechanisms, in particular those that have not been well researched to date. The study is part of the Pan-Cancer Analysis of Whole Genomes (PCAWG).

The PCAWG researchers found DNA mutations that point to one of the two known mechanisms of telomere lengthening in only 13 percent of the cases studied. As lead author Lina Sieverling explained:

    In the vast majority of the 2,500 cancer cases studied, we observed increased activity of the telomerase gene but without any changes in the genome that could explain this. Epigenetic factors that do not leave any trace in the genome might be partly responsible here."

Of the 13 percent of those tumors whose DNA showed indications of telomere lengthening, only 64 cases pointed to the alternative mechanisms. The researchers discovered two peculiarities in these tumors: Telomeres usually consist of hundreds of repetitions of the same sequence of six DNA bases. In the telomeres with alternative lengthening mechanisms, however, variations of the normal telomere sequences are often found. Moreover, small fragments of the telomeres are very often integrated into other parts of the genome in these tumor cells.

In certain types of cancer, particularly in children, one of the factors that determine the aggressiveness of the tumor is known to be the mechanism by which the telomeres of the cancer cells are lengthened. This is the case in medulloblastomas, for example, which carry a worse prognosis if the cancer cells use the alternative mechanism.

"At the moment, we cannot tell whether and, if so, in what way these two findings are important or whether they affect the course of disease in cancer patients," principal investigator Lars Feuerbach explained. "Active lengthening of the telomeres is one of the weak points in all cancer cells and hence an important focus in developing targeted treatments," he added. "To do so, a precise knowledge of all the underlying molecular processes is vital."

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Exposure To Air Pollution Before Birth Could Be Affecting The DNA Of Newborn Babies

Air pollution is responsible for 5.5 million of the 9 million deaths caused by pollution every year, making it the main cause of death by pollution in the world. Now, researchers have begun to understand the terrible effects air pollution is having on babies exposed to it in the womb.

The latest research,  looked at the DNA in umbilical cord blood from newborn babies born in a country, before and after a coal-burning power plant was closed in 2004. Several findings suggest that the pollution has affected the children’s DNA.

The team observed that babies born before the plant was shut down had shorter telomeres than those born afterward. Telomeres are a specialized section of DNA that allows chromosomes to be copied faithfully. After each copy, during cell division, the telomeres get shorter. Eventually, the shortened telomeres lead the copies to be less faithful and this has been linked to aging, cancer, heart disease, cognitive decline, and even premature death.   

The team confirmed that the shorter telomeres observed in those born before the coal plant shut down are associated with the presences of polycyclic aromatic hydrocarbons, a toxic component of air pollution from coal plants, and that they also led to a lower level of brain-derived neurotrophic factor, a protein involved in neuronal growth.

"An individual's telomere length at birth is known to influence their risk for disease decades later during adulthood," co-author said in a statement. However, "Further follow-up is needed to assess the role telomere length plays in health outcomes in the context of early life exposure to air pollution."

Out of the 255 children tested at birth in the study (half born before, and half after the shutdown), 210 were tested again at age 2 to check if the telomeres length was associated with neurodevelopment issues. They did not find any link, though this doesn’t exclude telomere length-associated development issues at a later age.

"The new study adds to the evidence that closing this coal-burning power plant was beneficial to the health and future well-being of newborns there," said lead author. "Moreover, we know that lowering exposure to air pollution anywhere will be beneficial to children's health and long-term potential."

The role of coal power plants in producing toxic fumes is undeniable and it is important to tackle this environmental danger to safeguard our health and the health of future generations.

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Ageing reversed in old human cells

In a breakthrough, scientists have discovered a way to rejuvenate old human cells, not only making them look physically younger, but also coaxing them to behave like young cells and start dividing.
Researchers  worked with senescent cells, which have stopped dividing. 

Within hours of treatment the older cells started to divide, and had longer telomeres - the caps on the chromosomes which shorten as we age. 

This discovery builds on earlier findings which showed that a class of genes called splicing factors are progressively switched off as we age. 

Researchers found that splicing factors can be switched back on with chemicals, making senescent cells not only look physically younger, but start to behave more like young cells and start dividing. 

They applied compounds called reversatrol analogues, chemicals based on a substance naturally found in red wine, dark chocolate, red grapes and blueberries, to cells in culture. 

The chemicals caused splicing factors, which are progressively switched off as we age to be switched back on. 

Within hours, the cells looked younger and started to rejuvenate, behaving like young cells and dividing.

The research, has the potential to lead to therapies which could help people age better, without experiencing some of the degenerative effects of getting old. 

Most people by the age of 85 have experienced some kind of chronic illness, and as people get older they are more prone to stroke, heart disease and cancer. 

"This is a first step in trying to make people live normal lifespans, but with health for their entire life. Our data suggests that using chemicals to switch back on the major class of genes that are switched off as we age might provide a means to restore function to old cells," said a professor.

"This demonstrates that when you treat old cells with molecules that restore the levels of the splicing factors, the cells regain some features of youth," Prof. said. 

"They are able to grow, and their telomeres - the caps on the ends of the chromosomes that shorten as we age - are now longer, as they are in young cells," she said.

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