Advancement in Understanding Aging and Cancer Relationship

Evidence has long shown that the likelihood of a person to succomb to any of the various types of cancers increases with age.  Scientists around the world spend countless hours hovering over powerful microscopes in hopes of furthering their understanding between this link.  Occasionally, their willful persistance pays off and invaluable headway toward further understanding and eventual solution is made.   

Scientists at the Institute for Biological Studies in Jolla, California, recently made newsworthy progress while studying the chromosomes of cells in patients with Werner Syndrome, a heritable premature aging disease.  In this study, a technique called FISH-ing (chromosome painting) was used, allowing the 46 chromosomes in cells taken from a Werner Syndrome patient, to be more easily isolated and thereby documented.

Jan Karlseder, Ph.D., the leader in this research, stated that, “Cancer is almost always related to chromosomal instability.”  What Karlseder and the team of assisting researchers found in this study is that by rebuilding structures called telomeres, the genetic damage that was seen in these Werner Syndrome patient’s cells could be significantly blocked.

Telomeres are the long end sequence of a DNA strand which occur at the tip of chromosomes.  According to an Answers.com definition, “A telomere is a region of highly repetitive DNA at the end of a linear chromosome that functions as a disposable buffer.”  Without telomeres, genetic information would be lost as chromosomes are replicated.

In this new study, researchers at the Salk Institute teamed up with their colleagues at the Institute of Human Genetics in Heidelberg, Germany, and grew cells from Werner Syndrome patients.  Using the FISH-ing technique, breakage or fusion of chromosomes characteristic of damaged DNA could then easily be seen under the microscope.

These cells were supplied with either a functional copy of the WRN gene, which is nonfunctional in Werner Syndrome, or a gene encoding telomerase, which is a protein that elongates short or missing telomeres.  After the cells divided several times, they were then observed for damage associated with aging and cancer.

Those cells that were supplied with the functional WRN gene predictably showed decreased DNA damage.  Most interesting was the finding that those cells receiving telomerase showed the suppression of the accumulation of mutations and showed an elongating of the short telomeres seen in the Werner Syndrome cells.” 

Though this research is exciting, further studies are needed and will certainly follow.  Karlseder is optimistic about the result of the study and goes on to say, “I predict that cancer in older people has precisely the same basis as that seen in Werner Syndrome patients.”

Others involved in this study were graduate student Colleen Naeger in Jolla, and Anna Jauch, Ph.D., and Heidi Holgreve-Grez, Ph.D, in Heidelberg.