In a study recently published in Molecular Cell, two molecular biologists at Tufts have used yeast artificial chromosomes to show that there is a highly flexible DNA sequence that increases fragility and stalls replication, causing the chromosome to break. The site that is prone to breaking lies in the middle of a tumor suppressor gene and breakage is highly associated with cancer.

According to Catherine Freudenreich, lead author on the study, "If you delete that gene or delete part of that gene so it doesn't work anymore, that can lead to tumors. The fact that there is fragility in the same region that this gene is located is a bad coincidence."

Being susceptible to a particularly aggressive form of prostate cancer could be in your genes, according to this. Scientists have identified a genetic marker called 8q24 that ups your chances of getting prostate cancer or having a family member that will by a significant amount. The presence of the marker can be determined by a blood test, and those with it will have to ensure they're more careful about getting screened for cancer. Furthermore, African American men are more likely to be carriers than those of European ancestry.

I've had several family members who've been diagnosed with prostate cancer, and it's scary stuff, boys! Get yourself checked out for the sake of yourself and your loved ones.

Childhood acute lymphoblastic leukemia (ALL) is being studied in a way to examine the chromosomes present in the diseased cells. Extra numbers of specific chromosomes are present and can arise according to a predictable pattern.

What does this mean? Our chromosomes carry the genes in all cells, which normally have 46 chromosomes. The ALL cells that are being studied can have more than 80 chromosomes.

This could help to understand what early events can cause this type of leukemia. The researchers also want to understand why children with ALL that have 51 or more chromosomes generally respond better to treatment than those with 50 or fewer chromosomes.

One of the authors of the study, Nyla A. Heerema, professor of pathology, states "The fact that an excess of certain chromosomes is associated with the particular overall number of chromosomes tells us that something significant happens when that first abnormal cell divides and initiates the disease"

Researchers are trying to figure out why these certain patterns occur and whether it can help guide decisions about therapy.

One or more extra or missing chromosomes can both fuel tumor growth and act to suppress tumor growth, according to University of California, San Diego (UCSD) School of Medicine researchers.

Heralded as a discovery that solves a 100-year-old genetic puzzle because the hypothesis was first suggested by German biologist Theodor Bover that long ago, researchers sought to determine if the wrong number of chromosomes contributed to tumor growth, or was a consequences of damage in cancerous cells.

While studying aneuploidy -- which is what the occurrence of one or more extra or missing chromosomes is called -- in mouse models, the researchers found that the same genetic mechanism that promotes tumor growth can slow tumor growth.

"This study opens up a whole series of potential therapeutic targets for cancer," said Beth A.A. Weaver, of the Ludwig Institute for Cancer Research and UCSD Department of Cellular and Molecular Medicine, the study's first author. "By increasing the level of genetic damage, we can kill tumor cells."