Tag Archives: Georgetown

Cancer gene link

A gene has been linked to at least three cancers in different tissues in the body, US researchers say.

Their findings, reported in the journal Science, showed a fifth of melanomas (skin cancer), Ewing’s sarcomas (bone) and glioblastomas (brain) had a defective copy of the gene STAG2.

It controls the way genetic material is divided between cells.

A cancer charity said the study provided researchers with new ways of tackling the disease.

Human genetic information is bound up in 23 pairs of chromosomes. When a cell divides in two, there should be 23 pairs in each of the two cells produced.

However, this does not always happen. Too many or too few chromosomes – known as aneuploidy – is common in cancer.

Cancer cells

Cancer cells

Researchers at the Georgetown University School of Medicine, Washington, have found a gene which controls that separation of genetic material.

Defective copies of STAG2 were found in 21% of Ewing’s sarcoma tumours, 19% of glioblastoma and 19% of melanoma.

Professor Todd Waldman said: “In the cancers we studied, mutations in STAG2 appear to be a first step in the transformation of a normal cell into a cancer cell.

“We are now looking at whether STAG2 might be mutated in breast, colon, lung, and other common human cancers.”


Researchers believe that if they can find a drug which targets cells with defective STAG2 they will be able to stop some cancers forming.

A separate study, also published in Science, looked at the affect of aneuploidy in yeast.

Researchers at the Massachusetts Institute of Technology created 13 strains of yeast with an extra chromosome. In all cases, the yeast’s genetic code become less stable and more susceptible to mutation.

The study’s authors suggest the “instability could facilitate the development of genetic alternations that drive malignant growth in cancer.”

Dr Julie Sharp, senior science information manager at Cancer Research UK, said: “Scientists have known for more than 100 years that having too many or too few chromosomes is linked to cancer and these results suggest that this is not just a characteristic but a cause of the disease.

“Their discovery sheds light on how chromosome numbers can be altered when cells divide and presents researchers with new ways to tackle cancer by designing drugs to upset this chain of events.”

Prostate cancer drug news

A new study has found that a drug developed to treat Ewing”s Sarcoma, a rare childhood cancer, may also help prevent human prostate cancer from spreading.

Researchers at Georgetown Lombardi Comprehensive Cancer Center have said that if the drug continues to work well – as they found in their lab- in further laboratory and pre-clinical studies, it may be the first prostate cancer drug specifically designed to stop cancer spread, or metastasis.

“This agent does not kill prostate cancer cells, but limits their ability to spread, which could be hugely beneficial in patients,” said the study”s lead investigator, Aykut Uren, an associate professor at Georgetown Lombardi.

The agent, YK-4 279, was designed in the GUMC Drug Discovery Program, directed by Milton Brown, a co-author on the paper.

prostate cancer

Prostate cancer

YK-4 279 is also being investigated for the treatment of Ewing”s sarcoma and is expected to move quickly into a clinical study.

Recent research has shown that 40 to 70 percent of prostate cancer cells express novel proteins when normal genes such as ETV1 and ERG break off from a chromosome and fuse in to a new location. These new genes produce proteins that push prostate cancer cells to become more aggressive and spread.


Noting that a similar fusion gene produces Ewing’s sarcoma, the researchers decided to check if their drug would work in prostate cancer cells.

They applied the agent to prostate cancer cells with chromosomal translocations that expressed either an ERG protein or an ETV1 protein and found that the YK-4 279 did inhibit functions of these proteins, which reduced their motility and invasiveness.

The finding was published online April 29 in PLoS ONE.