Prostate Cancer Update: New Gene

A genetic pattern (variation) found on human chromosome 8 has been found to have an association with a 5x risk increase for developing prostate cancer. It is thought to cause 2/3 of African-American cases and 1/3 of Caucasian-American cases of the disease.

Another biomarker might be coming! Pharmacogenomics companies: ready … go!

Full story at

New Pre-Cancer Biomarker Found

MIT scientists just discovered the function of 14-3-3 sigma protein, and also, what happens if it isn’t present in cells. This is a HUGE discovery toward preventative measures in cancer screening technology. It won’t be long before there are a new set of diagnostics out that screeen for a wide range of cancer precursor biomarkers that increase risk of cancer to a give tissue.

So, what do scientists propose that 14-3-3 sigma does? It plays a role in cell division. Specifically, it helps cells finish cytokinesis and separate into two distinct cells, right at the end of cell division. Michael Yaffe, an associate professor of biology and biological engineering and leader of the research team said “The cells try to divide and try to divide, and they just give up. They can’t finish cytokinesis.” This results in a single cell with two nuclei.

Key information not to be missed from the article:

  • Fused, or binucleate, cells have recently been shown to be precursors to cancer cells. They are often found in so-called “dysplastic” tissue, which consists of cells that are not fully normal but are not cancerous. Comparing tumors to weeds, Yaffe explained that those tissues act as fertile “soil” for tumor development. “Tumors grow in epithelial tissues that are already deranged for some reason, and something about that soil makes it better able to grow weeds.”
  • Loss of 14-3-3 sigma in dysplastic tissue could serve as a marker to help doctors predict whether tumors will develop. “Our hope is that it will be possible to monitor 14-3-3 expression in these ‘benign’ conditions, a subset of which may not be so benign,” said Yaffe.
  • The researchers were initially intrigued by the fact that 14-3-3 sigma is missing in normal tissue that surrounds tumors, which suggested that its function is lost very early in tumor development. Once the researchers started investigating the protein, they eventually unraveled a complex signaling pathway whose disruption leads to the failure of cell division.
  • They discovered that 14-3-3 sigma is most active during mitosis, when it helps control production of proteins necessary for division.
  • 14-3-3 sigma interacts with a translation factor known as eIF4B, whichforms part of an enzyme that allows mRNA to unwind so the ribosome can read its sequence.
  • When 14-3-3 sigma is knocked out, eIF4B is not produced, and mRNA for the protein p58 cannot be translated. p58 plays a critical role in the final splitting of one cell into two during mitosis, so when it is missing, the cells cannot fully divide.
  • When p58 function is restored, the cells resume normal division.

    The story was orginally issued by MIT, and covered by ScienceDaily under the title: MIT Identifies Role Of Key Protein In Tumor Growth