Group items tagged

In the study, published Monday (May 1) in Nature Biotechnology,  Luo and colleagues set their sights on two fusions genes they had previously found to be associated with prostate cancer and various forms of rapid and invasive cancer, including liver tumors. Using a modified CRISPR-Cas9 tool that creates a single- rather than double-stranded break in DNA, they targeted the chromosomal breakpoints that form these fusion genes and replaced fusion DNA with a gene encoding the enzyme HSV1-tk. This enzyme effectively kills tumor cells by converting the drug ganciclovir into its active form, which then blocks DNA synthesis and leads to cell death. (Ganciclovir is used to treat cytomegalovirus in humans.)

New immune system-boosting cancer drugs have in clinical trials saved the lives of many people with seemingly untreatable melanoma or lung cancer, but the drugs seem useless against colon cancer. One exception-a man with colon cancer whose metastatic tumors vanished for several years after he was treated in 2007-piqued researchers' interest. They suspected his recovery might have to do with the large number of mutations in his tumors. Now, a small clinical trial suggests that even cancer patients with types of tumors that were thought to be impervious to the new drugs could benefit if those malignancies have the right error-riddled DNA signature, a result that could help 3% to 4% of cancer patients.

Panobinostat is a new type of drug that works by blocking an enzyme responsible for modifying DNA at the epigenetic level. Epigenetics refers to chemical marks on DNA itself or on the protein "spools" called histones that package DNA. These marks influence the activity of genes without changing the underlying sequence, essentially acting as volume knobs for genes. Earlier genomic studies showed that about 80 percent of DIPG tumors carry a mutation that alters a histone protein, resulting in changes to the way DNA is packaged and tagged with those chemical marks. This faulty epigenetic regulation results in activation of growth-promoting genes that should have been turned off, and shutdown of others that should have acted as brakes to cell multiplication. Cancer is the result. Panobinostat appears to work by restoring proper functioning of the cells' chemical tagging system.

In this activity, we will work with the two groups of genes that control the cell cycle, proto-oncogenes and tumor suppressor genes. We will also add a new group of genes that are in charge of the maintenance of our DNA, the DNA repair system.

Vanderbilt-Ingram Cancer Center has become the first cancer center in the Southeast and one of the first in the nation to offer adult cancer patients routine "genotyping" of their tumors at the DNA level.

This 8-minute video is derived from the 2013 Holiday Lectures on Science. In it, Dr. Charles Sawyers explains the difference between proto-oncogenes, oncogenes, and tumor suppressor genes, and how mutations in these genes drive cancer development. "Cancer genes" can affect several cellular processes that he groups into three categories: cell growth and survival (i.e., genes involved in the cell cycle, cell fate (i.e., genes involved in cell differentiation), and genome maintenance (i.e, genes involved in DNA repair.)

In this video Paul Andersen answers the very simple question: What is cancer? He explains how damage to the DNA can create uncontrolled cell growth. He explains how malignant tumors can spread the disease throughout the body and gives possible treatments.

The idea of a general, quick and simple blood test for a diverse range of cancers just came closer to reality with news of a new study published in Nature Medicine.

One of these days, there could well be a simple blood test that can help diagnose and track cancers. We aren't there yet, but a burst of research in this area shows we are getting a lot closer.