A single gene that promotes initial development of the most common form of lung cancer and its lethal metastases has been identified by researchers at Mayo Clinic in Florida. Their study suggests other forms of cancer may also be driven by this gene, matrix metalloproteinase-10 (MMP-10). The study, published in the journal PLoS ONE, shows that MMP-10 is a growth factor secreted and then used by cancer stem-like cells to keep themselves vital. These cells then drive lung cancer and its spread, and are notoriously immune to conventional treatment. The findings raise hope for a possible treatment for non-small cell lung cancer, the leading cause of U.S. cancer deaths. Researchers discovered that by shutting down MMP-10, lung cancer stem cells lose their ability to develop tumors. When the gene is given back to the cells, they can form tumors again.
The development of more effective cancer drugs could be a step nearer thanks to the discovery, by scientists at Warwick Medical School, of how an inbuilt 'security check' operates to guarantee cells divide with the correct number of chromosomes. Most cells in our bodies contain 23 pairs of chromosomes that encode our individual genetic identities. The process of chromosome segregation is monitored by a system called the spindle checkpoint that ensures daughter cells receive the correct number of chromosomes. If daughter cells receive an unequal number of chromosomes, known as 'aneuploidy', this drives normal cells to become cancerous. Indeed, the cells of aggressive human tumours are frequently 'aneuploid' with many components of the spindle checkpoint being mutated or mis-expressed. Therefore, determining how the spindle checkpoint operates is vital to understanding what causes, and what can prevent, the formation of tumours.
The most commonly diagnosed cancer amongst women is breast cancer. There are various types of breast cancers, for instance, HER2-positive cancer in which the tumor's cells produce excess quantities of HER2, a particular protein called the human epidermal growth factor, whilst those with normal production are called HER2-negative. According to a systematic review in The Cochrane Library, women with HER2-positive breast cancer have a substantially higher chance of prolonging life and reducing the risk of cancer recurrence after completion of therapy if they add trastuzumab ( Herceptin ) to their standard treatment. Trastuzumab is a new-generation antibody based medicine that inhibits the receptor and stops it from initiating excessive cell growth, which causes tumors. About one-fifth of women with early breast cancer have HER2-positive tumors, which are linked to a worse outlook than HER2-negative tumors if left untreated.
Dramatic Gene Variation Between Patients With The Same Disease Has Implications For Personalized Medicine
Researchers at the Hebrew University of Jerusalem and other institutions have identified two distinguishable groups of genes: those that produce very abundant biochemical products in the cell and function properly in the majority of biological processes, and a flexible subset that might have abnormal function in a disease. They demonstrated that these two groups can be found among various organisms and cell types, including stem cells and cancer cells. One set of genes is a robust network that conducts the basic functions of all cells, such as producing energy and biochemical building blocks. This group represents the "hard core" of different organisms. The biochemical products produced by the other group of genes are less abundant in organisms, and their amount might vary significantly between different types of normal and diseased cells and even between different cancer cells derived from patients with the same type of cancer.
New research confirms an association between smoking and a reduced risk for a rare benign tumor near the brain, but the addition of smokeless tobacco to the analysis suggests nicotine is not the protective substance. The study using Swedish data suggests that men who currently smoke are almost 60 percent less likely than people who have never smoked to develop this tumor, called an acoustic neuroma. But men in the study who used snuff, which produces roughly the same amount of nicotine in the blood as smoking, had no reduced risk of tumor development. "We see this effect with current smokers but don't see it with current snuff users, so we think that maybe the protective effect has something to do with the combustion process or one of the other chemicals in cigarettes that are not in snuff, " said Sadie Palmisano, a doctoral student in epidemiology at Ohio State University and lead author of the study.