As cancer researchers continue to identify genetic mutations driving different cancer subtypes, they are also creating a catalog of possible targets for new treatments. The University of Michigan Comprehensive Cancer Center and Michigan Center for Translational Pathology (MCTP) recently completed a pilot study aimed at solving the practical challenges involved in quickly and systematically sequencing genetic material from patients with advanced or treatment-resistant cancer in order to match them with existing clinical trials based on the biomarkers identified. "We're talking about more than just examining a few genes where mutations are known to occur, or even about a hundred genes, " says co-lead investigator Dan Robinson, Ph.D., a post-doctoral fellow at MCTP. "We're talking about the ability to sequence more than 20, 000 genes and look not just for individual genetic mutations, but at combinations of mutations.
Combination treatment with everolimus, an inhibitor of the mammalian target rapamycin (mTOR), and octreotide has shown to improve progression-free survival for patients with advanced neuroendocrine tumors and a history of carcinoid syndrome, according to researchers at The University of Texas MD Anderson Cancer Center. Results of the international, randomized, placebo-controlled Phase III study were published in the journal Lancet. The treatment combination of everolimus and octreotide long-acting repeatable (LAR), a somatostatin analogue that has shown antitumor activity, led to a clinically meaningful five-month delay in tumor growth, compared to octreotide alone. Neuroendocrine tumors, also known as carcinoids, are uncommon tumors arising from various primary sites. Frequently, carcinoids spread to the liver, causing a variety of symptoms termed carcinoid syndrome.
Worldwide, approximately 15% of cancer survivors are diagnosed with a second primary cancer. A study published in the Canadian Medical Association Journal (CMAJ) reveals that those who have survived cancer are at more than double the risk of a second primary cancer of the same type, but the risk of developing a second cancer of a different type is only marginally higher. To establish whether the risk of secondary cancer is associated to the first diagnosed cancer, Danish researchers evaluated data for the entire Danish population (7, 493, 705 people) from 1980 to 2007. They established from a total of 843, 118 diagnoses, that approximately 10% (765, 255) had one or more diagnoses of primary cancer. They discovered that cancer survivors had a 2.2-fold risk of developing a second primary cancer of the same type as the first and a 1.
Cancer survivors have more than double the risk of a second primary cancer of the same type, according to a study published in CMAJ (Canadian Medical Association Journal).. Danish researchers looked at data for the entire population of Denmark (7 493 705 people) from 1980 to 2007 to determine whether the risk of secondary cancer is linked to the type of cancer found in the first instance. About 10% - 765 255 people - had one or more diagnoses of primary cancer for a total of 843 118 diagnoses. About 15% of cancer survivors worldwide are diagnosed with a second primary cancer. The researchers found a 2.2-fold risk of a second primary cancer of the same type as the first in cancer survivors. The risk of a different type of second primary cancer was 1.1-fold. Risk varied depending on the type of cancer.
Researchers of the Swedish medical university Karolinska Institutet and the University of Cologne, Germany, have identified a new protein involved in a defense mechanism against cancer. The VCP/p97 complex is best known for its role in protein destruction and is involved in a type of familial dementia and ALS. In a novel study the researchers now describe how this complex also plays an important role in regulating the recruitment of the tumor suppressor protein 53BP1 to damaged DNA suggesting an important role for VCP/p97 in our body's defense against cancer. Damage of DNA is potentially very dangerous and linked to the development of cancer. Since DNA damage is unavoidable, our cells are equipped with a sophisticated defense system that activates repair mechanisms. This process is initiated by binding of sensor proteins to the damaged DNA that in turn bind and activate other proteins responsible for repairing the damage.