Drugs already approved for clinical use across a variety of therapeutic categories can be screened to identify effective agents for thyroid cancer according to a recent study accepted for publication in the Endocrine Society's Journal of Clinical Endocrinology & Metabolism (JCEM). These findings could rapidly be implemented into a clinical trial to test how effective the treatment would be.

A new study shows that it is possible to selectively target and block a particular microRNA that is important in liver cancer. The finding might offer a new therapy for this malignancy, which kills an estimated 549,000 people worldwide annually.

The animal study, by researchers at The Ohio State University Comprehensive Cancer Center - Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC - James) and at Mayo Clinic, focused on microRNA-221 (miR-221), a molecule that is consistently present at abnormally high levels in liver cancer.

Either heart failure or diabetes alone is bad enough, but oftentimes the two conditions seem to go together. Now, researchers reporting in the January Cell Metabolism appear to have found the culprit that leads from heart failure to diabetes and perhaps a novel way to break that metabolic vicious cycle.

"Our findings clarify the reasons why the incidence of heart failure is high among diabetic patients, why the prevalence of insulin resistance is increased in heart failure patients, and why treatment of insulin resistance improves the prognosis of heart failure patients," says Tohru Minamino of Chiba University Graduate School of Medicine.

It is vital that the body's own immune system does not overreact. If its key players, the helper T cells, get out of control, this can lead to autoimmune diseases or allergies. An immune system overreaction against infectious agents may even directly damage organs and tissues.

Immune cells called regulatory T cells ("Tregs") ensure that immune responses take place in a coordinated manner: They downregulate the dividing activity of helper T cells and reduce their production of immune mediators.

Ever wondered how meteorologists can accurately predict the weather? They use complex spatiotemporal weather models, i.e. mathematical equations that track the motions of the atmosphere through time and space, and combine them with incoming data streams from weather stations and satellites. Now, an innovative new study published in BioMed Central's open access journal Biology Direct has determined that the mathematical methodology used to assimilate data for weather forecasting could be used to predict the spread of brain tumors.

In a major step that could revolutionize biomedical research, scientists have discovered a way to keep normal cells as well as tumor cells taken from an individual cancer patient alive in the laboratory - which previously had not been possible. Normal cells usually die in the lab after dividing only a few times, and many common cancers will not grow, unaltered, outside of the body.

Cancer growth normally follows a lengthy period of development. Over the course of time, genetic mutations often accumulate in cells, leading first to pre-cancerous conditions and ultimately to tumour growth. Using a mathematical model, scientists at the Max Planck Institute for Dynamics and Self-Organization in Göttingen, University of Pennsylvania and University of California San Francisco, have now shown that spatial tissue structure, such as that found in the colon, slows down the accumulation of genetic mutations, thereby delaying the onset of cancer. Their model could help in the assessment of tissue biopsies and improve predictions of the progression of certain cancer types.

Finding ways to counteract or disrupt the invasive nature of cancer cells, called "metastasis," has been a long-term goal of cancer researchers. Now, researchers at Moffitt Cancer Center in Tampa, Fla., have identified an interactive pathway that regulates metastases in some cancers that may be vulnerable to chemical targeting in order to prevent cancer cell proliferation and tumor growth.

Ongoing collaboration by researchers in Moffitt's Departments of Tumor Biology and Drug Discovery has revealed the potential for combating metastatic disease by disrupting the interaction between the retinoblastoma tumor suppressor protein (Rb) and Raf-1 (a gene with a potential to cause cancer) with RRD-251, a selective, chemical disrupter of Rb-Raf-1 interaction.

Scientists have discovered a new way to target cancer through manipulating a master switch responsible for cancer cell growth.

The findings, published in the journal Cancer Cell, reveal how cancer cells grow faster by producing their own blood vessels.

Cancer cells gain the nutrients they need by producing proteins that make blood vessels grow, helping deliver oxygen and sugars to the tumour. These proteins are vascular growth factors like VEGF - the target for the anti-cancer drug Avastin. Making these proteins requires the slotting together of different parts of genes, a process called splicing.