Howard Hughes Medical Institute researchers have developed a small molecule that can turn the survival signal for a variety of cancer cells into a death signal. The molecule mimics the activity of Smac, a protein that triggers the suicide of some types of cancer cells.

A mechanism that creates an “invisibility cloak” for certain cancer cells and allows them to hide from the immune system has been uncovered by a team of researchers at the University of British Columbia.

While some targeted therapies – drugs developed to attack specific molecules in the critical chemical pathways occurring within cancer cells – work well by themselves, increasingly researchers are finding that they work better when teamed with other targeted and conventional therapies.

With the discovery of suitable molecular targets – cellular molecules along pathways crucial for sustaining the life of cancer cells – comes the perplexing dilemma of where to find the next therapeutics that will bind to and disable those targets. While the possibilities for drug designs are near-limitless, the methods to screen drug databases and repositories are often problematic or ill-suited for the particular needs of researchers.

MIT and University of Rochester researchers report important advances toward a therapeutic device that has the potential to capture cells as they flow through the blood stream and treat them. Among other applications, such a device could zap cancer cells spreading to other tissues, or signal stem cells to differentiate.

Laboratory experiments have previously shown that cancer cells overproduce an enzyme, heparanase, which splits the body’s own polysaccharide heparan sulfate into shorter fragments.

Researchers have discovered new small molecules that may prevent prostate cancer cells from turning off normal genes in a process that transforms normal cells into cancer cells. This significant discovery in the field of epigenetics has immediate implications in the development of new diagnostic tests and cancer medications.

A group working at the Swiss Institute for Experimental Cancer Research (ISREC) in collaboration with the University of Pavia has discovered that telomeres, the repeated DNA-protein complexes at the end of chromosomes that progressively shorten every time a cell divides, also contain RNA.

Researchers have uncovered a new way in which a cell protein protects cancer cells from a wide range of chemotherapeutic drugs, identifying a possible target for improving treatment outcomes for patients.

A strong skeleton is less likely to be penetrated by metastasizing cancer cells, so a fortified glass of milk might be the way to block cancer’s spread, according to researchers at the ANZAC Research Institute in Concord, Australia.

The jury is in: microRNAs can cause tumors to metastasize. These tiny molecules fine-tune protein production and play a powerful role in biological processes ranging from development to aging. Now scientists have proved that they can prompt otherwise sedentary cancer cells to move and invade other tissues.

A team, led by researchers at the Carnegie Institution,* has found a key biochemical cycle that suppresses the immune response, thereby allowing cancer cells to multiply unabated. The research shows how the biomolecules responsible for healthy T-cells, the body’s first defenders against hostile invaders, are quashed, permitting the invading cancer to spread.