Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors that play essential roles in the regulation of cellular differentiation, development and metabolism. Since the introduction of the thiazolidinedione class of PPAR-γ activators in the late 1990s to treat type 2 diabetes, the use of PPAR-γ ligands to treat other conditions, including cancer, has been investigated. Researchers at the Mayo Clinic discovered that human anaplastic thyroid tumour cells treated with the PPAR-γ activator, RS5444, express a protein known as p21 that inhibits cell replication and suppresses tumour growth, but the underlying mechanism was not understood.
The group has now shown that activation of PPAR-γ with RS5444 (also known as CS-7017) turns on the RhoB tumor suppressor gene, which in turn induces p21 expression, thereby shutting down the cell cycle and blocking tumour growth. The researchers say that it is unusual for a cancer drug to be able to cause re-expression of a suppressed gene in this way, and hope that other cancers in which RhoB is deactivated, such as head and neck, brain, and lung cancers, might respond to RS5444 or to similar drugs. RS5444 is undergoing phase I/II clinical trials (in combination with paclitaxel) in patients with anaplastic thyroid cancer and phase II trials (in combination with carboplatin/paclitaxel) in patients with metastatic non-small cell lung cancer.
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It has been estimated that as many as 50 million people worldwide suffer from schizophrenia and many of these will be treated with antipsychotic medicines. The so-called typical antipsychotics have been available since the mid-1950s and a number of newer agents, the atypical antipsychotics, have been introduced since 1990. Increased dopaminergic activity is thought to be a contributory factor in schizophrenia and all of the antipsychotic medicines interact with the dopamine D2 receptor although they have different affinities and modulate the receptor in different ways.