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Basic research and clinical studies are underway to identify genetic polymorphisms that underlie drug effects. What obstacles must we overcome before we can use genetic analysis to predict the ability of patients to respond to certain treatments?
Most drugs are metabolized by CYP3A enzymes, and variations in expression levels of these enzymes are believed to determine whether patients will have a positive or adverse drug response. Little is known about the mechanisms that underlie inter-individual differences in CYP3A expression, but the mapping of human genome sequence variations will facilitate the search for answers.
One of the major challenges of the mad cow disease epidemic is the need for a good diagnostic test, to identify people and animals that have been infected with the infectious form of prion before symptoms appear. Differential display analysis may have revealed a good candidate marker (pages 361-364).
Most research into the function of the cystic fibrosis transmembrane conductance regulator has focused on its role in Cl− transport. New findings suggest that we may have been focusing on the wrong ion.
Many genetic loci have been associated with autoimmune diseases through linkage analyses, but it has been a major challenge to isolate actual disease genes. The sequencing of the human genome and mapping of single nucleotide polymorphisms will speed the identification of these genes, and may also help explain how environmental factors such as bacteria and viruses can induce autoimmunity.
The sequencing of the human genome is likely to speed the discovery of factors involved in cancer pathogenesis and lead to an age of individually tailored anti-cancer drugs. But does the ability to obtain an abundance of genetic information mean that we necessarily know how to use it?
The completion of the Human Genome Project will provide much needed insight into the molecular basis of monogenic or complex cardiac disorders. But what are the prospects for using genomic information in diagnosis and treatment of cardiac diseases?
Plasma fibronectin has been proposed to play a role in wound healing. Studies with conditional knockout mice, however, indicate that fibronectin has more to do with protecting cells from ischemic damage after stroke (pages 324-330).
Pathogenic bacteria use a variety of mechanisms to combat the host immune response. New data indicate that Shigella spp. make a preemptive strike against the deployment of host antibacterial peptides (pages 180–185).
Triclosan, an antibacterial agent found in mouthwashes, acne medicines and deodorants, also prevents the growth of Plasmodium falciparum. If properly developed, this type II fatty acid biosynthesis inhibitor may be a promising new antimalarial agent (pages 167–173).
Vascular endothelial growth factors are well-known angiogenic agents and targets for anti-cancer therapies. Now it appears that this signaling pathway is also involved in developmental and tumor-induced lymphangiogenesis (pages 186-191, 192-198, 199-205).
The BCR-ABL oncoprotein of chronic myeloid leukemia can be converted into an active killer of the malignant cell when allowed to enter the nucleus. Could this lead to a three-step strategy to improve molecular targeting in the treatment of leukemia (pages 228–234)?
The clot-busting drug tissue plasminogen activator (tPA) is currently the only FDA-approved therapy for acute stroke. However, increasing evidence suggests that tPA can also contribute to excitotoxic neuronal damage in animal models of stroke. (pages 59–64)
