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Kinase inhibitors such as imatinib (Gleevec) have improved the outlook for many people with chronic myeloid leukemia and related blood disorders. But such drugs do not target the leukemia stem cell population and may not be curative. Krause and Van Etten discuss several clinical studies that suggest that interferon-α may provide a solution by selectively eliminating leukemic stem cells—although only more basic research will tell us whether this is true and how it may happen.
Three postmortem studies examine long-term fetal transplants in subjects with advanced Parkinson's disease. The findings—such as the development of parkinsonian pathology in some transplanted neurons—underscore the limitations of this approach.
About 25% of the African-American population carries a gene variant that seems to protect against heart failure. The findings may have implications for the use of β-blockers (pages 510–517).
Allergens stimulate lymphocytes to become factories for secreted proteins that cause organ dysfunction in allergic diseases. Allergens are now shown to target dendritic cells, the cells responsible for processing and presenting antigens to T cells (pages 565–573).
The search is on for for vaccine adjuvants that boost the innate immune response and complement existing adjuvants. Mast cell activators may be one option (pages 536–541).
Three studies examine how resistance to chemotherapy develops in cancers deficient in BRCA1 and BRCA2. The mechanism involves restoration of BRCA1 and BRCA2 activity. Shah examines the implications for the clinic, such as the potential value of continuing treatment with cisplatin and similar agents even after drug resistance develops.
A strain of Escherichia coli that causes urinary tract infections seems to take hold in the body by interfering with signaling through Toll-like receptors (TLRs). The mechanism involves a secreted bacterial protein that is taken up by cells and clogs up the TLR signaling mechanism (pages 399–406).
Robo4 expression in emerging blood vessels can neutralize signaling through the angiogenic factor vascular endothelial growth factor (VEGF) and maintain vessel integrity. The findings could lead to new therapeutic targets for angiogenesis and vascular leakage (pages 448–453).
Only one drug is widely used to treat schistosomiasis, a chronic, neglected tropical disease caused by parasitic blood flukes. Fears of potential drug resistance have accelerated the search for new classes of antischistosome drugs. A promising candidate has now emerged (pages 407–412).
Two studies examine the cellular origins of peripheral nervous system tumors in mouse models of neurofibromatosis type 1 and conclude that stem cells may not be the culprits. Instead, more differentiated cells may give rise to and drive the tumors.
Inhibition of the Notch pathway reverses damage in a mouse model of kidney disease (pages 290–298). The findings suggest that blockade of the Notch pathway through inhibition of γ-secretase activity may be an approach to combating glomerular failure.
Matrix metalloproteases (MMPs) are shedding their traditional roles in tissue remodeling and appearing as players in diseases of the nervous system. MMP2 and MMP9 provide the latest example, with converging roles in chronic pain after peripheral nerve injury (pages 331–336).
Interleukin-22, a component of the immune system most studied for its role in autoimmunity, has a more beneficial side. Two studies show how this cytokine fights off microbes in the mucosa of the lung and gut (pages 275–281 and 282–289).
A recent theory about the basis for fragile X syndrome is now validated in a mouse model. The findings point the way to treatment options targeting group 1 metabotropic glutamate receptors.
