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In this issue, Gause and colleagues report the first evidence that alternatively activated macrophages are important effector cells mediating clearance of intestinal helminths. Alternatively activated macrophages have previously been implicated mainly in dampening and resolving pathology. This image shows alternatively activated macrophages (orange and yellow) surrounding invasive helminth parasite larvae in the small intestine of a mouse. Image courtesy of Robert Anthony and William Gause.
The most infamous pesticide in history is also the most effective weapon against malaria. Ready or not, DDT is on its way back to Africa. Apoorva Mandavilli reports.
Armed with facts and a flair for the dramatic, Amir Attaran is a master at bringing global health agencies to task—even when his views make enemies out of friends.
The high cell density, rapid growth rate and large population size of cancer are conventionally attributed to a pathologically high ratio of cell production to cell death. Yet these features might also or instead result from inappropriate cell movement, already understood to underlie invasion and metastasis. This integrating concept could induce a broadening of our existing anticancer pharmacopoeia, which, with mitosis as its predominant target, is now seldom curative.
Tyrosine kinase inhibitors, widely hailed for their success as treatments for cancer, are also plagued by the issue of cardiotoxic side effects. The mechanism behind the heart damage now comes to light for one such inhibitor, imatinib mesylate, also known as Gleevec (pages 908–916).
Transplantation of metastatic melanoma cells into zebrafish embryo disrupts development—and identifies a potential new drug target for this deadly cancer (pages 925–932).
The key developmental regulator Notch was first characterized in flies but has since been implicated in diseases ranging from cancer to migraine. Experiments in a rat model now suggest that activation of Notch can also promote neurogenesis and healing after stroke.
The role of inflammatory mechanisms in amyotrophic lateral sclerosis is a hotly debated topic. Findings in a mouse model now add weight to arguments that targeting of inflammatory cells might be a fruitful therapeutic approach.
Controlling the growth of cancer cells at metastatic sites is one goal of cancer drug development. Studies of metastasis suppressor function bring this long-sought goal closer (pages 933–938).
Mycobacterium leprae, the bacterium that causes leprosy, causes the breakdown of myelin. This breakdown is now shown to occur through the ErbB2 receptor, a process that can be blocked by Herceptin and kinase inhibitors (pages 961–966).
Certain antibiotics prompt Streptococcus pneumoniae to take up DNA from the environment, which may enable the microbe to acquire genes for antibiotic resistance.
Metastatic disease is the primary cause of death for most cancer patients. Complex and redundant pathways involving the tumor cell and the microenvironment mediate tumor invasion at the primary site, survival and arrest in the bloodstream, and progressive outgrowth at a distant site. Understanding these pathways and their dynamic interactions will help identify promising molecular targets for cancer therapy and key obstacles to their clinical development.