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ONCOLOGY: New insight into brain tumor aggressiveness Malignant gliomas are the most common and lethal of all human braintumors that originate in the brain. Patients with malignant gliomashave a poor prognosis because it is a highly aggressive form of cancer that is commonly resistant to current therapies. New therapeuticapproaches are much needed, but deeper understanding of themechanisms underlying malignant glioma aggressiveness is needed ifthey are to be developed. In this context, a team of researchersled by Erwin Van Meir, at Emory University, Atlanta, has gained newinsight into how the protein P14ARF - expression of which is lostin approx 60% of malignant gliomas - suppresses tumor developmentand progression. Specifically, they find that P14ARF inhibitsmalignant glioma-induced formation of new blood vessels that bringin nutrients required for tumor growth. Van Meir and colleaguestherefore suggest that restoring P14ARF activity or targetingmolecules that function in the pathway downstream of P14ARF toinhibit blood vessel formation could provide a new approach toblock the growth of malignant gliomas and potentially other tumors. TITLE: P14ARF inhibits human glioblastoma-induced angiogenesis byupregulating the expression of TIMP3 View this article at: articles/view/38596?key=7beeb4e23ccc74350b3e BACTERIOLOGY: Unraveling the chain of events leading to virulencedeterminant activity Persistent infection with Helicobacter pylori , a bacterium that can be found colonizing the stomach lining ofalmost half the world's population, increases an individual's riskof developing stomach cancer. Individuals infected withHelicobacter pylori strains carrying the virulence determinant CagAare at substantially greater risk of developing stomach cancer thanthose that harbor CagA-negative strains. This suggests that CagAhas an important role in cancer initiation and development. Many ofthe functions of CagA require it to be phosphorylated by proteinsin the host cell. A team of researchers led by Steffen Backert, atUniversity College Dublin, Ireland, has now shed light on thephosphorylation process, revealing it to be a tightly regulated andcoordinated sequential process. The data also provide insight intohow differential phosphorylation patterns affect CagA function andlead Anne M ller, at the University of Z rich, Switzerland, tosuggest in an accompanying commentary that detailed analysis ofCagA phosphorylation status could help determine a Helicobacter pylori -infected individual's level of risk of developing stomach cancer. TITLE: c-Src and c-Abl kinases control hierarchic phosphorylationand function of the CagA effector protein in Western and East Asian Helicobacter pylori strains View this article at: articles/view/61143?key=05d7a989d0fb9e6ac91f ACCOMPANYING COMMENTARY TITLE: Multistep activation of the Helicobacter pylori effector CagA View this article at: articles/view/61578?key=95ade54944224b05ef08 IMMUNOLOGY: Stairway to T cell development found in the humantonsil Central to the effective functioning of the immune system is thepresence of a broad repertoire of immune cells known as T cells,which develop in an organ known as the thymus. There is someevidence to suggest that T cells can also develop in tissues otherthan the thymus, but no complete program of human T celldevelopment has been described in an extrathymic tissue. Now, ateam of researchers led by Michael Caligiuri, at The Ohio StateUniversity, Columbus, has uncovered clear evidence that a stepwiseprogram of T cell development occurs outside the thymus within thehuman tonsil. Although it is not clear how significant acontribution T cell development in the tonsil makes to generatingthe T cell repertoire in healthy individuals, Caligiuri andcolleagues suggest that it might be important in the setting ofpoor thymic function or congenital deficit and in the context ofautoimmunity, cancer, or regenerative medicine. TITLE: Evidence for a stepwise program of extrathymic T celldevelopment within the human tonsil View this article at: articles/view/46125?key=f22c42a5fd52764465f0 HEPATOLOGY: Understanding how acetaminophen kills liver cells Overdoses of acetaminophen (also known as paracetamol) account formost drug overdoses in a number of countries, including the UnitedStates. Such overdoses damage the liver, causing acute liverfailure, which can be fatal. A team of researchers led by HartmutJaeschke, at the University of Kansas Medical Center, Kansas City,has now provided new insight into the mechanisms by whichacetaminophen causes liver damage in mice and humans. Specifically,they find that in liver cells, acetaminophen damages the cellularcompartments that generate power (mitochondria) and causes the DNAin the nucleus to fragment, leading to cell death by a processknown as necrosis. These data are important, as it had previouslybeen suggested that acetaminophen-induced liver cell toxicity was aresult of cellular events that lead to an alternative cell deathprocess known as apoptosis. TITLE: The mechanism underlying acetaminophen-inducedhepatotoxicity in humans and mice involves mitochondrial damage andnuclear DNA fragmentation View this article at: articles/view/59755?key=50f5172399a45b6295df Additional References Citations. 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