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ONCOLOGY: Answers to age-old questions surrounding fat cell cancer Myxoid round cell liposarcoma (MRCLS) is a cancerous tumor thattypically arises in deep fat tissues of the limbs or abdomen. Itwas shown almost 20 years ago to be characterized by a chromosomalchange that generates a fusion protein known as TLS:CHOP. Despitethis, neither the cell from which MRCLS arise nor the mechanism(s)by which TLS:CHOP induces tumor formation have been definitivelydetermined. A team of researchers led by Igor Matushansky, atColumbia University, New York, has now provided some answers tothese questions; in doing so, they identified a potential newcombination therapy for the treatment of MRCLS. A compound isolated from the sea squirt Ecteinascidia turbinate, ET-743, is a highly effective therapy for patients with MRCLS, buthow it works has not been determined. Using a new mouse model ofMRCLS that they developed, Matushansky and colleagues found thatexpression of TLS:CHOP in endogenous mesenchymal stem cells led to the in vivo development of MRCLS and that ET-743 worked bydecreasing expression of TLS:CHOP. Moreover, combining ET-743treatment with administration of agonists of the protein PPAR-gammaimproved survival of the mice. Matushansky and colleagues thereforesuggest that ET-743 plus PPAR-gamma agonist could provide arational combination for treating MRCLS. TITLE: PPAR-gamma agonists enhance ET-743-induced adipogenicdifferentiation in a transgenic mouse model of myxoid round cellliposarcoma View this article at: articles/view/60015?key=ace2cdfd6a47aee95dac TUMOR IMMUNOLOGY: Access denied: dense matrix blocks immune cellpath to cancer cells An individual's immune system does respond to a tumor. However, inindividuals diagnosed with cancer , the antitumor response was obviously inadequate to clear thetumor. It is hoped that understanding how tumors escape theantitumor immune response will identify candidate therapeuticapproaches, with the rationale being that if the escape mechanismcan be blunted then an individual's immune system will be able todestroy the tumor. In this context, a team of researchers led byEmmanuel Donnadieu, at Institut Cochin, France, has determined thatin human lung tumors, immune cells known as T cells are rarelyfound in the clusters of cancer cells. Rather, they accumulate inthe stromal region of the tumors (that is, the tissue thatsurrounds and supports the cancer cells). Moreover, Donnadieu andcolleagues found that the T cells could not enter the cancer cellregions because a dense matrix that the T cells could not penetratesurrounded these regions. Treating human lung tumor slices withmatrix-degrading compounds increased the ability of T cells toenter the cancer cell clusters. Donnadieu and colleagues hope thatfuture studies will increase understanding of the mechanisms bywhich the dense matrix is generated and thereby identify potentialnew therapeutic approaches. TITLE: Matrix architecture defines the preferential localizationand migration of T cells into the stroma of human lung tumors View this article at: articles/view/45817?key=3f332821bf27bc9a78d3 VIROLOGY: Finally, experimental transformation of a primary cellinto a tumor cell by the cancer-causing virus KSHV Kaposi sarcoma herpesvirus (KSHV) is the causative agent of several cancers thatarise most commonly in individuals with HIV/AIDS. Developingtherapeutic approaches to treat individuals with these cancers ishampered by a lack of understanding of the mechanisms by which KSHVtransforms normal cells into cancerous cells. This is poorlyunderstood in part because researchers have been unable toexperimentally infect a primary cell with KSHV and turn it into acancer cell. However, Shou-Jiang Gao and colleagues, at theUniversity of Texas Health Science Center at San Antonio, SanAntonio, have now done just that. Gao and colleagues found that KSHV efficiently infects primary ratembryonic metanephric mesenchymal precursor cells and transformsthem into cells that form tumors when injected into mice. They hopeto use this model to study the molecular mechanisms by which KSHVtransforms normal cells into cancerous cells, although they cautionthat additional analysis would be required to determine whethermechanisms uncovered using transformed rat cells are relevant tohuman cancers caused by KSHV. TITLE: Direct and efficient cellular transformation of primary ratmesenchymal precursor cells by KSHV View this article at: articles/view/58530?key=b593e40b17636db485f1 ONCOLOGY: Taking on features of cancer cells The protein p27Kip1 has a role in suppressing tumor development andprogression. It does so by inhibiting the activity of proteincomplexes that promote cell proliferation (cyclin-cyclin-dependentkinase complexes). In contrast, mutant forms of p27Kip1 that cannotinhibit cyclin-cyclin-dependent kinase complexes promote tumordevelopment in mice. Now, a team of researchers led by ArnaudBesson, at INSERM UMR1037, France, has identified a mechanism bywhich mutant forms of p27Kip1 that cannot inhibitcyclin-cyclin-dependent kinase complexes promote cells to take onfeatures of cancer cells. Future studies will determine whethernormal p27Kip1 protein can regulate the same mechanism ifmislocalized, as it often is in human tumors. TITLE: p27Kip1 controls cytokinesis via the regulation of citronkinase activation View this article at: articles/view/60376?key=2721832273bd35b1e9f0 Additional References Citations. We are high quality suppliers, our products such as Modern Islamic Clothing Manufacturer , Video Game Accessories Manufacturer for oversee buyer. 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