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ONCOLOGY: Answers to age-old questions surrounding fat cell cancer
Myxoid round cell liposarcoma (MRCLS) is a cancerous tumor that typically arises in deep fat tissues of the limbs or abdomen. It was shown almost 20 years ago to be characterized by a chromosomal change that generates a fusion protein known as TLS:CHOP. Despite this, neither the cell from which MRCLS arise nor the mechanism(s) by which TLS:CHOP induces tumor formation have been definitively determined. A team of researchers led by Igor Matushansky, at Columbia University, New York, has now provided some answers to these questions; in doing so, they identified a potential new combination 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, but how it works has not been determined. Using a new mouse model of MRCLS that they developed, Matushansky and colleagues found that expression of TLS:CHOP in endogenous mesenchymal stem cells led to the in vivo development of MRCLS and that ET-743 worked by decreasing expression of TLS:CHOP. Moreover, combining ET-743 treatment with administration of agonists of the protein PPAR-gamma improved survival of the mice. Matushansky and colleagues therefore suggest that ET-743 plus PPAR-gamma agonist could provide a rational combination for treating MRCLS.
TITLE: PPAR-gamma agonists enhance ET-743-induced adipogenic differentiation in a transgenic mouse model of myxoid round cell liposarcoma
View this article at: http://www.jci.org/articles/view/60015?key=ace2cdfd6a47aee95dac
TUMOR IMMUNOLOGY: Access denied: dense matrix blocks immune cell path to cancer cells
An individual's immune system does respond to a tumor. However, in individuals diagnosed with cancer, the antitumor response was obviously inadequate to clear the tumor. It is hoped that understanding how tumors escape the antitumor immune response will identify candidate therapeutic approaches, with the rationale being that if the escape mechanism can be blunted then an individual's immune system will be able to destroy the tumor. In this context, a team of researchers led by Emmanuel Donnadieu, at Institut Cochin, France, has determined that in human lung tumors, immune cells known as T cells are rarely found in the clusters of cancer cells. Rather, they accumulate in the stromal region of the tumors (that is, the tissue that surrounds and supports the cancer cells). Moreover, Donnadieu and colleagues found that the T cells could not enter the cancer cell regions because a dense matrix that the T cells could not penetrate surrounded these regions. Treating human lung tumor slices with matrix-degrading compounds increased the ability of T cells to enter the cancer cell clusters. Donnadieu and colleagues hope that future studies will increase understanding of the mechanisms by which the dense matrix is generated and thereby identify potential new therapeutic approaches.
TITLE: Matrix architecture defines the preferential localization and migration of T cells into the stroma of human lung tumors
View this article at: http://www.jci.org/articles/view/45817?key=3f332821bf27bc9a78d3
VIROLOGY: Finally, experimental transformation of a primary cell into a tumor cell by the cancer-causing virus KSHV
Kaposi sarcoma herpesvirus (KSHV) is the causative agent of several cancers that arise most commonly in individuals with HIV/AIDS. Developing therapeutic approaches to treat individuals with these cancers is hampered by a lack of understanding of the mechanisms by which KSHV transforms normal cells into cancerous cells. This is poorly understood in part because researchers have been unable to experimentally infect a primary cell with KSHV and turn it into a cancer cell. However, Shou-Jiang Gao and colleagues, at the University of Texas Health Science Center at San Antonio, San Antonio, have now done just that.
Gao and colleagues found that KSHV efficiently infects primary rat embryonic metanephric mesenchymal precursor cells and transforms them into cells that form tumors when injected into mice. They hope to use this model to study the molecular mechanisms by which KSHV transforms normal cells into cancerous cells, although they caution that additional analysis would be required to determine whether mechanisms uncovered using transformed rat cells are relevant to human cancers caused by KSHV.
TITLE: Direct and efficient cellular transformation of primary rat mesenchymal precursor cells by KSHV
View this article at: http://www.jci.org/articles/view/58530?key=b593e40b17636db485f1
ONCOLOGY: Taking on features of cancer cells
The protein p27Kip1 has a role in suppressing tumor development and progression. It does so by inhibiting the activity of protein complexes that promote cell proliferation (cyclin-cyclin-dependent kinase complexes). In contrast, mutant forms of p27Kip1 that cannot inhibit cyclin-cyclin-dependent kinase complexes promote tumor development in mice. Now, a team of researchers led by Arnaud Besson, at INSERM UMR1037, France, has identified a mechanism by which mutant forms of p27Kip1 that cannot inhibit cyclin-cyclin-dependent kinase complexes promote cells to take on features of cancer cells. Future studies will determine whether normal p27Kip1 protein can regulate the same mechanism if mislocalized, as it often is in human tumors.
TITLE: p27Kip1 controls cytokinesis via the regulation of citron kinase activation
View this article at: http://www.jci.org/articles/view/60376?key=2721832273bd35b1e9f0
Additional References Citations Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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