Leukemia (2009) 23, 870-876; doi:10.1038/leu.2008.390; selleck kinase inhibitor published online 15 January 2009″
“Altered expression of major histocompatibility

complex (MHC) class I molecules can be caused by defects in genes of the antigen-processing machinery (APM), and is often correlated to progression in solid tumours. However, little is known about expression of the APM components in blasts from patients with acute myeloid leukaemia (AML). In this study, we investigated the expression of the APM components large multifunctional peptidases (LMP) 2 and 7, transporter-associated with antigen processing (TAP) 1 and 2, beta-2-microglobulin (beta 2m) and MHC class I heavy chain in situ by tissue microarray from bone marrow biopsies of 30 AML patients. APM components were heterogeneously expressed in all AML samples tested, but no significant correlation ICG-001 cost with the AML subtype according to the French-American-British classification

was found. Depending on the APM component tested, up to 90% of the trephines showed no or weak expression, whereas the LMP7 protein was detected in 66% of all samples. By following disease progression in individual AML patients, we found severe downregulation of APM components in two out of four patients from initial diagnosis to relapse. We conclude that downregulation of APM find more components may play a role in the failure of immunosurveillance and may therefore contribute to relapse in acute leukaemia. Leukemia 2009) 23, 877-885; doi:10.1038/leu.2008.391; published online 15 January 2009″
“alpha B-crystallin is a member of the small heat shock proteins, which is abundantly expressed in various vertebrate tissues including

the central nervous system. In our previous report, we showed alpha B-crystallin induction in activated astrocytes in the postischemic brain and in H(2)O(2)-treated primary astrocyte cultures. To investigate the functional significance of alpha B-crystallin induction in astrocytes, we generated a stable C6 astroglioma cell line overexpressing alpha B-crystallin. In these cells, hydrogen peroxide-induced apoptosis was reduced by 60% compared to parent cells. Furthermore, the repression of aB-crystallin expression by alpha B-crystallin siRNA transfection suppressed this protective effect, indicating that alpha B-crystallin is responsible for the protection against H(2)O(2)-induced apoptosis in C6 astroglioma cells. Similar level of aggravation in H(2)O(2)-induced apoptosis was observed in primary astrocyte cultures when alpha B-crystallin expression was suppressed by alpha B-crystallin siRNA transfection, confirming the importance of alpha B-crystallin.