Rabbit anti-Human Bcl-2 polyclonal antibody

Mesenchymal chondrosarcoma (MC) is a rare aggressive mesenchymal sarcoma. Specific markers for the differential diagnosis of MCs remain to be developed. OLIG2 expression has been reported only in neuroepithelial tumors. Recently, OLIG2 expression was found to be involved in the development of NCOA2 fusion-positive alveolar rhabdomyosarcomas. Therefore, we investigated whether OLIG2 expression could be used as a diagnostic marker for MC. We report the clinical pathological and immunohistochemical features of 14 MCs. All tumors showed typical pathological features including biphasic patterns with sheets of primitive round mesenchymal cells and interspersed islands of cartilage. These tumors expressed BCL2, SOX9, and CD99. OLIG2 was robustly expressed in 12/14 of MCs. NCOA2 rearrangement was found in 12 cases. OLIG2 expression was not found in the NCOA2 rearrangement-negative MCs. Notably, OLIG2 expression was not detected in 52 neoplasms (8 Ewing sarcomas, 23 hemangiopericytomas, and 21 chondrosarcomas) that are frequently misdiagnosed as MC. Our findings provide convincing evidence that OLIG2 can serve as a reliable marker in the differential diagnosis of MC and may be a unique neurodevelopmental gene expression signature for the NCOA2 rearranged MCs.

Alzheimer's disease (AD) is a multifactorial and severe neurodegenerative disorder characterized by progressive memory decline, the presence of A beta plaques and tau tangles, brain atrophy, and neuronal loss. Available therapies provide moderate symptomatic relief but do not alter disease progression. This study demonstrated that PaPE-1, which has been designed to selectively activate non-nuclear estrogen receptors (ERs), has anti-AD capacity, as evidenced in a cellular model of the disease. In this model, the treatment of mouse neocortical neurons with A beta (5 and 10 mu M) induced apoptosis (loss of mitochondrial membrane potential, activation of caspase-3, induction of apoptosis-related genes and proteins) accompanied by increases in levels of reactive oxygen species (ROS) and lactate dehydrogenase (LDH) as well as reduced cell viability. Following 24 h of exposure, PaPE-1 inhibited A beta-evoked effects, as shown by reduced parameters of neurotoxicity, oxidative stress, and apoptosis. Because PaPE-1 downregulated A beta-inducedFas/FAS expression but upregulated that of A beta-inducedFasL, the role of PaPE-1 in controlling the external apoptotic pathway is controversial. However, PaPE-1 normalized A beta-induced loss of mitochondrial membrane potential and restored the BAX/BCL2 ratio, suggesting that the anti-AD capacity of PaPE-1 particularly relies on inhibition of the mitochondrial apoptotic pathway. These data provide new evidence for an anti-AD strategy that utilizes the selective targeting of non-nuclear ERs with PaPE-1.