β-Estradiol Enhanced Secretion of Lipoprotein Lipase from Mouse Mammary Tumor FM3A Cells.

The role of β-estradiol (E) in lipoprotein metabolism in mammary tumors is unclear, therefore, we investigated the effect of E on the secretion of lipoprotein lipase (LPL) from mouse mammary tumor FM3A cells. E-treated cells increased the secretion of active LPL from FM3A cells in a time- and dose-dependent manner. Activity of mitogen-activated protein kinase (MAPK) was increased in the tumor cells treated with E, and enhanced secretion of LPL was suppressed by MAPK kinase 1/2 inhibitor, PD98059, extracellular signal-regulated kinase (ERK) 1/2 inhibitor, FR180204, p38 MAPK inhibitor, SB202190, and phosphatidyl inositol 3-kinase (PI3K) inhibitor, LY294002.

Pro-inflammatory cytokinemia is frequently found in Down syndrome patients with hematological disorders.

Down syndrome (DS) patients are frequently complicated with infections, autoimmune phenomena and hematological disorders, including transient abnormal myelopoiesis (TAM) in infancy and acute megakaryoblastic leukaemia (AMKL) in later life. In this study, serum levels of cytokines from 23 TAM and 15 AMKL patients were examined using the highly sensitive microsphere fluorescence system. Statistical differences between DS neonates with or without TAM were found in IL-1beta [median 7.

Mutations of the PTPN11 and RAS genes in rhabdomyosarcoma and pediatric hematological malignancies.

PTPN11 has been identified as a causative gene in Noonan syndrome (NS), responsible for about 50% of cases of NS. Given the association between NS and an increased risk of some malignancies, notably leukemia and probably some solid tumors including neuroblastoma (NB) and rhabdomyosarcoma (RMS), recent studies have reported that gain-of-function somatic mutations in PTPN11 occur in some hematological malignancies, especially de novo juvenile myelomonocytic leukemia (JMML) and in some solid tumors such as NB, although at a low frequency. In a screen for mutations of PTPN11 in 7 cell lines and 30 fresh tumors of RMS and in 25 cell lines and 40 fresh tumors of NB, we identified a missense mutation (A72T) in an embryonal RMS patient.

Mn(III)/Cu(II)-mediated oxidative radical cyclization of alpha-(Methylthio)acetamides leading to erythrinanes.

Treatment of N-[2-(3,4-dimethoxyphenyl)ethyl]-alpha-(methylthio)acetamide 3 with Mn(OAc)3 in the presence of Cu(OAc)2 gave tetrahydroindol-2-one 4, which then cyclized with Mn(OAc)3 to give 4-acetoxyerythrinane 5. A similar reaction of the 3,4-methylenedioxyphenyl congener 8 also gave tetrahydroindol-2-one 9, which, however, gave only a trace amount of the Mn(OAc)3-mediated cyclization product 11 and afforded the oxidation product 10. On the basis of these results, formation of 5 from 4 was thought to proceed via nucleophilic attack of the pyrrole ring on the cation-radical lX, generated by a single electron-transfer reaction of the acetoxy-substituted intermediate V.