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41.
Karuna Mittal Angela Ogden Michelle D Reid Padmashree CG Rida Sooryanarayana Varambally Ritu Aneja 《Cell cycle (Georgetown, Tex.)》2015,14(17):2798-2809
Centrosome amplification (CA), the presence of centrosomes that are abnormally numerous or enlarged, is a well-established driver of tumor initiation and progression associated with poor prognosis across a diversity of malignancies. Pancreatic ductal adenocarcinoma (PDAC) carries one of the most dismal prognoses of all cancer types. A majority of these tumors are characterized by numerical and structural centrosomal aberrations, but it is unknown how CA contributes to the disease and patient outcomes. In this study, we sought to determine whether CA was associated with worse clinical outcomes, poor prognostic indicators, markers of epithelial-mesenchymal transition (EMT), and ethnicity in PDAC. We also evaluated whether CA could precipitate more aggressive phenotypes in a panel of cultured PDAC cell lines. Using publicly available microarray data, we found that increased expression of genes whose dysregulation promotes CA was associated with worse overall survival and increased EMT marker expression in PDAC. Quantitative analysis of centrosomal profiles in PDAC cell lines and tissue sections uncovered varying levels of CA, and the expression of CA markers was associated with the expression of EMT markers. We induced CA in PDAC cells and found that CA empowered them with enhanced invasive and migratory capabilities. In addition, we discovered that PDACs from African American (AA) patients exhibited a greater extent of both numerical and structural CA than PDACs from European American (EA) patients. Taken together, these findings suggest that CA may fuel a more aggressive disease course in PDAC patients. 相似文献
42.
Cadmium (Cd) is an industrial and environmental pollutant that produces toxic effects on gametogenesis, pre- and post-implantation embryos, and the placenta. Because the effects of acute Cd intoxication on the placenta are not well understood, we investigated changes in its glycosylated components in Cd treated dams at days 4, 7, 10 and 15 of gestation using lectin histochemistry. CdCl2 was administered to pregnant rats; control animals received sterile normal saline. Placentas were processed for DBA, Con A, SBA, PNA, UEA-I, RCA-I and WGA lectin histochemistry to evaluate changes in the carbohydrate pattern of the placenta that might modify cell interactions and contribute to embryonic alterations. Lectin binding was analyzed in the yolk sac; trophoblast giant cells; trophoblast I, II and III; spongiotrophoblast cells and endovascular trophoblast cells in the chorioallantoic placenta. Our lectin binding patterns showed that Cd caused alteration of SBA and DBA labeling of trophoblast-derived cells, which suggested increased expressions of α and β GalNAc. Cd also caused decreased UEA-1 binding affinity, which indicated fewer α-L-Fuc residues in placentas of Cd treated dams. The nonreactivity in trophoblast I of the control placentas incubated with Con-A contrasted with the labeling in placentas of experimental dams, which indicated increased expression of terminal α-D-Man, and α-D-Glc residues. We found that Cd altered the reactivity of placenta to several lectins, which indicated modification of the glycotype presented by the fetal component of the placenta. We report that Cd exerts a deleterious effect on the glycosylation pattern of the placenta. 相似文献
43.
Phylogeny and biogeography of ratite birds inferred from DNA sequences of the mitochondrial ribosomal genes 总被引:7,自引:2,他引:5
The origin of the flightless ratite birds of the southern continents has
been debated for over a century. Whether dispersal or vicariance
(continental breakup) best explains their origin depends largely on their
phylogenetic relationships. No consensus has been reached on this issue
despite many morphological and molecular studies. To address this question
further we sequenced a 2.8-kb region of mitochondrial DNA containing the
ribosomal genes in representative ratites and a tinamou. Phylogenetic
analyses indicate that Struthio (Africa) is basal and Rhea (South America)
clusters with living Australasian ratites. This phylogeny agrees with
transferrin and DNA hybridization studies but not with sequence analyses of
some protein-coding genes. These results also require reevaluation of the
phylogenetic position of the extinct moas of New Zealand. We propose a new
hypothesis for the origin of ratites that combines elements of dispersal
and vicariance.
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