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GATA transcription factors are structurally-related zinc finger proteins that recognize the consensus DNA sequence WGATAA (the GATA motif), an essential cis-acting element in the promoters and enhancers of many genes. These transcription factors regulate cell fate specification and differentiation in a wide array of tissues. As demonstrated by genetic analyses of mice and humans, GATA factors play pivotal roles in the development, homeostasis, and function of several endocrine organs including the adrenal cortex, ovary, pancreas, parathyroid, pituitary, and testis. Additionally, GATA factors have been shown to be mutated, overexpressed, or underexpressed in a variety of endocrine tumors (e.g., adrenocortical neoplasms, parathyroid tumors, pituitary adenomas, and sex cord stromal tumors). Emerging evidence suggests that GATA factors play a direct role in the initiation, proliferation, or propagation of certain endocrine tumors via modulation of key developmental signaling pathways implicated in oncogenesis, such as the WNT/β-catenin and TGFβ pathways. Altered expression or function of GATA factors can also affect the metabolism, ploidy, and invasiveness of tumor cells. This article provides an overview of the role of GATA factors in endocrine neoplasms. Relevant animal models are highlighted., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Smoking reduces the expression of VEGFR-1 in non-pregnant women. In pregnant women it reduces the risk of pre-eclampsia, which in turn is associated with increased placental expression of VEGFR-1 and increased maternal circulating soluble VEGFR-1 (sVEGFR-1). We therefore hypothesized that smoking might affect VEGFR-1 expression in pregnant women. In maternal plasma sVEGFR-1 concentrations during the third trimester in both smoking (median 1088, range 834-1362ng/L, n=20) and non-smoking (728, 719-1336ng/L, n=19) women were higher than during the second trimester (smokers 374, 291-683ng/L, n=6, p>0.05; non-smokers 375, 290-667ng/L, n=22, p<0.001). No difference was observed between smokers and non-smokers. Secretion of sVEGFR-1 into the culture medium, as well as the pattern and intensity of immunostaining in first trimester placenta were similar in tissue from smoking (n=22) and non-smoking (n=20) women. Thus, contrary to our hypothesis, smoking does not affect circulating maternal sVEGFR-1 concentrations or placental secretion of sVEGFR-1 or expression of VEGFR-1 in vitro.