Publications by authors named "J A Lockefeer"

Background: Depressive symptoms, fatigue, and low sleep quality are common symptoms during and after breast cancer (BC) treatment. In the present study, the relationship between trait anxiety and these symptoms in a long follow-up period was examined.

Methods: This was a prospective study.

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Prolactin (PRL) is essential for a number of developmental events in the mammary gland. Work with PRL and PRL receptor knockout mice has shown that PRL indirectly regulates ductal side branching during puberty and directly controls lobuloalveolar development and lactogenesis during pregnancy. Anterior pituitary or placental PRL is thought to be responsible for these functions via an endocrine mechanism; however, PRL is also produced in a number of extrapituitary sites including the mammary gland.

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Prolactin (PRL) is necessary for the genesis of mammary alveolar buds and for lactation. A cDNA library enriched for PRL-dependent genes was made by suppression subtractive hybridization. Aldolase C/zebrin (AldC/zebrin), a brain-specific aldolase, was found to be PRL-dependent in the mouse mammary glands.

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We have previously performed suppression subtractive hybridization to identify genes that were induced during prolactin (PRL)-driven lobuloalveolar development of the mammary gland. This suggested that cortactin-binding protein 90 (CBP90), which is known to be a brain-specific protein that binds to cortactin, was expressed under the regulation of PRL in the mammary glands (preliminary observation). In this study, the expression of CBP90 was examined in the mammary glands of mice under manipulated hormonal circumstances.

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Glycosylation-dependent cell adhesion molecule 1 (GlyCAM 1), a mucin-like endothelial glycoprotein, was induced by PRL and suppressed by progesterone in the mammary gland of mice, and in HC11 mouse mammary epithelial cells. Complementary DNA microarray analysis revealed that expression of GlyCAM 1 was reduced in the mammary gland of PRL-gene disrupted mice (PRL-/-) compared with control (PRL+/-) littermates. This result was confirmed by in situ hybridization and immunostaining.

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