Galanin is a widely distributed regulatory peptide which modulates the pituitary secretion of PRL and GH. Estrogen administration strongly stimulates galanin gene expression in the rat anterior pituitary. In adult female Fischer 344 rats, estrogen also induces hyperplasia of lactotropes. We used immunocytochemical analysis to assess the effects of estrogen on galanin-like immunoreactivity (Gal-IR) in the rat pituitary and hypothalamus during sc diethylstilbestrol (DES) implantation and after its removal at 30 days. In the anterior pituitary, DES implantation increased the portion of Gal-IR-containing cells from less than 2% in the control rats to 18.3% after 3 days of DES and 36% after 30 days. These changes paralleled the lactotrope hyperplasia exhibited in response to DES exposure. Ten and 30 days after removal of the DES capsules, the percentage of Gal-IR-containing cells in the anterior pituitary decreased to 6.3% and 1.5%, respectively. Colocalization studies revealed that Gal-IR-containing cells were predominantly lactotropes. Immunoelectron microscopy demonstrated that Gal-IR was concentrated in the Golgi region of these hyperplastic lactotropes and suggests that little of the synthesized galanin is secreted. The distribution of Gal-IR in the hypothalamus, median eminence, and neurohypophysis was unaffected by DES treatment. These data demonstrate that galanin is synthesized by hyperplastic pituitary lactotropes of Fischer 344 rats and that peptide accumulation is dependent on the presence of circulating estrogens. In contrast, neuronal galanin synthesis in the hypothalamus does not appear to be regulated by estrogen.
Astrocytomas, including glioblastoma multiforme, represent the most frequent and deadly primary neoplasms of the human nervous system. Despite a number of previous cytogenetic and oncogene studies primarily focusing on malignant astrocytomas, the primary mechanism of tumor initiation has remained obscure. The loss or inactivation of "tumor suppressor" genes are thought to play a fundamental role in the development of many human cancers. Thus, we have analyzed astrocytomas of various histological malignancy grades with polymorphic DNA markers to search for specific chromosomal deletions potentially pointing to loci containing tumor suppressor genes. Loss of constitutional heterozygosity indicating chromosomal loss or deletions was most frequently seen for markers on the short arm of chromosome 17 in 50% of the informative tumors (5 of 10 informative cases) and, to a lesser extent, for markers on chromosomes 1 and 10. Deletions on chromosome 17p were seen in both low-grade and high-
Meningioma growth is thought to be stimulated by the sex hormones progesterone and possibly estrogen. We report here stimulation of growth of meningioma-derived cells in culture by prolactin. Fourteen human tumors taken from surgery were initially grown in Ham's medium F10 with 15% fetal calf serum. The tumors were then trypsinized and resuspended in medium in a multi-well plate with either prolactin or bombesin; the cells were incubated for 1 week, washed, and resuspended for cell counting. The growth-stimulating effect of prolactin at 10 and 200 micrograms/ml was compared with bombesin at 5 mM/ml or 15 mM/ml. A growth index compared cell count in the experimental well to the control well; growth at the rate of the control well was given an index of 1.0. The tumors included 7 meningiomas and 7 other neoplasms (3 astrocytomas, an ependymoma, a pineoblastoma, a hemangiopericytoma, and a metastatic adenocarcinoma). For meningiomas incubated in 10 micrograms/ml prolactin, the growth index was 3.08; for those incubated in 200 micrograms/ml prolactin, it was 2.28. Bombesin indices were 1.7 and 1.2 at 5 mM/ml and 15 mM/ml, respectively. By 2-tailed t-testing both prolactin concentrations stimulated the growth of meningiomas significantly (P < or = 0.02), while bombesin did not. Neither peptide enhanced the growth of the other tumors tested.
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