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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aetiology and pathogenesis of benign prostate hyperplasia (BPH) are still unresolved questions, although a number of hypotheses have been developed, most of which have still not been confirmed by experimentation. BPH has been regarded as a kind of adenoma, as a stromal disease, as the result of either hormonal imbalance (altered oestrogen/testosterone ratio) or testosterone or dihydrotestosterone stimulation, and finally as the result of oestrogen stimulation, perinatally or involutionally. More recently, scientific interest has focused on the presence and possible function of growth factors and their receptors in the human prostate and their autocrine or paracrine stimulatory effects in BPH development. Hypotheses on their hormonal regulation as well as their interplay during epithelial-stromal interaction have been developed. The intact human prostate produces epithelial (EGF) and basic fibroblast (bFGF) growth factors. Normally, they do not appear to have autocrine or paracrine effects. In androgen deficiency, however, as shown experimentally in castrated rats, the stromal cells express increased amounts of TGF beta, of TGF beta receptor, and of bFGF. Platelet-derived growth factor (PDGF), but not the corresponding receptor, has been shown in prostate. The growth factor receptor-associated tyrosine protein kinase is present in the human prostate in two different forms, but its functional significance in BPH development has not yet been elucidated. A more significant role may be attributed to the recently described growth factors in cultured human stromal cells, which exert multifarious mitogenic and non-mitogenic effects on prostatic epithelium as well as neuronal and non-neuronal cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Benign prostatic hyperplasia and growth factors: mechanisms and hypotheses]. 137 33

Pituitary adenoma originates from adenohypophysial cells producing various pituitary hormones. Some of pituitary adenomas are associated with pathological states including primary hypothyroidism, Nelson's syndrome, hypothalamic hormone-producing tumors, multiple endocrine neoplasia type 1, McCune-Albright syndrome and transgenic animals transfected with hypothalamic hormones (HP). These facts suggest that excessive secretion of HP induces hyperplasia of the adenohypophysial cells, leading to adenoma by additive effects of other unknown factors. The majority of the pituitary adenomas are associated with de novo genetic changes in the adenohypophysial cells, which induce growth factor independent proliferation and clonal expansion of the tumor cells, due to mutation of Gsa gene, activation of hst gene, expression of growth factors (HP, AT II, bFGF), loss of heterozygosity or loss of imprinting.
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PMID:[Pathogenesis of pituitary tumor]. 825 24

Localization and biochemical characteristics of acidic and basic fibroblast growth factor (aFGF and bFGF) were studied in the normal parotid gland (NPG) and in pleomorphic adenoma (PA). In addition, the effects of these factors on proliferation activity were investigated in cultured PA cells. aFGF and bFGF were detected immunohistochemically in 62% and 58% of NPG and 44% and 58% of PA, respectively, and they localized in the cytoplasm of the ductal segments of the NPG, and of the tubular, trabecular and squamous components of PA. Both aFGF and bFGF, each with a molecular weight of 18 kDa, were identified in PA using heparin-sepharose chromatography and Western blot analysis. Both recombinant human aFGF and bFGF stimulated [3H]-thymidine incorporation by cultured PA cells. These results indicated that aFGF and bFGF, probably produced by neoplastic cells, play important roles in the proliferation of PA of the parotid gland.
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PMID:Effects of acidic and basic fibroblast growth factors on cell proliferation in pleomorphic adenoma of the parotid gland. 928 26

Angiogenic cytokines in the plasma and serum of cancer patients may serve as 'surrogate' markers of tumour neoangiogenesis. Serum VEGF correlates with disease stage in colorectal cancer (CRC), but the role of bFGF in CRC is uncertain. This study aimed to assess plasma bFGF levels in CRC patients before treatment, during chemoradiotherapy and at one-year follow-up. Plasma samples were taken from 124 CRC patients, 26 polyp patients and 55 controls, and bFGF levels were measured by ELISA. 19 patients underwent pre-operative chemoradiotherapy. One-year follow-up samples were available from 48 disease-free patients and 18 patients with progressive disease. There were no detectable differences between plasma bFGF levels in polyp, Dukes' A or B patients (4.55, 5.77, 4.25 pg/ml, respectively), but there was a significant increase in metastatic CRC patients [Dukes' C and D (7.42 and 6.6 pg/ml; P = 0.004 and 0.048, respectively)], relative to median control levels of 4.14 pg/ml. At follow-up, there was a significant fall in plasma bFGF levels in disease-free patients (pre-op 6.09 and follow-up 3.45 pg/ml, P = 0.0004), but a non-significant rise in 18 patients with progressive disease (pre-treatment 5.90 and follow-up 9.99 pg/ml, P = 0.33). Pre-treatment plasma bFGF in patients receiving chemo-radiotherapy was similar in those with responsive and non-responsive tumours. There were no detectable changes in plasma bFGF through the adenoma-carcinoma sequence or patient groups with non-metastatic cancers. Elevated plasma bFGF was, however, associated with metastatic spread. The significant fall in bFGF in disease-free patients following therapy suggests that bFGF may be useful in clinical practice.
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PMID:Plasma basic fibroblast growth factor levels in colorectal cancer: a clinically useful assay? 1255 80

The identification of a subpopulation of brain tumor cells with potent tumorigenic capacity strengthens the cancer stem cell hypothesis of the origin of the tumors that has recently attracted the attention of many researchers. Reports have been published on the identification of tumor cells with stem cells characteristics in different types of tumors (acute myelogenic leukemia, breast cancer, prostate cancer, bone sarcomas, liver cancer, and melanomas). We and other groups have previously reported the isolation of cancer stem cells from adult glioblastoma multiforme. These cells express stem cell markers, and when differentiated they express glial and neuronal markers. In vivo they give a tumor that recapitulates the characteristics of the tumor in the patient. More recently we have isolated tumor stem-like cells also from benign tumors like pituitary adenomas. Cells derived from pituitary adenomas are able to grow as floating aggregates resembling the neurospheres (typical of normal stem cells) in a medium supplemented by growth factors (EGF and bFGF). The immunocytochemical analysis revealed that pituitary tumor stem-like cells are positives for nestin and, when grown for ten days in differentiation medium they express GFAP, BIII tubulin, and S-100. In vitro tumor stem-like cells derived from a patient with a somatotroph adenoma showed high production of growth hormone and prolactin, while cells derived from the same patient but grown in presence of fetal bovine serum showed no production of hormones.
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PMID:Pituitary adenoma stem cells. 1958 28

Klotho is a transmembranal protein highly expressed in the kidneys, choroid plexus, and anterior pituitary. Klotho can also be cleaved and shed and acts as a circulating hormone. Klotho-deficient mice (kl/kl mice) develop a phenotype resembling early aging. Several lines of evidence suggest a role for klotho in the regulation of growth hormone (GH) secretion. The kl/kl mice are smaller compared with their wild-type counterparts, and their somatotropes show reduced numbers of secretory granules. Moreover, klotho is a potent inhibitor of the IGF-I pathway, a negative regulator of GH secretion. Therefore, we hypothesized that klotho may enhance GH secretion. The effect of klotho on GH secretion was examined in GH3 rat somatotrophs, cultured rat pituitaries, and cultured human GH-secreting adenomas. In all three models, klotho treatment increased GH secretion. Prolonged treatment of mice with intraperitoneal klotho injections increased mRNA levels of IGF-I and IGF-I-binding protein-3 mRNA in the liver, reflecting increased serum GH levels. In accord with its ability to inhibit the IGF-I pathway, klotho partially restored the inhibitory effect of IGF-I on GH secretion. Klotho is known to be a positive regulator of basic bFGF signaling. We studied rat pituitaries and human adenoma cultures and noted that bFGF increased GH secretion and stimulated ERK1/2 phosphorylation. Both effects were augmented following treatment with klotho. Taken together, our data indicate for the first time that klotho is a positive regulator of GH secretion and suggest the IGF-I and bFGF pathways as potential mediators of this effect.
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PMID:The aging suppressor klotho: a potential regulator of growth hormone secretion. 2493 36