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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor progression of cancers is manifested by phenotypic property changes including development of hormone/growth factor independence and metastatic ability. The progression results from acquired genomic alterations leading to clonal heterogeneity and outgrowth of more aggressive and therapy-resistant sublines. Previously, a cultured rat "Nb2 lymphoma" cell line was established, whose viability depends critically on the hormone, prolactin, acting as the principal growth factor. By prolactin starvation, prolactin-independent sublines were generated which possessed the parent karyotype plus extra acquired chromosomal changes (clonal evolution). In this study, the parent line (Nb2-U17) and a cloned subline (SFJCD1) were compared for metastatic ability using single s.c. tumor transplants in Noble rats. Rats (22) bearing Nb2-U17 tumors showed no evidence of metastases at autopsy, even when tumors at implantation site reached a size of 9 cm (length + width). In contrast, rats (19) bearing SFJCD1 tumors showed multiple metastases (liver, kidney) when transplants exceeded 5 cm. This difference in metastatic ability may be related to the acquisition of an inversion in chromosome 1, i.e. inv(1)(q31q41). The 1q41 locus is adjacent to the reported H-ras-1 proto-oncogene locus (1q41-q42). In another subline, tetraploidization (flow cytometric analysis, karyotyping) occurred spontaneously following prolonged culturing (20 mo). Together, the parent Nb2 lymphoma line and its clonal derivatives provide a novel system for studying cellular and molecular mechanisms underlying tumor progression to the metastatic phenotype.
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PMID:The rat Nb2 lymphoma: a novel model for tumor progression. 787 71

Rats were administered the somatostatin analogue octreotide 15 micrograms intraperitoneally twice daily for 4 weeks after intraportal injection of somatostatin receptor-positive pancreatic tumour cells (CA-20948) and somatostatin receptor-negative colonic tumour cells (CC531). Octreotide significantly inhibited the growth and development of somatostatin receptor-positive tumour cells in the liver. The median number of liver tumours was 286 (range 146 to greater than 500) in the treated animals and more than 500 (range 250 to in excess of 500) in the controls (P < 0.05). This significant difference in tumour load was also represented in the mean(s.e.m.) liver weight (14.5(3.7) g in animals given octreotide versus 17.9(3.0) g in the controls). No effect of octreotide treatment was found on the growth and development of somatostatin receptor-negative tumour cells in the liver. The median (range) number of tumours was 6.5 (0-425) in the treated animals and 11.0 (0-475) in the controls. Mean(s.e.m.) liver weights were 14.0(5.7) g and 11.8(4.5) g respectively. There was no difference in serum levels of growth hormone, prolactin and insulin-like growth factor between control and octreotide-treated rats. The growth inhibition of somatostatin receptor-positive tumour cells was unlikely to be the result of suppressed secretion of one of these tumour growth factors. Octreotide may be useful for the treatment of patients with somatostatin receptor-positive hepatic metastases, which can be demonstrated by somatostatin receptor scintigraphy.
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PMID:Somatostatin receptor-dependent growth inhibition of liver metastases by octreotide. 795 4

Neuroendocrine cells are thought to have a regulatory role in prostatic epithelial growth and may be prognostically useful in prostatic adenocarcinoma. To determine the extent of neuroendocrine differentiation in high-grade prostatic intraepithelial neoplasia (PIN), a putative precursor of cancer, we studied the immunohistochemical expression of 10 markers in 26 radical prostatectomy specimens with PIN and adenocarcinoma. Expression was measured as mean percent of positive cases and positive high-power (x40) fields. The highest percentage of cases showed immunoreactivity for serotonin (73%, PIN; 54%, carcinoma), neuron-specific enolase (NSE) (67%, PIN; 46%, carcinoma), chromogranin (62%, PIN; 65%, carcinoma), and human chorionic gonadotropin (hCG) (30%, PIN; 22%, carcinoma); the remaining markers showed immunoreactivity in fewer than 5% of cases (somatostatin, calcitonin, corticotropin) or in no cases (thyrotropin, prolactin, and glucagon). At least one of the markers was present in 88% of cases of PIN and 92% of carcinoma. Non-neoplastic epithelial cells expressed serotonin, NSE, chromogranin, and hCG in every case, and the expression was significantly greater than in PIN and cancer. Stepwise regression analysis revealed the following positive correlations: chromogranin expression in PIN and patient age, NSE expression in cancer and number of lymph node metastases, and hCG expression in cancer and percentage of Gleason pattern 5; serotonin expression in PIN and cancer did not correlate with any of the clinical and pathologic factors. Neuroendocrine differentiation is downregulated in prostatic carcinogenesis, with intermediate levels of expression in PIN compared with normal cells and carcinoma.
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PMID:Neuroendocrine differentiation in prostatic intraepithelial neoplasia and adenocarcinoma. 797 47

The authors report a case of a pituitary carcinoma which was locally invasive and which metastasized to cervical lymph nodes more than 9 years after the initial presentation. Cells from the tumour and metastasis immunostained with antibodies to prolactin and growth hormone, even though there was no clinical or biochemical evidence that the tumour was secreting prolactin or growth hormone. In addition, ultrastructural studies showed a monomorphic tumour with secretory granules much smaller than those normally associated with prolactin and growth hormone secretion. The clinical and pathological features suggest that the tumour is probably an acidophil stem cell adenoma, which although known to be aggressive in its clinical behaviour has not been previously reported to metastasize.
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PMID:Cervical lymph nodes metastases from a pituitary carcinoma. 801 Dec 1

Only seven cases of metastatic prolactin-secreting pituitary tumour have been reported in world literature. The metastases were intra-cranial in five cases and extra-cranial in two cases. We report a further case with multiple intra-cranial metastases in the supra-tentorial compartment. Histologically, both primary and metastatic tumours were benign with strongly positive immuno-histochemical staining for prolactin. Our case exemplifies the inconsistent correlation between the histopathological appearance and biological behaviour of malignant pituitary tumours.
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PMID:Case report: multiple intra-cranial metastases from a prolactin-secreting pituitary tumour. 801 6

Primary intracranial tumours develop in 420 adult Norwegians each year. Of these tumours, gliomas are the most frequent, followed by meningiomas, pituitary adenomas and acoustic neurinomas. Glioblastomas represent more than 50% of the gliomas. Less than 10% of the patients with glioblastoma survive for two years, despite aggressive therapy (surgery, radiotherapy and chemotherapy). The prognosis for low grade gliomas is much better. In the case of meningiomas, 95% of the tumours are benign. The primary treatment for meningiomas is surgery. If surgery is impossible, radiosurgery should be considered. Pituitary adenomas are often hormone-secreting (e.g. prolactin, growth hormone, adrenocorticotrophic hormone). Many prolactinomas are treated with bromocriptine alone. The rest of the pituitary adenomas are treated by microsurgery and radiotherapy. The prognosis for patients with pituitary adenomas is good. Acoustic neurinomas, which in most cases are benign, are treated by microsurgery or radiosurgery. Postoperative morbidity due to cochlear nerve and facial nerve dysfunction is a problem. Brain metastases are far more frequent than primary intracranial tumours. Solitary metastases in patients with stable systemic disease should be treated by surgery or radiosurgery.
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PMID:[Intracranial tumors in adults (over 15 years)]. 833 22

The purpose of this study was to investigate a prognostic indicator that can differentiate node negative breast cancer patients (N = 39, T2N0M0) with high risk and low risk for the development of recurrence or metastases. Preoperative plasma prolactin (PRL) was estimated by radioimmunoassay. The expression of PRL, p53, nm23, and c-erbB2 was investigated by immunohistochemical (IHC) localization; cathepsin D (CD, Enzyme Linked Sorbant Assay) and estrogen- and progesterone-receptors (ER and PR, Dextran coated charcoal method) were estimated in the tumor cytosols. The follow-up period was 2-6 years. Statistical comparisons were made between each marker for relapse-free survival (RFS) and overall survival (OS). Of the 39 patients, 18 had hyperprolactinemia (PRL > 20.0 ng/ml plasma), whereas overexpression of p53 was observed in 55% (17/31) tumors. These were independently and in combination associated with a reduced RFS and OS. The rest of the investigated markers did not show promising results. Hyperprolactinemia and/or overexpression of p53 were associated with aggressiveness of the tumor, early disease relapse or metastases, and poor OS in patients with node negative breast cancer. These two markers may enhance our ability to identify node negative breast cancer patients with aggressive tumors, for whom the use of adjuvant chemo and/or endocrine therapy is unequivocally justified.
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PMID:Node negative breast carcinoma: hyperprolactinemia and/or overexpression of p53 as an independent predictor of poor prognosis compared to newer and established prognosticators. 864 46

Hormones of the hypothalamic-pituitary-adrenal system were studied in 31 patients with early stage breast cancer and patients with metastatic breast cancer. Both groups received tamoxifen as first-line treatment. As a control group 15 age-matched healthy women participated in the study. The results showed that breast cancer patients had significant elevations in basal cortisol levels compared to controls. Metastatic breast cancer patients had higher cortisol levels than early stage breast cancer patients. No significant differences between breast cancer patients and controls were found in basal plasma ACTH and prolactin levels. These data provide evidence that breast cancer is associated with a hyperactive adrenal gland, which may be due to the physiological stress associated with the presence of (micro)metastases or tumor cells in the circulation, in combination with administration of tamoxifen. In response to a behavioral challenge increases were observed in plasma ACTH and prolactin. Metastatic breast cancer patients had a faster prolactin response to acute stress than healthy women. However, metastatic breast cancer patients showed a blunted ACTH response compared to healthy women. Stress-induced ACTH responses and basal cortisol levels were negatively correlated in the metastatic group only. Thus, the blunted ACTH response to the behavioral challenge might be related to hypercortisolemia suggesting that the pituitary corticotroph cell in metastatic cancer is appropriately restrained possibly by the negative feedback effects of chronic cortisol elevations. Interestingly, the behavioral challenge induced decreases in cortisol levels in all three groups. However, metastatic breast cancer patients had a faster cortisol decline compared to healthy women. We hypothesize that this is caused by increased metabolic clearance of cortisol due to increased utilization of metabolic substrates often observed in the presence of a tumor.
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PMID:Elevated basal cortisol levels and attenuated ACTH and cortisol responses to a behavioral challenge in women with metastatic breast cancer. 884 75

Cancer patients who had been treated for early stage breast cancer and were diagnosed with either positive axillary lymph nodes or distant metastases were randomly assigned to either a 13-week experiential-existential group psychotherapy (EEGP) program or a waiting list control (WLC) condition. Endocrine and immune measures were obtained before and after the intervention period. The findings of this study are that, after the 13 weeks of the experiment, patients in the EEGP group showed lower levels of plasma cortisol and lower levels of prolactin as well as lower percentages of natural killer cells, CD8 cells, and CD4 cells in addition to a lower proliferative response to pokeweed mitogen than patients in the WLC group. Importantly, this was only found in those breast cancer patients presenting relatively high endocrine and immune baseline levels, suggesting that the patients' profile with regard to endocrine and immune function at the start of a program can have an important effect. If replicated on a larger scale, the current results may be relevant for the treatment of breast cancer.
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PMID:Effectiveness of a short-term group psychotherapy program on endocrine and immune function in breast cancer patients: an exploratory study. 919 18

Plasma levels of chromogranin A (CgA) were measured by ELISA in 22 patients with pheochromocytoma (18 non-metastatic, 3 metastatic, and 1 mixed neuroendocrine-neural tumor), 9 patients with primary hyperparathyroidism, and 9 patients with pituitary adenoma. The plasma levels of CgA were compared with norepinephrine, epinephrine, parathyroid hormone and pituitary hormones, i.e., growth hormone and prolactin. In pheochromocytoma, CgA in preoperative plasma of the patients without metastasis was 228 +/- 38 U/L (mean +/- SEM) and significantly higher than healthy controls (30 +/- 11 U/L, n = 40). Plasma CgA was decreased after removal of the tumors (28 +/- 6.0 U/L), except in three patients with metastatic pheochromocytoma and a mixed neuroendocrine neural tumor. The concentration of CgA in the patients with non-metastatic pheochromocytoma was significantly correlated with that of plasma norepinephrine (P < 0.005, r = 0.68) and urinary norepinephrine (P < 0.05, r = 0.65), but not with that of epinephrine. There was an exceptional case in which CgA was extremely high, but the CA level was normal. This tumor was a highly malignant pheochromocytoma with extensive metastases composed of small tumor cells which were occasionally positive for tyrosine hydroxylase immunohistochemically. These cells were considered to be poorly differentiated tumor cells and synthesized a very small amount of norepinephrine. Plasma levels of the patients with primary hyperparathyroidism and the patients with pituitary adenoma were 44 +/- 4 U/L and 48 +/- 8 U/L, respectively. Only one patient with a growth hormone-producing pituitary adenoma had a high level of CgA. Plasma CgA is a useful tumor marker for pheochromocytoma, even for malignant pheochromocytoma without elevated CA level, but not for hyperparathyroidism, or pituitary adenoma.
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PMID:Plasma chromogranin A in pheochromocytoma, primary hyperparathyroidism and pituitary adenoma in comparison with catecholamine, parathyroid hormone and pituitary hormones. 922 69


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