Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventy-eight patients with cytologically and/or histologically confirmed prostatic cancer were randomly allocated to orchidectomy (ORX, n = 37) or combined intramuscular and oral estrogen treatment (ESTR, n = 41). Serum levels of testosterone (T), 17 alpha-hydroxyprogesterone, dehydroepiandrosterone, dehydroepiandrosterone sulfate, total estrone (tE1; sum of unconjugated and conjugated estrone, greater than or equal to 85% estrone sulfate), cortisol, luteinizing hormone, follicle-stimulating hormone, prolactin, growth hormone, sex hormone-binding globulin (SHBG), and albumin were determined prior to treatment and 12, 24, and 36 months after initiation of treatment. Fifty patients responded to treatment or had stable disease, and 28 did not respond (12 in the ORX and 16 in the ESTR group). There was no association between pretreatment hormone or protein levels and outcome of the treatment, neither in the total material nor within either of the two treatment subgroups. Significantly higher pretreatment levels of cortisol and prolactin and significantly lower levels of T, tE1, and albumin and a significantly lower T/SHBG-ratio (index on biologically active T) were found in patients with metastatic disease, compared with the patients without metastases. There was no association between testicular or adrenal androgens, SHBG, T/SHBG, and albumin values during treatment and the clinical outcome. The differences found between metastatic and nonmetastatic disease probably simply reflect the more stressful and catabolic condition and generally poorer health in patients with disseminated malignant disease. Furthermore, the study does not lend any support to the hypothesis that indicates an important role of adrenal "rest androgen" in prostatic cancer tumor growth.
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PMID:Prognostic value of serum hormone concentrations in prostatic cancer. 321 6

A rare case of a patient with multiple intracranial metastases from a prolactin-secreting pituitary neoplasm is described. At the age of 14 years, the patient had been operated on for a sellar tumor; he presented 12 years later with severe headache, at which time computed tomographic and magnetic resonance imaging scans revealed multiple intracranial metastases. Histopathology examination showed pituitary neoplastic cells with positive immunostaining for prolactin. The patient was investigated with positron emission tomography (PET) and dopamine D2-receptor binding, and the amino acid metabolism of the tumor was characterized in vivo. High dopamine D2-receptor binding and high amino acid metabolism were found in the tumor. The patient was subsequently treated with bromocriptine injections that resulted in a decrease in serum prolactin levels, decreased dopamine D2-receptor binding, reduced amino acid metabolism, and a reduction in tumor volume. This case demonstrates a beneficial effect of bromocriptine treatment in a patient with prolactinoma with multiple intracranial metastases. It also illustrates the great potential of PET in the in vivo characterization of the D2-binding and the high sensitivity of 11C-labeled L-methionine in the follow-up of treatment in patients with pituitary adenomas.
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PMID:Malignant prolactinoma with multiple intracranial metastases studied with positron emission tomography. 325 13

Prolactin secreting tumors account for ten to twenty percent of all intracranial lesions. The patients harboring these tumors present with amenorrhea, galactorrhea, other ovulatory disorders, infertility, delays in puberty and mixed polyendocrinopathy. These tumors are diagnosed by the measurement of serum prolactin levels, Goldmann-Bowl perimetry, and either computed axial tomography or magnetic resonance imaging. Protein secreting tumors are usually benign lesions and historically have been treated by partial or total hypophysectomy or radiation therapy. Surgical resection of the lesion often is followed by recurrence and administration of proton beam radiation therapy results in the development of a panhypopituitary state. Growth of pituitary tumors is controlled with the administration of dopamine agonists such as bromocriptine and prospective studies have suggested that these drugs are now the preferred method of treatment for primary lesions and recurrences.
Cancer Metastasis Rev 1986
PMID:Diagnosis and management of prolactinomas. 354 32

Hourly blood sampling for CEA determination was performed in metastatic breast cancer patients before and during medical treatment. Rhythmic fluctuations of marker concentrations could be detected. These oscillations seemed to be independent of the localisation of metastases and the kind of treatment. No relation between cortisol or prolactin and CEA levels became apparent.
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PMID:Rhythmic fluctuations of CEA serum levels in breast cancer patients. 367 59

A 28 year old man presented with partial hypopituitarism and signs of a pituitary tumour. A chromophobe adenoma was partially removed by right frontal craniotomy. Seven years later complete hypopituitarism and hyperprolactinaemia were documented, at which time there was no evidence of tumour recurrence of CT scan. The patient was treated with bromocriptine but the pituitary tumour redeveloped a year later. Nine years after the original operation the first metastasis was demonstrated together with very high prolactin levels. The intracranial metastasis, and the pituitary tumour were removed at a second craniotomy following which the prolactin concentration fell. Further metastases developed subsequently and the patient died 12 years after the initial diagnosis. At autopsy multiple metastases were found in the brain, tumour cells were present in the subarachnoid space and in cerebral veins. The pituitary tumour and secondaries were shown by immunocytochemistry to contain prolactin but not ACTH or growth hormone. This appears to be the third well documented case of a metastasizing, prolactin secreting pituitary tumour.
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PMID:Multiple intracranial metastases from a prolactin secreting pituitary tumour. 397 26

A 37-year-old man developed a left frontal metastasis from a prolactin-secreting pituitary tumour, which had been operated on nine years before. The metastatic tumour was totally excised. One and a half years later he was found to have multiple left temporal and parietal subarachnoid metastases. Because treatment with bromocriptine for five months and subsequent radiation proved ineffective, the tumour nodules were removed surgically.
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PMID:Subarachnoid metastases from a prolactinoma. 408 58

Hypophysectomy was studied for its possible effects on cancer by alt eration of the endorcines at the New York Hospital-Cornell Medical Center beginning in 1953. The major effort has been the treatment of 850 cases of metastic breast cancer. In 80 patients with other types of metastatic cancer benefit was found only in 50 cases of prostatic cancer. Prolactin is mediated directly from the anterior pituitary to breast tissue where it aids and abets the growth of breast cancer; its secretion is largely dependent on the estrogen produced in ovaries and adrenals. In humans estrogen given after total hypophysectomy is found to be ineffective in altering metastases. Growth hormone is also produced in the anteriod lobe of the pituitary but its production is not dependent on an estrogen feed-back mechanism. If the primary cancer is dependent on the presence of prolactin, failures with hypophysectomy are explained the tumor having gained autonomy and being no longer so dependent. Contraindications to hypophysectomy include extensive pulmonary, liver, or brain metastases and any systemic disease that would preclude major surgery. Following a remission after oophorectomy, another remission with hypophysectomy may often be obtained. Neither the pathological type of a breast cancer nor the location of metastases alter the results. However the longer the interval between mastectomy and reactivation of the tumor, the more favorable the outlook. Maintenance substitution therapy following removal of the pituitary employs daily hydrocortisone, 17.5 mg orally, or equivalent steroid preparations. The mortality rate is 2% in the first 30 days after operation. In 88 patients evaluated 2 years after operation those who had received a remisssion lasting over 6 months survived nearly 5 times longer than those unbenefitted by the operation. The intracranial procedure is preferred. In cases of failure or when a remission terminates, male hormone therapy, chemotherapy, or radiation may have limited value.
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PMID:Hypophysectomy for metastatic cancer. 466 60

The effects of neuroadenolysis on plasma titres of beta-endorphin, beta-lipotropin, ACTH, TSH and prolactin have been investigated in five patients with metastatic cancer who responded to the treatment and have been in remission for more than four years and in five others who were undergoing the treatment for the first time for pain due to cancer metastases. beta-Endorphin, beta-lipotropin and ACTH titres were within the normal ranges of values in both categories of patients but post-neuroadenolysis titres of these peptides were higher than those before the treatment. The ability to secrete TSH and prolactin and to respond to thyroid stimulating hormone releasing hormone (TRH) remains intact following the treatment. However, whereas basal TSH titres and response to TRH was lower in the majority of patients, no such effect was observed on prolactin secretion. Plasma titres of prolactin and TSH were below the sensitivity of the method in the five patients who are in remission for more than four years. These preliminary findings suggest that neuroadenolysis probably affects some mechanism(s) associated with the control of beta-endorphin, beta-lipotropin and ACTH synthesis.
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PMID:Some aspects of pituitary function after neuroadenolysis in patients with metastatic cancer. 627 71

The effect of tamoxifen therapy on plasma hormones in the pre- and postmenopausal state was studied in a young patient with breast cancer. Tamoxifen therapy was carried out for metastatic disease prior to (premenopausal) and after oophorectomy (surgical menopause). Changes in luteinizing hormone, follicle-stimulating hormone, prolactin, and estrogen were noted and were corroborated with the therapy or oophorectomy. The findings support some of the previously reported changes in those hormones that were noted in conjunction with tamoxifen therapy.
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PMID:Plasma hormone responses to tamoxifen therapy and oophorectomy. 629 82

Biopsy specimens of 55 human mammary carcinomas (38 primary and 17 metastatic) were assayed for prolactin receptors (PrlR). Prolactin bound specifically to 32 (58%) of the tumor biopsy specimens. The apparent Kd for PrlR in individual tumors ranged from 15 pM to 2.3 nM (mean 600 pM, n = 5) and the concentration of PrlR ranged from 0 to 44.5 fmoles/mg protein. Estrogen receptors (ERP) were also detected in 28 of the 32 tumors which had PrlR. Overall, there was no correlation between PrlR and ERP. However, the mean concentration of PrlR was significantly higher (p less than 0.01) in tumors with 6-100 fmoles/mg protein ERP (approximately 13 fmoles PrlR) than in tumors with either less than 6 or greater than 250 fmoles ERP (4.0 +/- 0.4 and 6.5 +/- 1.8 respectively fmoles PrlR). Analysis of PrlR concentration as a function of patient age also showed no overall correlation, but the mean PrlR in tumors from women aged 60-70 was significantly higher (p less than 0.01) than in those from either younger or older women. A higher concentration of PrlR was observed in tumors which were classified histologically as medium or well differentiated (6.1 +/- 1.2 and 11.1 +/- 2.1, respectively) than in those classified as poorly differentiated (3.3 +/- 1.2) (p less than 0.03). There was a negative correlation between PrlR concentration and membrane yield from the tumors (r = 0.43, p less than 0.02). The membrane yield correlated with the ratio of tumor cells to stroma (histologically) (r = 0.63, p less than 0.001). In tumors from 12 patients with metastatic disease on whom follow up after endocrine-related therapy was available, the mean PrlR concentration was significantly higher in the non-responding group (8.2 +/- 3.0) than in the responding group (3.4 +/- 4.2, p = 0.05).
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PMID:Prolactin binding by human mammary carcinoma: relationship to estrogen receptor protein concentration and patient age. 629 28


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