Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a preliminary report we described the effects of rat prolactin on the incorporation of [14C]acetate into lipids by a cell line from a dimethylbenz(a)anthracene-induced rat mammary tumor. The characteristics of the response to prolactin were very similar to those described for the normal rat mammary gland; namely, insulin was required for full expression of the response, maximal activity was not seen until 36 hr after the addition of the hormones, and growth hormone was able to elicit the same response. However, we were unable to detect binding of 125I-labeled prolactin to these cells, and furthermore, other more purified prolactin preparations were inactive. Upon further investigation we discovered that the activity resided in a low-molecular-weight fraction of the rat prolactin B-1 preparation and was probably either vasopressin or oxytocin or both. These data suggest the possibility that vasopressin may play a role in rodent mammary tumorigenesis.
Cancer Res 1978 Nov
PMID:Vasopressin stimulation of acetate incorporation into lipids in a dimethylbenz(a)anthracene-induced rat mammary tumor cell line. 10 Feb 17

Two cases of small cell carcinoma of the lung associated with the ectopic production of multiple hormones are reported. Both tumors were shown to contain significant amounts of ADH, ACTH, and beta-MSH. Biologic, immunologic, and gel chromatographic properties of these ectopic hormones were found to be very similar to those of pituitary origin. The effect of excessive secretion of antidiuretic hormone (ADH) dominated the clinical manifestations in both cases, i.e., syndrome of inappropriate secretion of ADH (SIADH). The clinical manifestations of the ectopic ACTH-MSH syndrome were minimal. These data suggest that multiple hormone production without clinically overt sequelae of excess hormone is not uncommon in small cell (oat cell) carcinoma of the lung.
Cancer 1976 Dec
PMID:Two cases of multiple hormone-producing small cell carcinoma of the lung: coexistence of tumor ADH, ACTH, and beta-MSH. 18 19

Cyclophosphamide is used extensively to treat malignancies. A 5-year-old boy with stage IV neuroblastoma is described who developed a fatal syndrome of inappropriate antidiuretic hormone (ADH) secretion after high dose cyclophosphamide therapy.
Cancer 1979 Sep
PMID:A fatal case of inappropriate ADH secretion induced by cyclophosphamide therapy. 47 99

Thirteen leukemic patients with disease refractory to conventional chemotherapy were treated with 1.0 to 7.5 g/m2 of Cytosine Arabinoside (Ara-C) over 29 drug cycles. Drug infusions were spaced at 12-hour intervals; a maximum of four doses was administered over 36 hours. After single dose tolerance had been established, three or four dose cycles were given at 2- to 30-day intervals. There were three partial remissions (PR) and one complete remission (CR) in a treatment group of four patients with AML, five with ALL, two with lymphoma converted to leukemic phase, one CML in blast crisis, and one promyelocytic leukemia. Five of the patients were septic and considered terminally ill at the time of treatment. All other patients had evidence of drug responsiveness. The nadir of the white count occurred from 3 to 12 days after treatment, with subsequent recovery of the peripheral granulocyte count between days 12 and 28. Toxicity included nausea and vomiting (GI symptoms) in twelve patients, central nervous system (CNS) disturbances in eight patients, one episode of inappropriate antidiuretic hormone syndromes (SIADH), one of hyperuricemia, and fever in eleven patients. There was no evidence of hepatic or renal dysfunction. These high doses of Ara-C appear useful for treatment of patients with refractory leukemia. Hospitalization is brief and toxicity acceptable.
Cancer 1979 Oct
PMID:High dose cytosine arabinoside (HDARAC) in refractory acute leukemia. 49 9

A 12-year-old female with lymphosarcoma responding to treatment including vincristine and cyclophosphamide developed clinical and laboratory findings compatible with the syndrome of inappropriate secretion of antidiuretic hormone. Some additional findings were observed, i.e. uremia, hypopotassemia and alkalosis, that have not so far been recorded in that syndrome. All abnormalities were corrected upon water restriction. A similar episode occurred after a 2nd drug course. It too was corrected upon water restriction. The patient was clinically free from her malignancy in both episodes. It is suggested that our child had probably an expanded form of the syndrome of inappropriate secretion of antidiuretic hormone.
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PMID:Electrolyte abnormalities in lymphosarcoma after chemotherapy. 58 54

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) has been recognized to occur following treatment with vincristine. None of the reports have provided information regarding its potential for recurrence on further challenge with vincristine (VCR), an agent generally required for repeated use in patients with malignancies. Symptomatic hyponatremia and SIADH that occurred 8 days following administration of VCR in a child with acute lymphatic leukemia was documented with specific radioimmunoassay of urinary ADH levels. The further occurrence of recurrent elevations in ADH excretion 8-10 days following repeated treatment with VCR was also observed. However, SIADH was prevented by prophylactic rigorous fluid restriction. The occurrence of SIADH following VCR therefore does not preclude the further safe usage of this drug.
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PMID:Syndrome of recurrent increased secretion of antidiuretic hormone following multiple doses of vincristine. 105 63

Because small cell anaplastic carcinoma of the prostate is an uncommon tumor, it has remained a poorly defined entity. To elucidate further the clinical, pathological and immunohistochemical characteristics of this cancer the 27 patients who presented to the Mayo Clinic from 1960 to 1990 were reviewed. Of these patients 18 (67%) presented with pure small cell anaplastic carcinoma, and 9 (33%) were diagnosed with small cell anaplastic carcinoma and adenocarcinoma of the prostate. Twenty-six patients (96%) had either stage C or D disease at the time of diagnosis. Two patients presented with a paraneoplastic syndrome, including 1 man with inappropriate antidiuretic hormone secretion and 1 who suffered from thyroxine intoxication. Of 24 men with long-term followup 22 (92%) died of small cell anaplastic carcinoma of the prostate despite antiandrogen therapy and the remaining 2 are alive with active, progressive disease. The median survival time following diagnosis was 17.1 months (range 2 to 90 months). All tumors with tissue available for immunohistochemical staining reacted positive for neuron-specific enolase, indicating that small cell anaplastic carcinoma of the prostate is most likely a neuroendocrine neoplasm. No tumor stained positive for either prostatic acid phosphatase or prostate specific antigen. Pathologically, small cell anaplastic carcinoma of the prostate appears to be similar to oat cell carcinoma of the lung. This series of 27 patients emphasizes that small cell anaplastic carcinoma of the prostate is highly malignant, is frequently of advanced stage at presentation, responds poorly to antiandrogen therapy and has a poor prognosis.
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PMID:Small cell anaplastic carcinoma of the prostate: a clinical, pathological and immunohistological study of 27 patients. 131 95

Neuropeptides are increasingly implicated in the control of cell proliferation and their mechanisms of action are attracting intense interest. The early complex cascade of events initiated by peptides of the bombesin family including gastrin-releasing peptide is increasingly understood. The cause-effect relationships and temporal organization of these early signals and molecular events provide a paradigm for the study of other growth factors and mitogenic neuropeptides and illustrate the activation and interaction of a variety of signaling pathways. These peptides may also act as autocrine growth factors for certain small cell lung cancer cells. The results discussed here strongly suggest that the autocrine growth loop of bombesin-like peptides may be only a part of an extensive network of autocrine and paracrine interactions involving a variety of Ca(2+)-mobilizing neuropeptides in small cell lung cancer including bradykinin, cholecystokinin, galanin, neurotensin, and vasopressin. In this context, broad spectrum antagonists that prevent the function of multiple Ca(2+)-mobilizing receptors are of special interest. These antagonists block neuropeptide mediated signals and inhibit small cell lung cancer growth in vitro and in vivo. Thus, broad spectrum neuropeptide antagonists constitute potential anticancer agents.
Cancer Res 1992 May 01
PMID:Growth of small cell lung cancer cells: stimulation by multiple neuropeptides and inhibition by broad spectrum antagonists in vitro and in vivo. 131 36

We have described a patient who had lung carcinoma, syndrome of inappropriate antidiuretic hormone, and central pontine myelinolysis (CPM). Although this association is well-known, it appears to be the first report having radiographic documentation of both the intracranial and intrathoracic abnormalities. When searching for the cause of CPM, the possibility of an underlying malignancy should also be considered. This may be more common than the radiology literature would suggest.
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PMID:Central pontine myelinolysis as a manifestation of the paraneoplastic syndrome. 131 30

The clinical and laboratory findings in 76 patients with isolated corticotropin deficiency (10 of our own and 66 from literature) were analyzed with the following observations. With the exceptions of hyperpigmentation and hyperkalemia, the similarity of symptoms and signs to those of Addison's disease and their reversibility by glucocorticoids indicate that most, but not all, manifestation of isolated corticotropin deficiency is caused by glucocorticoid deficiency. Isolated corticotropin deficiency seems to be of pituitary origin in most patients, as shown by lack of corticotropin response to insulin-induced hypoglycemia, vasopressin, or corticotropin-releasing factor. Secretion of other pituitary hormones is frequently abnormal, which is mostly attributable to glucocorticoid deficiency. Although the pathogenesis of isolated corticotropin deficiency is unknown in most patients, association with other autoimmune endocrinopathies, postpartum onset in women, or serum antipituitary antibodies suggests an autoimmune pathogenesis in some patients. In two of our 10 patients, cancer developed during glucocorticoid treatment. More observations of complications and long-term prognosis following glucocorticoid therapy are needed for optimal clinical decision making.
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PMID:Isolated corticotropin deficiency in adults. Report of 10 cases and review of literature. 132 48


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