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)

The antitumor sesquiterpene lactone helenalin, which is found in species of the plant genus Helenium, caused a marked potentiation of the increases in intracellular free Ca2+ concentration ([Ca2+]i) produced by mitogens such as vasopressin, bradykinin, and platelet-derived growth factor in Swiss mouse 3T3 fibroblasts. Removing external Ca2+ partly attenuated the increased [Ca2+]i responses caused by helenalin. The increased [Ca2+]i responses occurred at concentrations of helenalin that inhibited cell proliferation. At higher concentrations, helenalin inhibited the [Ca2+]i responses. No change in resting [Ca2+]i was caused by helenalin even at high concentrations. Other helenalin analogues also increased the [Ca2+]i response. Helenalin did not inhibit protein kinase C (PKC) and PKC appeared to play a minor role in the effects of helenalin on [Ca2+]i responses in intact cells. Studies with saponin-permeabilized HT-29 human colon carcinosarcoma cells indicated that helenalin caused an increased accumulation of Ca2+ into nonmitochondrial stores and that the potentiating effect of helenalin on mitogen-stimulated [Ca2+]i responses was due in part to an increase in the inositol-(1,4,5)-trisphosphate-mediated release of Ca2+ from these stores.
Cancer Chemother Pharmacol 1994
PMID:Increased intracellular Ca2+ signaling caused by the antitumor agent helenalin and its analogues. 803 1

Four classical and three variant small-cell carcinoma of the lung (SCCL) cell lines were examined for vasopressin and vasopressin V1a-receptor immunoreactivity. One of these classical cell lines, NCI-H345, and one variant cell line, NCI-H82, were further investigated for binding of V1 and V2 vasopressin-receptor antagonists, vasopressin-induced calcium mobilization, and vasopressin-induced thymidine uptake. All classical and variant SCCL cell lines examined contained vasopressin and vasopressin-receptors as determined by immunocytochemistry. Both NCI-H82 and NCI-H345 demonstrated similar binding patterns with the V1 and V2 vasopressin-receptor antagonists, indicating the presence of both receptor subtypes. For the classical cell line (NCI-H345), vasopressin (1 microM) induced an increase in cytosolic free calcium, while the peptide was ineffective at increasing cytosolic calcium in the variant cell line (NCI-H82). However, vasopressin (0.1 or 1 microM) was unable to stimulate thymidine uptake in the classical (NCI-H345) or variant (NCI-H82) cell lines for the conditions used. These results indicate that both classical and variant SCCL produce vasopressin, and vasopressin V1a and V2 receptors. In the variant cell line, there appears to be a disruption in the activation cascade for V1a receptors as indicated by the lack of vasopressin-induced calcium mobilization.
Cancer Lett 1994 Jul 29
PMID:Vasopressin and vasopressin-receptor immunoreactivity in small-cell lung carcinoma (SCCL) cell lines: disruption in the activation cascade of V1a-receptors in variant SCCL. 805 87

We detected low level expression of the gastrin-releasing peptide and neuromedin-B receptor mRNAs in cultures of human bronchial epithelium from 4 of 6 individuals. Bombesin receptor subtype-3 mRNA was undetectable in these cells. An elevation of intracellular calcium concentration was observed in response to bradykinin (6 of 6) and neurotensin (1 of 5) but not to bombesin (0 of 6), vasopressin (0 of 6), or cholecystokinin (0 of 3). In contrast, such responses are frequently noted in lung cancer cell lines. Bombesin did not stimulate the in vitro growth of an immortalized human bronchial epithelium cell line expressing low levels of bombesin receptor mRNAs. We conclude that bombesin receptors are expressed at low levels in human bronchial epithelium cells which may acquire greater responsiveness to multiple neuropeptides in the course of multistep carcinogenesis.
Cancer Res 1994 Apr 01
PMID:Receptor subtype expression and responsiveness to bombesin in cultured human bronchial epithelial cells. 813 67

In previous studies we have demonstrated the high incidence of vasopressin gene expression as a characteristic feature of small-cell carcinoma of the lung. In the present study we examined expression of this gene in non-neuroendocrine tumors to determine if vasopressin production is a common feature of all lung tumors. We carried out the immunohistochemical evaluation of 22 non-neuroendocrine tumors (12 adenocarcinomas and 10 squamous-cell carcinomas) with antibodies to vasopressin, to oxytocin, and to their related neurophysins. The antibody preparations directed against vasopressin, oxytocin, or oxytocin-associated human neurophysin did not react with any of the tumors examined. Of two monoclonal antibodies to vasopressin-associated human neurophysin used, one did not react with any of the tumors, while the other stained neoplastic cells in only one adenocarcinoma and one squamous-cell carcinoma. These findings, taken with previous reports, indicate that among lung carcinomas, a high incidence of vasopressin/oxytocin gene expression is confined to neuroendocrine tumors.
Cancer Lett 1993 Dec 10
PMID:Vasopressin and oxytocin production by non-neuroendocrine lung carcinomas: an apparent low incidence of gene expression. 829 25

Small-cell neuroendocrine carcinoma of the lung is known to express products related to the vasopressin gene, although these products have been reported to sometimes differ from those generated by neurones of the hypothalamo-neurohypophyseal system. To further investigate vasopressin gene expression in neuroendocrine carcinomas, we performed immunohistochemistry on 24 histologically classified small-cell carcinomas using antibodies directed against different regions of the vasopressin precursor. All of the tumours examined contained at least two parts of the vasopressin precursor, suggesting that vasopressin might have a biological role in these tumours and indicating a role for these products in tumour diagnosis and treatment. Sixty-seven per cent of the tumours contained immunoreactivity for all major regions of the precursor: vasopressin, vasopressin-associated human neurophysin, the bridging region between the hormone and the neurophysin, and vasopressin-associated human glycopeptide. However, 33% of the tumours examined appeared to express only part of the vasopressin precursor, as evidenced by the absence of immunoreactivity for the neurophysin and/or the glycopeptide. These results support the proposition that both normal and abnormal vasopressin gene expression occurs in small-cell carcinoma of the lung.
Br J Cancer 1994 Feb
PMID:Products of vasopressin gene expression in small-cell carcinoma of the lung. 829 23

Paraendocrine syndromes are the remote effects of cancer that result from ectopic hormonal production. Recent investigations have concentrated in five areas that include the evaluation of diagnostic studies, the recognition of rare cases, the contribution of secondary hormones, the clinical distinctions of ectopic syndromes from endocrine disorders, and the efficacy of pharmaceutical agents in correcting hormonally induced biochemical imbalances. The three most common paraendocrine syndromes (humoral hypercalcemia of malignancy, the syndrome of inappropriate antidiuretic hormone production, and ectopic Cushing's syndrome) are the subject of this review.
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PMID:Paraendocrine syndromes. 836 80

We describe a patient who presented with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) 2 months before clinical evidence of bronchogenic malignancy. Because of the potential for the ectopic production of atrial natriuretic peptide (ANP) to mimic SIADH, both hormones were measured in this hyponatremic patient to seek a possible marker of tumor activity. A hypertonic saline infusion at presentation revealed excessive osmotically decoupled secretion of arginine vasopressin but a normal ANP response.
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PMID:Early diagnosis of ectopic arginine vasopressin secretion. 838 Mar 64

Teleocidin, a phorbol ester-type tumor promoter, inhibits cell proliferation and calcium mobilization induced by epidermal growth factor and vasopressin in PLC/PRF/5 hepatoma cells. These inhibitory effects of teleocidin were observed even after a prolonged exposure of the hepatoma cells to this promoter, suggesting the presence of down-regulation-resistant protein kinase C in this hepatoma cell line. Column chromatography of cytosolic fractions showed three separate peaks of protein kinase C activity, two being down-regulation-sensitive while one was down-regulation-resistant. This down-regulation-resistant PKC is suggested to be responsible for the inhibitory effect of teleocidin on cell proliferation and calcium mobilization induced by epidermal growth factor and vasopressin.
Cancer Lett 1993 Jul 30
PMID:Involvement of down-regulation-resistant protein kinase C in teleocidin inhibition of cell proliferation and calcium mobilization induced by epidermal growth factor and vasopressin in human hepatoma cells. 839 71

A 69-year-old female was admitted to the hospital because of fever, hyponatremia and anemia. Laboratory data showed hemoglobin 8.6 g/dl, indirect bilirubin 1.9 mg/dl and Na 122 mEq/l. Urine osmolality was elevated and urinary excretion of sodium was increased. Furthermore, antidiuretic hormone (ADH) level was elevated. Renal function and hormonal data were within normal limit. Therefore, she was diagnosed as having syndrome of inappropriate secretion of antidiuretic hormone (SIADH). On the other hand, bone marrow aspiration showed hemophagocytosis and the diagnosis of hemophagocytic syndrome (HPS) was also made. High dose prednisolone and pulse therapy of cyclophosphamide were administered, nevertheless high grade fever persisted. Fever alleviation was acquired by Etoposide. But she died of pneumonia. An autopsy revealed hemophagocytosis in bone marrow, lymphnodes and spleen, but malignant tumor was not detected. And hypophysis was intact. The pathogenesis of SIADH in this case was not clarified. This report is seemed to be the first case of HPS associated with SIADH.
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PMID:[Hemophagocytic syndrome with syndrome of inappropriate secretion of antidiuretic hormone (SIADH)]. 853 31

A case of syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a patient with suboptimally cytoreduced stage III papillary serous surface carcinoma of the peritoneum is described. After the primary surgery, the patient refused further therapy. Within a month bilateral pleural effusions and abdominal ascites compelled the patient to accept treatment with carboplatin and cyclophosphamide. Ten days following the chemotherapy, she was admitted in a disoriented state with serum sodium of 117-mEq/L. During the evaluation, treatment, and subsequent follow-up, the diagnosis of SIADH was confirmed. Numerous disease processes have been associated with the development of SIADH; however, there have been few reports in gynecologic malignancies. Possible etiology and clinical management of this patient are briefly discussed.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion in papillary serous surface carcinoma of the peritoneum. 854 63


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