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)

Ascitic fluid form ovarian cancer patients (n = 16), but not from patients with other cancers or with benign diseases, contains a growth-promoting activity which induces the proliferation of both fresh ovarian cancer cells (n = 5) and the ovarian cancer cell line HEY. The ascitic fluid growth factor(s) appears to signal cells through binding and activation of specific, saturable, high-affinity cell surface receptors. Incubation of fresh or cultured ovarian cancer cells with a partially purified preparation of ascitic fluid stimulates phosphatidylinositol turnover and increases cytosolic-free calcium. Each of these biochemical events has been implicated in the action of growth factors. Purified preparations of previously identified growth factors including epidermal growth factor, transforming growth factor-beta, tumor necrosis factor, platelet-derived growth factor, thrombin, insulin, interleukin-1, interleukin-2, vasopressin, angiotensin, alpha- and gamma-interferons, and fibroblast growth factor did not increase cytosolic-free calcium in either fresh ovarian cancer cells or HEY cells. Therefore, ascitic fluid appears to contain one or more previously unidentified growth factors which activate ovarian cancer cells through phosphatidylinositol hydrolysis and resultant changes in cytosolic-free calcium.
Cancer Res 1988 Mar 01
PMID:A putative new growth factor in ascitic fluid from ovarian cancer patients: identification, characterization, and mechanism of action. 342 89

There are a variety of water and electrolyte disorders in patients with cancer. These disorders occur during the growth of tumors, generally as a consequence of inadequate intake and absorption of electrolytes, renal failure secondary to tumor or rapid tumor destruction and production of metabolically active substances by the tumor. In this paper, the electrolyte abnormalities associated with cancer were reviewed. Hyponatremia is one of the most common clinical electrolyte abnormalities in advanced cancer. Some patients may have hyponatremia, in spite of increased total body sodium and absence of a defect in water diuresis. This status is designated as "sick cell syndrome" or "essential hyponatremia". In addition, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in association with various tumors has been described. This syndrome is principally due to water retention, but can also be due to continuous urinary loss of sodium, and hypo-osmolality. Hypercalcemia is associated with coexistent primary hyperparathyroidism, prostaglandin (PGE2) or osteoclast-activating factor. It now seems likely that ectopic PTH is rarely the cause of hypercalcemia in nonparathyroid cancer. There are no data supporting the ectopic production of vitamin D-like substance as an important factor in the hypercalcemia of cancer. There are three general categories in which patients with hypercalcemia and cancer may be placed: those with bone metastases, those without bone metastases of solid tumors and those with hematologic malignancies. Hypokalemia is associated with ectopic ACTH- and insulin--producing tumors, and is often found in patients with mucin-secreting, potassium-losing adenocarcinoma of the colon.
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PMID:[Electrolyte abnormalities associated with cancer: a review]. 352 93

A patient with B-cell chronic lymphocytic leukemia (CLL) is described who presented with fever, headache, and hyponatremia. Subsequent evaluation established the diagnoses of CLL meningitis and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Both findings resolved following therapy with intrathecal methotrexate. A brief citation of the literature of CLL meningitis is presented.
Cancer 1987 Jul 15
PMID:Chronic lymphocytic leukemic meningitis as a cause of the syndrome of inappropriate secretion of antidiuretic hormone. 359 56

We assessed the therapeutic efficacy and toxicity of continuous hepatic infusion of vinblastine in the treatment of breast cancer predominantly metastatic to the liver. Twenty-six patients previously treated with one or more chemotherapeutic regimens received vinblastine at a dose of 2.0 mg/m2 daily for 5 days, via percutaneously inserted intra-arterial catheters, at 3-4-week intervals. Nine of 25 evaluable patients (36%) achieved partial response and four (16%) had minor response. For responding patients, the median time to disease progression was 21 weeks (range, 12-99), with a median survival of 11 months (range, 4-29) from the beginning of hepatic arterial infusion. The toxicity of the treatment was acceptable, and drug-related effects were comparable to those seen in patients with breast cancer treated by iv continuous infusion of vinblastine at slightly lower doses. We observed two episodes of transient inappropriate antidiuretic hormone secretion. Percutaneous hepatic arterial infusion of vinblastine had significant activity in the treatment of breast cancer metastatic to the liver.
Cancer Treat Rep 1987 Nov
PMID:Continuous 5-day infusion of vinblastine for percutaneous hepatic arterial chemotherapy for metastatic breast cancer. 367 9

In a group of 10 patients with a cancer of the digestive tract, some investigations, performed before the surgical intervention, showed the evidence of an adrenal-postpituitary imbalance in favour of the second term. During a water loading, the plasmatic cortisol rates stayed more higher by cancerous subjects than by controls (but not the plasmatic aldosterone rates); nevertheless, the vasopressin secretion rates could be considered as more higher yet in cancerous subjects because the free water clearances were significantly lowered by these patients. Such results have to be put in relation with the opposite effects of vasopressin and corticoids on the cell mitosis, as well as with some therapeutical attempts that end to check this type of endocrine imbalance.
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PMID:[Adrenal-posterior pituitary imbalance in digestive cancer patients]. 370 May 1

Normal cells require growth factors to multiply. One group of growth factors such as platelet-derived growth factor, bombesin and vasopressin in fibroblasts or antigen in lymphocytes uses a specific inositol lipid as part of a transduction mechanism for generating intracellular mitogenic signals. These growth factors stimulate the hydrolysis of phosphatidylinositol 4,5-bisphosphate to give diacylglycerol (DG) and inositol 1,4,5-trisphosphate (Ins1,4,5P3). The DG remains within the plane of the membrane to activate protein kinase C, one function of which is to increase intracellular pH by switching on a Na+/H+ exchanger. The other product, Ins1,4,5P3, functions as a second messenger to mobilize calcium from intracellular stores. These two ionic events, the increase in pH and calcium, contribute to the onset of DNA synthesis. The hydrolysis of an inositol lipid is a key event in this signal pathway which mediates the action of competence factors. A separate signal pathway, perhaps based on tyrosine phosphorylation, carries out the effects of progression growth factors such as epidermal growth factor (EGF) and insulin. It is argued that oncogenes may be arranged into groups associated with specific signal pathways. For example, the sis oncogene encodes platelet-derived growth factor which might use the src gene product as part of its transduction mechanism to generate the second messengers DG, Ins1,4,5P3 and calcium. These last then act to stimulate the transcription of myc and fos. On the other hand, the erbB gene encodes a protein which resembles the receptor for EGF. The function of the ras protein remains a major unsolved problem but there is indirect evidence for proposing that it may mediate the action of progression factors such as EGF or insulin.
Cancer Surv 1986
PMID:Growth factors, oncogenes and inositol lipids. 377 62

A review is given on symptoms, etiology, pathogenesis and prognosis of central pontine myelinolysis (CPM). Since 1959, 315 cases of CPM have been reported in world literature, 41 per cent of the patients described developed their neurological symptoms in the course of chronic alcoholism. In about 32 per cent CPM was connected with electrolyte disturbance, especially hypo- or hypernatremia. Beside the complications of alcoholism, accompanying diseases were malignancies (9%) infections of the lung (10%) and diseases of the central nervous system (7%). Current theories about etiology and pathogenesis of CPM are reviewed with special reference to the syndrome of inappropriate secretion of the antidiuretic hormone (IADH). Own experiences with clinical diagnosis of CPM are reported. Seven patients with neurological symptoms in hyponatremia have been seen prospectively during one year. In three cases clinically, in one patient neuropathologically the diagnosis of CPM was made.
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PMID:[Central pontine myelinolysis]. 380 30

A sixth case in the world literature is reported of a 59-year-old male with diabetes insipidus (DI) associated with chronic myelogenous leukemia (CML). The patient is unique in that his CML was diagnosed 10 years before he presented with vasopressin-responsive DI. Radiation to the central nervous system failed to reduce the daily requirement of his need for vasopressin.
Cancer 1985 Sep 15
PMID:Case report of vasopressin-responsive diabetes insipidus associated with chronic myelogenous leukemia. 386 Dec 27

Melphalan is now being investigated as an intravenous (IV) bolus chemotherapeutic agent in children with resistant tumors involving the bone marrow. Two patients received 2 mg/kg melphalan, IV bolus; 10 patients received 1 mg/kg. Seven of the ten patients receiving 1 mg/kg had noticeable downward trends in the serum sodium concentrations, whereas both patients receiving 2 mg/kg developed hyponatremia (serum sodium concentration [SNa], mEq/l = 124-125) and inappropriate urinary sodium losses. Syndrome of inappropriate antidiuretic hormone (SiADH) is a previously unreported complication of high dose bolus melphalan therapy.
Cancer 1985 Jan 01
PMID:Syndrome of inappropriate antidiuretic hormone secretion. A complication of high-dose intravenous melphalan. 396 85

Serum proteins from hepatectomized or control rats were separated by gel permeation chromatography and assayed for stimulation of hepatocyte proliferation in primary cultures of hepatocytes. Two peaks of activity were seen in the areas of large (greater than 120,000) and small (less than 3,000) molecular weight. These activities are different from insulin, epidermal growth factor, or vasopressin and are empirically termed hepatopoietin A and B, respectively. The two activities interact in a synergistic manner to stimulate hepatocyte proliferation at rates comparable to that of the whole serum.
Cancer Res 1984 Oct
PMID:Control of hepatocyte replication by two serum factors. 623 12


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