Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. A patient presented with mild hypertension, a raised plasma total renin concentration but a normal plasma angiotensin II concentration. The discrepancy was due to a high concentration of inactive renin in the plasma. 2. A renal carcinoma was detected and removed. The tumour contained a higher proportion of inactive renin than was found in uninvolved areas of the kidney. After unilateral nephrectomy, the plasma concentration of inactive renin fell to normal. 3. Six months later, plasma inactive renin concentration again increased and a metastasis was detected in a rib. Excision of the rib together with radiotherapy resulted in a fall in plasma inactive renin to normal. 4. The inactive renin in plasma and tumour extracts was activated to the same extent by acid treatment and by trypsin.
Clin Sci Mol Med Suppl 1978 Dec
PMID:A renal carcinoma secreting inactive renin. 28 45

We evaluated density of the natural killer (NK) cell-associated CD56 antigen on circulating NK cells of 47 patients with advanced renal cell carcinoma. Patients received a combination of low-dose subcutaneous recombinant interleukin-2 (rIL-2) and recombinant interferon-alpha (rIFN-alpha) as home therapy. Antigen density of CD56 before therapy was 2.2-fold higher (P < 0.005) in patients who subsequently achieved a complete or partial remission when compared with patients who presented with progressive disease on therapy. After a 6-week treatment cycle, NK cells of treatment responders expressed significantly (2.1-fold; P < 0.005) more CD56 antigens than NK cells in nonresponding patients. These results suggested a potential role of both pre- and posttreatment NK antigen density levels as a biologic correlate to treatment response.
Mol Biother 1992 Dec
PMID:Pretreatment natural killer antigen density correlates to clinical response in tumor patients receiving long-term subcutaneous recombinant interleukin-2 and recombinant interferon-alpha. 128 26

We cloned the hamster cdc25C cDNA by using the human cdc25C cDNA as a probe and prepared an antibody to Escherichia coli-produced hamster cdc25C protein that is specific to the human cdc25C protein. The microinjected antibody inhibited a chromosome condensation induced by tsBN2 mutation, indicating that the cdc25C protein is required for an activation of p34cdc2 kinase caused by loss of RCC1 function. The hamster cdc25C protein located in the cytoplasm, prominently in a periphery of the nuclei of cells arrested with hydroxyurea, and seemed to move into the nuclei by loss of RCC1 function. Also, we found a molecular shift of the cdc25C protein in cells showing premature chromosome condensation (PCC), in addition to normal mitotic cells. This molecular-shift appeared depending on an activation of p34cdc2 kinase.
Mol Biol Cell 1992 Dec
PMID:Chromosome condensation caused by loss of RCC1 function requires the cdc25C protein that is located in the cytoplasm. 133 89

Our 3-year clinical experience using recombinant interferon (rIFN) alpha-C in patients with metastatic renal cell carcinoma (RCC) is summarized. This type of IFN is a new subspecies of the IFN-alpha protein family. Its specific activity is 1-2 x 10(9) U/mg protein, the highest among IFN-alpha species presently available. Pharmacokinetic study indicated good bioavailability of the preparation from the intramuscular injection. A phase II study was performed to assess the response rate related to rIFN-alpha C at a low dosage. A dose of 3 x 10(6) U daily was administered, followed by 3 x 10(6) U/m2 every other day to avoid severe toxicity. Among 33 treated patients, a partial remission rate of 9.7% and stable disease rate of 25.8% were achieved. Side effects were usually mild and the treatment was well tolerated by the patients. However, mental deterioration and behavioral changes were observed in five patients with RCC treated by rIFN-alpha C and were related to neurotoxicity of IFN. The role of vinblastine in addition to IFN in the treatment of RCC was assessed in nine patients who had failed on IFN alone. No response was observed. It appeared that vinblastine had little if any effect in being added to IFN as second-line therapy. We conclude that rIFN-alpha C has moderate activity in the treatment of RCC. Familiarity with the possible toxicity of this agent will lead to more careful management of patients.
Mol Biother 1992 Sep
PMID:Our experience with interferon alpha: renal cell carcinoma. 144 66

The success of adoptive immunotherapy using recombinant interleukin-2 (rIL-2) and lymphokine-activated killer (LAK) cells in several cancers has been hampered by severe toxicity associated with high doses of rIL-2. Methods that reduce the dosage of rIL-2 without loss of clinical efficacy are needed. In this study we determined the in vitro effect of a phytochemical immune modulator, Astragalus membranaceus (AM), and two fractions isolated by high-performance liquid chromatography on the cytotoxicity of rIL-2-generated LAK cells against a murine renal cell carcinoma. Our results indicated a 10-fold potentiation of rIL-2-generated LAK cell cytotoxicity manifested by tumor cell lysis of 88% in the group with 100 U/ml of rIL-2 plus AM versus 86% in the group with 1,000 U/ml of rIL-2 alone. Potentiation was obtained with the purified fractions as well. A significantly reduced number of LAK cells was required to achieve the tumor cytotoxicity after LAK cell generation with rIL-2 plus the phytochemicals as compared with rIL-2 alone. Our data indicate that AM is an effective immune modulator, capable of potentiating in vitro the antitumor activity of rIL-2-generated LAK cells.
Mol Biother 1992 Sep
PMID:Phytochemicals potentiate interleukin-2 generated lymphokine-activated killer cell cytotoxicity against murine renal cell carcinoma. 144 69

Blood-borne metastases to a skeletal muscle are rare and may originate in various primary tumors. Recurrent solitary metastasis of renal cell carcinoma, and metastatic lesion as part of disseminated malignant melanoma in skeletal muscles are reported in two patients. In both cases interferon treatment with or without chemotherapy failed in arresting the disease.
Mol Biother 1992 Jun
PMID:Metastases to skeletal muscles and interferon treatment. 151 1

Temperature-sensitive mutants in the RCC1 gene of BHK cells fail to maintain a correct temporal order of the cell cycle and will prematurely condense their chromosomes and enter mitosis at the restrictive temperature without having completed S phase. We have used Xenopus egg extracts to investigate the role that RCC1 plays in interphase nuclear functions and how this role might contribute to the known phenotype of temperature-sensitive RCC1 mutants. By immunodepleting RCC1 protein from egg extracts, we find that it is required for neither chromatin decondensation nor nuclear formation but that it is absolutely required for the replication of added sperm chromatin DNA. Our results further suggest that RCC1 does not participate enzymatically in replication but may be part of a structural complex which is required for the formation or maintenance of the replication machinery. By disrupting the replication complex, the loss of RCC1 might lead directly to disruption of the regulatory system which prevents the initiation of mitosis before the completion of DNA replication.
Mol Cell Biol 1992 Aug
PMID:RCC1, a regulator of mitosis, is essential for DNA replication. 163 Apr 49

The present study was designed to shed light on the extraordinary histochemical properties of the chromophobe cell renal carcinoma detected by Hale's colloidal iron reaction. Special emphasis was laid on the lectin histochemical analysis of cytoplasmic glycoconjugates. Binding of peanut agglutinin (PNA) and Erythrina cristagalli agglutinin (ECA) after enzymatic release of sialic acid and direct binding of Dolichos biflorus agglutinin (DBA) correlates well with the expression of binding sites for Sambucus nigra agglutinin (SNA) and Maackia amurensis agglutinin (MAA) revealing abundant sialylated carbohydrate moieties within the cytoplasm. This characteristic binding pattern differs considerably from the faint staining observed in the majority of other renal carcinomas, thus confirming that the chromophobe cell renal carcinoma is a distinct entity. However, the lectin binding pattern of renal oncocytoma obviously resembles that of chromophobe carcinoma indicating a close relationship between these renal tumors. Detailed analysis of adjacent renal parenchyma revealed a lectin binding pattern quite similar to that described in the chromophobe carcinomas exclusively in the intercalated cells lining the collecting duct. This finding suggests that the chromophobe cell renal carcinoma originates from the collecting duct epithelium. The detection of small complexes consisting of altered epithelia which display the morphological characteristics of chromophobe carcinoma and the histochemical properties of intercalated cells probably indicates the emergence of preneoplastic lesions preceding the development of chromophobe carcinoma. Even though further studies are clearly needed to elucidate the physiological role of the cellular glycoconjugates detected, the present results already provide valuable insight into the histogenesis and pathogenesis of the chromophobe cell renal carcinoma.
Virchows Arch B Cell Pathol Incl Mol Pathol 1991
PMID:Sialylated glycoconjugates in chromophobe cell renal carcinoma compared with other renal cell tumors. Indication of its development from the collecting duct epithelium. 168 20

Fifty-four patients with advanced malignancies were treated on this phase I trial of coumarin and cimetidine. The dose of coumarin was escalated, with three patients treated at each dose level, while the cimetidine dose was held constant at 300 mg four times daily. Patients received coumarin alone as a single daily oral dose for 14 days; on day 15, cimetidine was added and both drugs were continued until progression of disease. This trial was initiated with patients receiving coumarin at 400 mg daily and closed at 7 g daily with four of five patients on this dose experiencing nausea and vomiting. Treatment was generally well tolerated over a wide range of coumarin doses. Symptomatic side effects were few, mild, and usually self limited. Side effects included insomnia, nausea, vomiting, diarrhea, and dizziness. Two patients withdrew from therapy because of daily nausea and vomiting. Typically, nausea, vomiting, and dizziness occurred 2.5-3 hours after a dose of coumarin. In most patients, these side effects abated spontaneously with continuation of therapy. There was no significant hematologic or renal toxicity. Hepatotoxicity occurred in only one patient and was manifested by asymptomatic abnormal elevations of serum hepatic transaminases. This toxicity was reversible upon interruption of therapy. Objective tumor regressions were observed in six patients with renal cell carcinoma. Responses occurred at coumarin doses ranging from 600 mg to 5 g daily. Coumarin is a relatively nontoxic, oral, outpatient therapy that warrants further investigations for the treatment of human malignancies. Because of its low toxicity, there is potential for combining coumarin with chemotherapeutic and/or biological agents in an attempt to improve on efficacy.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Biother 1991 Sep
PMID:Phase I evaluation of coumarin (1,2-benzopyrone) and cimetidine in patients with advanced malignancies. 176 68

Coumarin (1,2-benzopyrone) is a natural substance that appears to have some clinical activity against renal cell carcinoma and malignant melanoma. Preliminary evidence from in vitro and in vivo studies suggests that coumarin possesses immunomodulatory activity. It was reported previously that coumarin therapy resulted in augmented DR antigen expression by peripheral blood monocytes in cancer patients. The purpose of the present study was to examine the effects of coumarin on DR and DQ antigen expression by normal donor peripheral blood mononuclear cells in vitro. Using monoclonal antibody labeling techniques and FACS analysis, it was shown that both DR and DQ antigen expression by peripheral blood mononuclear cells were enhanced over controls after 48 hours of exposure to coumarin. While monocytes normally express these antigens, enhanced expression is consistent with an activated state. These results support the hypothesis that coumarin acts, at least in part, through immune augmentation.
Mol Biother 1991 Dec
PMID:Coumarin (1,2-benzopyrone) enhances DR and DQ antigen expressions by peripheral blood mononuclear cells in vitro. 176 72


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