Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:007401 (MCP)
 1,571 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Levels of the membrane complement regulatory proteins, C3b/C4b receptor (CR1, CD35), membrane cofactor protein (MCP, CD46), and decay-accelerating factor (DAF, CD55), expressed on cells from patients with haematological malignancies and normal subjects were assessed by flowcytometry using the respective monoclonal antibodies (mAbs). All myeloid and most lymphoid leukaemia samples tested were CR1-negative: two of the 42 leukaemia samples expressed minute amounts of CR1. Lack of CR1 in leukaemia cells was confirmed with two mAbs raised against CR1, 31R, and 243R, which recognized different epitopes and induced different degrees of CR1-mediated fluorescent shift on flow-cytometry in granulocytes and erythrocytes. MCP was increased in most chronic myelogenous leukaemia (CML) and chronic lymphocytic leukaemia (CLL), and was also increased in majority of acute nonlymphocytic leukaemia (ANLL), acute lymphocytic leukaemia (ALL) and non-Hodgkin's lymphoma (NHL). Levels of DAF were also high in CML and CLL, and were variable in other types of leukaemia: some were DAF-negative while others expressed extremely high levels of DAF. In CML patients, the high level of MCP and the lack of CR1 were normalized after medical treatment. These results are in agreement with the data obtained with human leukaemia cell lines, and support the hypothesis that CR1 is essentially a differentiated cell antigen and that a high level of MCP reflects some malignant transformation or an immature stage in blood cells.
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PMID:Levels of complement regulatory proteins, CD35 (CR1), CD46 (MCP) and CD55 (DAF) in human haematological malignancies. 138 49

Tumor-derived chemotactic factors (TDCF) have been identified and thought to play a role in the regulation of macrophage infiltration in neoplastic tissues. The present study was designed to assess the in vivo relevance of the TDCF molecularly identified as monocyte chemotactic protein/JE, by investigating murine sarcoma clones expressing different levels of MCP/JE. The 1D3 clone derived from the B77 RSV-induced sarcoma expressed appreciable levels of MCP/JE mRNA and, concomitantly, chemotactic activity for mononuclear phagocytes. In contrast, the 5B11 clone from the same tumor had undetectable levels of MCP/JE transcripts and little or no chemotactic activity. The chemotactic activity of 1D3 cells was blocked by an appropriate specific antiserum. The in vitro growth rate of the 2 sarcoma lines was identical. Upon in vivo transplantation, the 1D3 clone showed a substantially higher level of tumor-associated macrophages (28.9%; range 21%-34%) than the 5B11 clone (16.6%; range 13%-20%). 5B11-induced tumors appeared earlier and grew faster than those induced by 1D3. The difference in growth rate and in macrophage infiltration between 1D3 and 5B11 clones was also evident upon transplantation into nude mice. These results are consistent with the hypothesis that TDCF, identified as MCP/JE, is one important determinant of macrophage infiltration in tumors.
Int J Cancer 1991 Sep 30
PMID:Macrophage infiltration and growth of sarcoma clones expressing different amounts of monocyte chemotactic protein/JE. 165 61

Twenty-five patients with acute nonlymphoblastic leukemia undergoing 41 cycles of chemotherapy with daunorubicin/cytosine arabinoside (ara-C) or with etoposide/ara-C received metoclopramide (MCP; 0.5 mg/kg 6 hourly i.v.) or MCP (same dose) plus oral lorazepam (1 mg/d) during and 24 hours following the chemotherapy as antiemetic medication. Control of vomiting was achieved is 55% (complete 5%, partial 50%) of the patients receiving MCP alone and in 100 percent (complete 76.1%; partial 23.8%) of those receiving MCP plus lorazepam (p less than 0.001). Eighteen of the 21 patients (85.7%) receiving MCP plus lorazepam opted for the same antiemetic regimen as compared to six of the 20 (30%) receiving MCP alone (p less than 0.01). One patient in each group developed mild sedation during the treatment. It is concluded that oral lorazepam is an effective and safe adjuvant to MCP for the control of vomiting during cancer chemotherapy.
Indian J Cancer 1991 Jun
PMID:Low dose, oral lorazepam: a safe and effective adjuvant to antiemetic therapy. 193 45

Sixty-nine patients with malignant tumors receiving cancer chemotherapy, 90% including cis-platinum, were evaluated in a randomized crossover study for the antiemetic efficacy and the side effects of two antiemetic regimens: chlorpromazine (CPM) 2.5 mg/kg in 5 doses plus dexamethasone (DXM) 0.2 mg/kg in 2 doses, and high-dose metoclopramide (HD-MCP) 10 mg/kg in 5 doses plus the same dose of DXM. In 69% of 173 courses of chemotherapy, antiemetic response was achieved, and in 26% emesis was completely prevented. There was no statistical difference in the response to the antiemetic regimens, but 65% of the patients who completed 3 courses of chemotherapy preferred HD-MCP plus DXM. The main side effects of the treatment were drowsiness, nervousness, diarrhea and extrapyramidal reactions. HD-MCP plus DXM is recommended as a first line antiemetic treatment in patients receiving cancer chemotherapy. Patients resistant to this treatment should receive CPM plus DXM treatment.
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PMID:Chlorpromazine and dexamethasone versus high-dose metoclopramide and dexamethasone in patients receiving cancer chemotherapy, particularly cis-platinum: a prospective randomized crossover study. 265 92

One hundred and two patients with advanced solid tumors receiving chemotherapy were treated with metoclopramide (MCP; 100 mg) to prevent emesis. Twenty-six of 102 patients who had more than five episodes of vomiting were considered MCP-resistant and were randomized to receive MCP (100 mg) plus placebo versus MCP plus dexamethasone (DM; 48 mg) iv in a double-blind, crossover trial. The median number of vomiting episodes was 18 after MCP plus placebo and five after MCP plus DM (P less than 0.001). The median duration of vomiting episodes was 40 hours after MCP plus placebo and 10 hours after MCP plus DM. Immediate toxicity of the antiemetics was not enhanced by the addition of DM to MCP.
Cancer Treat Rep 1983 Apr
PMID:Improved control of chemotherapy-induced emesis by the addition of dexamethasone to metoclopramide in patients resistant to metoclopramide. 634 70

GB24 is a mouse monoclonal antibody raised against a common trophoblast-lymphocyte cross-reactive antigen. GB24 detects the membrane cofactor protein (MCP, CD46), a member of the complement regulatory protein family, which serves as a cofactor for factor 1 mediated cleavage of C3b. This study investigated the reactivity of GB24 on 38 breast carcinomas and 34 normal/benign breast tissues by immunochemistry as well as the reactivity of F2B7-2, an antibody specific to the decay accelerating factor (DAF, CD55) of the complement. GB24 staining was present on both normal tissue and benign lesions, but very strong diffuse reactivity was observed on carcinomas. This reactivity increased with the tumor grade. By contrast, malignant tumor cells lacked DAF expression. F2B7-2 antibody reacted weakly with benign epithelial cells. Results were studied by computer assisted image analysis to accurately define the mean optical densities. The densitometric analysis of MCP positive carcinomas showed a high intensity of the staining. Expression of MCP and DAF on MCF-7 cell lines was analyzed by flow cytometry. MCF-7 cell lines were strongly stained by mAb GB24 only. These data suggest that selectively enhanced expression of the antigen recognized by GB24 is associated with malignant breast disorders. This high expression, which may reflect a protective mechanism by which tumor cells survive complement activation, may prove useful as a marker of malignant transformation.
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PMID:High expression of the antigen recognized by the monoclonal antibody GB24 on human breast carcinomas: a preventive mechanism of malignant tumor cells against complement attack? 753 66

Normal human sera contained 10-60 ng/ml of soluble membrane cofactor protein (MCP, CD46) whereas sera of > 50% of the cancer patients contained > 60 ng/ml. MCP purified by immunoaffinity chromatography from both normal and cancer patients' sera consisted of three bands of 56, 47 and 29 kDa on SDS-PAGE/immunoblotting. The upper two components were increased in cancer patient sera. The 56 and 47 kDa soluble forms served as a cofactor for factor I-mediated cleavage of C3b. MCP expressed on Chinese hamster ovary (CHO) cells protects host cells from human C3 deposition and complement-mediated cytolysis, especially by activation of the alternative pathway. In this same assay system, exogenously added soluble MCP also protected untransfected CHO cells; however, its potency was much less than that of the endogenous membrane form. For example, 8 micrograms/ml of soluble MCP was equal to 10(4) copies/cell of the expressed MCP. Recombinant soluble forms possessed similar activity to the naturally occurring soluble forms and high doses (> 150 micrograms) blocked Arthus-like reaction induced in guinea-pigs by anti-Forssman antibody. These data establish that soluble forms of MCP are present in human sera that possess cofactor activity and their concentrations, especially the 56 and 47 kDa forms, are increased in sera of cancer patients. High doses of the recombinant soluble forms may be therapeutically useful for suppressing inflammatory responses.
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PMID:Purification and functional properties of soluble forms of membrane cofactor protein (CD46) of complement: identification of forms increased in cancer patients' sera. 754

Oncology of the hypertrophic prostate and histogenesis of the cancer. Histological examine of 286 hypertrophic prostates collected by suprapubic way, on histologic macrosections including the whole visceral area, with the "step section technique". N. 286 hypertrophic prostates collected through suprapubic way have been examined on histologic macrosections including the whole visceral area, with the step section technique. There have been used object holders slides measuring cm. 12 x 9 and cover objects measuring cm. 5 x 7. Colourings: hematoxylin-eosin , Goldner. Localisation of the tumours has been determined in the prostate area. The cases with the presence of tumours-microcarcinoma (MCP), with maximum axis up to 1 millimeter; small carcinoma (PCP), maximum axis from mm. 1.1 to mm. 5, and the classic carcinoma (CPcl) have been 232 (81%). CPcl appeared in 33 cases (11.53%). Histogenesis of the MCP has been ascertained (from terminal secretory micro-ducts of the prostate). Of PCP (from groups of MCP n. 56 in picture 7), and of CPcl (from PCP in progressive growth) or from grouping of MCP (in picture 14, 101 MCP of the 235 present in the area of mm2 40). CPcl has shows invading growth in ten cases; in 23 cases it consisted in infiltrating growth but limited, the border towards the prostatic tissue appears circumscribed by pseudocapsule, the cells show nucleoli of varying sizes. In seven cases it turned out to be adenocarcinoma with limited growth as said before, partly with pseudocapsules, and the cells appear seriously atypical, hypertrophic, hyperstained nuclei, thickening of the nuclear membrane, prominent nucleoli, in the absence of any invading tendency. Specific oncogenic agents are thought to transform the prostate cells into definite morphologic malignancy, while another oncogenic agent causes the invading proliferation.
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PMID:[Oncology of the hypertrophic prostate and study of the histogenesis of carcinoma. Histological analysis of 286 prostates obtained using the suprapubic route and examined using macro-sections including the entire visceral surface using the step-section technique]. 768 75

The levels of complement-regulatory molecules (complement receptor type one [CR1], decay-accelerating factor [DAF], membrane cofactor protein [MCP], and an inhibitor of membrane attack complex [CD59]) in lung cancer cells were analyzed to investigate the relation between their expression and histological subtypes, and the possibility of homologous complement deposition on cancer cells. In 25 cell lines (10 adenocarcinoma, 3 large-cell carcinoma, 7 small-cell lung cancer [SCLC], and 5 squamous cell carcinoma), flow cytometric analysis revealed that MCP was expressed in all cell lines, whereas none of the cell lines was CR1-positive. CD59 was detected in all cells. The DAF epitope defined by IA10 was expressed in all cells except one large cell carcinoma cell line. However, another epitope for anti-DAF monoclonal antibody, D17, was not detected in 5 (71.4%) SCLC and in 4 (22.2%) non-small-cell lung cancer. This disparity was seen in most cell lines, irrespective of histological subtypes. The loss of D17 reactivity seemed to be pertinent to malignant phenotype, because most of the normal pulmonary cells possessed the D17 epitope. Furthermore, a cell line lacking DAF (IA10-/D17-) allowed alternative pathway-mediated homologous complement (C3) deposition after pretreatment with anti-MCP antibody. This raises a new possibility for immunotargeting of cancer. These cell lines should be useful in studying the biology of lung cancer.
Jpn J Cancer Res 1993 Jul
PMID:Levels of complement regulatory molecules in lung cancer: disappearance of the D17 epitope of CD55 in small-cell carcinoma. 769 Mar 55

CD59 (protectin) and CD46 (membrane cofactor protein, MCP) are membrane-bound complement regulator proteins which inhibit complement-mediated cytolysis of autologous cells. CD59, a phosphatidyl-inositol-anchored glycoprotein, inhibits the formation of the terminal membrane attack complex (MAC) of complement and was found to be a second ligand for CD2 contributing to T-cell activation. In 20 colorectal normal mucosa samples, in ten adenomas, 71 carcinomas and in ten liver metastases derived thereof, CD59 was inconsistently expressed in the epithelial compartment. In carcinomas CD59 expression in the whole neoplastic compartment was more often found in well- and moderately differentiated tumours. By contrast, focal expression or even complete lack of CD59 was more often found in poorly differentiated tumours (P = 0.021). In addition, carcinomas without metastases at the time of operation (Dukes A/B) more often expressed CD59 in the entire neoplastic population compared to those carcinomas which had already metastasised (P = 0.018). There was no correlation between the mode of CD59 expression in colorectal carcinomas and the tumour type or location. CD46 has C3b/C4b binding and factor-I dependent cofactor activity and is broadly expressed in various cells and tissues. In the epithelial compartment of normal colorectal mucosa, of all adenomas, carcinomas and their liver metastases, CD46 was expressed throughout the epithelial compartment. Since CD46 was consistently expressed in colorectal carcinomas the low expression or even lack of CD59 in a subset of tumours might not lead to critical complement-mediated attack of CD59-negative tumour cells. Regarding CD59 as a natural T-cell ligand involved in cognate T-cell-target-cell interaction, however, loss of CD59 might well be a selection advantage, provided that tumour antigen-mediated T-cell toxicity in colorectal carcinoma exists.
Br J Cancer 1993 Nov
PMID:Expression of CD59, a complement regulator protein and a second ligand of the CD2 molecule, and CD46 in normal and neoplastic colorectal epithelium. 769 19


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