Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0027651 (tumor)
685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many reports have emphasized the role of gastrin as a growth factor for normal gastrointestinal mucosa and gastrointestinal cancers. Recent studies have pointed out that this peptide acts also as a growth factor for the pancreatic cancer cell line AR42J. This effect is mediated by gastrin [cholecystokinin (CCK)-B] receptors. In the present study, we investigated gastrin (CCK-B) receptor expression in the azaserine-induced rat pancreatic carcinoma DSL-6, comparing it to normal rat pancreas, and we also characterized CCK receptor subtypes in this tumor. The results showed that there is extensive gastrin binding to the DSL-6 pancreatic carcinoma. No evidence of specific gastrin binding to normal pancreas was found. Analysis of the ability of gastrin-17-I to inhibit 125I-gastrin-I binding demonstrated that gastrin bound to a single class of receptors with a Kd of 0.21 +/- 0.04 nM and a binding capacity of 184 +/- 29 fmol/mg protein. 125I-Gastrin-I binding was inhibited by the specific CCK-B receptor antagonist L365,260 approximately 40 times more effectively than by the specific CCK-A receptor antagonist L364,718. Analysis of the ability of cholecystokinin octapeptide (CCK-8) to inhibit 125I-Bolton-Hunter-CCK-8 binding revealed two CCK binding sites, i.e., a high affinity site and a low affinity site. The observed binding affinities of CCK-8 were then introduced into the computer analysis of the dose-inhibition curve of the ability of gastrin-17-I to inhibit binding of 125I-Bolton-Hunter-CCK-8, which was significantly better fit by a three-site model than by a two-site model. The three sites meet the criteria for CCK-B, high affinity CCK-A, and low affinity CCK-A receptors. The binding capacity of CCK-B receptors constitutes 34% of the total high affinity CCK binding sites. This study demonstrated that DSL-6 pancreatic carcinoma expresses three subtypes of CCK receptors. Gastrin (CCK-B) receptors, which were not detected in normal rat pancreas, constitute about one third of the total high affinity CCK receptors. We suggest that novel expression of gastrin (CCK-B) receptors may be generated by gene mutation or amplification during carcinogenesis and may play an important role in promoting tumor growth.
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PMID:Novel expression of gastrin (cholecystokinin-B) receptors in azaserine-induced rat pancreatic carcinoma: receptor determination and characterization. 145 79

In order to analyze the results of treatment of patients with locoregional recurrence after intentional curative resection of pancreatic cancer, a retrospective study was performed. During the period 1978-1988, 108 patients underwent an intentional curative resection fo the pancreas. In 34 patients locoregional recurrence occurred, all within a period of three years (cumulative recurrence rate 56%). Sixty-eight percent of the patients presented with upper abdominal pain, and 62% with weight loss. Survival was significantly better (p = 0.02) in the group of 18 patients without distant metastases (1-year survival 22%) than in the 16 patients with distant metastases (1-year survival 0%). Five patients without proven distant metastases were treated by resection or chemotherapy. The mean survival was 33 months (range 6-74) in the treated group, and 4 months (0.4-7 months) in the untreated group, p = 0.002. In this retrospective study the longest survival was seen after radical resection of locoregional tumor recurrence. We therefore recommend that patients with locoregional recurrence without distant metastases after intentional curative resection of pancreatic cancer be treated.
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PMID:Treatment of locoregional recurrence after intentional curative resection of pancreatic cancer. 145 25

We have been using external beam radiotherapy (EBRT) and intraoperative radiotherapy (IORT) for both resectable and unresectable pancreatic cancer patients. EBRT (50-60 Gy) was combined with IORT (25-33 Gy) whenever possible, but otherwise EBRT or IORT was given alone. In patients with unresectable tumor but no distant metastasis, the median survival time (MST) was 7.5 months (M) for the EBRT group and 9 M for the EBRT+IORT group. These MST's were significantly longer than the MST of 3 M of patients who had been treated without radiation (historical control). In non-Stage IV patients undergoing non-curative resection, the MST was 12.5 M for the EBRT group, 15.5 M for the EBRT+IORT group, and 7 M for the historical control. In patients undergoing macroscopic curative resection, the MST was 14 M for the EBRT group, 10 M for the EBRT+IORT group, and 10.5 M for the historical control. In Stage IV patients (with distant metastasis), the MST was 4.5 M for the EBRT group, 4 M for the EBRT+IORT group, 2 M for the IORT group, and 2.5 M for the historical control. Thus, radiotherapy appeared useful especially in non-Stage IV patients undergoing non-curative or no resection. A decrease or relief of pain was obtained in 90% of patients with unresectable lesions. Radiotherapy seems to play an important role in the treatment of pancreatic cancer but more aggressive combined treatment seems to be necessary to further improve the dismal prognosis of pancreatic cancer patients.
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PMID:[Radiation therapy of pancreatic cancer]. 146 40

An anti lung adenocarcinoma murine monoclonal antibody (MoAb), KM195 (IgG1), was generated using mice which underwent tolerance treatment to normal lung tissues. KM195 was selected from among a number of hybridoma clones because of its advantageous reactivity such as high binding to cell membranes of lung adenocarcinoma tissues and low binding to cell membranes of major normal tissues. In a binding assay using cultured cell lines KM195 was found to bind cytoplasmic antigen in many adenocarcinoma cells. Detailed immunohistochemical analysis using paraffin-fixed tissue sections showed that many adenocarcinoma cells such as gastric cancer, colorectal cancer, pancreatic cancer, mammary cancer, ovary cancer and cervical cancer reacted positively with KM195, as well as lung adenocarcinoma cells. KM195 also positively stained a small number of normal cells found in adult and fetal tissues like lung, intestine, pancreas, liver and kidney. Western blot analysis using membrane fraction of lung adenocarcinoma tissues revealed two major KM195-positive bands which were electrophoresed nearby at molecular weights (M.W.) of 40 Kd. The protein corresponding to the two major bands was purified by immuno-affinity chromatography and sequenced. The amino-terminal 19 residues of the lower band was identified as VLEVDPNIQAVXTQEXEQI, which is identical to that of the human cytokeratin 8 (residues 77 to 95), M.W. 52Kd. The amino-terminal sequence of the upper band was blocked and not determined. To examine the ability of KM195 for tumor imaging, 125I-labeled KM195 was injected i.v. into nude mice bearing SW1116 xenografts. Significantly higher radioactivity was observed in the tumor compared with major organs at days 3 and 5. These data indicate that KM195, which recognizes cytokeratin 8-like cytoplasmic antigen, could be a potential MoAb for use in the immunohistochemical diagnosis and radioimmunodetection of adenocarcinoma.
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PMID:Application of anti lung adenocarcinoma monoclonal antibody recognizing cytokeratin-like cytoplasmic antigen for tumor diagnosis. 150 2

Specific and nonspecific stimulation of the host immune system to reject cancer is an attractive concept that is just beginning to mature. Results with crude extracts and nonspecific immune stimulation have been variable. However, the recent observations of improved survival after administration of levamisole plus 5-fluorouracil in the adjuvant setting have made an impact on the treatment of colorectal cancer. Animal studies consistently show that immune therapies are most effective for disease that is not advanced. Thus, the small benefit seen with levamisole, a low toxicity immunomodulator, suggests that much more impressive results can be anticipated with more potent and specific agents. Postsurgical autologous tumor cell vaccine has been effective in some prospective randomized trials; in others, no benefit was found. The identification and purification of allogeneic tumor-associated antigens has lead to enhanced antigen-specific host cell-mediated immunity; this may result in more consistent antitumor effects. The current development of chemically defined immune adjuvants of low toxicity allows tumor-specific immune stimulation to be tested in high-risk apparently healthy patients after resection of colorectal cancer (Stages II and III). The influx of information regarding immune cell populations, cell-surface markers, and cytokines has fostered extensive exploration of lymphocyte stimulation, in vitro cell growth and expansion, and in vivo evaluation in patients with advanced cancer. Modest tumor response rates have been documented with adoptive transfer of lymphokine-activated killer cells and interleukin-2. Improved results are anticipated with the more potent tumor-infiltrating lymphocytes and specific in vitro sensitization of draining lymph node cells to autologous and allogeneic tumor antigens. Murine monoclonal antibodies specific for cell-surface markers, such as carcinoembryonic antigen, have been tested for their value in the diagnosis and therapy of colorectal cancer. A small response rate has been seen with single and multiple injections of C017-1A, a monoclonal antibody specific for colonic and pancreatic cancer. The development of antiidiotypic antibodies in these patients may have been important in those that responded to this type of therapy. However, laboratory evidence suggests that monoclonal antibody conjugated to a cytotoxic agent (i.e., radionuclide, drug, or toxin) should be much more effective. Radioimmunotherapy trials in the nude mouse model bearing human colon cancer xenografts showed good tumor incorporation of the radionuclide (yttrium 90 or iodine 131), inhibition of tumor growth, and long-term survival.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunotherapy of colorectal cancer. 151 94

Thirty-six patients (21 male, 15 female) with ductal pancreatic cancer were treated with the long-acting synthetic luteinizing hormone releasing hormone (LH-RH) analogue buserelin. All patients had advanced tumor stages (stage II: 7 patients; stage III: 11 patients; stage IV: 18 patients). A monthly follow-up including clinical status, computed tomography scan, or ultrasonography and the tumor markers carcinoembryonic antigen (CEA) and H carbohydrate antigen 19-9 (CA19-9) was carried out. There were no severe side effects apart from impotency in men and hot flashes and outbreaks of perspiration in three patients. No partial or complete remission was seen. Twenty-six patients showed tumor progression with a median survival time of 4 months (range 0.5-11 months). In 10 patients a "no change" evaluation with a median survival time of 10 months (range 8-17 months) was registered. In only two of these patients there was no increase in the serum tumor markers CA19-9 and CEA during this time. In conclusion, LH-RH analogue treatment cannot be recommended in this selected group of patients suffering from advanced tumor stages of pancreatic cancer.
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PMID:Treatment of duct carcinoma of the pancreas with the LH-RH analogue buserelin. 151

Cholecystokinin (CCK) exerts an influential effect on the growth of normal pancreas. It is postulated that carcinoma arising from the pancreas may retain some normal pancreatic properties as far as hormone dependency is concerned. In an effort to examine the effect of CCK on the growth of pancreatic cancer, we evaluated the effect of CCK receptor antagonist on the growth of a transplantable adenocarcinoma of the pancreas. For this study we utilized three groups of hamsters with adenocarcinoma of the pancreas transplanted subcutaneously on the right flank. Group I (n = 15) served as control. Group II (n = 15) received CCK receptor antagonist (L-364,718), 0.1 mg/100 g body wt subcutaneously BID. Group III received CCK receptor antagonist in the same dose but treatment was started after tumors became palpable. All animals were examined daily. Latency for tumor growth, tumor size, and body weight were recorded. Animals were sacrificed after 3 weeks and final tumor volume and weight were measured. CCK receptor antagonist (L-364,718) significantly reduced pancreatic carcinoma growth when given immediately after transplantation and also in animals with established tumor. However, this inhibitory effect of L-364,718 was only partial and effective only for a brief time. This finding suggests CCK may have only a minimal influence on the biologic behavior of exocrine pancreatic cancer.
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PMID:Effect of CCK receptor antagonist on growth of pancreatic adenocarcinoma. 152 48

Nineteen patients with metastatic liver tumor (9 of gastric cancer, 5 of colon cancer, 2 of pancreatic cancer, one each of mammary cancer, cholecystic cancer, carcinoid of biliary tract) and one patient with primary liver cancer were treated by endogenously induced LAK therapy consisting of transhepatic arterial infusion with ADM or MMC for induction therapy and OK-432 and rIL-2 (TGP-3) for immunotherapy. The following results were obtained. 1) Clinical response for liver tumor showed no CR but 8 cases of PR, for an overall response rate of 42.1%. 2) Reduced tumor marker value was noted in 76.5% cases, and 50% survival term became 349 days after the therapy. 3) Many CD4 and CD8 positive mononuclear cells had infiltrated around liver tumor after therapy by immuno-histochemical staining of surface marker. 4) NK activity of peripheral blood lymphocytes was markedly reduced soon after the therapy and continued for about 4-7 days, while in cases of combined subcutaneous administration with OK-432, NK activity showed only a slight decrease.
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PMID:[Significance of antitumor effects and immunological response on endogenously induced LAK therapy for primary or metastatic liver tumor]. 153 Feb 92

This is a retrospective study to evaluate arterial infusion chemotherapy and radiotherapy for non-resectable pancreatic cancer without liver metastasis. Intra-arterial chemotherapy of the pancreas was performed for 17 patients, and 5 additionally received irradiation therapy. Five patients received radiation therapy alone. Both pain relief and tumor-reduction were more successful compared to the systemic chemotherapy group. In the locoregional treatment group, the patient survival rate was 50% at 1 year and 16% at 2 years. These rates were significantly higher than in the systemic chemotherapy group (p less than 0.01). Among the locoregional treatment groups, the median survival period was 7 months in radiation alone, 12 months in intra-arterial chemotherapy group, and 11 months in intra-arterial chemotherapy plus radiation group. These results suggested that locoregional treatment for pancreatic tumor is effective in increasing survival period and improving the quality of life.
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PMID:[Evaluation of radiation therapy combined with intra-arterial infusion chemotherapy in patients with non-resectable pancreatic cancer]. 153 Mar 31

The adhesive properties of tumor cells to basement membranes are known to play a crucial role in the complex process of tumor invasion and metastasis. Therefore, the interaction between the rat pancreatic acinar cell line AR42J and various extracellular matrix components along the route of differentiation induced by glucocorticoids was investigated. AR42J cells displayed a significantly higher affinity to laminin than to type IV collagen and fibronectin. Flow cytometric analysis showed expression of the 67-kilodalton laminin receptor and the integrin VLA-6 as potential laminin binding proteins in AR42J cells. Cell adhesion inhibition studies revealed that binding of undifferentiated AR42J cells to laminin was mediated predominantly by the 67-kilodalton laminin receptor. Dexamethasone pretreatment, which results in a more differentiated phenotype of AR42J cells, reduced the adhesion to laminin. In contrast to undifferentiated cells, interaction of differentiated AR42J cells to laminin was mediated by VLA-6. Dexamethasone-induced differentiation of pancreatic AR42J cells was paralleled by a decreased expression of 67-kilodalton laminin receptors, most likely because of a downregulation of the steady-state concentration of 67-kilodalton laminin receptor messenger RNA induced by dexamethasone. The hormonal modulation of cell matrix interactions opens interesting perspectives to the potential regulation of infiltrative growth and metastasis in pancreatic cancer.
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PMID:Laminin binding in membranes of a rat pancreatic acinar cell line are targets for glucocorticoids. 153 Jul 83


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