Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because of the limited effects of single-agent chemotherapy for solid tumors, combination therapy was employed in an attempt to enhance the clinical effects. Following our former report in which the combination effects of mitomycin C (MMC) and 5'-deoxy-5-fluorouridine (5'-DFUR) were clarified, combined applications of 4 drugs, vindesine (VDS), methotrexate (MTX), cisplatin (CDDP) and 5'-DFUR against 3 lines of human breast cancer (H-62, H-31, H-71), and one line each of gastric cancer (H-55) and colon cancer (H-110) xenografted into nude mice were evaluated in comparison with CAF (cyclophosphamide, adriamycin and 5-FU) therapy which is commonly used for breast cancer. Treatment was initiated in groups of 7 mice each when the mean tumor volume of subcutaneous tumors had reached about 100mm3, and the therapeutic effect was evaluated in terms of the inhibition rate (I.R.). A synergistic effect is said to exist when the combination therapy is superior to each single drug therapy at the maximal tolerated dose. Combination therapy with 3 drugs (VDS, CDDP and 5'-DFUR) or 4 drugs (VDS, CDDP, MTX and 5'-DFUR) achieved an I.R. of over 98%, i.e., a marked effect with tumor shrinkage, in 3 lines of tumors (H-55, H-31 and H-62). Moreover, remarkable effects were shown even in the other 2 lines which were insensitive to every single-agent therapy, the I.R. values being 85.7% (H-71) and 78.5% (H-110). A synergistic effect was obtained in 3 of the 5 lines examined. These combination therapies were histologically superior to therapies employing each single-drug therapy or CAF therapy. The side effects for combination of these 3 or 4 drugs evaluated by body weight loss were transient and equivalent to maximal dose of VDS or CDDP. Clinically, it is thought that these combined therapies of 3 or 4 drugs will bring about a considerable response in practice.
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PMID:[Combination chemotherapy with 3 or 4 drugs on human breast and gastrointestinal cancer xenografts in nude mice (II)]. 295 10

We conducted a case-control study to evaluate the effect of Helicobacter pylori (HP) infection on the risk of gastric cancer in Tokyo, Japan. The sera at the time of diagnosis from 282 gastric cancer cases and 767 sex- and age-matched cancer-free controls were tested for the presence of anti-HP IgG antibody (HM-CAP ELISA kit) and serum pepsinogen (PG) level (PG I and PG II Riabead). No significant association was observed in all sets [matched odds ratio (OR) = 1.04, 95% confidence interval: 0.73-1.49]. In subgroup analyses, however, an association was suggested in females [OR = 1.57], a younger population (< 50 years) [OR = 1.86], early cancer [OR = 1.53] and small cancer (< 40 mm) [OR = 1.55]. Furthermore, we observed a tendency for odds ratios to decrease with an increase in age or cancer growth (depth of tumor invasion and tumor size). Considering that the spontaneous disappearance of HP due to extended mucosal atrophy may lead to these decreasing odds ratios, we applied the conditional logistic model adjusted for the PG I/II ratio as a measure of atrophic gastritis. This analysis showed a positive association with HP infection in all sets [OR = 1.69; 1.01-2.81], distal cancer [OR = 1.88; 1.07-3.31] and intestinal-type cancer [OR = 3.76; 1.39-10.18]. We concluded that the risk of cancer associated with HP infection may be underestimated in studies with cross-sectional exposure because of spontaneous disappearance of HP due to extended mucosal atrophy.
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PMID:Helicobacter pylori infection, serum pepsinogen level and gastric cancer: a case-control study in Japan. 773 12

KL-6, a circulating mucin-like glycoprotein, is a pulmonary adenocarcinoma-associated antigen and is also regarded as an indicator of disease activity of interstitial pneumonitis. KL-6 has extensive heterogeneous antigenic determinants and consists of multiple heterogeneous antigen molecules. We have searched for circulating KL-6-associated glycoproteins with superior diagnostic value to KL-6 as a tumor marker for pulmonary adenocarcinoma. A new murine monoclonal antibody EH-123 reacting with an asialosugar chain on KL-6 was established. A new KL-6-associated molecule detected by a bimonoclonal bideterminant sandwich assay using the EH-123 antibody as a catcher and horseradish peroxidase-labeled KL-6 as a tracer was designated as CAM 123-6. In 59% (22 of 37) of patients with pulmonary adenocarcinoma, serum levels of CAM 123-6 were abnormally elevated and the positive rate increased with the progression of clinical stage. Elevated levels were not detected in normal individuals or in patients with benign lung diseases, other histologic types of lung cancer, gastric cancer, colon cancer or breast cancer. CAM 123-6 was more specific to pulmonary adenocarcinoma than carcinoembryonic antigen (CEA), but the sensitivity of CAM 123-6 for pulmonary adenocarcinoma was similar to that of CEA. CAM 123-6 is a promising candidate as a serum tumor marker for pulmonary adenocarcinoma.
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PMID:A new serum tumor marker, CAM 123-6, highly specific to pulmonary adenocarcinoma. 814 2

The relationship between Helicobacter pylori (H. pylori) infection and gastric cancer becomes the topics in the world, since some reports thereon in 1991. The purpose of this study was to know the prevalence of H. pylori infection in many patients with gastric cancer. We examined the H. pylori IgG antibody in 507 patients with gastric cancer resected surgically in our hospital from 1989 to 1991, retrospectively. For the test of H. pylori IgG antibody, HM-CAP EIA kit (Italy, ENTERIC PRODUCTS Co.) was used. The overall detection rate of H. pylori IgG antibody was 75% (378/507). H. pylori infection was significant significantly frequent in early cancer (80%, 231/288) than advanced cancer (67%, 147/219). But, the other clinicopathological features such as sex, age, histological type, location and the degree of intestinal metaplasia were not significantly correlated with H. pylori infection. To evaluate the risk of H. pylori infection for gastric cancer, we are going to plan a matched-pair case-control study.
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PMID:[Helicobacter pylori infection in gastric cancer]. 828 40

Although no serological tumor marker has yet been shown to be sufficiently sensitive and specific to be used in screening for colorectal, gastric, or pancreatic cancers, elevated pre-operative levels of carcinoembryonic antigen and carbohydrate antigen (CA) 19-9 correlate with advances stages of disease and a poorer clinical outcome. Monitoring of serum carcinoembryonic antigen after primary resection of colorectal cancer may identify a small percentage of asymptomatic patients with recurrent disease who are amenable to a second surgical procedure with curative intent. A new class of tumor markers that recognize cytokeratins, which comprise the intermediate filaments of the cytoskeletons of epithelial cells, is being evaluated as a prognostic factor in colorectal and gastric cancer. Elevated mRNA expression of matrix metalloproteinases and their inhibitors in tumor tissue compared with normal intestinal mucosa predicts for a poor prognosis after primary management of colorectal cancer. CA 19-9, CA 72-4, and CYFRA 21-1 may convey prognostic information in gastric cancer. CA 19-9 appears to be the best overall tumor marker for pancreatic cancer, and a subsequent rise after postoperative normalization may precede clinical detection of recurrent disease. CAM 17.1 is a new marker that has similar sensitivity but better specificity than CA 19-9 in pancreatic cancer. The utility of serial monitoring of these tumor markers in patients with advanced disease is less well established but may become helpful if more effective systemic therapy is developed.
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PMID:The prognostic importance of tumor markers in adenocarcinomas of the gastrointestinal tract. 925 89

We have evaluated the use of proteinase K (PK)-treated cells isolated from Helicobacter pylori as lipopolysaccharide (LPS) antigens in an immunoblot assay and an enzyme-linked immunosorbent assay (ELISA) for the serodiagnosis of H. pylori infection. The sera from patients with chronic gastritis, gastric ulcer, duodenal ulcer or gastric cancer, and from healthy adults with or without H. pylori infection were assayed with three commercial serodiagnostic kits (HM-CAP, Helico-G, and G.A.P. II) and novel methods relying on the use of PK-treated cells. The PK-treated cells used in these assays were selected on the basis of their possibility to possess a common epitope in the O-polysaccharides of H. pylori, which is known to be highly immunogenic in humans. Of the sera from these patients, 71-94% were positive with the commercial kits, 97% with immunoblot assay, and 90% with ELISA. On the other hand, of the healthy adults infected with H. pylori, 72-97% were positive with the commercial kits, 86% with immunoblot assay, and 72% with ELISA. PK-treated cells that did not contain the common epitope were unsuitable as an antigen for immunoblot assay or ELISA. Furthermore, the reactivity of these sera reacted specifically with H. pylori PK-treated cells but not with LPSs from other gram-negative bacteria, such as Campylobacter, Proteus, Bordetella, and Salmonella. These results demonstrate that the serological assays relying on the use of H. pylori PK-treated cells possessing a highly antigenic epitope are potentially useful as a serodiagnostic test for H. pylori infection.
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PMID:Utilization of proteinase K-treated cells as lipopolysaccharide antigens for the serodiagnosis of Helicobacter pylori infections. 971 4

The independent prognostic significance of isolated tumour cells in bone marrow is still a matter of debate. This study evaluated the possible association of bone marrow micrometastases with tumour progression and prognosis in patients affected by gastric cancer. Bone marrow aspirates from both iliac crests were obtained from 114 consecutive patients operated on for gastric cancer. The specimens were stained with monoclonal antibody CAM 5.2 which reacts predominantly with cytokeratin filaments 8 and 19. Among 114 cases analysed, 33 cases (29%) had cytokeratine-positive cells in the bone marrow. There was no significant relationship between the presence of bone marrow micrometastases and site, depth of tumour invasion, lymph node metastases, presence of metastases. Patients with cytokeratine-positive cells had a trend towards a diffuse type histology (P=0.06). Among the 88 curatively resected patients, median survivals were 40 months and 36 months for cytokeratine-negative and cytokeratine-positive subsets respectively (P=0.9). Recurrence of the disease was observed in 39 cases (44.3%); 11 of 24 (45.8%) in the cytokeratine-positive subset and 28 of 64 (43.7%) in the cytokeratine-negative subset. In conclusion in our experience the presence of cytokeratine-positive cells in the bone marrow of curatively resected gastric cancer patients did not affect outcome and its independent prognostic significance remains to be proven before its official acceptance in the TNM classification.
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PMID:The presence of bone marrow cytokeratin-immunoreactive cells does not predict outcome in gastric cancer patients. 1195 46

BACKGROUND: We conducted a case-control study to evaluate whether patients with severe gastric atrophy (indicated by serum pepsinogen concentration) have a high risk of gastric cancer.METHODS: At the time of diagnosis of gastric cancer, sera from 301 patients (cases) and 602 sex- and age-matched cancer-free individuals (controls) were tested for the presence of anti- Helicobacter pylori IgG antibody (HM-CAP enzyme-linked immunoassay [ELISA] kit; Kyowa Medix, Tokyo, Japan) and serum pepsinogen (PG) levels (PG I and II Riabead Kits; Dainabot, Tokyo, Japan). We defined positivity for pepsinogen a pepsinogen I concentration of less than 70 ng/mL and a PG I/II ratio of less than 3.0. We categorized the subjects according to serum pepsinogen levels and anti- Helicobacter pylori IgG antibody, creating four categories.RESULTS: Of the 301 cancer cases, 177 had positive serum pepsinogen levels, and 172 were positive for anti- Helicobacter pylori IgG antibody. The category in which subjects had positive serum pepsinogen levels and were negative for anti- Helicobacter pylori IgG antibody had the highest proportion (76.9%) of individuals with gastric cancer and the highest odds ratio (4.20) of the four categories. The odds ratios were 2.55 (95% confidence interval; 1.92-3.88) for positive serum pepsinogen levels and 0.93 (95% confidence interval; 0.63-1.27) for positive anti- Helicobacter pylori IgG antibody.CONCLUSION: These results suggest that patients with positive serum pepsinogen levels who are negative for IgG antibody to Helicobacter pylori, constitute a high-risk group for gastric cancer. Helicobacter pylori infection is associated with the development of gastric cancer by providing a suitable environment i.e., severe gastric atrophy, for carcinogenesis of the gastric mucosa.
Gastric Cancer 1998 Mar
PMID:Severe atrophic gastritis with Helicobacter pylori infection and gastric cancer. 1195 55

BACKGROUND: In cases of pT3 gastric cancer, even when standard histological staining reveals no evidence of metastases in the regional lymph nodes, patients still may die of postoperative recurrence of the tumor. An attempt was made in the present study to explain the unfavorable outcome of such patients by investigating the presence of occult cancer cells in lymph nodes by immunostaining of cytokeratin.METHODS: We examined 2310 lymph nodes that had been removed from 83 patients with stage II gastric cancer (pT3, N0, M0). Two consecutive sections of 4 &mgr;m thick were prepared for simultaneous staining with hematoxylin and eosin and immunostaining with the CAM 5.2 monoclonal antibody against cytokeratin, respectively.RESULTS: Evidence of occult involvement was found in 299 of 2310 (13%) lymph nodes and in 54 of 83 (65%) patients with pT3 gastric cancer. An analysis of survival demonstrated the limited 5-year survival of patients with occult involvement in their resected lymph nodes, as compared with that of patients without involvement ( P < 0.01). Moreover, the patients in whom group 2 lymph nodes had occult cancer cells had a significantly poorer prognosis than those in whom occult involvement was limited to group 1 lymph nodes ( P < 0.05).CONCLUSIONS: The accuracy of predictions of prognosis of patients with pT3 gastric cancer should be greatly enhanced if cytokeratin-specific immunostaining is performed in conjunction with routine histopathological examination of lymph nodes.
Gastric Cancer 1999 Aug
PMID:Clinicopathological value of immunohistochemical detection of occult involvement in pT3N0 gastric cancer. 1195 80

BACKGROUND: Endoscopic mucosal resection is frequently used in the treatment of mucosal gastric cancer. Micrometastasis in the lymph nodes of mucosal gastric cancer remains unclear.METHODS: We examined 2526 lymph nodes from 84 patients with mucosal gastric cancer. Two consecutive sections were prepared, for simultaneous staining with hematoxylin and eosin and immunostaining with CAM 5.2 monoclonal antibody against cytokeratin (CK), respectively. A clinicopathological comparison was made between patients with and without lymph node involvement.RESULTS: Lymph node involvement was detected in 45 of 2526 (1.8%) lymph nodes. The incidence of nodal involvement was significantly increased, from 1.2% (1/84 patients) with hematoxylin and eosin staining, to 19% (16/84 patients) with CK immunostaining. Although no significant difference was found, micrometastasis to lymph nodes was more frequently detected in tumors larger than 1.0 cm (15/72 patients, 21%) than in those less than or equal to 1.0 cm (1/12 patients; 8%, P = 0.307). However, discrete CK-positive cancer cells or clusters of CK-positive cancer cells were detected only in tumors larger than 2 cm.CONCLUSION: Because mucosal gastric cancer of more than 1.0 cm in superficial diameter may indicate a risk of micrometastasis to lymph nodes, endoscopic mucosal resection is not recommended for these patients.
Gastric Cancer 2000 Sep 29
PMID:Micrometastasis in lymph nodes of mucosal gastric cancer. 1198 17


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