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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intercellular adhesion molecule-1 (ICAM-1), a molecule bound to the cell surface, is a ligand for leukocyte function antigen-1 (LFA-1), and the ICAM-1/LFA-1 system mediates various cell-cell interactions involved in immunity. Soluble ICAM-1 (sICAM-1) is a circulating substance and binds with LFA-1 of leukocytes, thus, making leukocytes less available for binding with cell surface ICAM-1 on target cells. The serum level of soluble ICAM-1 (sICAM-1) was found to be significantly elevated (p<0.01) in patients with early and advanced gastric cancer compared with healthy controls. Natural killer activity (NK activity) was assessed by measuring the cytotoxicity of peripheral blood mononuclear cells (PBMCs) for K562 cells. There was no significant difference in NK activity between gastric cancer patients and healthy controls when heat-inactivated fetal calf serum was used in assays. However, addition of patient serum significantly decreased (p<0.05) NK activity when the serum was from patients with advanced gastric cancer compared with healthy volunteers. Addition of anti-ICAM-1 monoclonal antibody 0 to 5.0 microg/ml caused little change in NK activity in healthy controls, but its addition at 10 microg/ml remarkably decreased NK-activity in gastric cancer patients, probably through antibody binding with ICAM-1 on target cells. In other experiments, liver metastasis was induced in mice by inoculation of colon 26 murine colon cancer cells. In vitro pretreatment of colon 26 cells with the anti-ICAM-1 monoclonal antibody significantly increased the number of metastatic nodules. These results suggest that both sICAM-1 and anti-ICAM-1 monoclonal antibody act as immunosuppressive factors by inhibiting the ICAM-1/LFA-1 system.
Res Commun Mol Pathol Pharmacol 1998 Jun
PMID:Soluble intercellular adhesion molecule-1 and natural killer cell activity in gastric cancer patients. 973 8

The purpose of this study is to extract common features of an environmental hormone-oriented neoplasia by comparatively investigating the epidemiological characteristics of testicular cancer in Denmark with those of other cancers, of which the age-adjusted incidence rates (AAIRs) underwent remarkable increase or decrease in the time range of early 1960's to mid 1980's. Practically, the log-transformed (log) AAIRs and the corresponding log ASIRs (age-specific incidence rates) were used in parallel to investigate the dynamic aspect of cancer risk changes in time and space. The present study includes cancers of the testis, lung, bladder and stomach as study subjects, and followed the chronological transition of cancer risk for each tumor type and for each population unit from early 1960's to mid 1980's. In space, the present study includes the data for 6 population units as follows: Denmark, Birmingham-England, the State of New York less New York city, Miyagi-Japan, Puerto Rico and Cali-Colombia. Since 3 neoplasias other than testicular cancer were associated with male predominance of cancer risk, 1st order regression analysis was applied to a set of 5 chronologically consecutive data of log AAIRs for a given tumor to comparatively investigate the sex discrimination of cancer risk for each of 3 neoplasia types. Results obtained are as follows: a) the ASIR profile of testicular cancer in Denmark (a high-risk country) was a composite of an adult type surge and an infant type surge (a product of in utero carcinogenic insult). Consistent ascension of both the adult type surge and the infant type surge of the ASIR profile was observed in parallel with the straight line increase of log AAIR of testicular cancer in Denmark. b) The ASIR profiles of testicular cancer for Miyagi-Japan (a low-risk country with steady increase of log AAIR) experienced new emergence of the infant type surge that was detectable in the profile for the years 1968-1971 and 1983-1987, but not in the profile for the years 1959-1960. c) The ASIR profiles of testicular cancer for Cali-Colombia (a low-risk country with no sign of risk increase) was free of the infant type surge throughout the study period. d) Temporary emergence of the infant type surge was experienced in cancers of the lung and bladder in early 1970's. In space, the infant type surge had preference of occurrence for a high-risk country to a low-risk country, and for a male population to a female population. e) Another feature of environmental hormone-oriented tumor was found in the recent risk decrease of gastric cancer of which the rate of risk decrease was distinct in Western countries and Japan, but not in Cali-Colombia. Puerto Rico was ranked as an in-between existence--a violation to the rules of Westernization effect for cancer risk. f) The relation between the male log AAIR and the male log AAIR less female log AAIR for a given tumor type was found to have a good fitness to the equilibrium model of which the members are destined to interact with each other under the law of mass action. The above mathematical strictness was found to be valid with all of cancers of the liver, skin, lung, bladder, stomach and esophagus--a finding to indicate that the relation between the changes of male cancer risk and that of female cancer risk in time and space is defined by the law of mass action regardless of the presence or absence of environmental hormone impact, and that no marker is available to detect possible implication of the environmental hormones with this system. g) The significance of the last finding in cancer etiology was discussed in the light of the steroid criminal hypothesis of human carcinogenesis in general. In conclusion, the recent risk changes of cancers of all the testis, lung, bladder and stomach in high-risk areas are in part to be explained in terms of the environmental hormone impact.
Int J Mol Med 1998 Dec
PMID:Comparative epidemiology of cancers of the testis, lung, bladder and stomach with special reference to the possible implication of environmental hormones in the recent risk changes of the 4 neoplasia types. 985 Jul 40

Activated T lymphocytes release a soluble form of IL-2R (SoIL-2R) into the bloodstream, which can be detected by CD25 monoclonal antibody. Perioperative changes of serum levels of SoIL-2R and the number of CD25-positive cells were monitored simultaneously to clarify the clinical implications of SoIL-2R in patients with gastric cancer (n=91). Preoperative levels of SoIL-2R were significantly higher than in normal controls and levels were a useful indicator of possible lymph node involvement. Postoperative levels of SoIL-2R increased independently of the number of CD25-positive cells. Patients with progressive postoperative increases in levels of SoIL-2R had both a significantly high frequency of postoperative relapse and a poor prognosis. Increased SoIL-2R may reduce the availability of IL-2 by binding to it. Postoperative progressive increases in SoIL-2R appear to be a good indicator for a poor prognosis in patients with gastric cancer.
Int J Mol Med 1998 Jan
PMID:A progressive postoperative increase in the serum level of soluble receptors for interleukin-2 is an indicator of a poor prognosis in patients with gastric cancer. 985 7

We describe a simple and sensitive method for detection of low number of cancer cells in the blood. The method is based on FACS sorting of leukocytes labelled with anti-CD45 monoclonal antibody and examining CD45- cells by conventional cytology and immunostaining for cytokeratin 18. In a model study, cancer cells seeded at the frequency of 1 per 106 and 1 per 107 leukocytes were detected in CD45- population. Sensitivity of this method was comparable to reverse transcription polymerase chain reaction (RT-PCR) used for detection of cancer cells expressing CD44 variants-mRNA. In a pilot study, cancer cells were also isolated from the blood of some patients with locally advanced gastric cancer. This method may be useful for detection of circulating tumour cells in cancer patients.
Int J Mol Med 1998 Mar
PMID:Detection of cancer cells in the blood by FACS sorting of CD45- cells. 985 65

The exposure of human stomach cancer KATO III cells to black tea theaflavin extract, free theaflavin, and theaflavin digallate that are main components of the extract, led to both growth inhibition and the induction of programmed cell death (apoptosis). Morphological changes showing apoptotic bodies were observed in the cells treated with black tea theaflavin extract, theaflavin and theaflavin digallate. The fragmentations by these theaflavin compounds of DNA to oligonucleosomal-sized fragments that are characteristics of apoptosis were observed to be concentration- and time-dependent. These data suggest that drinking of black tea in large amounts is recommended to protect humans from stomach cancer.
Int J Mol Med 1998 Apr
PMID:Black tea theaflavins induce programmed cell death in cultured human stomach cancer cells. 985 88

Thymidine phosphorylase (dThdPase) is identical to platelet-derived endothelial cell growth factor (PD-ECGF), an angiogenesis factor. We investigated the correlation between dThdPase activity in gastric cancer tissue and clinicopathological factors. Thirty-three cancer tissue specimens and 23 adjacent normal gastric mucosal specimens were obtained from surgery. Measurement of dThdPase activity was based on the amount of 5-fluorouracil formed from 5'-deoxy-5-fluorouridine by dThdPase. Mean dThdPase activity in cancer tissue was approximately 3.2 times higher than that in normal tissue. Cancerous tissues with venous invasion had about twice the dThdPase activity as cancerous tissues without venous invasion. Other clinicopathological features were not related to dThdPase activity. A correlation between dThdPase activity and immunosuppressive acidic protein level was observed (r = 0.532, P = 0.005). dThdPase activity in gastric cancer cells was found to be correlated with venous invasion, supporting previous findings that it plays a role in tumor angiogenesis.
Int J Mol Med 1998 Oct
PMID:Thymidine phosphorylase activity in tumor correlates with venous invasion. 985 35

Precise correlation of histomorphology with the results of molecular genetic analysis is difficult in gastric cancer tissue composed of intestinal and diffuse types. A novel microdissection procedure was applied to correlate p53 and APC allelic loss with histologic type and tumor stage (mucosal vs. invasive cancer) in formalin-fixed, paraffin-embedded specimens of 25 gastric cancers. In addition, mucosal and invasive lesions were dissected from each of 11 invasive gastric cancers to study progression, and allelic loss of the p53 and APC genes was assessed. The p53 gene underwent loss of heterozygosity (LOH) in 4 of 4 informative cases of intestinal-type gastric cancer with mucosal lesions associated with invasion. By contrast, no p53 LOH was found among 6 informative cases with mucosal cancer. LOH of the APC gene in both intestinal and diffuse types of cancer was detected in 4 of 7 and 5 of 6 informative cases, respectively. These data suggest that allelic deletion of the p53 gene in intestinal-type gastric carcinoma predicts the invasive potential of mucosal cancer, and that inactivation of the APC gene plays a role in the genetic tumorigenesis of both intestinal and diffuse types of gastric cancer. Microdissection can correlate genetic alterations with histologic morphology in gastric cancer.
Diagn Mol Pathol 1998 Oct
PMID:Correlation of histologic morphology and tumor stage with molecular genetic analysis using microdissection in gastric carcinomas. 999 Apr 80

Inherited mutations in the E-cadherin gene ( CDH1 ) were described recently in three Maori kindreds with familial gastric cancer. Familial gastric cancer is genetically heterogeneous and it is not clear what proportion of gastric cancer susceptibility in non-Maori populations is due to germline CDH1 mutations. Therefore, we screened eight familial gastric cancer kindreds of British and Irish origin for germline CDH1 mutations, by SSCP analysis of all 16 exons and flanking sequences. Each family contained: (i) two cases of gastric cancer in first degree relatives with one affected before age 50 years; or (ii) three or more cases of gastric cancer. Novel germline CDH1 mutations (a nonsense and a splice site) were detected in two families (25%). Both mutations were predicted to truncate the E-cadherin protein in the signal peptide domain. In one family there was evidence of non-penetrance and susceptibility to both gastric and colorectal cancer; thus, in addition to six cases of gastric cancer, a CDH1 mutation carrier developed colorectal cancer at age 30 years. We have confirmed that germline mutations in the CDH1 gene cause familial gastric cancer in non-Maori populations. However, only a minority of familial gastric cancers can be accounted for by CDH1 mutations. Loss of E-cadherin function has been implicated in the pathogenesis of sporadic colorectal and other cancers, and our findings provide evidence that germline CDH1 mutations predispose to early onset colorectal cancer. Thus, CDH1 should be investigated as a cause of inherited susceptibility to both gastric and colorectal cancers.
Hum Mol Genet 1999 Apr
PMID:Germline E-cadherin gene (CDH1) mutations predispose to familial gastric cancer and colorectal cancer. 1007 28

The development, maintenance and repair of tissue requires an exquisite balance between cell proliferation, cell adhesion and cell motility. Equally, tumour initiation and progression are characterized by not only the abnormal expression of genes involved in cell proliferation and survival but also by genes responsible for the control of cell adhesion and cell motility. Central to the process of cell-cell adhesion in epithelial tissues is E-cadherin. Loss of E-cadherin function in tumours results in the rapid progression of relatively benign adenomas to invasive, metastatic carcinomas. Germline mutation of the E-cadherin gene predisposes to diffuse, poorly differentiated gastric cancer, and its downregulation in sporadic tumours is associated with poor clinical prognosis.
Mol Med Today 1999 Apr
PMID:E-cadherin downregulation in cancer: fuel on the fire? 1043 Nov 65

The presence of the carcinoembryonic antigen (CEA) gene and CEA expression in the liver was tested to identify their possible roles in the liver metastasis of colorectal carcinoma. The CEA gene in the liver was identified by amplifying the CEA-specific N-terminal domain exon with digoxigenin-dUTP labeling in 16 colorectal carcinomas with liver metastases. Next, CEA expression was tested by immunostaining using the anti-CEA monoclonal antibody (T84.66, ATCC). Liver tissues from 13 stomach cancer patients and 12 colorectal cancer patients without liver metastasis were also tested as control groups. Three grades (<25%, 25-50%, and 50%< or =) were given according to the proportion of positive cells. The CEA gene was amplified in the metastatic tumor cells of the liver (2.6 +/- 0.2, mean grade +/- SEM) and their surrounding hepatocytes (1.5 +/- 0.2) in all cases. CEA expression was found in all metastatic tumor cells and 14 cases of the surrounding hepatocytes. Among the control groups, the CEA gene of the hepatocytes was found in 9 cases each of the colorectal and the stomach cancers that did not exhibit CEA expression. The level of serum CEA was related with the numbers and volume of liver metastases, but not with CEA expression in tumor cells and surrounding hepatocytes. The CEA gene in the metastatic tumor cells, not in the hepatocytes, was closely associated with CEA expression in the surrounding hepatocytes (p<0.01). Although the precise mechanism of CEA gene regulation in hepatocytes remains to be proven, the CEA gene in the metastatic tumor of the liver seems to affect CEA expression in the surrounding hepatocytes facilitating liver metastasis in colorectal carcinoma.
Mol Cells 1999 Apr 30
PMID:Carcinoembryonic antigen gene and carcinoembryonic antigen expression in the liver metastasis of colorectal carcinoma. 1034 Apr 66


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