Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

California has 12% of the U.S. population. In 1991, the newly diagnosed cancer cases in California represented 10% of all new cancer cases in the country, and the yearly toll was 10% of all cancer deaths. Relative to all new cancer cases in the U.S., California had 10, 9.8, 9.8, and 9.3% of breast, lung, prostate, and colorectal cancers, respectively. Because of its large population and cancer incidence, the epidemiology of cancer in California is of particular interest. Epidemiological factors reviewed in this article include ethnicity, lifestyle, occupation, and environmental conditions. Ethnic factors: There is an increased incidence of cervical and gallbladder cancer among Hispanic women, and of stomach cancer in Hispanic men and women. In U.S.-born Chinese men, the most prevalent cancers are those of the lung and colon, which is also seen in American white men. In U.S.-born Chinese women, there is an upward displacement of breast cancer incidence. In U.S.-born Japanese men and women, the mortality rate is closer to that of American whites. Life-style: Members of the Mormon Church and Seventh-Day Adventists have only 50% of the U.S. standardized mortality rate for cancer associated with smoking. Increased coffee consumption has been found to be associated with increased occurrence of colon and bladder cancer; alcohol use has been reported to have a positive association with colorectal cancer. The large AIDS population in San Francisco has a 144-fold odds ratio of Kaposi's sarcoma and a fivefold odds ratio of lymphoma when compared with the general U.S. population. Occupational factors: An increased incidence of mesothelioma in asbestos workers, of gastric cancer, skin cancer, and lymphoma in men working in dusty environments, and of astrocytoma in individuals with prolonged exposure to low-frequency electric and magnetic fields has been recorded. Environmental factors: The drinking-water pool in northern California is contaminated with asbestos of the serpentine type, which is associated with mesothelioma of the peritoneum and carcinoma of the lung, gallbladder, and pancreas. Petrochemical fumes in the heavily industrialized San Francisco Bay area have not been associated with an increased occurrence of cancer. No significant incidence in cancer has been noted in the counties surrounding the nuclear power plant at San Onofre during 18 years of close observation.
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PMID:Epidemiological factors of cancer in California. 146 11

The isolation of a cancer-associated, SCM-recognition, immunedefense-suppressing, and serine protease-protecting (CRISPP) peptide from the blood plasma of cancer patients is described. The amino acid sequences were determined on preparations from 12 different cancers. The peptide is composed in 9 cancers of 29 and in 3 cancers of 35 amino acid residues with molecular weights of 3410 and 4007 Da, respectively. A consensus, synthetic 29 amino acid CRISPP peptide (CRISPPs) has the same cancer SCM-recognition (CR) activity and SCM-response modifying effects as the natural peptide. The "cancer SCM-recognition epitope" of the CRISPP peptide was determined. Anti-CRISPPs antibodies were raised and used in immunoassays to confirm the presence of the CRISPP peptides in cancer blood plasmas, in supernatants of cancer cell growth media and in cultured human cancer cells. The amino terminal end sequences of peptides isolated from growth media of cultured breast and colon cancer cells corresponded to amino acid sequences of CRISPP peptides isolated from cancer blood plasmas of subjects with the respective cancers. The CRISPP peptides are between 83 to 100% homologous to the alpha 1-protease inhibitor amino acid sequence located at the carboxy terminal end between residues 358 and 393. The genetic origin of the CRISPP peptides and their selective advantage to cancer cell survival are discussed.
Cancer Detect Prev 1992
PMID:Cancer-associated SCM-recognition, immunedefense suppression, and serine protease protection peptide. Part I. Isolation, amino acid sequence, homology, and origin. 147 20

In this study, we analyzed 149 surgical cases of colorectal cancer between January 1983 and August 1989. Thirteen cases (8.7 percent) of colorectal primary cancer associated with extracolonic primary malignancy of 14 lesions and 10 cases (6.7 percent) of multiple primary colorectal cancers were included. Among the 14 lesions of extracolonic primary malignancy, there were 6 gastric carcinomas, 2 endometrial carcinomas, 2 urinary bladder carcinomas, and one each in the esophagus, liver, bile duct and jejunum. The second tumor was not detected preoperatively in 3 of 4 cases of synchronous multiple primary colorectal carcinoma. A curative resection was done in 10 (77 percent) out of 13 cases of colorectal cancer associated with extracolonic malignancy, while 7 (88 percent) out of 8 cases of multiple colorectal cancers had a curative resection. Nine patients (69 percent) with colorectal cancer associated with extracolonic malignancy were disease-free for 2 months to 14 years. Seven patients (88 percent) with multiple colorectal cancers were disease-free for one to 22 years. We recommend, therefore, that in any patient with colorectal cancer, the entire large bowel should be thoroughly searched for any other primary tumors, by taking the existence of extracolonic tumors into account. A curative resection should be performed, and the follow-up period should be life-long.
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PMID:Multiple colorectal carcinomas and colorectal carcinoma associated with extracolonic malignancies. 149 1

The sialosyl-Tn (STn) antigen is a mucin-associated carbohydrate antigen expressed by a variety of adenocarcinomas. In the colon, expression of this antigen has been associated with a poor prognosis, independent of tumor stage or histology. The present study was performed to determine whether this adverse clinical outcome might be due to an interaction between STn-positive mucin and natural killer (NK) cell cytotoxicity. Ovine submaxillary mucin (OSM), a mucin highly rich in STn antigen, partially inhibited NK cell cytotoxicity against K562 target cells, but only at high concentrations. Low concentrations of OSM were not inhibitory but became markedly inhibitory in the presence of ammonium ions. Two other STn-positive submaxillary mucins also markedly inhibited NK cytotoxicity when combined with ammonium ions. Removal of sialic acid from OSM reversed the OSM/ammonium-mediated inhibition of NK cell activity. Unlike the submaxillary mucins, two mucins derived from human breast and lung cancer cells which lack the STn antigen, did not inhibit NK cell activity in this system. Likewise, four other non-mucin glycoproteins which lack STn expression did not inhibit NK cells despite having levels of sialic acid that were, in some cases, comparable to submaxillary mucin. These results indicate that mucins bearing the cancer-associated STn antigen can effectively inhibit NK cell cytotoxicity in the presence of ammonium ions. While this NK cell inhibition is likely to be caused by ammonium, mucin markedly enhances this effect, thereby implicating a novel immunomodulatory property of mucin.
Cancer Res 1992 Sep 01
PMID:Mucins bearing the cancer-associated sialosyl-Tn antigen mediate inhibition of natural killer cell cytotoxicity. 151 39

The effect of voluntary exercise on azoxymethane-induced hepatocarcinogenesis was investigated in male F344 rats. Beginning at 5 weeks of age, all animals were divided into two groups (sedentary and exercise) and fed AIN-76A semipurified diet ad libitum. At 7 weeks of age, animals were given azoxymethane (AOM) s.c. at a dose level of 15 mg/kg of body weight, once weekly for 2 weeks. Four days after the second dose of AOM, all animals in the exercise group were housed in individual wheel-cage units and the animals in the sedentary group were housed in plastic cages. The experiment was terminated at 38 weeks post-AOM treatment. Body weights of animals in the exercise and sedentary groups were comparable. Immunohistochemical staining of glutathione S-transferase placental form (GST-P) was performed in the liver and measured GST-P positive foci. Density (number of GST-P positive foci/cm2 area of liver section), average area of foci and unit area of foci were significantly inhibited in the exercise group, although the incidence of neoplastic nodules and GST-P positive foci were unaffected by the exercise. Thus, energy expenditure due to exercise may reduce hepatocarcinogenesis in a laboratory animal model.
Cancer Lett 1992 Mar 31
PMID:Effect of voluntary exercise on azoxymethane-induced hepatocarcinogenesis in male F344 rats. 155 8

From 1967 to 1990, 96 previously untreated patients with cervicovaginal cancer associated with a history of vaginal pessary use to control uterovaginal prolapse were referred to eight radiation therapy departments in France. Sixty-eight patients had cervical cancer, and 28 had vaginal cancer. The mean interval between pessary insertion and cancer diagnosis was 18 years, with a range of 1 to 41 years. Most patients received radiation therapy and brachytherapy. Few (5%) had Grade 3 treatment side effects. The overall 5-year relative survival rate was 54%; nonsurvival was related to locoregional recurrence. Because almost all tumors occurred at the site of pessary insertion, foreign body chronic inflammation in association with viral infection may be the cause of the tumors.
Cancer 1992 May 15
PMID:Cervical and vaginal cancer associated with pessary use. 156 72

Hereditary non-polyposis colorectal cancer (HNPCC) probably constitutes 5% of all the cases of sporadic colorectal cancer. At present, the diagnosis can only be established on the basis of a family history which should fulfill the "Amsterdam criteria": 1) Colorectal cancer in at least three family members, 2) One family member must be a close relative of the other two, and 3) The diagnosis must have been established prior to the age of 50 years in at least one relative. Other forms of cancer also occur in the HNPCC syndrome, particularly endometrial cancer. The syndrome has a dominant inheritance and, therefore, all close relatives should be submitted to control examinations for the most important forms of cancer associated with the syndrome.
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PMID:[Hereditary non-polyposis colorectal cancer]. 158

Fucosyltransferase (FT) is considered to be one of the most important glycosyltransferases responsible for the synthesis of cancer-associated carbohydrate chains such as CA19-9 and SLX. To determine whether FT is a sensitive tumor marker, we measured the enzyme activity of FT in sera from 136 cancer patients, 14 patients with benign diseases and 59 healthy controls, by using PA (pyridylamino)-labeled type II biantennary oligosaccharide derived from human serotransferrin as an acceptor substrate. Serum FT activity was significantly elevated in patients with cancer compared to healthy controls. Analysis of the enzyme products using HPLC and various fucosidases with different specificity revealed that alpha 1----3 FT was responsible for most of the elevation of the enzyme activity in sera from cancer patients. It should be stressed that the alpha 1----3FT derived from cancer patients transferred fucose to terminal lactosamine residues of type II biantennary oligosaccharides already attached to sialic acid. This indicates that the substrate specificity is clearly different from that reported in normal sera and tissues. In addition to alpha 1----3FT, some glycosidases including fucosidase were also elevated in sera from cancer patients.
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PMID:[Elevation of serum fucosyltransferase activities in malignant diseases--a sensitive tumor marker?]. 158 92

The cause of cancer cachexia is unclear. Tumors may be competing with the host for ingested nutrients or may be releasing some factor that actively inhibits energy utilization. To explore these questions, plasma was sterilely collected and pooled from 103 terminally cachectic Fischer 344 rats implanted with an experimental sarcoma. Control plasma was collected in similar fashion from 138 nontumor-bearing rats (NTBP). Plasma from tumor-bearing rats (TBP) or NTBP was continuously infused in a randomized, blinded fashion for 4 days into 20 normal rats. During infusion, food intake and nitrogen excretion were measured daily. At sacrifice, body weight and organ masses were determined. Rats receiving TBP demonstrated an immediate and profound anorexia compared with those receiving NTBP. Total food intake during treatment was 31.2 +/- 3.3 (g +/- SEM) in the TBP group versus 48.2 +/- 2.8 in the NTBP group (P less than 0.001 by t test). Likewise, the total decline in body weight was greater in the TBP group as compared with the NTBP group (-35.2 +/- 3.4 versus -14.6 +/- 4.0, P less than 0.001). Mean daily nitrogen balance during treatment was negative in the rats receiving TBP (-14.5 +/- 20.1 mg +/- SEM) while remaining highly positive in the rats receiving NTBP (110.7 +/- 19.3, P less than 0.002). Finally, cardiac and gastrocnemius muscle masses were decreased, while hepatic mass was unaffected. These data demonstrate that the syndrome of cancer-associated cachexia is transmissible in plasma and therefore may be mediated by a circulating molecule or molecules. Identification and purification of the molecule(s) responsible for this effect would have obvious clinical benefits.
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PMID:Cancer cachexia is transmissible in plasma. 159 73

Seven different tumor cell lines (human melanoma SK MEL 28; hamster melanoma HM29; murine melanomas B16F10 and amelanotic melanoma B16a; human colon carcinoma HCT8; murine colon carcinoma CT26; and murine Lewis lung carcinoma) were treated with thrombin at 0.5-1 unit/ml and examined for their ability to bind to adherent platelets; HM29 was studied for its ability to bind to fibronectin and von Willebrand factor; CT26, B16F1, B16F10, and B16a were studied for their ability to form pulmonary metastasis after i.v. injection of thrombin-treated tumor cells; CT26 was studied for its ability to grow s.c. Five of 7 thrombin-treated tumor cell lines increased their adhesion to adherent platelets 2-to 3-fold. HM29 increased its adherence to fibronectin and von Willebrand factor 2- to 3-fold. CT26, B16F1, B16F10, and B16a increased experimental pulmonary metastasis 10- to 156-fold. Thrombin-treated CT26 cells demonstrated 2-fold greater growth in vivo after s.c. injection. The mechanism of enhanced adhesion of thrombin-treated tumor cells to platelets required the platelet integrin GPIIb-GPIIIa since it could be inhibited by agents known to block adhesion of ligands to GPIIb-GPIIIa (monoclonal antibody 10E5, tetrapeptide RGDS, disintegrin Albolabrin); as well as a "GPIIb-GPIIIa-like" structure on tumor cells since it could be inhibited by treatment of thrombin-treated tumor cells with 10E5 and RGDS. The thrombin effect on tumor cells was optimum at 1 h of incubation with thrombin, did not require active thrombin on the tumor cell surface, and did not require protein synthesis (not inhibited by cycloheximide). Thus, thrombin-treated tumor cells markedly enhance pulmonary metastasis. It is suggested that this may be secondary to thrombin-induced enhanced adhesion as well as growth of tumor cells.
Cancer Res 1992 Jun 15
PMID:Effect of thrombin treatment of tumor cells on adhesion of tumor cells to platelets in vitro and tumor metastasis in vivo. 159 84


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