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)

Although the hamster pancreas does not express A, B or H blood group antigens, all hamster pancreatic ductal adenocarcinomas induced by treatment with N-nitrosobis(2-oxopropyl)amine express blood group-A antigen. Thus, the acquisition of blood group-A antigen expression in this system is a cancer-associated alteration. We have purified three major blood group-A antigen bearing glycoproteins (gp120, gp135 and gp150) from hamster pancreatic cancer cell membrane preparations using affinity chromatography on DBA (Dolichos biflorus) agglutinin-agarose. When assayed by immunoblotting, gp120 and gp135 showed strong blood group-A reactivity, which was removed by treating membrane samples with peptide-N-glycosidase F. Blood group-A reactivity was unchanged by treatment of the membrane fractions with endoglycosidases F and H. In addition, these two glycoproteins bearing blood group-A antigen also bound L-PHA (Phaseolus vulgaris leucoagglutinin). These results demonstrate that gp120 and gp135 express blood group-A antigen on Asn-linked multi-antennary complex type glycan structures. The gp150 showed weak blood group-A expression. This is the first demonstration of the neoexpression of cancer-associated blood group-A determinants which reside on Asn-linked glycan structures.
Carcinogenesis 1992 Oct
PMID:Purification and analysis of glycoproteins bearing blood group-A determinants from hamster pancreatic ductal adenocarcinomas. 138 1

Several rodent studies based on molecular biology have suggested that accumulation of genetic alterations in cancer-associated genes is required to convert a normal cell into a malignant cell. Activation of oncogenes and inactivation of tumor suppressor genes appear to be involved in carcinogenesis. In renal cell carcinomas, we have recently implied that the presence of tumor suppressor genes at chromosome 3p13-14.3 and 21.3, the regions where are also commonly deleted in adenocarcinoma of the lung; at chromosome 5q21, the region where the MCC (mutated in colorectal cancer) gene and APC (adenomatous polyposis coli) gene are located; at chromosome 6q27; and at 10q 21-23. We have also indicated that genes on 3p is probably important for development of RCCs and genes on 5q, 6q, and 10q may be associated with progression of RCCs.
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PMID:[Tumor suppressor genes associated with development of human renal cell carcinoma]. 149 60

We have demonstrated that S-2-(3-aminopropylamino)ethylphosphorothioic acid (WR2721) administered to mice 30 min prior to a relatively low dose of ionizing radiation is effective in protecting against radiation-induced carcinogenesis and subsequent life shortening. Female C57BL/6JANL x BALB/cJANL F1 mice, 200 per group, were exposed to gamma radiation at a dose of 206 cGy. Additional groups of 200 animals were sham treated, given injections of 400 mg/kg of WR2721, or administered WR2721 and the irradiated with 60Co photons at doses of 206 cGy or 417 cGy. Mice were treated at 110 days of age. They were housed five to a cage and were checked daily throughout life. All deceased animals were necropsied, and tissues were removed and fixed for histopathological analysis. Over 90% of the animal deaths were due to tumor involvement. WR2721 afforded significant protection (P = 0.0016) against radiation-induced malignancies (i.e., a total of 164 tumor codes were used) following a dose of 206 cGy. Protection against lymphoreticular tumors in particular was significant (P = 0.0165). Subsequent survival time in WR2721-protected animals (compared with matched irradiated controls) was extended by 65 days. Mice irradiated with 417 cGy following administration of WR2721 exhibited a response similar to those irradiated without the protector at a dose of 206 cGy (P = 0.26). Cumulative survival curves for unirradiated mice were unaffected by a single dose of WR2721. These data indicate a potential novel benefit for radioprotectors in cancer therapy. WR2721 and similar aminothiols may be effective adjuvants for reducing the risk of therapy-induced secondary cancers in patients who have an excellent prognosis for cure and long-term survival.
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PMID:Protection against late effects of radiation by S-2-(3-aminopropylamino)-ethylphosphorothioic acid. 165 Nov 55

Citral is a widely used flavoring and scenting agent which is employed in numerous food, industrial, and household products. Although the current regulatory status of citral lists it as a GRAS chemical on the FDA list, the chemical is a reactive beta-substituted vinyl aldehyde that has been shown to induce irritations of skin and mucous membranes, and to exhibit a dose-dependent teratogenic effect on embryos of white leghorn chickens. Because of these factors, citral was nominated by the National Toxicology Program for carcinogenesis study. Stability studies of dose formulations of citral (0.02%) in NIH-07 rodent diet indicated a loss of 41% of the citral after 1 day in a rat cage, due mainly to volatility and reactivity with diet components. The chemical was subsequently microencapsulated using a shell medium of food-grade modified cornstarch and sucrose, and then formulated into NIH-07 diet (0.02%) for various stability studies. Results after 7 days in a rat cage showed 95% retention of chemical; diet that had been stored 21 days retained 95% at 5 degrees C storage and 89% at room temperature. An assessment of the purity of the citral in the microcapsules indicated that total impurities increased from 0.7% in the neat chemical to 1.1% in the encapsulated chemical.
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PMID:Application of microencapsulation technology to improve the stability of citral in rodent diets. 179 63

The mutagenic and carcinogenic properties of fission-spectrum neutrons (KERMA-weighted mean energy of 0.85 MeV) from Argonne National Laboratory's JANUS reactor are substantially greater than those of low-LET radiation sources such as X-ray and 60Co photons. However, in contrast to the vast amount of work focused on chemical protection against damage induced by low-LET radiation, studies on the prevention of carcinogenic damage induced by fission neutrons have been limited. We have investigated the protective properties of the thiophosphorate compound S-3-(3-methylaminopropylamino)propylphosphorothioic acid (WR-151327) against carcinogenesis and life shortening in the B6CF1 hybrid mouse strain. Male and female mice, 200 of each sex per experimental group, were irradiated individually at 110 days of age. WR-151327 was administered intraperitoneally at a dose of 580 mg/kg 30 min prior to irradiation with a dose of 10 cGy. Animals were housed five to a cage; cage locations in holding rooms were controlled by computer and randomized. Mice were checked daily and all deceased animals were necropsied. A neutron dose of 10 cGy significantly altered the patterns of death of male and female animals compared to corresponding unirradiated control groups (logrank P values of 0.01 and 0.07, respectively). This was evidenced by a shortening of the life span due to tumor induction in the irradiated groups. WR-151327, when administered 30 min prior to irradiation, effectively protected both male and female animals from these effects. The life curves of irradiated male and female animals and those of corresponding unirradiated control groups were not significantly different (logrank P values of 0.63 and 0.25, respectively).
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PMID:Protection by WR-151327 against late-effect damage from fission-spectrum neutrons. 192 38

Karyotypic abnormalities have been described in more than 10,000 human neoplasms analyzed by means of chromosome banding. These aberrations are of three different kinds: primary abnormalities, which are essential in establishing the tumor; secondary abnormalities, which develop only after the neoplasm is established but which nevertheless may be important in tumor progression; and cytogenetic noise, which is the background level of nonconsequential aberrations. These latter changes are, in contrast to the primary and secondary aberrations, randomly distributed throughout the genome. The primary abnormalities, of which more than 100 have been identified, are strictly correlated with particular neoplastic disorders and even with histopathological subgroups within a given tumor type. To these purely cytogenetic data implicating specific genetic changes in carcinogenesis may now be added the growing evidence of molecular specificity emerging from recombinant DNA studies. It appears that both currently known classes of directly cancer-relevant genes, the dominant oncogenes and the recessive anti-oncogenes, are located at precisely those genomic sites that are visibly involved in neoplasia-associated chromosomal rearrangements. The molecular genetic data thus support the cytogenetic conclusion that the distribution of consistently cancer-associated breakpoints reflects the genomic position of genes that, either directly or through the control function they exert, are essential in the proliferation and differentiation of human cells.
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PMID:Chromosome abnormalities in cancer. 222 17

A complex network of proteins having attachment sites with DNA are known to exist in mammalian cells and have been referred to as a nuclear cage, matrix, scaffold and nucleoid. Since ionizing radiation is known to induce DNA--protein crosslinks as well as DNA single- and double-stranded breaks, an investigation of the sedimentation of the nucleoid in Chinese hamster ovary (CHO)* cells before, during and after treatments with ionizing radiation was undertaken. Using neutral sucrose gradient sedimentation, it was possible to reproducibly separate the protein and DNA components of interphase nucleoids. Under conditions of radiation damage, the DNA and protein components of the nucleoid were shifted to a coincident position in the gradients consistent with the generation of single- and double-stranded DNA scissions. During DNA damage repair, an apparent recruitment of protein to the nucleoid occurred and a rearrangement of the protein sedimentation was observed as the repair of DNA progressed. These data suggest that the protein component of the nucleoid was dynamic under conditions of DNA damage repair.
Carcinogenesis 1989 May
PMID:Nuclear protein organization and the repair of radiation damage. 270 45

Advances in the understanding of biochemical and molecular processes associated with cellular growth and differentiation, as well as colonic carcinogenesis hold promise for the development of new diagnostic and therapeutic modalities for this disease. Altered glycosylation of cell surface and secreted glycoconjugates appear to be useful markers in differentiating normal from malignant colonic tissue. New information regarding deletion and inappropriate expression of several blood group-related carbohydrate antigens as well as the synthesis of unique cancer-related carbohydrate structures has been derived from the use of monoclonal antibody technology, and may lead to more sensitive and specific screening tests and targeted therapies. Several glycoprotein markers for colon cancer have been studied whose diagnostic accuracy may surpass the limited sensitivity and specificity of traditional markers such as CEA. Colorectal cancers contain numerous quantitative and qualitative differences in metabolic and synthetic enzyme activities compared with normal colonic mucosa, which may be of potential importance in designing chemotherapeutic regimens or for following disease activity. Other cancer-associated markers, such as increases in orthinine decarboxylase activity and crypt cell labeling reflect abnormal proliferative activity and may be correlated with premalignant states. Studies of protooncogene expression and certain chromosomal deletions will provide insight into mechanisms of carcinogenesis and may also serve to define high-risk individuals. It is likely that as the biochemical and molecular mechanisms underlying malignancy are further delineated, cancer-associated markers will be defined that will improve diagnostic and more importantly, therapeutic efficacy.
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PMID:Biochemical and other markers of colon cancer. 306 43

The effect of voluntary exercise on azoxymethane (AOM; CAS: 25843-45-2)-induced colon carcinogenesis was investigated in male F344 rats. Beginning at 5 wk of age, all animals were divided into two groups (sedentary and exercise) and fed AIN-76A semipurified diet ad libitum. At 7 wk of age, animals were given AOM s.c. at a dose level of 15 mg/kg of body weight, once weekly for 2 wk. 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 wk post-AOM treatment. Body weights of animals in the exercise and sedentary groups were comparable. The incidence (percentage of animals with tumors) and multiplicity (tumors/animal) of colon adenocarcinomas were significantly inhibited in the exercise group, but the incidence and multiplicity of colon adenomas were unaffected by the exercise. The incidence of small intestinal adenocarcinomas and liver foci was also inhibited in the exercise group.
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PMID:Effect of voluntary exercise on azoxymethane-induced colon carcinogenesis in male F344 rats. 319 84

The three-dimensional distribution of nuclear DNA damage induced by dibenzo(a,e)fluoranthene (DBF), a potent carcinogen for mouse fibroblasts, has been examined. The intact supercoiled nuclear DNA obtained from nucleoids of mouse fibroblasts incubated with DBF was fractionated into loop DNA attached to the matrix (10%) and bulk loop DNA (90%). Preferential binding of DBF to the DNA of the extremities of loops, which are rich in regulatory sequences, was observed in all experiments. An increase of the preferential DBF binding was seen when fibroblasts were incubated with both DBF and novobiocin or hydroxyurea. The excess damage seen in loop DNA attached to the cage may be due to the kinetics of diffusion to the interior of the nucleus of hydrophobic DBF metabolites accumulated in lipid-rich nuclear membrane.
Carcinogenesis 1988 Aug
PMID:Non-random distribution of dibenzo[a,e]fluoranthene-induced DNA adducts in DNA loops in mouse fibroblast nuclei. 340 34


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