A potent carcinogen and neurotoxic compound. It is particularly effective in inducing colon carcinomas.
Tumors or cancer of the COLON.
Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included.
Clusters of colonic crypts that appear different from the surrounding mucosa when visualized after staining. They are of interest as putative precursors to colorectal adenomas and potential biomarkers for colorectal carcinoma.
The segment of LARGE INTESTINE between the CECUM and the RECTUM. It includes the ASCENDING COLON; the TRANSVERSE COLON; the DESCENDING COLON; and the SIGMOID COLON.
Pathological processes that tend eventually to become malignant. (From Dorland, 27th ed)
Long-chain polymer of glucose containing 17-20% sulfur. It has been used as an anticoagulant and also has been shown to inhibit the binding of HIV-1 to CD4-POSITIVE T-LYMPHOCYTES. It is commonly used as both an experimental and clinical laboratory reagent and has been investigated for use as an antiviral agent, in the treatment of hypolipidemia, and for the prevention of free radical damage, among other applications.
Tumors or cancer of the INTESTINES.
Agents that reduce the frequency or rate of spontaneous or induced tumors independently of the mechanism involved.
Lining of the INTESTINES, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. In the SMALL INTESTINE, the mucosa is characterized by a series of folds and abundance of absorptive cells (ENTEROCYTES) with MICROVILLI.
A plant genus of the family BIGNONIACEAE that is a source of lapachol.
The combination of two or more different factors in the production of cancer.
Inflammation of the COLON section of the large intestine (INTESTINE, LARGE), usually with symptoms such as DIARRHEA (often with blood and mucus), ABDOMINAL PAIN, and FEVER.
The aglycone of CYCASIN. It acts as a potent carcinogen and neurotoxin and inhibits hepatic DNA, RNA, and protein synthesis.
Oil from ZEA MAYS or corn plant.
Hydrazine substituted by one methyl group.
A cyclooxygenase inhibiting, non-steroidal anti-inflammatory agent (NSAID) that is well established in treating rheumatoid arthritis and osteoarthritis and used for musculoskeletal disorders, dysmenorrhea, and postoperative pain. Its long half-life enables it to be administered once daily.
A benign epithelial tumor with a glandular organization.
Tumors or cancer of the DUODENUM.
An inducibly-expressed subtype of prostaglandin-endoperoxide synthase. It plays an important role in many cellular processes and INFLAMMATION. It is the target of COX2 INHIBITORS.
Oils high in unsaturated fats extracted from the bodies of fish or fish parts, especially the LIVER. Those from the liver are usually high in VITAMIN A. The oils are used as DIETARY SUPPLEMENTS. They are also used in soaps and detergents and as protective coatings.
A multi-functional catenin that participates in CELL ADHESION and nuclear signaling. Beta catenin binds CADHERINS and helps link their cytoplasmic tails to the ACTIN in the CYTOSKELETON via ALPHA CATENIN. It also serves as a transcriptional co-activator and downstream component of WNT PROTEIN-mediated SIGNAL TRANSDUCTION PATHWAYS.
A malignant epithelial tumor with a glandular organization.
The chromosome region which is active in nucleolus formation and which functions in the synthesis of ribosomal RNA.
Hydrazines substituted with two methyl groups in any position.
Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.
Complexing agent for removal of traces of heavy metal ions. It acts also as a hypocalcemic agent.
The origin, production or development of cancer through genotypic and phenotypic changes which upset the normal balance between cell proliferation and cell death. Carcinogenesis generally requires a constellation of steps, which may occur quickly or over a period of many years.
A flavonol glycoside found in many plants, including BUCKWHEAT; TOBACCO; FORSYTHIA; HYDRANGEA; VIOLA, etc. It has been used therapeutically to decrease capillary fragility.
Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.
A pyridoxal-phosphate protein, believed to be the rate-limiting compound in the biosynthesis of polyamines. It catalyzes the decarboxylation of ornithine to form putrescine, which is then linked to a propylamine moiety of decarboxylated S-adenosylmethionine to form spermidine.
The use of chemical compounds to prevent the development of a specific disease.
Regular course of eating and drinking adopted by a person or animal.
An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic.
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
A DNA alkylating agent that has been shown to be a potent carcinogen and is widely used to induce colon tumors in experimental animals.
A sulfinylindene derivative prodrug whose sulfinyl moiety is converted in vivo to an active NSAID analgesic. Specifically, the prodrug is converted by liver enzymes to a sulfide which is excreted in the bile and then reabsorbed from the intestine. This helps to maintain constant blood levels with reduced gastrointestinal side effects.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms.
A 16-kDa peptide hormone secreted from WHITE ADIPOCYTES. Leptin serves as a feedback signal from fat cells to the CENTRAL NERVOUS SYSTEM in regulation of food intake, energy balance, and fat storage.
Cell surface receptors for obesity factor (LEPTIN), a hormone secreted by the WHITE ADIPOCYTES. Upon leptin-receptor interaction, the signal is mediated through the JAK2/STAT3 pathway to regulate food intake, energy balance and fat storage.
Any of several BRASSICA species that are commonly called mustard. Brassica alba is white mustard, B. juncea is brown or Chinese mustard, and B. nigra is black, brown, or red mustard. The plant is grown both for mustard seed from which oil is extracted or used as SPICES, and for its greens used as VEGETABLES or ANIMAL FEED. There is no relationship to MUSTARD COMPOUNDS.
A plant genus of the family BRASSICACEAE. The common name of white mustard sometimes refers to other plants (MUSTARD PLANT).
A large increase in oxygen uptake by neutrophils and most types of tissue macrophages through activation of an NADPH-cytochrome b-dependent oxidase that reduces oxygen to a superoxide. Individuals with an inherited defect in which the oxidase that reduces oxygen to superoxide is decreased or absent (GRANULOMATOUS DISEASE, CHRONIC) often die as a result of recurrent bacterial infections.
A specialty concerned with the nature and cause of disease as expressed by changes in cellular or tissue structure and function caused by the disease process.
The science concerned with the detection, chemical composition, and biological action of toxic substances or poisons and the treatment and prevention of toxic manifestations.
Societies whose membership is limited to scientists.
Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system.
One of the two major classes of cholinergic receptors. Muscarinic receptors were originally defined by their preference for MUSCARINE over NICOTINE. There are several subtypes (usually M1, M2, M3....) that are characterized by their cellular actions, pharmacology, and molecular biology.
An alkaloid from SOLANACEAE, especially DATURA and SCOPOLIA. Scopolamine and its quaternary derivatives act as antimuscarinics like ATROPINE, but may have more central nervous system effects. Among the many uses are as an anesthetic premedication, in URINARY INCONTINENCE, in MOTION SICKNESS, as an antispasmodic, and as a mydriatic and cycloplegic.
An antimuscarinic agent that inhibits gastric secretion at lower doses than are required to affect gastrointestinal motility, salivary, central nervous system, cardiovascular, ocular, and urinary function. It promotes the healing of duodenal ulcers and due to its cytoprotective action is beneficial in the prevention of duodenal ulcer recurrence. It also potentiates the effect of other antiulcer agents such as CIMETIDINE and RANITIDINE. It is generally well tolerated by patients.
Repair or renewal of hepatic tissue.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.

Effect of meat (beef, chicken, and bacon) on rat colon carcinogenesis. (1/492)

High intake of red meat or processed meat is associated with increased risk of colon cancer. In contrast, consumption of white meat (chicken) is not associated with risk and might even reduce the occurrence of colorectal cancer. We speculated that a diet containing beef or bacon would increase and a diet containing chicken would decrease colon carcinogenesis in rats. One hundred female Fischer 344 rats were given a single injection of azoxymethane (20 mg/kg i.p.), then randomized to 10 different AIN-76-based diets. Five diets were adjusted to 14% fat and 23% protein and five other diets to 28% fat and 40% protein. Fat and protein were supplied by 1) lard and casein, 2) olive oil and casein, 3) beef, 4) chicken with skin, and 5) bacon. Meat diets contained 30% or 60% freeze-dried fried meat. The diets were given ad libitum for 100 days, then colon tumor promotion was assessed by the multiplicity of aberrant crypt foci [number of crypts per aberrant crypt focus (ACF)]. The ACF multiplicity was nearly the same in all groups, except bacon-fed rats, with no effect of fat and protein level or source (p = 0.7 between 8 groups by analysis of variance). In contrast, compared with lard- and casein-fed controls, the ACF multiplicity was reduced by 12% in rats fed a diet with 30% bacon and by 20% in rats fed a diet with 60% bacon (p < 0.001). The water intake was higher in bacon-fed rats than in controls (p < 0.0001). The concentrations of iron and bile acids in fecal water and total fatty acids in feces changed with diet, but there was no correlation between these concentrations and the ACF multiplicity. Thus the hypothesis that colonic iron, bile acids, or total fatty acids can promote colon tumors is not supported by this study. The results suggest that, in rats, beef does not promote the growth of ACF and chicken does not protect against colon carcinogenesis. A bacon-based diet appears to protect against carcinogenesis, perhaps because bacon contains 5% NaCl and increased the rats' water intake.  (+info)

Coordinate regulation of cyclooxygenase-2 and TGF-beta1 in replication error-positive colon cancer and azoxymethane-induced rat colonic tumors. (2/492)

Evidence is accumulating which indicates that cyclooxygenase-2 (COX-2) is involved in the pathogenesis of colorectal cancer. We evaluated the expression of COX-2 in replication error-positive (RER) colon cancers, colon cancers metastatic to liver and azoxymethane (AOM)-induced rat colonic tumors. Immunohistochemistry showed that COX-2 was low to undetectable in normal human mucosa, but abundant in the RER adenocarcinomas we examined. COX-2 immunoreactivity in metastatic colon cancers was less abundant, but clearly detectable. In the colon of AOM-treated rats, COX-2 protein was not detectable in normal mucosa, but present in most of the epithelial cells comprising the tumors. The TGF-beta1 staining pattern in these human and rat tumors was similar to that observed for COX-2. The role of TGF-beta in RER adenocarcinomas is complex because of the increased mutation rate of TGF-beta type II receptors. Northern analysis showed abundant TGF-beta1 mRNA in AOM-induced tumors, but not in paired mucosa. TGF-beta1 induced the expression of COX-2 mRNA and protein in intestinal epithelial cells (IEC-6). Chronic TGF-beta1 treatment caused a TGF-beta-dependent overexpression of COX-2 in rat intestinal epithelial cells (RIE-1). TGF-beta1 may regulate COX-2 expression during the colonic adenoma to carcinoma sequence.  (+info)

Effect of retinoids on AOM-induced colon cancer in rats: modulation of cell proliferation, apoptosis and aberrant crypt foci. (3/492)

We have previously reported that the retinoids, 4-(hydroxyphenyl)retinamide (4-HPR) and 9-cis-retinoic acid (RA) prevented azoxymethane (AOM)-induced colon tumors and along with 2-(carboxyphenyl)retinamide (2-CPR) prevented aberrant crypt foci (ACF). In this study, we evaluated the effect of 2-CPR on AOM-induced colon tumors and the effect of the three retinoids on apoptosis and cell proliferation. Male F344 rats were administrated 15 mg/kg AOM at weeks 7 and 8 of age. 2-CPR (315 mg/kg) was administered in the diet starting either 1 week before or at week 12 after the first dose of AOM. The rats continued to receive the 2-CPR until killed at week 46. Unlike the demonstrated prevention of colon cancer by the other two retinoids, both dosing schedules of 2-CPR resulted in an approximate doubling of the yield of colon tumors. In adenomas, 2-CPR, 4-HPR and 9-cis-RA were equally effective in reducing mitotic activity, while only 4-HPR and 9-cis-RA but not 2-CPR enhanced apoptosis. When administered for only the 6 days prior to killing 4-HPR but not 2-CPR decreased the Mitotic Index and increased the Apoptotic Index in adenomas. In non-involved crypts, chronic exposure to 4-HPR and 9-cis-RA in contrast to 2-CPR reduced the Mitotic Index and enhanced the Apoptotic Index. In concurrence with our previous study, both 2-CPR and 4-HPR were very potent in preventing ACF when administered in the diet starting 1 week before the first dose of AOM and continuing for the 5 weeks of the study. Hence, unlike the other two retinoids, 2-CPR, although very potent in preventing ACF, enhanced rather than prevented AOM-induced colon cancer. Furthermore, our results suggest that the effect of 2-CPR on tumor yield is different from 4-HPR and 9-cis-RA because, unlike them, it does not enhance apoptosis.  (+info)

Prevention by aspirin and its combination with alpha-difluoromethylornithine of azoxymethane-induced tumors, aberrant crypt foci and prostaglandin E2 levels in rat colon. (4/492)

The dose-response relationship in male F344 rats was determined for the ability of aspirin administered in the diet to prevent azoxymethane (AOM)-induced colon cancer and aberrant crypt foci (ACF) and to reduce prostaglandin E2 (PGE2) levels. Starting at either 7 or 22 weeks of age, the rats received aspirin. All rats received two doses of AOM (15 mg/kg each on days 7 and 14) and were killed on day 36. The lowest concentrations of aspirin to prevent ACF or reduce PGE2 levels were 600 and 400 mg/kg, respectively. To evaluate the prevention of tumors, rats received either 0 or 400 mg/kg aspirin for a total of 39 weeks with AOM (30 mg/kg) administered 7 days after the start of treatment. Aspirin had no effect on the yield of colon tumors. In a second experiment, rats started to receive 0, 200, 600 or 1800 mg/kg aspirin or 1000 mg/kg alpha-difluoromethylornithine (DFMO) +/- aspirin. Eight and 15 days later, all the rats received 15 mg/kg AOM. Eleven weeks later, animals that were receiving the control diet started to receive 0, 200, 600 or 1800 mg/kg aspirin; 1000 or 3000 mg/kg DFMO; or 1000 mg/kg DFMO + 200 or 600 mg/kg aspirin. The animals were killed 32 weeks later. DFMO effectively reduced the yield of colon tumors when administered starting either before or after AOM while aspirin was much weaker. The combination of aspirin + DFMO administered after AOM was synergistic. Both aspirin and DFMO decreased the Mitotic Index, while apoptosis was increased only by DFMO. Our results demonstrated that aspirin and DFMO could prevent colon cancer when administered after AOM. Furthermore, aspirin reduced ACF, PGE2 levels and mitosis at concentrations that did not prevent cancer. In contrast, the ability to enhance apoptosis did correlate with the prevention of cancer.  (+info)

Chemoprevention of colonic aberrant crypt foci by an inducible nitric oxide synthase-selective inhibitor. (5/492)

Inducible nitric oxide synthase (iNOS) is overexpressed in colonic tumors of humans and also in rats treated with a colon carcinogen. iNOS appear to regulate cyclooxygenase-2 (COX-2) expression and production of proinflammatory prostaglandins, which are known to play a key role in colon tumor development. Experiments were designed to study the inhibitory effects of S,S'-1,4-phenylene-bis(1,2-ethanediyl)bis-isothiourea (PBIT) a selective iNOS-specific inhibitor, measured against formation of azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF). Beginning at 5 weeks of age, male F344 rats were fed experimental diets containing 0 or 50 p.p.m. of PBIT, or 2000 p.p.m. of curcumin (non-specific iNOS inhibitor). One week later, rats were injected s.c. with AOM (15 mg/kg body wt, once weekly for 2 weeks). At 17 weeks of age, all rats were killed, colons were evaluated for ACF formation and colonic mucosa was assayed for isoforms of COX and NOS activities. Both COX and iNOS activities in colonic mucosa of the AOM-treated rats were significantly induced. Importantly, 50 p.p.m. PBIT suppressed AOM-induced colonic ACF formation to 58% (P < 0.0001) and crypt multiplicity containing four or more crypts per focus to 78% (P < 0.0001); it also suppressed AOM-induced iNOS activity. Curcumin inhibited colonic ACF formation by 45% (P < 0.001). These observations suggest that iNOS may play a key regulatory role in colon carcinogenesis. Developing iNOS-specific inhibitors may provide a selective and safe chemopreventive strategy for colon cancer treatment.  (+info)

Preliminary analysis of azoxymethane-induced colon tumorigenesis in mouse aggregation chimeras. (6/492)

Inbred mice exhibit differential susceptibility to colon carcinogens. The following study addresses the possibility that differences are intrinsic to colonic mucosa (cell autonomous) or are mediated by extracolonic systemic factors (e.g. liver activation of carcinogens). Our approach was to construct mouse aggregation chimeras, mice whose tissues are a mosaic of cells derived from two parental genotypes, from a susceptible (SWR) and a resistant (DBA/2) strain. Forty-five embryo aggregations yielded 11 viable pups, four of which were chimeric by coat color. Six-week-old SWR<-->BA/2 chimeras were injected i.p. with azoxymethane (AOM) once a week for 8 weeks (5 and 7.5 mg/kg body wt for 2 weeks followed by 10 mg/kg for 6 weeks) and tumor incidence in distal colon was evaluated 15 weeks after the last injection. Additional groups of parental mice received the same treatment. In the parental SWR treatment group, 1.7 +/- 0.82 tumors/colon were found. No tumors were observed in AOM-treated DBA/2 mice. In SWR<-->DBA/2 chimeras exposed to AOM, 2.8 +/- 2.1 tumors/colon were found. Tumor lineage was examined in paraffin sections stained with Dolichos biflorus agglutinin-peroxidase, a cell surface specific marker that stains intestinal endothelial cells of SWR and epithelial cells of DBA/2. Cellular lineage of tumors was further evaluated by microsatellite analysis of DNA isolated by microdissection. There was no significant difference in tumor incidence between SWR parental and chimera treatment groups. Histochemical analysis of tumor tissue in chimeras suggested that most tumors were derived from SWR. However, subsequent genetic analysis of tumors indicated mixed parental composition. These preliminary studies suggest that DBA/2 resistance mechanisms are not sufficient to protect adjacent SWR-derived epithelium from the tumorigenic effects of AOM.  (+info)

Carcinogen and dietary lipid regulate ras expression and localization in rat colon without affecting farnesylation kinetics. (7/492)

Epidemiological and experimental data suggest that dietary fiber and fat are major determinants of colorectal cancer. However, the mechanisms by which these dietary constituents alter the incidence of colon cancer have not been elucidated. Evidence indicates that dominant gain-of-function mutations short-circuit protooncogenes and contribute to the pathogenesis of cancer. Therefore, we began to dissect the mechanisms whereby dietary fat and fiber, fed during the initiation, promotion and progression stages of colon tumorigenesis, regulate ras p21 localization, expression and mutation frequency. Male Sprague-Dawley rats (140) were provided with corn oil or fish oil and pectin or cellulose plus or minus the carcinogen azoxymethane (AOM) in a 2 x 2 x 2 factorial design and killed after 34 weeks. We have previously shown adenocarcinoma incidence in these animals to be 70.3% (52/74) for corn oil + AOM and 56.1% (37/66) for fish oil + AOM (P < 0.05). Total ras expression as well as ras membrane:cytosol ratio was 4- to 6-fold higher in colon tumors than in mucosa from AOM- or saline-injected rats. Expression of ras in the mucosal membrane fraction was 13% higher for animals fed corn oil compared with fish oil feeding (P < 0.05), which is noteworthy since ras must be localized at the plasma membrane to function. The elevated ras membrane:cytosol ratio in tumors was not due to increased farnesyl protein transferase activity or prenylation state, as nearly all detectable ras was in the prenylated form. Phosphorylated p42 and p44 mitogen activated protein kinase (ERK) expression was two-fold higher in tumor extracts compared with uninvolved mucosa from AOM- and saline-injected rats (P < 0.05). The frequency of K-ras mutations was not significantly different between the various groups, but there was a trend toward a greater incidence of mutations in tumors from corn oil fed rats (85%) compared with fish oil fed rats (58%). Our results indicate that the carcinogen-induced changes in ras expression and membrane localization are associated with the in vivo activation of the ERK pathway. In addition, suppression of tumor development by dietary n-3 polyunsaturated fatty acids may be partly due to a combined effect on colonic ras expression, membrane localization, and mutation frequency.  (+info)

Polyethylene-glycol, a potent suppressor of azoxymethane-induced colonic aberrant crypt foci in rats. (8/492)

Bulking fibers and high water intake may decrease colon carcinogenesis in rats, and the risk of colorectal cancer in humans. We speculated that a non-fermented polymer, polyethylene-glycol (PEG) 8000, which increases stool moisture, might protect rats against colon carcinogenesis. Thirty female F344 rats were given a single injection of azoxymethane (20 mg/kg), and 7 days later randomized to AIN76 diets containing PEG (to provide 3 g/kg body wt/day), or no PEG (control). Diets were given ad libitum for 105 days, then colon carcinogenesis was assessed by the aberrant crypt foci (ACF) test. ACF were scored blindly by a single observer. Dietary feeding of PEG almost suppressed ACF larger than one crypt, and strikingly decreased the total number of ACF per rat. PEG-fed rats had 100 times less large ACF than controls (0.8 and 83 respectively, P = 0.00001). PEG-fed rats had 20 times less total ACF than control (six and 107 ACF/rat, respectively; P < 0.0001). Two treated rats had no detectable ACF. PEG is 10 times more potent than other chemopreventive agents in this model. Since PEG is generally recognized as safe, its cancer-preventive features could be tested in humans.  (+info)

The effect of 30% caloric restriction on azoxymethane (AOM)-induced colon carcinogenesis was investigated in male F344 rats. Starting at 5 weeks of age, groups of animals were fed ad libitum a high-fat (23.5%) semipurified diet. At 7 weeks of age, all animals except the vehicle-treated groups were s.c. injected with AOM (15 mg/kg body wt, once weekly for 2 weeks). Four days after the second AOM injection, groups of animals were continued on high-fat diet and fed ad libitum (ad libitum group) whereas other groups were restricted to 70% of total calories (calorie-restricted group) consumed by the ad libitum group, but received same amounts of fiber, vitamins, and minerals. Thirty-two weeks after AOM injections, all animals were necropsied. The animals in the calorie-restricted group developed significantly fewer colon tumors and had a lower colon tumor incidence than did the rats in the ad libitum group. The size of colon tumors was also reduced in the calorie-restricted group.. ...
TY - JOUR. T1 - Effect of diets fortified with tomatoes or onions with variable quercetin-glycoside content on azoxymethane-induced aberrant crypt foci in the colon of rats. AU - Femia, A.P.. AU - Caderni, G.. AU - Ianni, M.. AU - Salvadori, M.. AU - Schijlen, E.G.W.M.. AU - Collins, G.. AU - Bovy, A.G.. AU - Dolara, P.. PY - 2003. Y1 - 2003. N2 - Background: Onion and tomato are vegetables widely consumed by humans and epidemiological studies show an inverse association between vegetable consumption and colon cancer risk; however, the effect on colon cancer of diets containing high levels of vegetables like onion and tomato are not clear. Aims of the study: To investigate whether tomatoes and onions,with low or high quercetin-glycoside content, could reduce azoxymethane (AOM)-induced Aberrant Crypt Foci (ACF), preneoplastic lesions in the colon of rats. Methods: Male Fisher 344 rats were fed the following diets: a) high fat (HF) diet (control diet); b) HF diet containing 20 % (w/w) tomatoes ...
Background and aims: The molecular mechanisms underlying the promotion of colorectal carcinogenesis by a high-fat diet (HFD) remain unclear. We investigated the role of the insulin-signal pathway and the c-Jun N-terminal kinase (JNK) pathway, which reportedly play crucial roles in insulin resistance, during colorectal carcinogenesis in the presence of hyperinsulinemia induced by a HFD.. Methods: Azoxymethane-induced aberrant crypt foci formation and cell proliferation in the colonic epithelium were compared between mice fed a normal diet (ND) and mice fed a HFD. A western blot analysis was performed to elucidate the mechanism affecting colorectal carcinogenesis by a HFD.. Results: The number of aberrant crypt foci and the colonic epithelial cell proliferative activity were significantly higher in the HFD group than in the ND group. While the plasma insulin level was significantly higher in the HFD group than in the ND group, a western blot analysis revealed the inactivation of Akt, which is ...
β-Catenin is a key regulator of the cadherin-mediated cell-cell adhesion system and an important element in the Wnt signal transduction pathway. Stabilization and accumulation of cytoplasmic β-catenin, which result from mutations in either the adenomatous polyposis coli or β-catenin genes, are causatively associated with colon carcinogenesis. In the present study, we examined the expression of β-catenin in rat colon tumors induced by azoxymethane in comparison with adjacent normal colon mucosa by immunostaining and immunoblotting. Cytoplasmic and nuclear immunostaining was pronounced in all colon adenoma and carcinoma tissues, whereas antibody binding was limited to membranes at the intercellular borders in normal colon epithelial cells. Increase of the free β-catenin fraction in tumor cells was also indicated by immunoblot analysis of fractionated tissue lysates. Investigation of mutations in the glycogen synthase kinase-3β phosphorylation consensus motif of the β-catenin gene by ...
Severe combined immunodeficiency (Scid) mice have defects in V(D)J recombination and DNA double-strand breaks repair caused by an inherited genetic defect in the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs). Scid mice are highly susceptible to development of T-cell lymphomas, and because of the nature of its association with DNA repair and recombination, DNA-PKcs is considered to belong to the caretaker class of tumor suppressor genes. In the present study, the susceptibility of Scid mice to colon carcinogenesis due to administration of azoxymethane (AOM) was investigated. Significantly higher susceptibility in terms of induction of both aberrant crypt foci (ACFs), putative pre-cancerous lesions of the colon and colon cancers was observed as compared with the isogenic strain, C.B-17 mice. The incidences of colon tumors, either adenomas or adenocarcinomas, in Scid and C.B-17 mice after administration of AOM (10 mg/kg body weight/week) for 6 weeks were 87% (26 of 30) and 50% (15 of ...
Cell cycle variations and DNA aneuploidy, were investigated in different phases of azoxymethane (AOM)-induced colon carcinogenesis in rats by flow cytometry. K-ras gene mutations (transitions Gright curved arrow A) were frequently detected in aberrant crypt foci (ACF) initial pre-neoplastic lesions. The fraction of cells in the G2M-phase of the cell cycle was higher in ACF compared to the normal mucosa of control rats. A similar modification of the cell cycle was found in adenomas and adenocarcinomas but, unexpectedly, also in morphologically normal mucosa from AOM-treated animals indicating that AOM treatment permanently modifies cell cycle control in rat colon mucosa. These alterations, however, were not associated with DNA aneuploidy as reported in human sporadic colorectal cancer, suggesting that tumour development in AOM-treated rats is less dependent on aneuploidy.. ...
Purpose: Colon cancer is a major cause of cancer deaths. Dietary factors contribute substantially to the risk of this malignancy. Western-style diets promote development of azoxymethane-induced colon cancer. Although we showed that epidermal growth factor receptors (EGFR) controlled azoxymethane tumorigenesis in standard fat conditions, the role of EGFR in tumor promotion by high dietary fat has not been examined.. Experimental Design: A/J × C57BL6/J mice with wild-type Egfr (Egfrwt) or loss-of-function waved-2 Egfr (Egfrwa2) received azoxymethane followed by standard (5% fat) or western-style (20% fat) diet. As F1 mice were resistant to azoxymethane, we treated mice with azoxymethane followed by one cycle of inflammation-inducing dextran sulfate sodium to induce tumorigenesis. Mice were sacrificed 12 weeks after dextran sulfate sodium. Tumors were graded for histology and assessed for EGFR ligands and proto-oncogenes by immunostaining, Western blotting, and real-time PCR.. Results: Egfrwt mice ...
Inducible nitric oxide synthase (iNOS) is potential target for inflammation and cancer. Previously, we have shown that S,S′‐1,4‐Phenylenebis(1,2‐ethanediyl)bisisothiourea (PBIT) inhibit colon carcinogenesis induced by azoxymethane (AOM). Although, colon cancer inhibitory efficacy of PBIT has been significant, selective iNOS inhibitors do not completely abrogate NO production due to the exogenous bioavailability and NO generation by eNOS in tumor tissues. To create an iNOS selective and multi‐targeted molecule, we have developed a novel isosteric analogue of PBIT, namely PBISe in which sulfur was replaced with selenium. We examined the chemopreventive efficacy of PBISe on AOM‐induced rat colon carcinogenesis model using aberrant crypt foci (ACF) as end point. At seven weeks of age, rats (12/group) were fed the control diet (AIN 76A) and colonic ACF were induced by AOM. Three days after second AOM treatment, rats were fed the diets containing 0, 10 and 20 ppm of PBI‐Se and continued ...
Azoxymethane (AOM) is a colon carcinogen that is used to study the pathogenesis of sporadic colorectal cancer. We have evaluated differential susceptibility to AOM in inbred mice used as progenitors of recombinant/transgenic lines. In experiment 1, male FVB/N, 129/SvJ, C57Bl/6J mice were treated i.p. with 10 mg/kg AOM once per week for 4 weeks and sacrificed after 20 weeks. Only AOM-treated FVB/N mice developed tumors (3.6 tumors/mouse) in distal colon. In experiment 2, A/J, AKR/J, Balb/CJ mice were treated with AOM for 6 weeks and sacrificed after 24 weeks. AOM-treated A/J and Balb/CJ mice developed 9.2 and 1 tumor/mouse, respectively. Despite these differences, tumors had similar morphology regardless of strain. Immunohistochemistry with β-catenin resulted in marked nuclear and cytoplasmic staining of tumor cells in FVB/N. However, fainter and heterogeneous β-catenin staining was observed in A/J tumors, suggesting distinct pathways of tumorigenesis in different strains. Irrespective of ...
Results A single bout of exercise increased the expression and secretion of SPARC in skeletal muscle in both mice and humans. In addition, in an azoxymethane-induced colon cancer mouse model, regular low-intensity exercise significantly reduced the formation of aberrant crypt foci in wild-type mice but not in SPARC-null mice. Furthermore, regular exercise enhanced apoptosis in colon mucosal cells and increased the cleaved forms of caspase-3 and caspase-8 in wild-type mice but not in SPARC-null mice. Culture experiments showed that SPARC secretion from myocytes was induced by cyclic stretch and inhibited proliferation with apoptotic effect of colon cancer cells.. ...
The preventive effect of polysaccharide of Larimichthys crocea swimming bladder (PLCSB) and the increase of this effect by use of resistant starch (RS3) as the carrier for PLCSB on azoxymethane (AOM) and dextran sulfate sodium (DSS)-inducing colon carcinogenesis in C57BL/6 mice has been studied. RS3 microspheres carrying PLCSB (RS3 + PLCSB) were produced and evaluated as a potentially improved colon carcinogenesis therapy for this study. The body weight, colon length, and colon weight of mice were determined, and colonic tissues were histologically observed. The serum levels of proinflammatory cytokines and the inflammation and apoptosis-related genes in colonic tissue were also tested. The PLCSB or RS3 + PLCSB significantly suppressed AOM and DSS-induced body weight loss, colon length shortening and decreased the colon weight to length ratio. PLCSB or RS3 + PLCSB reduced the levels of the serum pro-inflammatory cytokines IL-6, IL-12, TNF-α, and IFN-γ to a greater extent compared with the control
The main objective of this proposal was to investigate the effect of vitamin B6 on colon carcinogenesis in vivo. Two in vivo studies were conducted to determine the role of vitamin B6 as a biological modifier of colon carcinogenesis. It is hypothesized that vitamin B6 may serve as an antioxidant in vivo and will modulate colon carcinogenesis. In the first study, a 2X3 factorial experimental design was used to determine if three different levels of vitamin B6, classified as low, normal and high in conjunction with two different levels of protein intake, classified as normal or high, will affect post-initiation stages of colon carcinogenesis, in Sprague-Dawley rats. Male Sprague-Dawley male were injected with azoxymethane for two weeks (15mg/kg/week) and then one week later they were allocated to different dietary treatment groups. After eight weeks, the effects of dietary treatment on hematological status, oxidative stress markers and antioxidant enzymes, as well as enumeration of preneoplastic ...
Previous work suggests that vagus nerve disruption reduces hepatocyte and oval cell expansion following liver injury. The role of post-neuronal receptor activation in response to liver injury has not been ascertained. We investigated the actions of scopolamine, a non-selective muscarinic receptor antagonist, and specific genetic ablation of a key cholinergic receptor, muscarinic subtype-3 (Chrm3), on azoxymethane (AOM)-induced liver injury in mice. Animal weights and survival were measured as was liver injury using both gross and microscopic examination. To assess hepatocyte proliferation and apoptosis, ductular hyperplasia and oval cell expansion, we used morphometric analysis of BrdU-, activated caspase-3-, H&E-, CK-19- and EpCAM-stained liver sections. Sirius red staining was used as a measure of collagen deposition and its association with oval cell reaction. In AOM-treated mice, both muscarinic receptor blockade with scopolamine and Chrm3 ablation attenuated hepatocyte proliferation and ...
As the Dietitians Association of Australia (DAA) kicks off Australias Healthy Weight Week today, new research shows that cooking at home more often means Australians will up their fruit and vegetable intake, helping win the war on weight.. The research, involving more than 1,300 people, found those who spent the most time preparing and cooking meals ate more fruit and vegetables and spent less money on food away from home, compared with those who spent the least amount of time in the kitchen.. Given more than nine in 10 Australians dont eat the recommended five serves of vegetables a day, and 63 per cent of adults are overweight or obese, and that number is rising, this is important research, Dietitians Association of Australia (DAA) spokesperson and Co-Director of the Priority Research Centre in Physical Activity and Nutrition at the University of Newcastle, Professor Clare Collins said.. Professor Collins said the quality of a persons diet was a good way of predicting weight; and ...
Healthy Weight Week signifies the importance of balance diet and healthy lifestyle. Being healthy does not mean losing weight and going on a diet. It means pursuing livable and sustainable healthy lifestyle through eating well, living actively and feeling good. Bentham Science publishes important research publications that promote this idea. Click here to find related…
Chronic inflammation characterizing patients with inflammatory bowel disease (IBD) represents a major risk factor for the development of colorectal cancer. Mechanisms underlying this neoplastic transformation are not fully understood though studies in experimental models of colon carcinogenesis suggest that inflammatory cell-derived cytokines either directly or indirectly stimulate the uncontrolled growth of cancer cells. Nevertheless, under specific inflammatory conditions, immune cells can boost an anti-tumor immune response with the down-stream effect of eliminating dysplastic and cancerous cells. This review outlines the beneficial and detrimental role of inflammation in colon carcinogenesis.
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Mustard seeds (MS), which are consumed in considerable amounts by the Japanese people that, interestingly, have the longest life expectancy in the world, are known to contain a number of yet not fully defined but quite powerful anti-oxidants. A suspension of extracted MS was found to suppress oxidized-LDL-induced macrophage respiratory burst in vitro, to prevent growth, and to induce apoptotic death of SW480 cells (a human colon cancer cell line), while no such effects were found for normal 3T3 cells. A diet enriched with MS decreased plasma levels of the lipid peroxidation product malonaldehyde in mice exposed to the colon cancer-inducer azoxymethane (AOM). Such a diet also dose-dependently enhanced the activity of several anti-oxidant enzymes, such as superoxide dismutase (SOD), catalase, and GSH-peroxidase and, moreover, reduced AOM-mediated formation of colon adenomas by about 50%. Further studies are required to detail and explore the beneficial effects of MS and their rich content of ...
Dietary artepillin C suppresses the formation of aberrant crypt foci induced by azoxymethane in mouse colon.. Shimizu K, Das SK, Baba M, Matsuura Y, Kanazawa K.. Source. Department of Life Science, Graduate School of Science and Technology, Kobe University, Rokkodai, Nada-ku, Kobe 657-8501, Japan.. Abstract. Artepillin C, a prenylated phenylpropanoid found specifically in Brazilian propolis, has been shown to be a bioavailable antioxidant. In this study, artepillin C was tested for colon cancer-preventing activity using azoxymethane-challenged ddY mice. Oral doses of 80 and 160 mg/kg body weight of propolis or 10mg/kg of artepillin C (equi-amounts to 160 mg propolis) reduced significantly the frequency of colonic aberrant crypt foci (ACF) by 39.2, 43.7 and 43.4%, respectively. In liver of the mice, glutathione S-transferase and NADPH:quinone reductase activity increased with the doses of propolis or artepillin C, and an antioxidant-responsive element (ARE) was found to be activated for binding ...
The influence of bovine lactoferrin (bLf) on colon carcinogenesis was investigated in male F344 rats treated with azoxymethane (AOM). In experiment I, 2% and 0.2% bLf, and Bifidobacterium longum (B. longum) as a positive control at 3% were given in the diet for 4 weeks, along with two s.c. 15 mg/kg …
Preventive intervention of colorectal cancer has become essential as a major portion of the population may develop the disease at some points during their lives. Diet and nutrition play an important role during this multistep colon carcinogenic process. Inhibitory activity of aqueous suspensions of garlic and tomato, individually and in combination, were tested on azoxymethane induced colon carcinogenesis in Sprague-Dawley rats. The effect was observed on aberrant crypt foci (ACF), the preneoplastic lesion. To investigate the mechanism of action of the agents used, cell proliferation and the level of apoptosis were determined and the expression of cyclooxygenase-2 (COX-2) protein was analyzed in the colon. Following treatment, significant inhibition of the level of cell proliferation (P|0.01 in garlic; P|0.001 in tomato and P|0.001 in combination treatment group with respect to the carcinogen control group), significant induction of apoptosis (P|0.01 in garlic treated; P|0.01 in tomato treated and P|0
The dose-response relationship in male F344 rats was determined for the ability of aspirin administered in the diet to prevent azoxymethane (AOM)-induced colon cancer and aberrant crypt foci (ACF) and to reduce prostaglandin E2 (PGE2) levels. Starting at either 7 or 22 weeks of age, the rats received aspirin. All rats received two doses of AOM (15 mg/kg each on days 7 and 14) and were killed on day 36. The lowest concentrations of aspirin to prevent ACF or reduce PGE2 levels were 600 and 400 mg/kg, respectively. To evaluate the prevention of tumors, rats received either 0 or 400 mg/kg aspirin for a total of 39 weeks with AOM (30 mg/kg) administered 7 days after the start of treatment. Aspirin had no effect on the yield of colon tumors. In a second experiment, rats started to receive 0, 200, 600 or 1800 mg/kg aspirin or 1000 mg/kg α-difluoromethylornithine (DFMO) +/- aspirin. Eight and 15 days later, all the rats received 15 mg/kg AOM. Eleven weeks later, animals that were receiving the control ...
It is generally assumed that inflammatory bowel disease (IBD)-related carcinogenesis occurs as a result of chronic inflammation. We previously developed a novel colitis-related mouse colon carcinogenesis model initiated with azoxymethane (AOM) and followed by dextran sodium sulfate (DSS). In the present study we investigated whether a cyclooxygenase (COX)-2 inhibitor nimesulide and ligands for peroxisome proliferator-activated receptors (PPARs), troglitazone (a PPARγ ligand) and bezafibrate (a PPARα ligand) inhibit colitis-related colon carcinogenesis using our model to evaluate the efficacy of these drugs in prevention of IBD-related colon carcinogenesis. Female CD-1 (ICR) mice were given a single intraperitoneal administration of AOM (10 mg/kg body weight) and followed by one-week oral exposure of 2% (w/v) DSS in drinking water, and then maintained on the basal diets mixed with or without nimesulide (0.04%, w/w), troglitazone (0.05%, w/w), and bezafibrate (0.05%, w/w) for 14 weeks. The inhibitory
Aspirin, naproxen, and other nonsteroidal anti-inflammatory drugs (NSAIDs) are promising chemopreventive agents for individuals at high risk for colorectal cancer (CRC). However, uptake of chronic and continuous NSAID administration to reduce CRC risk is limited by unwanted side effects. Employing novel dosing regimens and an azoxymethane-induced rat colon cancer model, Mohammed and colleagues found that intermittent use of either aspirin or naproxen was highly effective in preventing the progression of colonic adenoma to adenocarcinoma without serious side effects (see the study beginning on page 751). These findings could ultimately impact the standard of preventive care for patients at the adenoma stage (i.e., in high-risk cohorts) to protect against advancement to invasive adenocarcinoma with intermittent NSAID use. The micrograph on the cover depicts hematoxylin and eosin staining of rat colon crypt, hyperplasia, adenoma, and adenocarcinomas that recapitulate the histological progression of ...
It is pertinent however to determine wholesome cooking strategies in addition to consuming habits in methods to not intervene with the nutritious worth of meals Mother Nature intended. Have you ever ever gone through a grueling weight reduction program for a very long time, solely to seek out out later that youve hit a wall when it comes to outcomes. You wont end up tempted almost as much if your forbidden foods arent simply accessible. Correctly, chances are youll need to do additional than merely discovering a meals plan reply program. He did it greater than 50 years earlier. One factor to remember when deciding how one can go about shedding pounds is that there is no such thing as a single greatest way to lose weight. This can be a weight loss program thats loaded with numerous greens and fruits, chemopreventive effects of dietary canola oil on colon cancer development with the lean meats and likewise other protein sources. Due to this actuality, it is best to avoid excessive consumption ...
The goal of this study was to characterize p53 tumor suppressor pathway in colon-specific carcinogen azoxymethane (AOM)-induced mouse colon tumor and to assess the usefulness of this animal model to evaluate novel anti-cancer drugs. The acute exposure of mice to AOM showed no overall induction of p53-regulated genes. Subdued p53 gene activation in the colon corresponded to a drop in the expression of its transcriptional co-activator, p300. The status of p53 pathway was further analyzed using AOM-induced mouse colon tumor and the cell line (AJ02-NM0) generated from the primary tumor. Wild type p53 protein, constitutively expressed in this model, showed no detectable DNA binding activity nor did it activate p21 expression. The cell line studies revealed that p53 activity was inhibited by a constitutive interaction with Mdm2. The p53-activating p19/ARF protein did not appear to have significant effect on the standing of p53 pathway in this cell line. p53 was activated by Doxorubicin, 5-FU and the recently
But early in colon cancer development, these growth-controlling hormones are lost and not expressed, disrupting GCCs activity, and, Dr. Waldman believes, contributing to tumor formation. Using two separate mouse models that mimic the development of colon cancer in people, his team showed that GCC signaling blocks such tumors from forming. According to Dr. Waldman, the group found that GCC stops tumors from forming through two different mechanisms. In one case, it controls cell growth, while in the other, it maintains regulation of genomic integrity.. In one mouse cancer model, the animals carried mutations in the APC gene, which causes colon polyps that frequently lead to colon cancer. Mice in the other cancer-development model were exposed to a commonly used experimental cancer-causing agent, azoxymethane. We modeled both ways that humans develop colon cancer, and studied the effects of a lack of GCC on the incidence of colon cancer development, he explains.. We found that in animals ...
Background: The group IIA secretory phospholipase A2 gene, Pla2g2a, confers resistance to intestinal tumorigenesis in the ApcMin/+ mouse model. However, it is unclear how Pla2g2a exerts its tumor-suppressive effects and whether its mode of action dep
Myeloid Translocation Gene, Related-1 (MTGR1) CBFA2T2 is a member of the Myeloid Translocation Gene (MTG) family of transcriptional corepressors. The remaining two family members, MTG8 (RUNX1T1) and MTG16 (CBFA2T3) are identified as targets of chromosomal translocations in acute myeloid leukemia (AML). Mtgr1(-/-) mice have defects in intestinal lineage allocation and wound healing. Moreover, these mice show signs of impaired intestinal stem cell function. Based on these phenotypes, we hypothesized that MTGR1 may influence tumorigenesis arising in an inflammatory background. We report that Mtgr1(-/-) mice were protected from tumorigenesis when injected with azoxymethane (AOM) and then subjected to repeated cycles of dextran sodium sulfate (DSS). Tumor cell proliferation was comparable, but Mtgr1(-/-) tumors had significantly higher apoptosis rates. These phenotypes were dependent on epithelial injury, the resultant inflammation, or a combination of both as there was no difference in aberrant ...
Interestingly, in the investigated effect of consumption of standard diets supplemented with freeze-dried vegetables (peas, spinach, sprouts and broccoli) and carotenoids (all-trans beta-carotene and palm oil carotenoid extract) on surrogate end-point markers for colorectal cancer in an azoxymethane-induced rat model, researchers at the Unilever Research Vlaardingen, illustrated ...
Tanaka Takuji , Sugie Shigeyuki Journal of toxicologic pathology 20(4), 215-235, 2007-12-25 J-STAGE 医中誌Web 参考文献192件 ...
Bielas and colleagues first set out to analyze mutation rates in mitochondrial DNA because they wanted to see if it could act as a surrogate for nuclear DNA as a cancer biomarker. Cells contain a thousandfold more mitochondrial genetic material than nuclear DNA, so theoretically youd need a thousand times less tissue to get the same genetic information to predict clinical outcomes such as how fast a tumor would progress or whether it would be resistant to therapy, Bielas said.. While mitochondrial DNA proved to be an unreliable stand-in for nuclear DNA as a cancer biomarker, it offers promise as a new drug target.. If we could increase DNA damage and mutation within the mitochondrial genome, theoretically we could decrease cancer, Bielas said. Thats what were testing now. This is a whole new hypothesis.. The way mitochondria maintain genetic stability in the face of cancer, Bielas suggests, may be because unlike normal cells, cancer cells do not need oxygen to survive. In fact, cancer ...
Sedlis, A and Stone, D F., Experimental carcinogenesis in pregnant mice, a preliminary report. (1965). Subject Strain Bibliography 1965. 820 ...
Stanford University School of Medicine found that 63 percent of participants in a study who had a positive body image were more successful at losing and maintaining weight for a year compared to a 26 percent success rate for those who were dissatisfied with their appearance (Source: Shape). How can you work toward develop a positive body image? By realizing that fitness is not a number; it is a way of life. Avoid choosing a perfect weight for yourself. Instead, think of your ideal weight as a zone, or a range of weight in which you feel comfortable and beautiful. If you focus on healthy lifestyle instead of a number or a measurement, you can feel truly satisfied ...
The characteristic features of cancer cells are aberrant (acidic) intracellular pH and elevated levels of phosphatidylserine. The primary focus of cancer research is concentrated on the discovery of biomarkers directed towards early diagnosis and therapy. It has been observed that azoxymethane-treated mice demonstrate an increased expression of calnuc (a multi-domain, Ca2+- and DNA-binding protein) in their colon, suggesting it to be a good biomarker of carcinogenesis. We show that culture supernatants from tumor cells have significantly higher amounts of secreted calnuc compared to non-tumor cells, selectively packaged into exosomes. Exosomal calnuc is causal for epithelial-mesenchymal transition and atypical migration in non-tumor cells, which are key events in tumorigenesis and metastasis. In vitro studies reveal a significant affinity for calnuc towards phosphatidylserine, specifically to its C-terminal region, leading to the formation of molten globule conformation. Similar structural ...
Dr. Mathew Meeneghan joins Debbie Bosque at KULM-FM 98.3 to discuss colon cancer on The Doctors Point of View radio show. Dr. Meeneghan talks about colon cancer development, treatment and screening procedures like colonoscopies.
Physicians have long suspected a link between carbohydrate intake and colon cancer development, and a recent study may have illuminated the sought-after link.
If you havent been eating healthy since the week began you must try to catch up. Why? Because its Healthy Weight Week (HWW), is why. The annual HWW is A Kenyan lifestyle platform for digital storytelling.
In their pioneering work on essential fatty acids, Burr, Burr and Miller compared the nutritional properties of α-eleostearic acid (ELA) to that of its isomer alpha-linolenic acid (ALA). ALA relieved essential fatty acid deficiency; ELA did not.[1] In rats, α-eleostearic acid is converted to a conjugated linoleic acid.[2] The compound has been found to induce programmed cell death of fat cells,[3] and of HL60 leukemia cells in vitro at a concentration of 20 μM.[4] Diets containing 0.01% bitter gourd seed oil (0.006% as α-eleostearic acid) were found to prevent azoxymethane-induced colon carcinogenesis in rats.[5] ...
The incidence and mortality rates of colorectal cancer (CRC) continue to increase worldwide. Therefore, new preventive strategies are needed to lower the burden of this disease. Previous studies reported that aspirin could suppress the development of sporadic colorectal adenoma. In addition, metformin is a biguanide derivative that is long widely used for the treatment of diabetes mellitus and has recently been suggested to have a suppressive effect on carcinogenesis and cancer cell growth. Both drugs exhibit a chemopreventive effect, but their efficacy is limited. Aberrant crypt foci (ACF), defined as lesions containing crypts that are larger in diameter and stain more darkly with methylene blue than normal crypts, are more prevalent in patients with cancer and adenomas, and considered a reliable surrogate biomarker of CRC. Thus, we designed a prospective trial as a preliminary study prior to a CRC chemoprevention trial to evaluate the chemopreventive effect of aspirin combined with metformin on
Routine fortification of food with folic acid was implemented in the U.S. in 1996 to reduce the risk of birth defects in newborns. Widespread fortification in c...
US28 is a constitutively active chemokine receptor encoded by CMV (also referred to as human herpesvirus 5), a highly prevalent human virus that infects a broad spectrum of cells, including intestinal epithelial cells (IECs). To study the role of US28 in vivo, we created transgenic mice (VS28 mice) in which US28 expression was targeted to IECs. Expression of US28 was detected in all IECs of the small and large intestine, including in cells expressing leucine rich repeat containing GPCR5 (Lgr5), a marker gene of intestinal epithelial stem cells. US28 expression in IECs inhibited glycogen synthase 3β (GSK-3β) function, promoted accumulation of β-catenin protein, and increased expression of Wnt target genes involved in the control of the cell proliferation. VS28 mice showed a hyperplastic intestinal epithelium and, strikingly, developed adenomas and adenocarcinomas by 40 weeks of age. When exposed to an inflammation-driven tumor model (azoxymethane/dextran sodium sulfate), VS28 mice developed a
Natural killer (NK) cells are an essential component of innate immunity against cancer development. Many studies have been conducted to evaluate immune-modulating effects using dietary compounds. Our laboratory has been investigating the chemopreventive potential of black raspberries (BRBs) and previously demonstrated their beneficial modulation of genetic and epigenetic biomarkers in patients with colorectal cancer (CRC). The current study investigated their potential on modulating NK cells. To avoid the excessive inflammation caused by the dextran sulfate sodium (DSS) treatment that leads to colitis, we treated the mice with overnight DSS so that it would slightly irritate the colon but still promote colon carcinogenesis with 100% incidence in both the Apc(Min/+) mice and azoxymethane (AOM)-treated mice ...
Cardiac fibrosis is a pathophysiologic hallmark of the aging heart. In the uninjured heart, cardiac fibroblasts exist in the quiescent state, but little is known about how proliferation rates and fibroblast transcriptional programs change throughout the lifespan of the organism from the immediate postnatal period to adult life and old age. Using EdU pulse labeling, we demonstrate that more than 50% of cardiac fibroblasts are actively proliferating in the first day of post-natal life. However, within 4 weeks of birth in the juvenile animal, only 10% of cardiac fibroblasts are proliferating. By early adulthood, the fraction of proliferating cardiac fibroblasts further decreases to approximately 2%, where it so remains throughout the rest of the organisms life span. Examination of absolute cardiac fibroblast numbers demonstrated concordance with age related changes in fibroblast proliferation with no significant differences in absolute cardiac fibroblast numbers between animals 14 weeks and 1.5 ...
Everyone needs a wakeup call Kylie. I got mine when I went to my doctor, and my cholesterol was very high. She said loose weight, or go on medication. I hate medication, and so have started seeing a dietician and have currently lost around 10 kilos. I actually lost all my weight years ago, after having Michael, but then put it all back on again after he got his diagnosis! Have discovered I am a stress eater, and it is very hard not to eat when stressed, but I am getting better! Good luck Kylie, it is not an easy battle! xx. ReplyDelete ...
Recent research from the laboratory of Michael Karin, PhD, at the University of California, San Diego School of Medicine - the first researcher to demonstrate a molecular link between inflammation and cancer - has identified ...
Pterostilbene : The official website. Everything to know about Pterostilbene : Health benefits ? Dosage ? Where to order the best quality ? And more...
In observance of Healthy Weight Week January 16-20, we asked our members what they are currently doing in regards to the overwhelming levels of obesity around us. View the links below to see what our members are doing.. ...
Hi mamas I was wondering if anyone knew much about weight gain in pregnancy. Ive lost 2lbs since my booking weight but am consistently staying at the same weight week after week now. Im nearly 16 weeks. Im not too worried but just curious if its ok that Im not gaining…
Pterostilbene has many healthful properties that you discover article after article through your site pterostilbene.com. Some of its healthful properties
It promotes colon cancer development in Azoxymethane-induced and APC gene knockout mice. 3) It promotes hypertension in ...
"A bitter diterpenoid furanolactone columbin from Calumbae Radix inhibits azoxymethane-induced rat colon carcinogenesis". Cancer ...
Azoxymethane (AOM) is a genotoxic colonic carcinogen and is routinely used to induce colon tumours in mice. The AOM-induced ... Treatment of this mouse model with the procarcinogen azoxymethane (AOM) leads to formation of dysplastic microadenomas in the ... "A novel inflammation-related mouse colon carcinogenesis model induced by azoxymethane and dextran sodium sulfate". Cancer Sci. ...
Inhibits Azoxymethane-Induced Colon Carcinogenesis in Male F344 Rats". Nutrition and Cancer. 49 (2): 170-3. doi:10.1207/ ...
... a significant increase in tumor formation was observed in mice overexpressing progastrin and treated with azoxymethane (AOM), a ... expression of mutant and wild-type progastrin significantly increases colon carcinogenesis in response to azoxymethane in ...
Falcarinol on Development of Azoxymethane-Induced Preneoplastic Lesions in the Rat Colon". Journal of Agricultural and Food ...
... on azoxymethane-induced colon preneoplastic lesions in male F344 rats". Cancer Letters. 205 (2): 133-141. doi:10.1016/j.canlet. ...
Diets containing 0.01% bitter gourd seed oil (0.006% as α-eleostearic acid) were found to prevent azoxymethane-induced colon ... "Dietary seed oil rich in conjugated linolenic acid from bitter melon inhibits azoxymethane-induced rat colon carcinogenesis ...
However, stressful treatment of mice with azoxymethane and dextran sulphate caused more than four colonic tumors per MGMT ...
"Dietary seed oil rich in conjugated linolenic acid from bitter melon inhibits azoxymethane-induced rat colon carcinogenesis ...
... a store building web application for Amazon Associates Azoxymethane, a potent carcinogen Academy of Music (disambiguation) ...
... azoxymethane, methylnitrosourea, and hydroxybutylnitrosamine in the brain, spinal cord, intestine, mammary gland, and urinary ...
... azoxymethane - AZQ - AZT B cell - B lymphocyte - B3 antigen - B43-PAP immunotoxin - B7-1 - Bacillus Calmette Guérin - bacterial ...
The molecular formula C2H6N2O (molar mass: 74.08 g/mol) may refer to: Azoxymethane (AOM) Glycinamide N-Nitrosodimethylamine ( ...
... azoxymethane are suspected to be genotoxic. IUPAC, Compendium of Chemical Terminology, 2nd ed. (the "Gold Book") (1997). Online ...
... (AOM) is a carcinogenic and neurotoxic chemical compound used in biological research. It is the oxide of ... Azoxymethane at Sigma-Aldrich CID 33184 from PubChem. ...
"Dietary seed oil rich in conjugated linolenic acid from bitter melon inhibits azoxymethane-induced rat colon carcinogenesis ...
Katsuhisa Sakano, Mami Takahashi, Mitsuaki Kitano, Takashi Sugimura, Keiji Wakabayashi: Suppression of Azoxymethane-induced ...
Azoxymethane (AOM) is a carcinogenic and neurotoxic chemical compound used in biological research. It is the oxide of ... Azoxymethane at Sigma-Aldrich CID 33184 from PubChem. ...
Suppression of azoxymethane-induced colonic premalignant lesion formation by coenzyme Q10 in rats.. Sakano K1, Takahashi M, ... In the present study, effects of CoQ10 on development of azoxymethane (AOM)-induced aberrant crypt foci (ACF) and mucin- ...
Serial endoscopy in azoxymethane treated mice using ultra-high resolution optical coherence tomography.. Hariri LP1, Qiu Z, ... OCT to serially image the lower colon of azoxymethane (AOM) treated A/J mouse models of CRC in order to monitor the progression ...
Azoxymethane (AOM) induces tumorigenesis in the colon of laboratory animals. Used to study chemoprevention in colon cancer ...
Unexpectedly, in azoxymethane-treated rats, leptin significantly inhibited aberrant crypt foci formation in the middle and ... Leptin reduces the development of the initial precancerous lesions induced by azoxymethane in the rat colonic mucosa ... azoxymethane-induced colonic lesions study). The effects of injections or continuous infusion of leptin into the colon were ...
Anti-oxidants, Azoxymethane, Colon cancer, Mustard seeds National Category Medical and Health Sciences Identifiers. URN: urn: ... Mustard seeds (Sinapis Alba Linn) attenuate azoxymethane-induced colon carcinogenesis. Yuan, Haifeng Nanfang Hospital. ... plasma levels of the lipid peroxidation product malonaldehyde in mice exposed to the colon cancer-inducer azoxymethane (AOM). ...
Effects of modulating M3 muscarinic receptor activity on azoxymethane-induced liver injury in mice.. [Sandeep Khurana, ... Previously, we reported that azoxymethane (AOM)-induced liver injury is robustly exacerbated in M3 muscarinic receptor (M3R)- ...
The carcinogen azoxymethane (AOM) was diluted in 0.9% (v/v) saline. The rats received intraperitoneal injections once weekly ( ... B. L. Tan, N. M. Esa, H. S. Rahman, H. Hamzah, and R. Karim, "Brewers rice induces apoptosis in azoxymethane-induced colon ... C. H. F. Chan, D. Cook, and C. P. Stanners, "Increased colon tumor susceptibility in azoxymethane treated CEABAC transgenic ... Brewers Rice: A By-Product from Rice Processing Provides Natural Hepatorenal Protection in Azoxymethane-Induced Oxidative ...
... azoxymethane (AOM), and a 1-week oral exposure (2% in drinking water) to a non-genotoxic car … ... A novel inflammation-related mouse colon carcinogenesis model induced by azoxymethane and dextran sodium sulfate Cancer Sci. ... azoxymethane (AOM), and a 1-week oral exposure (2% in drinking water) to a non-genotoxic carcinogen, dextran sodium sulfate ( ...
Sulindac Sulfone Inhibits Azoxymethane-induced Colon Carcinogenesis in Rats without Reducing Prostaglandin Levels. Gary A. ... Rats received two s.c. injections of azoxymethane (15 mg/kg) for 2 weeks and were fed either experimental or control diets ... Sulindac Sulfone Inhibits Azoxymethane-induced Colon Carcinogenesis in Rats without Reducing Prostaglandin Levels ... Sulindac Sulfone Inhibits Azoxymethane-induced Colon Carcinogenesis in Rats without Reducing Prostaglandin Levels ...
At 4 and 5 weeks of age, rats received subcutaneous injections (100 μL) of either 15 mg/kg of azoxymethane (AOM) prepared in ... The azoxymethane- (AOM-) induced colon cancer model in rodents has been utilized extensively to examine dietary influences on ... Figure 1: Tumor incidence in rats treated with the carcinogen azoxymethane and fed either a casein (AIN control), black bean- ( ... J. Chen and X. F. Huang, "The signal pathways in azoxymethane-induced colon cancer and preventive implications," Cancer Biology ...
Regressive Effects of Various Chemopreventive Agents on Azoxymethane-induced Aberrant Crypt Foci in the Rat Colon * * MORISHITA ... Piroxicam-induced regression of azoxymethane-induced aberrant crypt foci and prevention of colon cancer in rats PEREIRA M. A. ... Suppression of azoxymethane-induced colonic aberrant crypt foci by dietary exposure to a novel synthesized retinoidal ... Aberrant crypts correlate with tumor incidence in F344 rats treated with azoxymethane and phytate PRETLOW T. P. ...
Effect of Restricted Caloric Intake on Azoxymethane-induced Colon Tumor Incidence in Male F344 Rats. Bandaru S. Reddy, Chung- ... The effect of 30% caloric restriction on azoxymethane (AOM)-induced colon carcinogenesis was investigated in male F344 rats. ... Effect of Restricted Caloric Intake on Azoxymethane-induced Colon Tumor Incidence in Male F344 Rats ... Effect of Restricted Caloric Intake on Azoxymethane-induced Colon Tumor Incidence in Male F344 Rats ...
Feeding azoxymethane (AOM)-induced rats with carrots and purified FaOH have previously been shown to inhibit neoplastic ... Feeding azoxymethane (AOM)-induced rats with carrots and purified FaOH have previously been shown to inhibit neoplastic ... isolated from carrots prevents the formation of neoplastic lesions in the colon of azoxymethane-induced rats M. Kobaek-Larsen, ... isolated from carrots prevents the formation of neoplastic lesions in the colon of azoxymethane-induced rats ...
... we reported that azoxymethane (AOM)-induced liver injury is robustly exacerbated in M3 muscarinic receptor (M3R)-deficient mice ... Graphical abstractPreviously, we reported that azoxymethane (AOM)-induced liver injury is robustly exacerbated in M3 muscarinic ... Effects of modulating M3 muscarinic receptor activity on azoxymethane-induced liver injury in mice ...
Scopolamine Treatment and Muscarinic Receptor Subtype 3 Gene Ablation Augment Azoxymethane-Induced Murine Liver Injury. Sandeep ... Scopolamine Treatment and Muscarinic Receptor Subtype 3 Gene Ablation Augment Azoxymethane-Induced Murine Liver Injury. Sandeep ... Scopolamine Treatment and Muscarinic Receptor Subtype 3 Gene Ablation Augment Azoxymethane-Induced Murine Liver Injury. Sandeep ... Scopolamine Treatment and Muscarinic Receptor Subtype 3 Gene Ablation Augment Azoxymethane-Induced Murine Liver Injury ...
... instead of azoxymethane, an equal volume of normal saline. Two weeks after the second injection of azoxymethane or normal ... injections of azoxymethane (15 mg/kg body weight). Two weeks after azoxymethane treatment, rats (48 per group) were fed ... In contrast, azoxymethane led to the formation of colon tumors, with 75% incidence and 1.58 ± 0.23 (mean ± SE for this and all ... Groups of male F344 rats fed control diet beginning in 8 and 9 wks of age, azoxymethane (AOM) was given at dose levels of 15 mg ...
Study of the antineoplastic action of Tabebuia avellanedae in carcinogenesis induced by azoxymethane in mice Estudo da ação ... METHODS: Fifty (n=50) mice were divided into five groups: in group I azoxymethane (AOM) was administered, in Group II - β- ... PURPOSE: To study the antitumor action of Tabebuia avellanedae in experimentally induced colon carcinogenesis by azoxymethane ... Study of the antineoplastic action of Tabebuia avellanedae in carcinogenesis induced by azoxymethane in mice ...
... ... In the present study, we found that consumption of MG significantly deteriorated azoxymethane (AOM)-induced colonic ...
We used azoxymethane (AOM) treated A/J Min/+ mice, which developed a significantly higher tumor load in the colon than in the ... Effect of Dietary Fibers on Cecal Microbiota and Intestinal Tumorigenesis in Azoxymethane Treated A/J Min/+ Mice. ... Effect of Dietary Fibers on Cecal Microbiota and Intestinal Tumorigenesis in Azoxymethane Treated A/J Min/+ Mice ... Effect of Dietary Fibers on Cecal Microbiota and Intestinal Tumorigenesis in Azoxymethane Treated A/J Min/+ Mice ...
Pla2g2a attenuates colon tumorigenesis in azoxymethane-treated C57BL/6 mice; expression studies reveal Pla2g2a target genes and ... Pla2g2a strongly inhibited colon tumorigenesis in mice following treatment with the DNA alkylating agent azoxymethane (AOM). ...
Protein expression profiles that underpin the preventive and therapeutic potential of Moringa oleifera Lam against azoxymethane ... Protein expression profiles that underpin the preventive and therapeutic potential of Moringa oleifera Lam against azoxymethane ... Protein expression profiles that underpin the preventive and therapeutic potential of Moringa oleifera Lam against azoxymethane ... Protein expression profiles that underpin the preventive and therapeutic potential of Moringa oleifera Lam against azoxymethane ...
As F1 mice were resistant to azoxymethane, we treated mice with azoxymethane followed by one cycle of inflammation-inducing ... Epidermal Growth Factor Receptor Is Required for Colonic Tumor Promotion by Dietary Fat in the Azoxymethane/Dextran Sulfate ... Epidermal Growth Factor Receptor Is Required for Colonic Tumor Promotion by Dietary Fat in the Azoxymethane/Dextran Sulfate ... Epidermal Growth Factor Receptor Is Required for Colonic Tumor Promotion by Dietary Fat in the Azoxymethane/Dextran Sulfate ...
Effect of Aloe vera gel extract on antioxidant enzymes and azoxymethane-induced oxidative stress in rats. ... for 30 days on azoxymethane (AOM)-induced oxidative stress in rats. It was observed that AOM administration resulted in a ...
Nrf2-Dependent Suppression of Azoxymethane/Dextran Sulfate Sodium-Induced Colon Carcinogenesis by the Cinnamon-Derived Dietary ... Nrf2-Dependent Suppression of Azoxymethane/Dextran Sulfate Sodium-Induced Colon Carcinogenesis by the Cinnamon-Derived Dietary ... Nrf2-Dependent Suppression of Azoxymethane/Dextran Sulfate Sodium-Induced Colon Carcinogenesis by the Cinnamon-Derived Dietary ... Nrf2-Dependent Suppression of Azoxymethane/Dextran Sulfate Sodium-Induced Colon Carcinogenesis by the Cinnamon-Derived Dietary ...
The combination of 1α, 25(OH)2 - Vitamin D3, calcium and acetylsalicyclic acid affects azoxymethane-induced aberrant crypt foci ... The combination of 1α, 25(OH)2 - Vitamin D3, calcium and acetylsalicyclic acid affects azoxymethane-induced aberrant crypt foci ... The combination of 1α, 25(OH)2 - Vitamin D3, calcium and acetylsalicyclic acid affects azoxymethane-induced aberrant crypt foci ... T1 - The combination of 1α, 25(OH)2 - Vitamin D3, calcium and acetylsalicyclic acid affects azoxymethane-induced aberrant crypt ...
In this study, we evaluated the chemopreventive effect of RGO in a mouse model of azoxymethane/dextran sulfate sodium (AOM/DSS ... In this study, we evaluated the chemopreventive effect of RGO in a mouse model of azoxymethane/dextran sulfate sodium (AOM/DSS ... Chemopreventive Activity of Red Ginseng Oil in a Mouse Model of Azoxymethane/Dextran Sulfate Sodium-Induced Inflammation- ... article{Truong2019ChemopreventiveAO, title={Chemopreventive Activity of Red Ginseng Oil in a Mouse Model of Azoxymethane/ ...
Consumption of Black Beans and Navy Beans (Phaseolus vulgaris) Reduced Azoxymethane-Induced Colon Cancer in Rats. Tagged: * ... Consumption of Black Beans and Navy Beans (Phaseolus vulgaris) Reduced Azoxymethane-Induced Colon Cancer in Rats.pdf. 61.6 KB. ...
Selected fruits reduce azoxymethane (AOM)-induced aberrant crypt foci (ACF) in Fisher 344 male rats. Food Chem Toxicol 2007;45: ... Inhibition of Azoxymethane-Induced Colonic Aberrant Crypt Foci Formation by Silibinin in Male Fisher 344 Rats. Balaiya ... Gene mutations and altered gene expression in azoxymethane-induced colon carcinogenesis in rodents. Cancer Sci 2004;95:475-80. ... Suppression of azoxymethane-induced colon cancer development in rats by a cyclooxygenase-1 selective inhibitor, mofezolac. ...
... using azoxymethane (AOM)-induced colon cancer mice model. Male BALB/c mice were administrated with AOM without or with AR ... using azoxymethane (AOM)-induced colon cancer mice model. Male BALB/c mice were administrated with AOM... ...
  • Azoxymethane (AOM) is an active metabolite of the colon-specific carcinogen 1,2-dimethylhydrazine (DMH) that effectively induces colon tumors in susceptible rodents. (hindawi.com)
  • To develop an efficient animal model for colitis-related carcinogenesis, male Crj: CD-1 (ICR) mice were given a single intraperitoneal administration (10 mg/kg body weight) of a genotoxic colonic carcinogen, azoxymethane (AOM), and a 1-week oral exposure (2% in drinking water) to a non-genotoxic carcinogen, dextran sodium sulfate (DSS), under various protocols. (nih.gov)
  • Aberrant crypt foci (ACF), putative preneoplastic lesions, are early morphological changes induced by the colon carcinogen azoxymethane (AOM). (oup.com)
  • Azoxymethane (AOM) is a colon carcinogen that is used to study the pathogenesis of sporadic colorectal cancer. (spandidos-publications.com)
  • Apc Min/+ mutation or carcinogen treatment with azoxymethane (AOM), respectively. (aacrjournals.org)
  • The etiology of CRC is known to be multifactorial, responding to family, environmental and dietary agents 2 , 3 , 4 putative preneoplastic lesions, are early morphological changes induced by the colon carcinogen azoxymethane (AOM. (isciii.es)
  • We therefore developed a novel colitis-related mouse colorectal cancer model initiated with a colon carcinogen azoxymethane and promoted by DSS. (aacrjournals.org)
  • That model consists of using the colon carcinogen azoxymethane (AOM) along with the colon inflammatory agent dextran sodium sulfate (DSS) to produce colitis-associated pre-neoplastic aberrant crypts in the colon ( 10 ) that are blocked by aspirin or Aspirin-PC treatments. (spandidos-publications.com)
  • After treatment with azoxymethane (AOM), a carcinogen that induces colon cancer, germ-free Il10 −/− mice mono-associated with the colitis-inducing E. coli NC101 strain developed invasive mucinous carcinomas, while mice mono-associated with Enterococcus faecalis , another colitis-inducing bacterial strain, did not. (elifesciences.org)
  • In the present study, we first induced colon adenocarcinoma with azoxymethane, a carcinogen agent, and then investigated the potentiality of polyamidoamine (PAMAM) dendrimer to improve capecitabine therapeutic index and decrease its adverse side effects on healthy tissues like liver and bone marrow. (magiran.com)
  • In the present study, we found that consumption of MG significantly deteriorated azoxymethane (AOM)-induced colonic preneoplastic lesions in ICR mice, in which biomarkers of oxidative stress and inflammation within the body and feces induced by MG-fueled carbonyl stress may have played important roles. (ovid.com)
  • To evaluate red propolis , gum arabic and L-lysine activity on colorectal preneoplastic lesions induced by azoxymethane (AOM). (bvsalud.org)
  • natalensis Berger (designated as 'ALOE') on azoxymethane (AOM)-induced aberrant crypt foci (ACF), putative preneoplastic lesions, in the rat colorectum. (fujita-hu.ac.jp)
  • Aims of the study: To investigate whether tomatoes and onions,with low or high quercetin-glycoside content, could reduce azoxymethane (AOM)-induced Aberrant Crypt Foci (ACF), preneoplastic lesions in the colon of rats. (wur.nl)
  • 0.05) reductions in the incidence of ACF in azoxymethane induced preneoplastic lesions. (cranberryinstitute.org)
  • Therefore, the present study aimed to explore the protein expression profiles responsible for the suppressive effect of bMO supplementation on azoxymethane (AOM)/dextran sodium sulfate (DSS)‑induced mouse colon carcinogenesis. (spandidos-publications.com)
  • Phannasil P, Roytrakul S, Phaonakrop N, Kupradinun P, Budda S, Butryee C, Akekawatchai C and Tuntipopipat S: Protein expression profiles that underpin the preventive and therapeutic potential of Moringa oleifera Lam against azoxymethane and dextran sodium sulfate‑induced mouse colon carcinogenesis. (spandidos-publications.com)
  • As F 1 mice were resistant to azoxymethane, we treated mice with azoxymethane followed by one cycle of inflammation-inducing dextran sulfate sodium to induce tumorigenesis. (aacrjournals.org)
  • Chemopreventive Activity of Red Ginseng Oil in a Mouse Model of Azoxymethane/Dextran Sulfate Sodium-Induced Inflammation-Associated Colon Carcinogenesis. (semanticscholar.org)
  • In this study, we evaluated the chemopreventive effect of RGO in a mouse model of azoxymethane/dextran sulfate sodium (AOM/DSS)-induced colitis and explored its underlying mechanisms. (semanticscholar.org)
  • In this study, we investigated the chemopreventive efficacy of PEITC and DBM in the azoxymethane (AOM)-initiated and dextran sodium sulfate (DSS)-promoted colon cancer mouse model and to compare their potential in vivo mechanisms leading to chemoprevention. (qxmd.com)
  • The epigenetic effects of aspirin: the modification of histone H3 lysine 27 acetylation in the prevention of colon carcinogenesis in azoxymethane- and dextran sulfate sodium-treated CF-1 mice. (qxmd.com)
  • BACKGROUD/OBJECTIVES: The objective of this study was to investigate the effects of vitamin C on inflammation, tumor development, and dysbiosis of intestinal microbiota in an azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced inflammation-associated early colon cancer mouse model. (koreascience.or.kr)
  • The present study investigated the potential molecular mechanisms for the protective effect of glutamine in a murine model of azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced CAC. (mdpi.com)
  • Male ICR mice were given a single ip injection of azoxymethane (AOM, 10 mg/kg body weight), followed by the addition of 2% (w/v) dextran sodium sulfate (DSS) to their drinking water for 7 days, starting 1 week after the AOM injection. (qxmd.com)
  • Dose-dependent promoting effect of dextran sodium sulfate on mouse colon carcinogenesis initiated with azoxymethane. (qxmd.com)
  • Sequential observations on the occurrence of preneoplastic and neoplastic lesions in mouse colon treated with azoxymethane and dextran sodium sulfate. (qxmd.com)
  • Chemoprevention of azoxymethane/dextran sodium sulfate-induced mouse colon carcinogenesis by freeze-dried yam sanyaku and its constituent diosgenin. (qxmd.com)
  • Strain differences in the susceptibility to azoxymethane and dextran sodium sulfate-induced colon carcinogenesis in mice. (qxmd.com)
  • A gamma-tocopherol-rich mixture of tocopherols inhibits colon inflammation and carcinogenesis in azoxymethane and dextran sulfate sodium-treated mice. (qxmd.com)
  • We modeled this relationship by "treating mice lacking TNF receptors with a colon cancer causing combination of azoxymethane followed by repeated dextran sulphate sodium exposures (AOM + DSS regime). (scirp.org)
  • The role of selenium (Se) in modulating colon carcinogenesis induced by azoxymethane (AOM) followed by dextran sodium sulfate (DSS) was investigated in mice . (bvsalud.org)
  • This study was aimed to investigate the protective role of BF in a colorectal cancer (CRC) model induced by azoxymethane (AOM) and dextran sulfate sodium (DSS) in germ-free (GF) mice. (elsevier.com)
  • This model consists of initiation induced by azoxymethane (AOM) and promoted by sodium dextran sulfate (DSS), simulating human colonic carcinogenesis in a rat model. (isciii.es)
  • Here we show that colitis induced with azoxymethane via intraperitoneal injection + 2% dextran sulfate sodium in the drinking water is suppressed by Cl-amidine (also given in the drinking water). (aspetjournals.org)
  • In this study, an experimental colitis and colitis-associated colorectal carcinogenesis mouse model, chemically induced by azoxymethane/dextran sodium sulfat. (hica.co.za)
  • Male CD-1 mice were given a single i.p. injection of azoxymethane followed by 1-week oral exposure of 1% dextran sodium sulfate in drinking water. (aacrjournals.org)
  • This study was to evaluate the effects of SBS on azoxymethane (AOM) and dextran sodium sulfate (DSS) induced colitis associated CRC (caCRC) and to analyze the underlying mechanism of SBS in preventing CRC. (biomedcentral.com)
  • iv) C + 0.5% B. longum + 2.5% lactulose (C+Bl+L). All animals received a s.c. injection of azoxymethane at 16 mg/kg body wt at 7 and 8 weeks of age. (uoi.gr)
  • Two weeks after azoxymethane treatment, rats (48 per group) were fed experimental diets containing NO-indomethacin (0, 40, or 80 ppm), or NO-aspirin (1,500 or 3,000 ppm), representing 40% and 80% of the maximum tolerated dose. (aacrjournals.org)
  • All rats were killed 48 weeks after azoxymethane treatment and assessed for colon tumor efficacy and molecular changes in colonic tumors and normally appearing colonic mucosa of different dietary groups. (aacrjournals.org)
  • However, azoxymethane treated Cdx2 +/− mice developed tumours specifically in the distal colon 12 weeks after azoxymethane treatment whereas no tumours were found in wild-type littermates at this stage. (bmj.com)
  • Unexpectedly, in azoxymethane-treated rats, leptin significantly inhibited aberrant crypt foci formation in the middle and distal colon compared with controls (P = 0.006). (nih.gov)
  • Inhibition of azoxymethane-induced aberrant crypt foci formation in rat colorectum by whole leaf Aloe arborescens Miller var. (fujita-hu.ac.jp)
  • Fingerprint Dive into the research topics of 'Inhibition of azoxymethane-induced aberrant crypt foci formation in rat colorectum by whole leaf Aloe arborescens Miller var. (fujita-hu.ac.jp)
  • We used azoxymethane (AOM) treated A/J Min/+ mice, which developed a significantly higher tumor load in the colon than in the small intestine, to compare the effects of dietary inulin (IN), cellulose (CE) or brewers spent grain (BSG) on intestinal tumorigenesis and cecal microbiota. (nofima.no)
  • Results: Pla2g2a strongly inhibited colon tumorigenesis in mice following treatment with the DNA alkylating agent azoxymethane (AOM). (iospress.com)
  • Although we showed that epidermal growth factor receptors (EGFR) controlled azoxymethane tumorigenesis in standard fat conditions, the role of EGFR in tumor promotion by high dietary fat has not been examined. (aacrjournals.org)
  • The effect of 30% caloric restriction on azoxymethane (AOM)-induced colon carcinogenesis was investigated in male F344 rats. (aacrjournals.org)
  • Seven-week-old male F344 rats were fed control diet, and 1 week later, rats received two weekly s.c. injections of azoxymethane (15 mg/kg body weight). (aacrjournals.org)
  • Effects of 1alpha,25(OH)(2)-vitamin D(3) and acetylsalicylic acid at various dietary levels of calcium (CaCO(3)) on development of aberrant crypt foci (ACF) and tumours in colon were examined in groups of 16 male F344 rats initiated with azoxymethane and observed for 16 weeks. (dtu.dk)
  • RESULTS: It was observed the presence of aberrant crypt foci in all animals of groups I and IV, 50% in group II and 90% in group V. CONCLUSION: The β-lapachone extracted from the Tabebuia avellanedae showed no protective effect of lesions induced by azoxymethane in colon of mice. (scielo.br)
  • The present work was undertaken with a view to study the effect of oral feeding of 2% Aloe vera gel extract (AGE) for 30 days on azoxymethane (AOM)-induced oxidative stress in rats. (niscair.res.in)
  • Dietary folate protects against azoxymethane-induced aberrant crypt foci development and oxidative stress in rat colon. (semanticscholar.org)
  • Modulatory influence of garlic and tomato on cyclooxygenase-2 activity, cell proliferation and apoptosis during azoxymethane induced colon carcinogenesis in rat. (semanticscholar.org)
  • Attenuation by the GABA receptor agonist baclofen of experimental carcinogenesis in rat colon by azoxymethane. (muscimol.xyz)
  • IMSEAR at SEARO: Inhibition of azoxymethane-induced DNA adduct formation by Aloe arborescens var. (who.int)
  • To clarify the possible mechanisms of inhibition of azoxymethane (AOM)-induced aberrant crypt foci (ACF) in the rat colorectum by freeze-dried whole leaves of Aloe arborescens var. (who.int)
  • After azoxymethane treatment, the gastric-like heteroplasias in the pericaecal region did not evolve into cancer indicating that they are not precancerous lesions. (bmj.com)
  • Accumulation of K-ras Codon 12 Mutations in the F344 Rat Distal Colon Following Azoxymethane Exposure. (fda.gov)
  • In addition, dietary heme, but not systemically delivered heme, contributed to the exacerbation of DSS-induced colitis and facilitated adenoma formation in the azoxymethane/DSS colorectal cancer (CRC) mouse model. (frontiersin.org)
  • Dietary artepillin C suppresses the formation of aberrant crypt foci induced by azoxymethane in mouse colon. (propolisscience.org)
  • Presentation] Chemopreventive effect of RAS inhibitor on azoxymethane-induced colorectal carcinogenesis. (nii.ac.jp)
  • Rats received two s.c. injections of azoxymethane (15 mg/kg) for 2 weeks and were fed either experimental or control diets until necropsy. (aacrjournals.org)
  • We previously demonstrated that black bean (BB) and soy flour (SF)-based diets inhibit azoxymethane (AOM)-induced colon cancer. (hindawi.com)
  • Western-style diets promote development of azoxymethane-induced colon cancer. (aacrjournals.org)
  • In all of the studies, starch diets were fed to Azoxymethane (AOM) - induced Fisher 344 rats for 8 weeks with 50-55% of the diet replaced with RS. (iastate.edu)
  • Rats were continued on respective experimental diets and sacrificed 8 weeks after the azoxymethane treatment. (aacrjournals.org)
  • Rats received the diets for 10 wk and were injected with azoxymethane (15 mg/kg) at wk 3 and 4. (tamu.edu)
  • The present study examined the effects of astaxanthin on the development of azoxymethane (AOM)-induced colonic premalignant lesions in C57BL/KsJ- db/db ( db/db ) obese mice. (biomedcentral.com)
  • Suppression of azoxymethane-induced colonic premalignant lesion formation by coenzyme Q10 in rats. (nih.gov)
  • The effects of the gamma-amino-n-butyric acid (GABA)A receptor agonist muscimol, and the GABAB receptor agonist baclofen, on colon carcinogenesis induced by azoxymethane in Wistar rats were tested. (muscimol.xyz)
  • Carcinogenesis was induced with azoxymethane in Wistar rats kept on a conventional diet or a hypercaloric diet containing unsaturated fat. (scielo.br)
  • los focos de criptas aberrantes (ACF) son lesiones preneoplásicas en colon que pueden ser utilizados como herramienta para estudiar procesos preventivos para el cáncer colorectal (CCR). (isciii.es)
  • Azoxymethane treated rats were fed either a standard rat diet or a rat diet supplemented with FaOH and FaDOH. (biomedcentral.com)
  • To test this hypothesis, we studied the effect of dietary sulindac sulfone (500-2000 ppm), a metabolite of sulindac reported to lack cyclooxygenase inhibitory activity, on tumor formation and PGE 2 levels in the azoxymethane model of colon carcinogenesis. (aacrjournals.org)
  • The azoxymethane- (AOM-) induced colon cancer model in rodents has been utilized extensively to examine dietary influences on colon cancer. (hindawi.com)
  • Herein, we investigated the mediation of AR in the formation of colonic preneoplastic aberrant crypt foci (ACF) using azoxymethane (AOM)-induced colon cancer mice model. (oup.com)
  • This study measured the potential mechanism(s) by which vitamin D3 could synergise the tumouricidal activities of 5-FU in azoxymethane (AOM) rat model of colon cancer. (biomedcentral.com)
  • Azoxymethane (AOM) is commonly used in rodents to create an experimental model of colon cancer that mimics the sporadic phenotype in human with high similarities in molecular, clinical and histopathological features of the disease between both species [ 2 - 4 ]. (biomedcentral.com)
  • The development of colorectal cancer in the azoxymethane-induced mouse model can be observed by using a miniaturized optical coherence tomography (OCT) imaging system. (elsevier.com)
  • We also examine the chemopreventive efficacy of β-ionone on azoxymethane-induced rat colon carcinogenesis model using colonic aberrant crypt foci (ACF) as endpoint biomarker. (aacrjournals.org)
  • Arthur and colleagues identified a genotoxic island in Escherichia coli NC101 that appeared to be responsible for causing neoplastic lesions in inflammation-induced IL10 −/− mice treated with azoxymethane. (elifesciences.org)
  • 3 R )-Falcarinol (FaOH) and (3 R ,8 S )-falcarindiol (FaDOH) have previously been shown to reduce the number of neoplastic lesions and the growth rate of polyps in the colon of azoxymethane (AOM) treated rats. (biomedcentral.com)
  • FaDOH], isolated from carrots, reduce the number of neoplastic lesions as well as the growth rate of the polyps in the colon of azoxymethane (AOM) treated rats. (biomedcentral.com)
  • Once a week for 2 weeks, animals on control groups received saline, while animals in experimental groups received azoxymethane (15 mg/kg i.p. (bvsalud.org)
  • We assessed the chemopreventive properties of NO-indomethacin (NCX 530) and NO-aspirin (NCX 4016) against azoxymethane-induced colon cancer. (aacrjournals.org)
  • This study investigated the chemopreventive properties and toxicity of KH in Sprague Dawley rats induced with azoxymethane (AOM). (hindawi.com)
  • FaOH and FaDOH have previously demonstrated a chemopreventive effect on precursor lesions of colorectal cancer (CRC) in azoxymethane (AOM)-induced rats. (aau.dk)
  • In this study, the chemopreventive potential of Cranberry was analyzed in reducing the Aberrant Crypt Foci (ACF) induced by Azoxymethane (AOM) in Fisher 344 male rats. (cranberryinstitute.org)
  • Chemoprevention of azoxymethane-induced rat colon carcinogenesis by a xanthine oxidase inhibitor, 1'-acetoxychavicol acetate. (qxmd.com)
  • Effects of modulating M3 muscarinic receptor activity on azoxymethane-induced liver injury in mice. (sigmaaldrich.com)
  • Previously, we reported that azoxymethane (AOM)-induced liver injury is robustly exacerbated in M3 muscarinic receptor (M3R)-deficient mice. (sigmaaldrich.com)
  • We investigated the actions of scopolamine, a non-selective muscarinic receptor antagonist, and specific genetic ablation of a key cholinergic receptor, muscarinic subtype-3 ( Chrm3 ), on azoxymethane (AOM)-induced liver injury in mice. (aspetjournals.org)
  • Given the reports of liver injury in humans and livestock fed cycad palm nuts on the island of Guam, we hypothesized that the active ingredient azoxymethane (AOM) could cause FHF. (elsevier.com)
  • 2) It promotes colon cancer development in Azoxymethane-induced and APC gene knockout mice. (wikipedia.org)
  • METHODS: Fifty (n=50) mice were divided into five groups: in group I azoxymethane (AOM) was administered, in Group II - β-lapachone, in group III - vehicle (diluent) and in group IV - vehicle + AOM and finally in group V - β-lapachone + AOM. (scielo.br)
  • Based on our recent silibinin efficacy studies in human colorectal cancer cells, we investigated the effects of its dietary feeding on azoxymethane (AOM)-induced aberrant crypt foci (ACF) formation and associated biomarkers in male Fisher 344 rats. (aacrjournals.org)
  • Heterozygous loss of PPARγ causes an increase in β-catenin levels and a greater incidence of colon cancer when animals are treated with azoxymethane. (pnas.org)
  • In the present study, effects of CoQ10 on development of azoxymethane (AOM)-induced aberrant crypt foci (ACF) and mucin-depleted foci (MDF) in F344 male rats were investigated. (nih.gov)
  • Heterozygous Cdx2 +/− mice were analysed for spontaneous malignant tumours and for tumour development after treatment with a DNA mutagen, azoxymethane. (bmj.com)