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.
F344 rats are an inbred strain of albino laboratory rats (Rattus norvegicus) that have been widely used in biomedical research due to their consistent and reliable genetic background, which facilitates the study of disease mechanisms and therapeutic interventions.
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.
Azo compounds are organic compounds characterized by the presence of one or more azo groups, -N=N-, linking two aromatic rings, which can impart various colors and are used in dyes, pharmaceuticals, and chemical research.
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.

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)

Azoxymethane is a chemical compound that is used primarily in laboratory research. It is an organodihydroazoxy compound, and it is known to cause colon cancer in experimental animals, particularly rats and mice. As such, it is often used as a tool in studies of carcinogenesis and chemically induced colon tumors.

In scientific studies, azoxymethane is typically administered to laboratory animals in order to induce colon tumors. This allows researchers to study the mechanisms of cancer development and test potential therapies or preventive measures. It is important to note that while azoxymethane has been shown to cause cancer in laboratory animals, it does not necessarily mean that it poses the same risk to humans.

The use of azoxymethane in research is subject to strict regulations and guidelines, as with any potentially hazardous chemical. Researchers are required to follow safety protocols and take appropriate precautions when handling this compound to minimize risks to themselves and the environment.

Colonic neoplasms refer to abnormal growths in the large intestine, also known as the colon. These growths can be benign (non-cancerous) or malignant (cancerous). The two most common types of colonic neoplasms are adenomas and carcinomas.

Adenomas are benign tumors that can develop into cancer over time if left untreated. They are often found during routine colonoscopies and can be removed during the procedure.

Carcinomas, on the other hand, are malignant tumors that invade surrounding tissues and can spread to other parts of the body. Colorectal cancer is the third leading cause of cancer-related deaths in the United States, and colonic neoplasms are a significant risk factor for developing this type of cancer.

Regular screenings for colonic neoplasms are recommended for individuals over the age of 50 or those with a family history of colorectal cancer or other risk factors. Early detection and removal of colonic neoplasms can significantly reduce the risk of developing colorectal cancer.

Carcinogens are agents (substances or mixtures of substances) that can cause cancer. They may be naturally occurring or man-made. Carcinogens can increase the risk of cancer by altering cellular DNA, disrupting cellular function, or promoting cell growth. Examples of carcinogens include certain chemicals found in tobacco smoke, asbestos, UV radiation from the sun, and some viruses.

It's important to note that not all exposures to carcinogens will result in cancer, and the risk typically depends on factors such as the level and duration of exposure, individual genetic susceptibility, and lifestyle choices. The International Agency for Research on Cancer (IARC) classifies carcinogens into different groups based on the strength of evidence linking them to cancer:

Group 1: Carcinogenic to humans
Group 2A: Probably carcinogenic to humans
Group 2B: Possibly carcinogenic to humans
Group 3: Not classifiable as to its carcinogenicity to humans
Group 4: Probably not carcinogenic to humans

This information is based on medical research and may be subject to change as new studies become available. Always consult a healthcare professional for medical advice.

F344 is a strain code used to designate an outbred stock of rats that has been inbreeded for over 100 generations. The F344 rats, also known as Fischer 344 rats, were originally developed at the National Institutes of Health (NIH) and are now widely used in biomedical research due to their consistent and reliable genetic background.

Inbred strains, like the F344, are created by mating genetically identical individuals (siblings or parents and offspring) for many generations until a state of complete homozygosity is reached, meaning that all members of the strain have identical genomes. This genetic uniformity makes inbred strains ideal for use in studies where consistent and reproducible results are important.

F344 rats are known for their longevity, with a median lifespan of around 27-31 months, making them useful for aging research. They also have a relatively low incidence of spontaneous tumors compared to other rat strains. However, they may be more susceptible to certain types of cancer and other diseases due to their inbred status.

It's important to note that while F344 rats are often used as a standard laboratory rat strain, there can still be some genetic variation between individual animals within the same strain, particularly if they come from different suppliers or breeding colonies. Therefore, it's always important to consider the source and history of any animal model when designing experiments and interpreting results.

Aberrant crypt foci (ACF) are abnormal, enlarged and dysplastic (abnormally developing) crypts in the lining of the colon or rectum. They are considered to be early preneoplastic lesions, meaning they have the potential to develop into colon cancer. ACF can be detected through a microscopic examination of tissue samples taken during a colonoscopy.

The presence and number of ACF have been associated with an increased risk for developing colorectal cancer. They are often found in individuals with inflammatory bowel disease, particularly those with long-standing ulcerative colitis or Crohn's colitis. The identification and removal of ACF during a colonoscopy may help prevent the development of colorectal cancer.

The colon, also known as the large intestine, is a part of the digestive system in humans and other vertebrates. It is an organ that eliminates waste from the body and is located between the small intestine and the rectum. The main function of the colon is to absorb water and electrolytes from digested food, forming and storing feces until they are eliminated through the anus.

The colon is divided into several regions, including the cecum, ascending colon, transverse colon, descending colon, sigmoid colon, rectum, and anus. The walls of the colon contain a layer of muscle that helps to move waste material through the organ by a process called peristalsis.

The inner surface of the colon is lined with mucous membrane, which secretes mucus to lubricate the passage of feces. The colon also contains a large population of bacteria, known as the gut microbiota, which play an important role in digestion and immunity.

Azo compounds are organic compounds characterized by the presence of one or more azo groups (-N=N-) in their molecular structure. The term "azo" is derived from the Greek word "azō," meaning "to boil" or "to sparkle," which refers to the brightly colored nature of many azo compounds.

These compounds are synthesized by the reaction between aromatic amines and nitrous acid or its derivatives, resulting in the formation of diazonium salts, which then react with another aromatic compound containing an active methylene group to form azo compounds.

Azo compounds have diverse applications across various industries, including dyes, pigments, pharmaceuticals, and agrochemicals. They are known for their vibrant colors, making them widely used as colorants in textiles, leather, paper, and food products. In addition, some azo compounds exhibit unique chemical properties, such as solubility, stability, and reactivity, which make them valuable intermediates in the synthesis of various organic compounds.

However, certain azo compounds have been found to pose health risks due to their potential carcinogenicity and mutagenicity. As a result, regulations have been imposed on their use in consumer products, particularly those intended for oral consumption or direct skin contact.

A precancerous condition, also known as a premalignant condition, is a state of abnormal cellular growth and development that has a higher-than-normal potential to progress into cancer. These conditions are characterized by the presence of certain anomalies in the cells, such as dysplasia (abnormal changes in cell shape or size), which can indicate an increased risk for malignant transformation.

It is important to note that not all precancerous conditions will eventually develop into cancer, and some may even regress on their own. However, individuals with precancerous conditions are often at a higher risk of developing cancer compared to the general population. Regular monitoring and appropriate medical interventions, if necessary, can help manage this risk and potentially prevent or detect cancer at an early stage when it is more treatable.

Examples of precancerous conditions include:

1. Dysplasia in the cervix (cervical intraepithelial neoplasia or CIN)
2. Atypical ductal hyperplasia or lobular hyperplasia in the breast
3. Actinic keratosis on the skin
4. Leukoplakia in the mouth
5. Barrett's esophagus in the digestive tract

Regular medical check-ups, screenings, and lifestyle modifications are crucial for individuals with precancerous conditions to monitor their health and reduce the risk of cancer development.

Dextran sulfate is a type of polysaccharide (a complex carbohydrate) that is made up of repeating units of the sugar dextran, which has been sulfonated (introduced with a sulfonic acid group). It is commonly used as a molecular weight standard in laboratory research and can also be found in some medical products.

In medicine, dextran sulfate is often used as a treatment for hemodialysis patients to prevent the formation of blood clots in the dialyzer circuit. It works by binding to and inhibiting the activity of certain clotting factors in the blood. Dextran sulfate may also have anti-inflammatory effects, and it has been studied as a potential treatment for conditions such as inflammatory bowel disease and hepatitis.

It is important to note that dextran sulfate can have side effects, including allergic reactions, low blood pressure, and bleeding. It should be used under the close supervision of a healthcare professional.

Intestinal neoplasms refer to abnormal growths in the tissues of the intestines, which can be benign or malignant. These growths are called neoplasms and they result from uncontrolled cell division. In the case of intestinal neoplasms, these growths occur in the small intestine, large intestine (colon), rectum, or appendix.

Benign intestinal neoplasms are not cancerous and often do not invade surrounding tissues or spread to other parts of the body. However, they can still cause problems if they grow large enough to obstruct the intestines or cause bleeding. Common types of benign intestinal neoplasms include polyps, leiomyomas, and lipomas.

Malignant intestinal neoplasms, on the other hand, are cancerous and can invade surrounding tissues and spread to other parts of the body. The most common type of malignant intestinal neoplasm is adenocarcinoma, which arises from the glandular cells lining the inside of the intestines. Other types of malignant intestinal neoplasms include lymphomas, sarcomas, and carcinoid tumors.

Symptoms of intestinal neoplasms can vary depending on their size, location, and type. Common symptoms include abdominal pain, bloating, changes in bowel habits, rectal bleeding, weight loss, and fatigue. If you experience any of these symptoms, it is important to seek medical attention promptly.

Anticarcinogenic agents are substances that prevent, inhibit or reduce the development of cancer. They can be natural or synthetic compounds that interfere with the process of carcinogenesis at various stages, such as initiation, promotion, and progression. Anticarcinogenic agents may work by preventing DNA damage, promoting DNA repair, reducing inflammation, inhibiting cell proliferation, inducing apoptosis (programmed cell death), or modulating immune responses.

Examples of anticarcinogenic agents include chemopreventive agents, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and retinoids; phytochemicals found in fruits, vegetables, and other plant-based foods; and medications used to treat cancer, such as chemotherapy, radiation therapy, and targeted therapies.

It is important to note that while some anticarcinogenic agents have been shown to be effective in preventing or reducing the risk of certain types of cancer, they may also have potential side effects and risks. Therefore, it is essential to consult with a healthcare professional before using any anticarcinogenic agent for cancer prevention or treatment purposes.

The intestinal mucosa is the innermost layer of the intestines, which comes into direct contact with digested food and microbes. It is a specialized epithelial tissue that plays crucial roles in nutrient absorption, barrier function, and immune defense. The intestinal mucosa is composed of several cell types, including absorptive enterocytes, mucus-secreting goblet cells, hormone-producing enteroendocrine cells, and immune cells such as lymphocytes and macrophages.

The surface of the intestinal mucosa is covered by a single layer of epithelial cells, which are joined together by tight junctions to form a protective barrier against harmful substances and microorganisms. This barrier also allows for the selective absorption of nutrients into the bloodstream. The intestinal mucosa also contains numerous lymphoid follicles, known as Peyer's patches, which are involved in immune surveillance and defense against pathogens.

In addition to its role in absorption and immunity, the intestinal mucosa is also capable of producing hormones that regulate digestion and metabolism. Dysfunction of the intestinal mucosa can lead to various gastrointestinal disorders, such as inflammatory bowel disease, celiac disease, and food allergies.

"Tabebuia" is a term that refers to a genus of trees and shrubs, primarily found in tropical regions of the Americas. While it is a common name in botany, it is not a medical term. The bark and wood of some species have been used in traditional medicine, but there is limited scientific evidence supporting their effectiveness or safety.

The bark has been used to treat various conditions such as fever, inflammation, and skin diseases. The wood has been used for making tools, furniture, and musical instruments. However, it's important to note that the use of these plants in traditional medicine does not equate to proven medical efficacy or safety.

Therefore, if you're considering using a Tabebuia species for medicinal purposes, it's crucial to consult with a healthcare provider first due to potential side effects and interactions with other medications.

Cocarcinogenesis is a term used in the field of oncology to describe a process where exposure to certain chemicals or physical agents enhances the tumor-forming ability of a cancer-causing agent (carcinogen). A cocarcinogen does not have the ability to initiate cancer on its own, but it can promote the development and progression of cancer when combined with a carcinogen.

In other words, a cocarcinogen is a substance or factor that acts synergistically with a known carcinogen to increase the likelihood or speed up the development of cancer. This process can occur through various mechanisms, such as suppressing the immune system, promoting inflammation, increasing cell proliferation, or inhibiting apoptosis (programmed cell death).

Examples of cocarcinogens include tobacco smoke, alcohol, certain viruses, and radiation. These agents can interact with carcinogens to increase the risk of cancer in individuals who are exposed to them. It is important to note that while cocarcinogens themselves may not directly cause cancer, they can significantly contribute to its development and progression when combined with other harmful substances or factors.

Colitis is a medical term that refers to inflammation of the inner lining of the colon or large intestine. The condition can cause symptoms such as diarrhea, abdominal cramps, and urgency to have a bowel movement. Colitis can be caused by a variety of factors, including infections, inflammatory bowel disease (such as Crohn's disease or ulcerative colitis), microscopic colitis, ischemic colitis, and radiation therapy. The specific symptoms and treatment options for colitis may vary depending on the underlying cause.

Methylazoxymethanol Acetate (MAM) is not a medication or therapeutic agent used in human medicine. It is a research tool, specifically a neurotoxin, that is used in laboratory studies to help understand the development and organization of the nervous system, particularly in relation to neurodegenerative disorders and brain injuries.

MAM is primarily used in animal models, often rats or mice, to study the effects of early life exposure to neurotoxic substances on brain development. It is known to cause widespread degeneration of nerve cells (neurons) and disruption of normal neural connections, which can provide valuable insights into the processes underlying various neurological conditions.

However, it's important to note that MAM is not used as a treatment or therapy in human medicine due to its neurotoxic properties.

Corn oil is a type of vegetable oil that is extracted from the germ of corn (maize). It is rich in polyunsaturated fat, particularly linoleic acid, and contains about 25% saturated fat. Corn oil has a high smoke point, making it suitable for frying and baking. It is also used as an ingredient in margarine, salad dressings, and other food products. In addition to its use as a food product, corn oil is sometimes used topically on the skin as a moisturizer or emollient.

Monomethylhydrazine (MMH) is not a medical term, but a chemical compound. It is commonly used in the medical field in relation to the chemistry and pharmacology of certain drugs or as a potential hazardous substance. Here's a definition from a chemistry perspective:

Monomethylhydrazine (MMH) is an organic compound with the formula CH3NHNH2. It is a colorless liquid, highly reactive, and toxic. Monomethylhydrazine is used as a rocket propellant due to its high performance, but it also has applications in chemical synthesis.

In medicine, MMH may be encountered in the context of occupational health and safety or in discussions about chemical hazards and their management in healthcare settings. It is essential for medical professionals to understand the properties and potential risks associated with this compound when handling or working around it.

Piroxicam is a non-steroidal anti-inflammatory drug (NSAID) that is used to treat pain, inflammation, and fever. It works by inhibiting the activity of cyclooxygenase (COX) enzymes, which are involved in the production of prostaglandins, chemicals that contribute to inflammation and pain.

Piroxicam is available as a prescription medication and is used to treat conditions such as osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis. It is typically taken orally in the form of tablets or capsules, and its effects can last for up to 12 hours.

Like other NSAIDs, piroxicam can cause side effects such as stomach ulcers, bleeding, and kidney problems, especially when used at high doses or for long periods of time. It is important to use piroxicam only as directed by a healthcare provider and to follow any recommended precautions.

An adenoma is a benign (noncancerous) tumor that develops from glandular epithelial cells. These types of cells are responsible for producing and releasing fluids, such as hormones or digestive enzymes, into the surrounding tissues. Adenomas can occur in various organs and glands throughout the body, including the thyroid, pituitary, adrenal, and digestive systems.

Depending on their location, adenomas may cause different symptoms or remain asymptomatic. Some common examples of adenomas include:

1. Colorectal adenoma (also known as a polyp): These growths occur in the lining of the colon or rectum and can develop into colorectal cancer if left untreated. Regular screenings, such as colonoscopies, are essential for early detection and removal of these polyps.
2. Thyroid adenoma: This type of adenoma affects the thyroid gland and may result in an overproduction or underproduction of hormones, leading to conditions like hyperthyroidism (overactive thyroid) or hypothyroidism (underactive thyroid).
3. Pituitary adenoma: These growths occur in the pituitary gland, which is located at the base of the brain and controls various hormonal functions. Depending on their size and location, pituitary adenomas can cause vision problems, headaches, or hormonal imbalances that affect growth, reproduction, and metabolism.
4. Liver adenoma: These rare benign tumors develop in the liver and may not cause any symptoms unless they become large enough to press on surrounding organs or structures. In some cases, liver adenomas can rupture and cause internal bleeding.
5. Adrenal adenoma: These growths occur in the adrenal glands, which are located above the kidneys and produce hormones that regulate stress responses, metabolism, and blood pressure. Most adrenal adenomas are nonfunctioning, meaning they do not secrete excess hormones. However, functioning adrenal adenomas can lead to conditions like Cushing's syndrome or Conn's syndrome, depending on the type of hormone being overproduced.

It is essential to monitor and manage benign tumors like adenomas to prevent potential complications, such as rupture, bleeding, or hormonal imbalances. Treatment options may include surveillance with imaging studies, medication to manage hormonal issues, or surgical removal of the tumor in certain cases.

Duodenal neoplasms refer to abnormal growths in the duodenum, which is the first part of the small intestine that receives digestive secretions from the pancreas and bile duct. These growths can be benign or malignant (cancerous).

Benign neoplasms include adenomas, leiomyomas, lipomas, and hamartomas. They are usually slow-growing and do not spread to other parts of the body. However, they may cause symptoms such as abdominal pain, bleeding, or obstruction of the intestine.

Malignant neoplasms include adenocarcinomas, neuroendocrine tumors (carcinoids), lymphomas, and sarcomas. They are more aggressive and can invade surrounding tissues and spread to other parts of the body. Symptoms may include abdominal pain, weight loss, jaundice, anemia, or bowel obstruction.

The diagnosis of duodenal neoplasms is usually made through imaging tests such as CT scans, MRI, or endoscopy with biopsy. Treatment depends on the type and stage of the tumor and may include surgery, chemotherapy, radiation therapy, or a combination of these modalities.

Cyclooxygenase-2 (COX-2) is an enzyme involved in the synthesis of prostaglandins, which are hormone-like substances that play a role in inflammation, pain, and fever. COX-2 is primarily expressed in response to stimuli such as cytokines and growth factors, and its expression is associated with the development of inflammation.

COX-2 inhibitors are a class of nonsteroidal anti-inflammatory drugs (NSAIDs) that selectively block the activity of COX-2, reducing the production of prostaglandins and providing analgesic, anti-inflammatory, and antipyretic effects. These medications are often used to treat pain and inflammation associated with conditions such as arthritis, menstrual cramps, and headaches.

It's important to note that while COX-2 inhibitors can be effective in managing pain and inflammation, they may also increase the risk of cardiovascular events such as heart attack and stroke, particularly when used at high doses or for extended periods. Therefore, it's essential to use these medications under the guidance of a healthcare provider and to follow their instructions carefully.

Fish oils are a type of fat or lipid derived from the tissues of oily fish. They are a rich source of omega-3 fatty acids, specifically eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These fatty acids have been associated with various health benefits such as reducing inflammation, decreasing the risk of heart disease, improving brain function, and promoting eye health. Fish oils can be consumed through diet or taken as a dietary supplement in the form of capsules or liquid. It is important to note that while fish oils have potential health benefits, they should not replace a balanced diet and medical advice should be sought before starting any supplementation.

Beta-catenin is a protein that plays a crucial role in gene transcription and cell-cell adhesion. It is a key component of the Wnt signaling pathway, which regulates various processes such as cell proliferation, differentiation, and migration during embryonic development and tissue homeostasis in adults.

In the absence of Wnt signals, beta-catenin forms a complex with other proteins, including adenomatous polyposis coli (APC) and axin, which targets it for degradation by the proteasome. When Wnt ligands bind to their receptors, this complex is disrupted, allowing beta-catenin to accumulate in the cytoplasm and translocate to the nucleus. In the nucleus, beta-catenin interacts with T cell factor/lymphoid enhancer-binding factor (TCF/LEF) transcription factors to activate the transcription of target genes involved in cell fate determination, survival, and proliferation.

Mutations in the genes encoding components of the Wnt signaling pathway, including beta-catenin, have been implicated in various human diseases, such as cancer, developmental disorders, and degenerative conditions.

Adenocarcinoma is a type of cancer that arises from glandular epithelial cells. These cells line the inside of many internal organs, including the breasts, prostate, colon, and lungs. Adenocarcinomas can occur in any of these organs, as well as in other locations where glands are present.

The term "adenocarcinoma" is used to describe a cancer that has features of glandular tissue, such as mucus-secreting cells or cells that produce hormones. These cancers often form glandular structures within the tumor mass and may produce mucus or other substances.

Adenocarcinomas are typically slow-growing and tend to spread (metastasize) to other parts of the body through the lymphatic system or bloodstream. They can be treated with surgery, radiation therapy, chemotherapy, targeted therapy, or a combination of these treatments. The prognosis for adenocarcinoma depends on several factors, including the location and stage of the cancer, as well as the patient's overall health and age.

The Nucleolus Organizer Region (NOR) is a specific region within the chromosomes, primarily in the short arm of the acrocentric chromosomes (chromosomes 13, 14, 15, 21, and 22). It consists of clusters of repetitive DNA sequences that encode ribosomal RNA (rRNA) genes. During interphase, these regions form the nucleolus, a distinct structure within the nucleus where rRNA transcription, processing, and ribosome assembly occur. The number of NORs in an individual can vary, which has implications in certain genetic conditions and aging processes.

Dimethylhydrazines are organic compounds that consist of two methyl groups (-CH3) bonded to a hydrazine molecule (N2H4). The most common dimethylhydrazine is 1,2-dimethylhydrazine, which is a colorless liquid with an unpleasant odor. It is used as a rocket fuel and in the synthesis of other chemicals.

Dimethylhydrazines are highly reactive and can be hazardous to handle. They can cause skin and eye irritation, and prolonged exposure can lead to more serious health effects such as damage to the respiratory system, liver, and kidneys. Ingestion or inhalation of large amounts of dimethylhydrazines can be fatal.

It is important to handle dimethylhydrazines with care and follow proper safety precautions when working with them. This may include wearing protective clothing, gloves, and eye protection, as well as using appropriate ventilation and storage methods.

Neoplastic cell transformation is a process in which a normal cell undergoes genetic alterations that cause it to become cancerous or malignant. This process involves changes in the cell's DNA that result in uncontrolled cell growth and division, loss of contact inhibition, and the ability to invade surrounding tissues and metastasize (spread) to other parts of the body.

Neoplastic transformation can occur as a result of various factors, including genetic mutations, exposure to carcinogens, viral infections, chronic inflammation, and aging. These changes can lead to the activation of oncogenes or the inactivation of tumor suppressor genes, which regulate cell growth and division.

The transformation of normal cells into cancerous cells is a complex and multi-step process that involves multiple genetic and epigenetic alterations. It is characterized by several hallmarks, including sustained proliferative signaling, evasion of growth suppressors, resistance to cell death, enabling replicative immortality, induction of angiogenesis, activation of invasion and metastasis, reprogramming of energy metabolism, and evading immune destruction.

Neoplastic cell transformation is a fundamental concept in cancer biology and is critical for understanding the molecular mechanisms underlying cancer development and progression. It also has important implications for cancer diagnosis, prognosis, and treatment, as identifying the specific genetic alterations that underlie neoplastic transformation can help guide targeted therapies and personalized medicine approaches.

Phytic acid, also known as phytate in its salt form, is a natural substance found in plant-based foods such as grains, legumes, nuts, and seeds. It's a storage form of phosphorus for the plant and is often referred to as an "anti-nutrient" because it can bind to certain minerals like calcium, iron, magnesium, and zinc in the gastrointestinal tract and prevent their absorption. This can potentially lead to mineral deficiencies if a diet is consistently high in phytic acid-rich foods and low in mineral-rich foods. However, it's important to note that phytic acid also has antioxidant properties and may have health benefits when consumed as part of a balanced diet.

The bioavailability of minerals from phytic acid-rich foods can be improved through various methods such as soaking, sprouting, fermenting, or cooking, which can help break down some of the phytic acid and release the bound minerals.

Carcinogenesis is the process by which normal cells are transformed into cancer cells. It is a complex, multi-step process that involves various genetic and epigenetic alterations in the cell's DNA. These changes can be caused by exposure to carcinogens, such as chemicals, radiation, or viruses, and can lead to the uncontrolled growth and division of cells, resulting in the formation of a tumor.

The process of carcinogenesis typically involves several stages: initiation, promotion, and progression. Initiation is the initial damage to the cell's DNA, which can be caused by exposure to a carcinogen. Promotion is the clonal expansion of the initiated cells due to the stimulation of cell growth and division. Progression is the accumulation of additional genetic changes that lead to the development of invasive cancer.

It is important to note that not all exposures to carcinogens will result in cancer, as the process of carcinogenesis depends on a variety of factors, including the dose and duration of exposure, the individual's genetic susceptibility, and the presence of co-carcinogens or protective factors.

Rutin is a flavonoid, a type of plant pigment that is found in various plants and foods including citrus fruits, buckwheat, and asparagus. It has antioxidant properties and is known to help strengthen blood vessels and reduce inflammation. In medical terms, rutin may be mentioned in the context of discussing treatments for conditions related to these effects, such as varicose veins or hemorrhoids. However, it's important to note that while rutin has potential health benefits, more research is needed to fully understand its effects and proper dosages.

Colorectal neoplasms refer to abnormal growths in the colon or rectum, which can be benign or malignant. These growths can arise from the inner lining (mucosa) of the colon or rectum and can take various forms such as polyps, adenomas, or carcinomas.

Benign neoplasms, such as hyperplastic polyps and inflammatory polyps, are not cancerous but may need to be removed to prevent the development of malignant tumors. Adenomas, on the other hand, are precancerous lesions that can develop into colorectal cancer if left untreated.

Colorectal cancer is a malignant neoplasm that arises from the uncontrolled growth and division of cells in the colon or rectum. It is one of the most common types of cancer worldwide and can spread to other parts of the body through the bloodstream or lymphatic system.

Regular screening for colorectal neoplasms is recommended for individuals over the age of 50, as early detection and removal of precancerous lesions can significantly reduce the risk of developing colorectal cancer.

Ornithine decarboxylase (ODC) is a medical/biochemical term that refers to an enzyme (EC 4.1.1.17) involved in the metabolism of amino acids, particularly ornithine. This enzyme catalyzes the decarboxylation of ornithine to form putrescine, which is a precursor for the synthesis of polyamines, such as spermidine and spermine. Polyamines play crucial roles in various cellular processes, including cell growth, differentiation, and gene expression.

Ornithine decarboxylase is a rate-limiting enzyme in polyamine biosynthesis, meaning that its activity regulates the overall production of these molecules. The regulation of ODC activity is tightly controlled at multiple levels, including transcription, translation, and post-translational modifications. Dysregulation of ODC activity has been implicated in several pathological conditions, such as cancer, neurodegenerative disorders, and inflammatory diseases.

Inhibitors of ornithine decarboxylase have been explored as potential therapeutic agents for various diseases, including cancer, due to their ability to suppress polyamine synthesis and cell proliferation. However, the use of ODC inhibitors in clinical settings has faced challenges related to toxicity and limited efficacy.

Chemoprevention is a medical term that refers to the use of chemical agents, usually in the form of drugs or dietary supplements, to prevent or delay the development of cancer. These agents are typically designed to interfere with the molecular processes involved in cancer initiation, promotion, or progression.

There are several different approaches to chemoprevention, depending on the specific type of cancer and the individual patient's risk factors. Some chemopreventive agents work by blocking the action of hormones that can promote cancer growth, while others may inhibit the activity of enzymes involved in DNA damage or repair.

Chemoprevention is often used in individuals who are at high risk of developing cancer due to inherited genetic mutations, a history of precancerous lesions, or other factors. However, it is important to note that chemopreventive agents can have side effects and may not be appropriate for everyone. Therefore, they should only be used under the close supervision of a healthcare provider.

A diet, in medical terms, refers to the planned and regular consumption of food and drinks. It is a balanced selection of nutrient-rich foods that an individual eats on a daily or periodic basis to meet their energy needs and maintain good health. A well-balanced diet typically includes a variety of fruits, vegetables, whole grains, lean proteins, and low-fat dairy products.

A diet may also be prescribed for therapeutic purposes, such as in the management of certain medical conditions like diabetes, hypertension, or obesity. In these cases, a healthcare professional may recommend specific restrictions or modifications to an individual's regular diet to help manage their condition and improve their overall health.

It is important to note that a healthy and balanced diet should be tailored to an individual's age, gender, body size, activity level, and any underlying medical conditions. Consulting with a healthcare professional, such as a registered dietitian or nutritionist, can help ensure that an individual's dietary needs are being met in a safe and effective way.

Ursodeoxycholic acid (UDCA) is a naturally occurring bile acid that is used medically as a therapeutic agent. It is commonly used to treat gallstones, particularly cholesterol gallstones, and other conditions associated with abnormal liver function, such as primary biliary cholangitis (PBC). UDCA works by decreasing the amount of cholesterol in bile and protecting liver cells from damage. It is also known as ursodiol or Ursotan.

Body weight is the measure of the force exerted on a scale or balance by an object's mass, most commonly expressed in units such as pounds (lb) or kilograms (kg). In the context of medical definitions, body weight typically refers to an individual's total weight, which includes their skeletal muscle, fat, organs, and bodily fluids.

Healthcare professionals often use body weight as a basic indicator of overall health status, as it can provide insights into various aspects of a person's health, such as nutritional status, metabolic function, and risk factors for certain diseases. For example, being significantly underweight or overweight can increase the risk of developing conditions like malnutrition, diabetes, heart disease, and certain types of cancer.

It is important to note that body weight alone may not provide a complete picture of an individual's health, as it does not account for factors such as muscle mass, bone density, or body composition. Therefore, healthcare professionals often use additional measures, such as body mass index (BMI), waist circumference, and blood tests, to assess overall health status more comprehensively.

1,2-Dimethylhydrazine is a chemical compound with the formula (CH3)2N-NH2. It is a colorless liquid with an ammonia-like odor. It is used in research and industry as a reducing agent and a rocket fuel component. It is also a potent carcinogen and is harmful if swallowed, inhaled, or comes into contact with the skin. Long-term exposure can lead to cancer, particularly of the liver and digestive system.

Sulindac is a non-steroidal anti-inflammatory drug (NSAID) that is used to treat pain, inflammation, and fever. It works by inhibiting the activity of cyclooxygenase (COX) enzymes, which are involved in the production of prostaglandins, chemicals that contribute to inflammation and pain.

Sulindac is a prodrug, meaning that it is converted into its active form, sulindac sulfide, in the body. Sulindac sulfide has both analgesic (pain-relieving) and anti-inflammatory effects, making it useful for treating conditions such as osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis.

Like other NSAIDs, sulindac can cause side effects such as stomach ulcers, bleeding, and kidney damage, especially when taken at high doses or for long periods of time. It should be used with caution in people with a history of gastrointestinal (GI) problems, kidney disease, or liver disease.

It is important to note that this information is intended to supplement, not substitute for, the expertise and judgment of healthcare professionals. It is always recommended to consult with a doctor or pharmacist for medical advice.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

Experimental neoplasms refer to abnormal growths or tumors that are induced and studied in a controlled laboratory setting, typically in animals or cell cultures. These studies are conducted to understand the fundamental mechanisms of cancer development, progression, and potential treatment strategies. By manipulating various factors such as genetic mutations, environmental exposures, and pharmacological interventions, researchers can gain valuable insights into the complex processes underlying neoplasm formation and identify novel targets for cancer therapy. It is important to note that experimental neoplasms may not always accurately represent human cancers, and further research is needed to translate these findings into clinically relevant applications.

... (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 (PubChem ID (CID) same as Wikidata, Articles needing additional references ...
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. ...
... azoxymethane are suspected to be genotoxic. IUPAC, Compendium of Chemical Terminology, 2nd ed. (the "Gold Book") (1997). Online ...
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 ...
... in while performing experiments in azoxymethane treated mice. The findings of the study found "...tumorigenesis by altering ...
... 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 ...
... mice were treated with dextran sulfate sodium to produce colitis and an intraperitoneal injection of azoxymethane, a colon ...
... 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, exact mass: 74.0480 u) may refer to: Azoxymethane (AOM) Glycinamide N- ...
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 (PubChem ID (CID) same as Wikidata, Articles needing additional references ...
Dietary cooked navy beans and their fractions attenuate colon carcinogenesis in azoxymethane-induced mice.Jan 01, 2008. ... Dry beans inhibit azoxymethane-induced colon carcinogenesis in rats.Dec 01, 1997. ...
Sepporta, M.V.; Fuccelli, R.; Rosignoli, P.; Ricci, G.; Servili, M. Oleuropein prevents azoxymethane-induced colon crypt dys- ... it prevented azoxymethane (AOM)-induced colon cancer and, in addition, reduced DNA damage in peripheral leukocytes [117]. ...
High fat diet-induced obesity increases the formation of colon polyps induced by azoxymethane in mice. Ann. Transl. Med. 3:679 ... High fat diet-induced obesity increases the formation of colon polyps induced by azoxymethane in mice. Ann. Transl. Med. 3:679 ... Enhancement of development of azoxymethane-induced colonic premalignant lesions in C57BL/KsJ-db/db mice. Carcinogenesis 25:5821 ... Enhancement of development of azoxymethane-induced colonic premalignant lesions in C57BL/KsJ-db/db mice. Carcinogenesis 25:5821 ...
Azoxymethane alters the plasma metabolome to a greater extent in mice fed a high fat diet compared to an AIN-93 diet - (Peer ... Azoxymethane alters the plasma metabolome to a greater extent in mice fed a high fat diet compared to an AIN-93 diet. ...
Yoshitani, S. I., Tanaka, T., Kohno, H., and Takashima, S. Chemoprevention of azoxymethane-induced rat colon carcinogenesis by ...
Chemopreventive Potential of Select Herbal Teas and Spices on Azoxymethane-Induced Aberrant Crypt Foci in Fisher 344 Male Rats ...
Yang K, Lamprecht SA, Liu Y. Chemoprevention studies of the flavonoids quercetin and rutin in normal and azoxymethane-treated ...
... azoxymethane, methylazoxymethanol, bis (2-oxopropyl) nitrosamine, benzopyrene, 1 methyl-1-nitrosourea and n-methyl-n-nitro- ...
... azoxymethane-induced colon carcinogenesis and decreased colonic and tumor phospholipase A2, phospholipase CyI, and PGE2 levels ... curcumin to rats inhibited azoxymethane-induced colon carcinogenesis and decreased colonic and tumor phospholipase A2, ...
In this context, other chemopreventive agents with antioxidant properties have been found to inhibit DMH and azoxymethane- ... Modifying effects of naturally occurring products on the development of colonic aberrant crypt foci induced by azoxymethane in ...
Inositol Hexaphosphate Inhibits Large Intestinal Cancer in F344 Rats 5 Months After Induction by Azoxymethane. Carcinogenesis. ...
BC supplementation inhibited tumor formation and the expression of M2 macrophage markers in an azoxymethane/dextran sodium ...
... are determined against colitis-associated mouse colon tumorigenesis induced by azoxymethane (AOM) and dextran sulfate sodium ( ...
Through this mechanism it was demonstrated that oroxylin A inhibits colitis-associated carcinogenesis in an azoxymethane/ ...
Given these unique attributes, we investigated the impact of enteric glia depletion on tumor development in azoxymethane/ ...
Methods: BALB/c mice with azoxymethane/dextran sodium sulfate (AOM/DSS)-induced colitis-associated colorectal cancer (CAC), we ... Methods: BALB/c mice with azoxymethane/dextran sodium sulfate (AOM/DSS)-induced colitis-associated colorectal cancer (CAC), we ... Methods: BALB/c mice with azoxymethane/dextran sodium sulfate (AOM/DSS)-induced colitis-associated colorectal cancer (CAC), we ...
... and a mouse model for colitis-induced colorectal tumors triggered by azoxymethane (AOM)/dextran sodium sulfate (DSS) treatment ...
Otsuka, K., Isobe, J., Asai, Y., Nakano, T., Hattori, K., Ariyoshi, T., Yamashita, T., Motegi, K., Saito, A., Kohmoto, M., Hosonuma, M., Kuramasu, A., Baba, Y., Murayama, M., Narikawa, Y., Toyoda, H., Funayama, E., Tajima, K., Shida, M., Hirasawa, Y., & 17 othersTsurui, T., Ariizumi, H., Ishiguro, T., Suzuki, R., Ohkuma, R., Kubota, Y., Sambe, T., Tsuji, M., Wada, S., Kiuchi, Y., Kobayashi, S., Horiike, A., Goto, S., Murakami, M., Kim, Y. G., Tsunoda, T. & Yoshimura, K., 2024 Feb, In: Cancer Immunology, Immunotherapy. 73, 2, 23.. Research output: Contribution to journal › Article › peer-review ...
Abbreviations: AMBRA1: autophagy and beclin 1 regulator 1; AOM: azoxymethane; ATG5: autophagy related 5; ATG7: autophagy ...
Evaluation of potential role of catharanthus roseus and acanthus ilicifolius in the prevention of azoxymethane-induced aberrant ... ilicifolius against azoxymethane (AOM) induced colonic aberrant crypt foci (ACF) in rats. The bioactivities of the crude ... Evaluation of potential role of catharanthus roseus and acanthus ilicifolius in the prevention of azoxymethane-induced aberrant ...
Inhibition of azoxymethane-induced colon cancer by orange juice. Nutr Cancer 36(2):224-229. ...
The Effect of Omega-3 Rich Fish Oil on the Kidney Changes in Mice Induced by Azoxymethane and Dextran Sodium Sulfate. 1 year 7 ...
were used azoxymethane to induce aberrant crypt loci in rats. They found that Bifidobacteria could inhibit colon carcinogenesis ... Inhibitory effect of Bifidobacterium longum cultures on the azoxymethane-induced aberrant crypt foci formation and fecal ... several metabolites that could influence the function of P450s and afterward have an effect on the conversion of azoxymethane ( ...
This graph shows the total number of publications written about "Diamide" by people in Harvard Catalyst Profiles by year, and whether "Diamide" was a major or minor topic of these publication ...
Effects of konjac glucomannan, inulin and cellulose on acute colonic responses to genotoxic azoxymethane,FOOD CHEMISTRY, vol. ...
Kimchi protects against azoxymethane/destran sulfate sodium-induced colorectal carcinogenesis in mice. J Med Food. 2014;17(8): ... Femia AP, Dolara P, Caderni G. Mucin-depleted foci (MDF) in the colon of rats treated with azoxymethane (AOM) are useful ... Beef meat and blood sausage promote the formation of azoxymethane-induced mucin-depleted foci and aberrant crypt foci in rat ...
2-related Factor 2 Knockout Suppresses the Development of Aggressive Colorectal Cancer Formation Induced by Azoxymethane/ ...
... non-tumor areas of azoxymethane/dextran sodium sulfate mice had less inflammation than those of CD4-dnTGFßRII/azoxymethane mice ... Although feasibility and reproducibility of azoxymethane/CD4-dbTGFßRII appear to be disadvantages compared to the azoxymethane/ ... METHODS: Azoxymethane (AOM)-treated, ApcMin/+ and germ-free mice were gavaged with feces from obese individuals and control ... The azoxymethane (AOM)/dextran sodium sulfate (DSS) mouse model reproduces human colitis-associated colorectal cancer. To ...
  • In vivo, BC supplementation inhibited tumor formation and the expression of M2 macrophage markers in an azoxymethane/dextran sodium sulfate-induced colitis-associated CRC mouse model. (physiciansweekly.com)
  • Methods: BALB/c mice with azoxymethane/dextran sodium sulfate (AOM/DSS)-induced colitis-associated colorectal cancer (CAC), we intraperitoneally treated with commercial preparation of human plasma AAT (4 mg per mouse). (lu.se)
  • METHODS: To investigate the effect of astragaloside IV against CAC and the underlying mechanism, C57 mice were treated with (20, 40, 80 mg/kg) astragaloside IV while CAC was induced by intraperitoneal injection of 10 mg/kg azoxymethane (AOM) and ad libitum consumption of 2% dextran sulfate sodium salt (DSS). (bvsalud.org)
  • The aim of current research is to assess the chemoprotective outcomes of ethanolic extracts of C. roseus and A. ilicifolius against azoxymethane (AOM) induced colonic aberrant crypt foci (ACF) in rats. (um.edu.my)
  • We also examined whether lactic acid bacteria increased the production of the cancer-specific anti-tumor cytokine, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), in human, and examined whether the RB-reactivating drinks with lactic acid bacteria decreased azoxymethane-induced rat colon aberrant crypt foci (ACF) and aberrant crypts (ACs) in vivo. (bvsalud.org)
  • In the present study, we developed a novel mouse model of malignant lesions in the biliary ducts induced by the administration of the carcinogen azoxymethane to obese C57BLKS/J-db/db mice. (bvsalud.org)
  • Consequently, we assessed the role of aberrant DNA methylation in the azoxymethane (AOM) rodent model of colon cancer. (nih.gov)
  • The effects of dietary selenomethionine on polyamines and azoxymethane-induced aberrant crypts. (nih.gov)
  • 1. Varying effect of dietary lipids and azoxymethane on early stages of colon carcinogenesis: enumeration of aberrant crypt foci and proliferative indices. (nih.gov)
  • 11. Ursodeoxycholic acid and F(6)-D(3) inhibit aberrant crypt proliferation in the rat azoxymethane model of colon cancer: roles of cyclin D1 and E-cadherin. (nih.gov)
  • 16. Diosgenin, a steroid saponin of Trigonella foenum graecum (Fenugreek), inhibits azoxymethane-induced aberrant crypt foci formation in F344 rats and induces apoptosis in HT-29 human colon cancer cells. (nih.gov)
  • 2008 The mouse style of colitis-associated cancer of the colon (CAC) which can be induced by administration of azoxymethane (AOM) accompanied by repeated dental administration of dextran sulfate sodium (DSS) continues to be highly informative. (biodiversityhotspot.org)
  • We all show aspects of your inflammasome are shielding throughout acute as well as recurring colitis as well as CAC within the dextran sulfate salt (DSS) and also azoxymethane + DSS types. (mek-inhibitors.com)
  • We evaluated the effects of dietary selenomethionine supplementation on colonic polyamine levels and the ability of L-selenomethionine supplementation to modulate the carcinogenic activity of azoxymethane (AOM) in the rat colon. (nih.gov)
  • At 5 and 6 weeks, the rats received 2 subcutaneous injections of azoxymethane. (medscape.com)
  • 13. Molecular changes in the early stage of colon carcinogenesis in rats treated with azoxymethane. (nih.gov)
  • 14. Effects of adlay on azoxymethane-induced colon carcinogenesis in rats. (nih.gov)
  • 20. Mucin-depleted foci (MDF) in the colon of rats treated with azoxymethane (AOM) are useful biomarkers for colon carcinogenesis. (nih.gov)
  • 4. Tan BL, Norhaizan ME, Huynh K, Heshu SR, Yeap, SK, Hazilawati, H, Roselina, K (2015) Water extract of brewers' rice induces apoptosis in human colorectal cancer cells via activation of caspase-3 and caspase-8 and downregulates the Wnt/β-catenin downstream signaling pathway in brewers' rice-treated rats with azoxymethane-induced colon carc. (ijrr.com)
  • Their more recent studies reported on the first intestinally targeted PPARD overexpression model, which showed the profound impact of PPARD on azoxymethane-induced colonic carcinogenesis and gastric carcinogenesis. (umich.edu)
  • The researchers investigated the effect of folic acid supplementation on colorectal cancer risk in the offspring of an azoxymethane rat model of colorectal cancer. (medscape.com)