Carcinogens environmental. Medical search

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.

A class of compounds that contain a -NH2 and a -NO radical. Many members of this group have carcinogenic and mutagenic properties.

A hepatic carcinogen whose mechanism of activation involves N-hydroxylation to the aryl hydroxamic acid followed by enzymatic sulfonation to sulfoxyfluorenylacetamide. It is used to study the carcinogenicity and mutagenicity of aromatic amines.

A potent mutagen and carcinogen. It is a public health concern because of its possible effects on industrial workers, as an environmental pollutant, an as a component of tobacco smoke.

Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes.

A class of chemicals that contain an anthracene ring with a naphthalene ring attached to it.

The products of chemical reactions that result in the addition of extraneous chemical groups to DNA.

Tests to experimentally measure the tumor-producing/cancer cell-producing potency of an agent by administering the agent (e.g., benzanthracenes) and observing the quantity of tumors or the cell transformation developed over a given period of time. The carcinogenicity value is usually measured as milligrams of agent administered per tumor developed. Though this test differs from the DNA-repair and bacterial microsome MUTAGENICITY TESTS, researchers often attempt to correlate the finding of carcinogenicity values and mutagenicity values.

An alkylating agent that forms DNA ADDUCTS at the C-8 position in GUANINE, resulting in single strand breaks. It has demonstrated carcinogenic action.

7,12-Dimethylbenzanthracene. Polycyclic aromatic hydrocarbon found in tobacco smoke that is a potent carcinogen.

Tests of chemical substances and physical agents for mutagenic potential. They include microbial, insect, mammalian cell, and whole animal tests.

A nitrosourea compound with alkylating, carcinogenic, and mutagenic properties.

The combination of two or more different factors in the production of cancer.

Biphenyl compounds substituted in any position by one or more amino groups. Permitted are any substituents except fused rings.

A potent mutagen and carcinogen. This compound and its metabolite 4-HYDROXYAMINOQUINOLINE-1-OXIDE bind to nucleic acids. It inactivates bacteria but not bacteriophage.

7,8,8a,9a-Tetrahydrobenzo(10,11)chryseno (3,4-b)oxirene-7,8-diol. A benzopyrene derivative with carcinogenic and mutagenic activity.

The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alterations may be divided into METABOLIC DETOXICATION, PHASE I and METABOLIC DETOXICATION, PHASE II.

Four fused benzyl rings with three linear and one angular, that can be viewed as a benzyl-phenanthrenes. Compare with NAPHTHACENES which are four linear rings.

A nitrosoguanidine derivative with potent mutagenic and carcinogenic properties.

Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms.

Compounds consisting of two or more fused ring structures.

A nitrosamine derivative with alkylating, carcinogenic, and mutagenic properties. It causes serious liver damage and is a hepatocarcinogen in rodents.

A very potent liver carcinogen.

A reagent used mainly to induce experimental liver cancer. According to the Fourth Annual Report on Carcinogens (NTP 85-002, p. 89) published in 1985, this compound "may reasonably be anticipated to be a carcinogen." (Merck, 11th ed)

A family of diphenylenemethane derivatives.

Experimentally induced tumors of the LIVER.

A potent hepatotoxic and hepatocarcinogenic mycotoxin produced by the Aspergillus flavus group of fungi. It is also mutagenic, teratogenic, and causes immunosuppression in animals. It is found as a contaminant in peanuts, cottonseed meal, corn, and other grains. The mycotoxin requires epoxidation to aflatoxin B1 2,3-oxide for activation. Microsomal monooxygenases biotransform the toxin to the less toxic metabolites aflatoxin M1 and Q1.

A N-hydroxylated derivative of 2-ACETYLAMINOFLUORENE that has demonstrated carcinogenic action.

1,2-Benzphenanthrenes. POLYCYCLIC COMPOUNDS obtained from coal tar.

Quinolines substituted in any position by one or more nitro groups.

A nitrosamine derivative with alkylating, carcinogenic, and mutagenic properties.

A carcinogen that is often used in experimental cancer studies.

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.

A transferase that catalyzes the addition of aliphatic, aromatic, or heterocyclic FREE RADICALS as well as EPOXIDES and arene oxides to GLUTATHIONE. Addition takes place at the SULFUR. It also catalyzes the reduction of polyol nitrate by glutathione to polyol and nitrite.

Agents that reduce the frequency or rate of spontaneous or induced tumors independently of the mechanism involved.

Pathological processes that tend eventually to become malignant. (From Dorland, 27th ed)

Benzopyrenes saturated in any two adjacent positions and substituted with two hydroxyl groups in any position. The majority of these compounds have carcinogenic or mutagenic activity.

Furano-furano-benzopyrans that are produced by ASPERGILLUS from STERIGMATOCYSTIN. They are structurally related to COUMARINS and easily oxidized to an epoxide form to become ALKYLATING AGENTS. Members of the group include AFLATOXIN B1; aflatoxin B2, aflatoxin G1, aflatoxin G2; AFLATOXIN M1; and aflatoxin M2.

A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).

A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.

Antineoplastic agent that is also used as a veterinary anesthetic. It has also been used as an intermediate in organic synthesis. Urethane is suspected to be a carcinogen.

A major group of unsaturated cyclic hydrocarbons containing two or more rings. The vast number of compounds of this important group, derived chiefly from petroleum and coal tar, are rather highly reactive and chemically versatile. The name is due to the strong and not unpleasant odor characteristic of most substances of this nature. (From Hawley's Condensed Chemical Dictionary, 12th ed, p96)

Tumors or cancer of the LUNG.

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 potent carcinogen and neurotoxic compound. It is particularly effective in inducing colon carcinomas.

An enzyme that catalyzes the transfer of acetyl groups from ACETYL-COA to arylamines. It can also catalyze acetyl transfer between arylamines without COENZYME A and has a wide specificity for aromatic amines, including SEROTONIN. However, arylamine N-acetyltransferase should not be confused with the enzyme ARYLALKYLAMINE N-ACETYLTRANSFERASE which is also referred to as SEROTONIN ACETYLTRANSFERASE.

Very toxic industrial chemicals. They are absorbed through the skin, causing lethal blood, bladder, liver, and kidney damage and are potent, broad-spectrum carcinogens in most species.

A liver microsomal cytochrome P-450 monooxygenase capable of biotransforming xenobiotics such as polycyclic hydrocarbons and halogenated aromatic hydrocarbons into carcinogenic or mutagenic compounds. They have been found in mammals and fish. This enzyme, encoded by CYP1A1 gene, can be measured by using ethoxyresorufin as a substrate for the ethoxyresorufin O-deethylase activity.

Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.

Reduction of pharmacologic activity or toxicity of a drug or other foreign substance by a living system, usually by enzymatic action. It includes those metabolic transformations that make the substance more soluble for faster renal excretion.

New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.

A member of the BENZODIOXOLES that is a constituent of several VOLATILE OILS, notably SASSAFRAS oil. It is a precursor in the synthesis of the insecticide PIPERONYL BUTOXIDE and the drug N-methyl-3,4-methylenedioxyamphetamine (MDMA).

An effective soil fumigant, insecticide, and nematocide. In humans, it causes severe burning of skin and irritation of the eyes and respiratory tract. Prolonged inhalation may cause liver necrosis. It is also used in gasoline. Members of this group have caused liver and lung cancers in rodents. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), 1,2-dibromoethane may reasonably be anticipated to be a carcinogen.

Experimentally induced mammary neoplasms in animals to provide a model for studying human BREAST NEOPLASMS.

Inhaling and exhaling the smoke of burning TOBACCO.

The aglycone of CYCASIN. It acts as a potent carcinogen and neurotoxin and inhibits hepatic DNA, RNA, and protein synthesis.

Hydrazines substituted by one or more methyl groups in any position.

A cytochrome P450 enzyme subtype that has specificity for relatively planar heteroaromatic small molecules, such as CAFFEINE and ACETAMINOPHEN.

A superfamily of hundreds of closely related HEMEPROTEINS found throughout the phylogenetic spectrum, from animals, plants, fungi, to bacteria. They include numerous complex monooxygenases (MIXED FUNCTION OXYGENASES). In animals, these P-450 enzymes serve two major functions: (1) biosynthesis of steroids, fatty acids, and bile acids; (2) metabolism of endogenous and a wide variety of exogenous substrates, such as toxins and drugs (BIOTRANSFORMATION). They are classified, according to their sequence similarities rather than functions, into CYP gene families (>40% homology) and subfamilies (>59% homology). For example, enzymes from the CYP1, CYP2, and CYP3 gene families are responsible for most drug metabolism.

A circumscribed benign epithelial tumor projecting from the surrounding surface; more precisely, a benign epithelial neoplasm consisting of villous or arborescent outgrowths of fibrovascular stroma covered by neoplastic cells. (Stedman, 25th ed)

A highly poisonous compound used widely in the manufacture of plastics, adhesives and synthetic rubber.

A large group of cytochrome P-450 (heme-thiolate) monooxygenases that complex with NAD(P)H-FLAVIN OXIDOREDUCTASE in numerous mixed-function oxidations of aromatic compounds. They catalyze hydroxylation of a broad spectrum of substrates and are important in the metabolism of steroids, drugs, and toxins such as PHENOBARBITAL, carcinogens, and insecticides.

The exposure to potentially harmful chemical, physical, or biological agents that occurs as a result of one's occupation.

The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals.

A genus of the family Muridae having three species. The present domesticated strains were developed from individuals brought from Syria. They are widely used in biomedical research.

Organic compounds with the general formula R-NCS.

A group of compounds derived from ammonia by substituting organic radicals for the hydrogens. (From Grant & Hackh's Chemical Dictionary, 5th ed)

Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases.

A gas that has been used as an aerosol propellant and is the starting material for polyvinyl resins. Toxicity studies have shown various adverse effects, particularly the occurrence of liver neoplasms.

The relationship between the dose of an administered drug and the response of the organism to the drug.

A trace element that plays a role in glucose metabolism. It has the atomic symbol Cr, atomic number 24, and atomic weight 52. According to the Fourth Annual Report on Carcinogens (NTP85-002,1985), chromium and some of its compounds have been listed as known carcinogens.

Derivatives of GLUCURONIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that include the 6-carboxy glucose structure.

Tumors or cancer of the URINARY BLADDER.

A nucleoside consisting of the base guanine and the sugar deoxyribose.

Salts of chromic acid containing the CrO(2-)4 radical.

Disinfectant used in vapor form to sterilize vaccines, grafts, etc. The vapor is very irritating and the liquid form is carcinogenic.

A plant genus of the family SOLANACEAE. Members contain NICOTINE and other biologically active chemicals; its dried leaves are used for SMOKING.

Family of retrovirus-associated DNA sequences (ras) originally isolated from Harvey (H-ras, Ha-ras, rasH) and Kirsten (K-ras, Ki-ras, rasK) murine sarcoma viruses. Ras genes are widely conserved among animal species and sequences corresponding to both H-ras and K-ras genes have been detected in human, avian, murine, and non-vertebrate genomes. The closely related N-ras gene has been detected in human neuroblastoma and sarcoma cell lines. All genes of the family have a similar exon-intron structure and each encodes a p21 protein.

A naphthalene derivative with carcinogenic action.

The art or practice of preparing food. It includes the preparation of special foods for diets in various diseases.

Tumors or cancer of the COLON.

The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.

Tumors or cancer of the SKIN.

Toxic, volatile, flammable liquid hydrocarbon byproduct of coal distillation. It is used as an industrial solvent in paints, varnishes, lacquer thinners, gasoline, etc. Benzene causes central nervous system damage acutely and bone marrow damage chronically and is carcinogenic. It was formerly used as parasiticide.

An ethanol-inducible cytochrome P450 enzyme that metabolizes several precarcinogens, drugs, and solvents to reactive metabolites. Substrates include ETHANOL; INHALATION ANESTHETICS; BENZENE; ACETAMINOPHEN and other low molecular weight compounds. CYP2E1 has been used as an enzyme marker in the study of alcohol abuse.

Mixture of 2- and 3-tert-butyl-4-methoxyphenols that is used as an antioxidant in foods, cosmetics, and pharmaceuticals.

The covalent bonding of an alkyl group to an organic compound. It can occur by a simple addition reaction or by substitution of another functional group.

Used in the form of its salts as a dye and as an intermediate in manufacture of Acid Yellow, diazo dyes, and indulines.

A barbituric acid derivative that acts as a nonselective central nervous system depressant. It potentiates GAMMA-AMINOBUTYRIC ACID action on GABA-A RECEPTORS, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations.

A colorless and flammable gas at room temperature and pressure. Ethylene oxide is a bactericidal, fungicidal, and sporicidal disinfectant. It is effective against most micro-organisms, including viruses. It is used as a fumigant for foodstuffs and textiles and as an agent for the gaseous sterilization of heat-labile pharmaceutical and surgical materials. (From Reynolds, Martindale The Extra Pharmacopoeia, 30th ed, p794)

Inorganic salts or organic esters of arsenious acid.

A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.

Organic compounds that include a cyclic ether with three ring atoms in their structure. They are commonly used as precursors for POLYMERS such as EPOXY RESINS.

The N-glucuronide conjugate of cotinine is a major urinary metabolite of NICOTINE. It thus serves as a biomarker of exposure to tobacco SMOKING. It has CNS stimulating properties.

A shiny gray element with atomic symbol As, atomic number 33, and atomic weight 75. It occurs throughout the universe, mostly in the form of metallic arsenides. Most forms are toxic. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), arsenic and certain arsenic compounds have been listed as known carcinogens. (From Merck Index, 11th ed)

Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).

A nitrosourea compound with alkylating, carcinogenic, and mutagenic properties.

Closed vesicles of fragmented endoplasmic reticulum created when liver cells or tissue are disrupted by homogenization. They may be smooth or rough.

A colorless, odorless, highly water soluble vinyl monomer formed from the hydration of acrylonitrile. It is primarily used in research laboratories for electrophoresis, chromatography, and electron microscopy and in the sewage and wastewater treatment industries.

An acid-base indicator which is colorless in acid solution, but turns pink to red as the solution becomes alkaline. It is used medicinally as a cathartic.

Regular course of eating and drinking adopted by a person or animal.

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.

Tumor suppressor genes located on the short arm of human chromosome 17 and coding for the phosphoprotein p53.

A method of measuring the effects of a biologically active substance using an intermediate in vivo or in vitro tissue or cell model under controlled conditions. It includes virulence studies in animal fetuses in utero, mouse convulsion bioassay of insulin, quantitation of tumor-initiator systems in mouse skin, calculation of potentiating effects of a hormonal factor in an isolated strip of contracting stomach muscle, etc.

Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.

Tumors or cancer of the LIVER.

A derivative of acetic acid, N(CH2COOH)3. It is a complexing (sequestering) agent that forms stable complexes with Zn2+. (From Miall's Dictionary of Chemistry, 5th ed.)

A flavoprotein that reversibly catalyzes the oxidation of NADH or NADPH by various quinones and oxidation-reduction dyes. The enzyme is inhibited by dicoumarol, capsaicin, and caffeine.

A potent nitrofuran derivative tumor initiator. It causes bladder tumors in all animals studied and is mutagenic to many bacteria.

Elements of limited time intervals, contributing to particular results or situations.

Carcinogenic nitrosamine that may be formed from preservatives in meats during their preparation or in the liver during metabolism.

Diseases caused by factors involved in one's employment.

Induction and quantitative measurement of chromosomal damage leading to the formation of micronuclei (MICRONUCLEI, CHROMOSOME-DEFECTIVE) in cells which have been exposed to genotoxic agents or IONIZING RADIATION.

An increase in the rate of synthesis of an enzyme due to the presence of an inducer which acts to derepress the gene responsible for enzyme synthesis.

Nitro-phenanthrenes occurring in ARISTOLOCHIACEAE and other plants. They derive from stephanine (APORPHINES) by oxidative ring cleavage. The nitro group is a reactive alkylator (ALKYLATING AGENTS) that binds to biological macromolecules. Ingestion by humans is associated with nephropathy (NEPHRITIS). There is no relationship to the similar named aristolochene (SESQUITERPENES).

Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke.

The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.

The presence in food of harmful, unpalatable, or otherwise objectionable foreign substances, e.g. chemicals, microorganisms or diluents, before, during, or after processing or storage.

Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.

A group of compounds that are derivatives of methoxybenzene and contain the general formula R-C7H7O.

A di-tert-butyl PHENOL with antioxidant properties.

A benign epithelial tumor with a glandular organization.

Agents that reduce the frequency or rate of spontaneous or induced mutations independently of the mechanism involved.

Substances or energies, for example heat or light, which when introduced into the air, water, or land threaten life or health of individuals or ECOSYSTEMS.

Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.

An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.

A 4-hydroxylated metabolite of AFLATOXIN B1, one of the MYCOTOXINS from ASPERGILLUS tainted food. It is associated with LIVER damage and cancer resulting from its P450 activation to the epoxide which alkylates DNA. Toxicity depends on the balance of liver enzymes that activate it (CYTOCHROME P-450) and others that detoxify it (GLUTATHIONE S TRANSFERASE) (Pharmac Ther 50.443 1991). Primates & rat are sensitive while mouse and hamster are tolerant (Canc Res 29.236 1969).

A group of condensed ring hydrocarbons.

Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.

Contamination of the air by tobacco smoke.

Aromatic diamine used in the plastics industry as curing agent for epoxy resins and urethane rubbers. It causes bladder, liver, lung, and other neoplasms.

The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.

Plants or plant parts which are harmful to man or other animals.

Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.

A family of enzymes accepting a wide range of substrates, including phenols, alcohols, amines, and fatty acids. They function as drug-metabolizing enzymes that catalyze the conjugation of UDPglucuronic acid to a variety of endogenous and exogenous compounds. EC 2.4.1.17.

That portion of the electromagnetic spectrum immediately below the visible range and extending into the x-ray frequencies. The longer wavelengths (near-UV or biotic or vital rays) are necessary for the endogenous synthesis of vitamin D and are also called antirachitic rays; the shorter, ionizing wavelengths (far-UV or abiotic or extravital rays) are viricidal, bactericidal, mutagenic, and carcinogenic and are used as disinfectants.

Tumors, cancer or other neoplasms produced by exposure to ionizing or non-ionizing radiation.

Negative ions or salts derived from bromic acid, HBrO3.

A malignant epithelial tumor with a glandular organization.

Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.

Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.

Asbestos. Fibrous incombustible mineral composed of magnesium and calcium silicates with or without other elements. It is relatively inert chemically and used in thermal insulation and fireproofing. Inhalation of dust causes asbestosis and later lung and gastrointestinal neoplasms.

Inorganic compounds that contain sodium as an integral part of the molecule.

Preclinical testing of drugs in experimental animals or in vitro for their biological and toxic effects and potential clinical applications.

Enzymes that catalyze reversibly the formation of an epoxide or arene oxide from a glycol or aromatic diol, respectively.

Products of the hydrolysis of chlorophylls in which the phytic acid side chain has been removed and the carboxylic acids saponified.

A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)

The monitoring of the level of toxins, chemical pollutants, microbial contaminants, or other harmful substances in the environment (soil, air, and water), workplace, or in the bodies of people and animals present in that environment.

A chemical by-product that results from burning or incinerating chlorinated industrial chemicals and other hydrocarbons. This compound is considered an environmental toxin, and may pose reproductive, as well as, other health risks for animals and humans.

A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.

An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.

An enzyme, sometimes called GGT, with a key role in the synthesis and degradation of GLUTATHIONE; (GSH, a tripeptide that protects cells from many toxins). It catalyzes the transfer of the gamma-glutamyl moiety to an acceptor amino acid.

Organic derivatives of thiocyanic acid which contain the general formula R-SCN.

Air pollutants found in the work area. They are usually produced by the specific nature of the occupation.

Procedures, such as TISSUE CULTURE TECHNIQUES; mathematical models; etc., when used or advocated for use in place of the use of animals in research or diagnostic laboratories.

Isocoumarins found in ASPERGILLUS OCHRACEUS and other FUNGI. Ochratoxin contaminated FOOD has been responsible for cases of FOODBORNE DISEASES.

A musculomembranous sac along the URINARY TRACT. URINE flows from the KIDNEYS into the bladder via the ureters (URETER), and is held there until URINATION.

Established cell cultures that have the potential to propagate indefinitely.

Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.

A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases.

Tumors or cancer of the INTESTINES.

Tumors or cancer of the NOSE.

Artifactual vesicles formed from the endoplasmic reticulum when cells are disrupted. They are isolated by differential centrifugation and are composed of three structural features: rough vesicles, smooth vesicles, and ribosomes. Numerous enzyme activities are associated with the microsomal fraction. (Glick, Glossary of Biochemistry and Molecular Biology, 1990; from Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)

The exposure to potentially harmful chemical, physical, or biological agents by inhaling them.

The qualitative or quantitative estimation of the likelihood of adverse effects that may result from exposure to specified health hazards or from the absence of beneficial influences. (Last, Dictionary of Epidemiology, 1988)

An exchange of segments between the sister chromatids of a chromosome, either between the sister chromatids of a meiotic tetrad or between the sister chromatids of a duplicated somatic chromosome. Its frequency is increased by ultraviolet and ionizing radiation and other mutagenic agents and is particularly high in BLOOM SYNDROME.

MAMMARY GLANDS in the non-human MAMMALS.

Exchange of substances between the maternal blood and the fetal blood at the PLACENTA via PLACENTAL CIRCULATION. The placental barrier excludes microbial or viral transmission.

The science concerned with the detection, chemical composition, and biological action of toxic substances or poisons and the treatment and prevention of toxic manifestations.

The use of chemical compounds to prevent the development of a specific disease.

An arsenical that has been used as a dermatologic agent and as an herbicide.

The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.

Defective nuclei produced during the TELOPHASE of MITOSIS or MEIOSIS by lagging CHROMOSOMES or chromosome fragments derived from spontaneous or experimentally induced chromosomal structural changes.

Hydrazine substituted by one methyl group.

A genotoxicological technique for measuring DNA damage in an individual cell using single-cell gel electrophoresis. Cell DNA fragments assume a "comet with tail" formation on electrophoresis and are detected with an image analysis system. Alkaline assay conditions facilitate sensitive detection of single-strand damage.

Viscous materials composed of complex, high-molecular-weight compounds derived from the distillation of petroleum or the destructive distillation of wood or coal. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.

Ring compounds having atoms other than carbon in their nuclei. (Grant & Hackh's Chemical Dictionary, 5th ed)

Tumors or cancer of the MOUTH.

The maximum exposure to a biologically active physical or chemical agent that is allowed during an 8-hour period (a workday) in a population of workers, or during a 24-hour period in the general population, which does not appear to cause appreciable harm, whether immediate or delayed for any period, in the target population. (From Lewis Dictionary of Toxicology, 1st ed)

Chemical compounds which pollute the water of rivers, streams, lakes, the sea, reservoirs, or other bodies of water.

The restriction of a characteristic behavior, anatomical structure or physical system, such as immune response; metabolic response, or gene or gene variant to the members of one species. It refers to that property which differentiates one species from another but it is also used for phylogenetic levels higher or lower than the species.

A group of pyrido-indole compounds. Included are any points of fusion of pyridine with the five-membered ring of indole and any derivatives of these compounds. These are similar to CARBAZOLES which are benzo-indoles.

A serotype of Salmonella enterica that is a frequent agent of Salmonella gastroenteritis in humans. It also causes PARATYPHOID FEVER.

A benzodiazepine used in the treatment of anxiety, alcohol withdrawal, and insomnia.

2-Amino-4-(ethylthio)butyric acid. An antimetabolite and methionine antagonist that interferes with amino acid incorporation into proteins and with cellular ATP utilization. It also produces liver neoplasms.

Elements, compounds, mixtures, or solutions that are considered severely harmful to human health and the environment. They include substances that are toxic, corrosive, flammable, or explosive.

Environmental factors as regulators and effectors of multistep carcinogenesis. (1/593)

This review highlights current knowledge of environmental factors in carcinogenesis and their cellular targets. The hypothesis that environmental factors influence carcinogenesis is widely supported by both epidemiological and experimental studies. The fact that only a small fraction of cancers can be attributed to germline mutations in cancer-related genes further buttresses the importance of environmental factors in carcinogenesis. Furthermore, penetrance of germline mutations may be modified by either environmental or other genetic factors. Examples of environmental factors that have been associated with increased cancer risk in the human population include chemical and physical mutagens (e.g. cigarette smoke, heterocyclic amines, asbestos and UV irradiation), infection by certain viral or bacterial pathogens, and dietary non-genotoxic constituents (e.g. macro- and micronutrients). Among molecular targets of environmental influences on carcinogenesis are somatic mutation (genetic change) and aberrant DNA methylation (epigenetic change) at the genomic level and post-translational modifications at the protein level. At both levels, changes elicited affect either the stability or the activity of key regulatory proteins, including oncoproteins and tumor suppressor proteins. Together, via multiple genetic and epigenetic lesions, environmental factors modulate important changes in the pathway of cellular carcinogenesis. (+info)

Heterocyclic aromatic amines induce DNA strand breaks and cell transformation. (2/593)

Heterocyclic aromatic amines (HAAs), formed during the cooking of foods, are known to induce tumours in rodent bioassays and may thus contribute to human cancer risk. We tested six HAAs in a morphological transformation assay and in three in vitro genotoxicity assays. The morphological transforming abilities of HAAs were tested, in the presence of rat-liver S9, in the C3H/M2 fibroblast cell line. Concentration levels of 50 microM 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (8-MeIQx), 100 microM 2-amino-3,4,8-trimethylimidazo-[4,5-f]quinoxaline (4,8-DiMeIQx), 50 microM 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 100 microM 2-amino-9H-pyrido[2,3-b]indole (AalphaC), 100 microM 2-amino-3-methyl-9H-pyrido[2,3-b]indole (MeAalphaC) and 15 microM 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) induced maximum transformation potencies of 5.5, 6.6, 6.3, 5.2, 7.3 and 9.2 transformed foci per 10(4) surviving cells, respectively. Bacterial mutagenic activity was determined in the presence of rat-liver S9 using the Salmonella typhimurium reverse-mutation assay employing strain YG1019. Mutagenic potencies of 3800 revertants (revs)/ng with 8-MeIQx, 2900 revs/ng with 4,8-DiMeIQx, 3480 revs/ng with IQ, 1.6 revs/ng with AalphaC, 2.9 revs/ng with MeAalphaC and 5 revs/ng with PhIP were observed. Clastogenic activity in vitro was analysed by the micronucleus assay in metabolically competent MCL-5 cells. Dose-dependent induction of micronuclei was observed for all HAAs tested with 1-5.4% of cells containing micronuclei at 10 ng/ml. Micronucleus induction was in the order 4,8-DiMeIQx > 8-MeIQx > IQ > MeAalphaC > PhIP > AalphaC. DNA strand-breaking activity in MCL-5 cells was measured by the alkaline single cell-gel (comet) assay. The lowest effect doses for significant increases (P < or = 0.0007, Mann-Whitney test) in comet tail length (microm) were 45.5 microg/ml (200 microM) for PhIP, 90.9 microg/ml (410-510 microM) for 4,8-DiMeIQx, IQ, MeAalphaC and AalphaC, and 454.5 microg/ml (2130 microM) for 8-MeIQx. It is not yet clear which of these assays most accurately reflects the genotoxic potential to humans of compounds of this class of environmental carcinogens. (+info)

Decreased expression of glutathione S-transferase M1 in HPV16-transfected human cervical keratinocytes in culture. (3/593)

Glutathione S-transferase (GST) M1 is a member of the GST mu family of cytosolic enzymes that have been hypothesized to catalyze the conjugation of glutathione to a large number of hydrophobic substances, including carcinogens such as polynuclear aromatic hydrocarbons present in tobacco smoke, leading to their excretion. Epidemiologic and experimental evidence suggests that the risk of cervical cancer is related to both human papillomavirus (HPV) infection and cigarette smoking. We compared the enzymatic activities and mRNA levels of GSTs in GSTM1-positive human cervical keratinocytes (HCKs) that had been transfected with HPV16 with those in the parental cells. The GSTM1 activity toward the substrate trans-stilbene oxide was 5- to 7-fold lower than in the parental cells. The relative mRNA level in HCK transfected with HPV16 E6/E7, as quantified by reverse transcriptase-polymerase chain reaction (RT-PCR) with normalization against endogenous glyceraldehyde-3-phosphate dehydrogenase (GAPDH) expression, was 6% that of the parental cells. It was 16 and 82%, respectively, in cells that were transfected with HPV16 E6 alone or HPV16 E7 alone. When quantified by competitive RT-PCR using an exogenous nuclease-resistant synthetic cyclophilin RNA transcript as control, the mRNA level in HCK transfected with HPV16 E6 was approximately 10-fold lower that that in the parental cells. It was approximately 5- to 7-fold lower in the HPV16 E7 or HPV16 E6/E7 cells. Our results suggest that viral infections, through the modulation of cellular xenobiotic-metabolizing enzymes, may play a role in the ability of cells to handle environmental carcinogens. (+info)

Histopathology and gene expression changes in rat liver during feeding of fumonisin B1, a carcinogenic mycotoxin produced by Fusarium moniliforme. (4/593)

Fumonisin B1 (FB1) is a carcinogenic mycotoxin produced by the fungus Fusarium moniliforme in corn. Feeding of FB1 to rats causes acute liver injury, chronic liver injury progressing to cirrhosis, and sometimes terminates in hepatocellular carcinoma or cholangiocarcinoma. This study describes the histolopathology and changes in gene expression in the rat liver during short-term feeding of FB1. Male Fischer rats were fed either FB1 250 mg/kg or control diet, and were killed weekly for 5 weeks. FB1 caused a predominantly zone 3 'toxic' liver injury, with hepatocyte death due to necrosis and apoptosis. Hepatocyte injury and death were mirrored by hepatic stellate cell proliferation and marked fibrosis, with progressive disturbance of architecture and formation of regenerative nodules. Despite ongoing hepatocyte mitotic activity, oval cell proliferation was noted from week 2, glutathione S-transferase pi-positive hepatic foci and nodules developed and, at later time points, oval cells were noted inside some of the 'atypical' nodules. Northern blot (mRNA) analysis of liver specimens from weeks 3 to 5 showed a progressive increase in gene expression for alpha-fetoprotein, hepatocyte growth factor, transforming growth factor alpha (TGF-alpha) and especially TGF-beta1 and c-myc. Immunostaining with LC(1-30) antibody demonstrated a progressive increase in expression of mature TGF-beta1 protein by hepatocytes over the 5 week feeding period. The overexpression of TGF-beta1 may be causally related to the prominent apoptosis and fibrosis seen with FB1-induced liver injury. Increased expression of c-myc may be involved in the cancer promoting effects of FB1. (+info)

Differential protection against benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide-induced DNA damage in HepG2 cells stably transfected with allelic variants of pi class human glutathione S-transferase. (5/593)

The pi class glutathione S-transferase (GSTP1-1), which is polymorphic in human populations, is believed to play an important role in detoxification of the ultimate carcinogen of widespread environmental pollutant benzo[a]pyrene [(+)-anti-benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide [(+)-anti-BPDE]]. The allelic variants of human GSTP1-1 (hGSTP1-1) differ in their structures by the amino acids in positions 104 (isoleucine or valine) and/or 113 (valine or alanine). Here, we have determined the protective effect of overexpression of allelic variants of hGSTP1-1, through stable transfection in HepG2 cells, against (+)-anti-BPDE-induced DNA modification. Clonal transfectants of HepG2 cells corresponding to the three allelic variants of hGSTP1-1 [(I104,A113), (V104,A113), and (V104,V113), denoted hGSTP1(IA), hGSTP1(VA), and hGSTP1(VV), respectively] with similar levels of hGSTP1 protein were identified and characterized for their GST activity and (+)-anti-BPDE-induced DNA modification. The glutathione S-transferase activity toward (+)-anti-BPDE was significantly higher (approximately 3.0-3.6-fold) in cells transfected with hGSTP1(VA) [HepG2(VA)] and hGSTP1(VV) [HepG2(VV)] compared with hGSTP1(IA) transfectant [HepG2(IA)]. The formation of (+)-anti-BPDE-DNA adducts was significantly reduced in HepG2(VA) and HepG2(VV) cells compared with cells transfected with insert-free vector (HepG2-vect). Maximum protection against (+)-anti-BPDE-induced DNA damage was afforded by the hGSTP1(VV) isoform. The results of this study indicate that the allelic variants of hGSTP1-1 significantly differ in their ability to provide protection against (+)-anti-BPDE-induced DNA damage. Thus, hGSTP1-1 polymorphism may be an important factor in differential susceptibility of individuals to tumorigenesis induced by benzo[a]pyrene. (+info)

Metabolic proficiency and benzo[a]pyrene DNA adduct formation in APCMin mouse adenomas and uninvolved mucosa. (6/593)

Tumour formation may involve interactions between genetic factors and environmental carcinogens. Adenoma formation in APCMin/+ mice is associated homozygous adenomatous polyposis coli (APC) gene mutation, but the effects on carcinogen susceptibility are unknown. This study tests the hypothesis that APCMin/+ adenoma formation is accompanied by changes in metabolic proficiency and carcinogen susceptibility. Cytochrome P450 (CYP)1A1/1A2, glutathione S-transferase (GST)alpha, mu and pi classes and DNA adduct formation were assayed in adenomas and uninvolved mucosa from APCMin/+ mice, before and after benzo[a]pyrene (B[a]P) treatment. In untreated adenomas and mucosa, CYP1A1/1A2 and B[a]P-DNA adducts were undetected but GSTalpha, mu and pi class enzymes were constitutively expressed. In adenomas, B[a]P only induced CYP1A1/1A2 to low level while GSTalpha and pi class enzymes were unaffected. A GST mu band which was absent from mucosa, was induced in adenomas. In mucosa, B[a]P induced CYP1A1/1A2 and GSTalpha and pi, to high levels. B[a]P-DNA adduct levels were 56 +/- 15/10(8) nucleotides (median +/- SE) in adenomas versus 89 +/- 19/10(8) nucleotides in mucosa (P < 0.0001). APCMin adenomas show reduced bioactivation capacity and sustain less DNA damage from B[a]P exposure, than APCMin uninvolved mucosa. These properties could influence mutagenesis and subsequent neoplastic transformation of adenomas. (+info)

Cytosine methylation in a CpG sequence leads to enhanced reactivity with Benzo[a]pyrene diol epoxide that correlates with a conformational change. (7/593)

Benzo[a]pyrene (B[a]P) is a widespread environmental carcinogen that must be activated by cellular metabolism to a diol epoxide form (BPDE) before it reacts with DNA. It has recently been shown that BPDE preferentially modifies the guanine in methylated 5'-CpG-3' sequences in the human p53 gene, providing one explanation for why these sites are mutational hot spots. Using purified duplex oligonucleotides containing identical methylated and unmethylated CpG sequences, we show here that BPDE preferentially modified the guanine in hemimethylated or fully methylated CpG sequences, producing between 3- and 8-fold more modification at this site. Analysis of this reaction using shorter duplex oligonucleotides indicated that it was the level of the (+)-trans isomer that was specifically increased. To determine if there were conformational differences between the methylated and unmethylated B[a]P-modified DNA sequences that may be responsible for this enhanced reactivity, a native polyacrylamide gel electrophoresis analysis was carried out using DNA containing isomerically pure B[a]P-DNA adducts. These experiments showed that each adduct resulted in an altered gel mobility in duplex DNA but that only the presence of a (+)-trans isomer and a methylated C 5' to the adduct resulted in a significant gel mobility shift compared with the unmethylated case. (+info)

Mutagenic activation of environmental carcinogens by microsomes of gastric mucosa with intestinal metaplasia. (8/593)

Coexpression of cytochrome P450 monooxygenases (CYPs) and reductase was found in human gastric mucosa with intestinal metaplasia. Immunohistochemistry showed reactivity to P450 reductase in metaplastic epithelial cells and in pyloric gland cells in glands showing intestinal metaplasia. These cells exhibit NADPH-diaphorase activity. Reverse transcription-PCR analysis and Western blotting showed that CYP1A1 and CYP1A2 were expressed in specimens with intestinal metaplasia. Tissue distribution of CYP1A1 coincided with that of P450 reductase. However, immunoreactivity to CYP1A2 protein was localized only in the pyloric gland cells near the intestinal metaplastic gland. Salmonella typhimurium mutagen assay definitively revealed that microsomes prepared from gastric mucosa with intestinal metaplasia, in particular in the pyloric gland, functionally activated benzo(a)pyrene and 2-amino-3-methylimidazo [4,5-f]quinoline. These results indicate that carcinogen activation by CYP enzymes expressed in the gastric mucosa may contribute to carcinogenesis of the stomach. (+info)

Cocarcinogenesis can occur through various mechanisms, such as:

1. Synergistic effects: The combined effect of two or more substances is greater than the sum of their individual effects. For example, smoking and exposure to asbestos can increase the risk of lung cancer more than either factor alone.
2. Antagonism: One substance may counteract the protective effects of another substance, leading to an increased risk of cancer. For example, alcohol consumption may antagonize the protective effects of a healthy diet against liver cancer.
3. Potentiation: One substance may enhance the carcinogenic effects of another substance. For example, smoking can potentiate the carcinogenic effects of exposure to certain chemicals in tobacco smoke.
4. Multistage carcinogenesis: Cocarcinogens can contribute to the development of cancer through multiple stages of carcinogenesis, including initiation, promotion, and progression.

Understanding cocarcinogenesis is important for developing effective cancer prevention strategies and for identifying potential co-carcinogens in our environment and diet. By identifying and avoiding co-carcinogens, we can reduce our risk of cancer and improve our overall health.

Types of experimental neoplasms include:

* Xenografts: tumors that are transplanted into animals from another species, often humans.
* Transgenic tumors: tumors that are created by introducing cancer-causing genes into an animal's genome.
* Chemically-induced tumors: tumors that are caused by exposure to certain chemicals or drugs.

The use of experimental neoplasms in research has led to significant advances in our understanding of cancer biology and the development of new treatments for the disease. However, the use of animals in cancer research is a controversial topic and alternatives to animal models are being developed and implemented.

Examples of experimental liver neoplasms include:

1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and can be induced experimentally by injecting carcinogens such as diethylnitrosamine (DEN) or dimethylbenz(a)anthracene (DMBA) into the liver tissue of animals.
2. Cholangiocarcinoma: This type of cancer originates in the bile ducts within the liver and can be induced experimentally by injecting chemical carcinogens such as DEN or DMBA into the bile ducts of animals.
3. Hepatoblastoma: This is a rare type of liver cancer that primarily affects children and can be induced experimentally by administering chemotherapy drugs to newborn mice or rats.
4. Metastatic tumors: These are tumors that originate in other parts of the body and spread to the liver through the bloodstream or lymphatic system. Experimental models of metastatic tumors can be studied by injecting cancer cells into the liver tissue of animals.

The study of experimental liver neoplasms is important for understanding the underlying mechanisms of liver cancer development and progression, as well as identifying potential therapeutic targets for the treatment of this disease. Animal models can be used to test the efficacy of new drugs or therapies before they are tested in humans, which can help to accelerate the development of new treatments for liver cancer.

Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.

Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.

In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.

It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.

See also: Cancer, Tumor

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Examples of precancerous conditions include:

1. Dysplasia: This is a condition where abnormal cells are present in the tissue, but have not yet invaded surrounding tissues. Dysplasia can be found in organs such as the cervix, colon, and breast.
2. Carcinoma in situ (CIS): This is a condition where cancer cells are present in the tissue, but have not yet invaded surrounding tissues. CIS is often found in organs such as the breast, prostate, and cervix.
3. Atypical hyperplasia: This is a condition where abnormal cells are present in the tissue, but they are not yet cancerous. Atypical hyperplasia can be found in organs such as the breast and uterus.
4. Lobular carcinoma in situ (LCIS): This is a condition where cancer cells are present in the milk-producing glands of the breasts, but have not yet invaded surrounding tissues. LCIS is often found in both breasts and can increase the risk of developing breast cancer.
5. Adenomas: These are small growths on the surface of the colon that can become malignant over time if left untreated.
6. Leukoplakia: This is a condition where thick, white patches develop on the tongue or inside the mouth. Leukoplakia can be a precancerous condition and may increase the risk of developing oral cancer.
7. Oral subsquamous carcinoma: This is a type of precancerous lesion that develops in the mouth and can progress to squamous cell carcinoma if left untreated.
8. Cervical intraepithelial neoplasia (CIN): This is a condition where abnormal cells are present on the surface of the cervix, but have not yet invaded surrounding tissues. CIN can progress to cancer over time if left untreated.
9. Vulvar intraepithelial neoplasia (VIN): This is a condition where abnormal cells are present on the vulva, but have not yet invaded surrounding tissues. VIN can progress to cancer over time if left untreated.
10. Penile intraepithelial neoplasia (PIN): This is a condition where abnormal cells are present on the penis, but have not yet invaded surrounding tissues. PIN can progress to cancer over time if left untreated.

It is important to note that not all precancerous conditions will develop into cancer, and some may resolve on their own without treatment. However, it is important to follow up with a healthcare provider to monitor any changes and determine the best course of treatment.

There are several types of lung neoplasms, including:

1. Adenocarcinoma: This is the most common type of lung cancer, accounting for approximately 40% of all lung cancers. It is a malignant tumor that originates in the glands of the respiratory tract and can be found in any part of the lung.
2. Squamous cell carcinoma: This type of lung cancer accounts for approximately 25% of all lung cancers and is more common in men than women. It is a malignant tumor that originates in the squamous cells lining the airways of the lungs.
3. Small cell lung cancer (SCLC): This is a highly aggressive form of lung cancer that accounts for approximately 15% of all lung cancers. It is often found in the central parts of the lungs and can spread quickly to other parts of the body.
4. Large cell carcinoma: This is a rare type of lung cancer that accounts for only about 5% of all lung cancers. It is a malignant tumor that originates in the large cells of the respiratory tract and can be found in any part of the lung.
5. Bronchioalveolar carcinoma (BAC): This is a rare type of lung cancer that originates in the cells lining the airways and alveoli of the lungs. It is more common in women than men and tends to affect older individuals.
6. Lymphangioleiomyomatosis (LAM): This is a rare, progressive, and often fatal lung disease that primarily affects women of childbearing age. It is characterized by the growth of smooth muscle-like cells in the lungs and can lead to cysts, lung collapse, and respiratory failure.
7. Hamartoma: This is a benign tumor that originates in the tissue of the lungs and is usually found in children. It is characterized by an overgrowth of normal lung tissue and can be treated with surgery.
8. Secondary lung cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
9. Metastatic cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
10. Mesothelioma: This is a rare and aggressive form of cancer that originates in the lining of the lungs or abdomen. It is caused by asbestos exposure and can be treated with surgery, chemotherapy, and radiation therapy.

Lung diseases can also be classified based on their cause, such as:

1. Infectious diseases: These are caused by bacteria, viruses, or other microorganisms and can include pneumonia, tuberculosis, and bronchitis.
2. Autoimmune diseases: These are caused by an overactive immune system and can include conditions such as sarcoidosis and idiopathic pulmonary fibrosis.
3. Genetic diseases: These are caused by inherited mutations in genes that affect the lungs and can include cystic fibrosis and primary ciliary dyskinesia.
4. Environmental diseases: These are caused by exposure to harmful substances such as tobacco smoke, air pollution, and asbestos.
5. Radiological diseases: These are caused by exposure to ionizing radiation and can include conditions such as radiographic breast cancer and lung cancer.
6. Vascular diseases: These are caused by problems with the blood vessels in the lungs and can include conditions such as pulmonary embolism and pulmonary hypertension.
7. Tumors: These can be benign or malignant and can include conditions such as lung metastases and lung cancer.
8. Trauma: This can include injuries to the chest or lungs caused by accidents or other forms of trauma.
9. Congenital diseases: These are present at birth and can include conditions such as bronchopulmonary foregut malformations and congenital cystic adenomatoid malformation.

Each type of lung disease has its own set of symptoms, diagnosis, and treatment options. It is important to seek medical attention if you experience any persistent or severe respiratory symptoms, as early diagnosis and treatment can improve outcomes and quality of life.

Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.

Types of Neoplasms

There are many different types of neoplasms, including:

1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.

Causes and Risk Factors of Neoplasms

The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:

1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.

Signs and Symptoms of Neoplasms

The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:

1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.

Diagnosis and Treatment of Neoplasms

The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.

The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:

1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.

Prevention of Neoplasms

While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:

1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.

It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.

Examples of 'Mammary Neoplasms, Experimental' in a sentence:

1. The researchers studied the effects of hormone therapy on mammary neoplasms in experimental animals to better understand its potential role in human breast cancer.
2. The lab used mice with genetic mutations that predispose them to developing mammary neoplasms to test the efficacy of new cancer drugs.
3. In order to investigate the link between obesity and breast cancer, the researchers conducted experiments on mammary neoplasms in rats with diet-induced obesity.

Papillomas can occur anywhere on the body, but they are most commonly found on the face, neck, and scalp. They may appear as small bumps or growths that look like a wart. In some cases, papillomas may be associated with human papillomavirus (HPV) infection.

Papillomas are typically diagnosed through a physical examination of the affected area. In some cases, a biopsy may be performed to confirm the diagnosis and rule out other potential causes. Treatment for papillomas usually involves removal of the growth through a minor surgical procedure or cryotherapy (freezing).

Papillomas are not cancerous and do not typically pose any long-term health risks. However, they may be unsightly and can cause psychological distress for some people. In these cases, treatment may be sought for cosmetic reasons. It is important to note that papillomas should not be confused with squamous cell carcinoma, a type of skin cancer that can resemble a papilloma in appearance but has the potential to be more aggressive and harmful.

These tumors can be benign or malignant, and their growth and behavior vary depending on the type of cancer. Malignant tumors can invade the surrounding tissues and spread to other parts of the body through the bloodstream or lymphatic system, causing serious complications and potentially life-threatening consequences.

The risk factors for developing urinary bladder neoplasms include smoking, exposure to certain chemicals, recurrent bladder infections, and a family history of bladder cancer. The symptoms of these tumors can include blood in the urine, pain during urination, frequent urination, and abdominal pain.

Diagnosis of urinary bladder neoplasms is typically made through a combination of imaging tests such as ultrasound, computed tomography (CT) scan or magnetic resonance imaging (MRI), and cystoscopy, which involves inserting a flexible tube with a camera into the bladder to visualize the tumor.

Treatment options for urinary bladder neoplasms depend on the type of cancer, stage, and location of the tumor. Treatment may include surgery to remove the tumor, chemotherapy, radiation therapy, or a combination of these modalities. Early detection and treatment can improve the prognosis for patients with urinary bladder neoplasms.

There are several types of colonic neoplasms, including:

1. Adenomas: These are benign growths that are usually precursors to colorectal cancer.
2. Carcinomas: These are malignant tumors that arise from the epithelial lining of the colon.
3. Sarcomas: These are rare malignant tumors that arise from the connective tissue of the colon.
4. Lymphomas: These are cancers of the immune system that can affect the colon.

Colonic neoplasms can cause a variety of symptoms, including bleeding, abdominal pain, and changes in bowel habits. They are often diagnosed through a combination of medical imaging tests (such as colonoscopy or CT scan) and biopsy. Treatment for colonic neoplasms depends on the type and stage of the tumor, and may include surgery, chemotherapy, and/or radiation therapy.

Overall, colonic neoplasms are a common condition that can have serious consequences if left untreated. It is important for individuals to be aware of their risk factors and to undergo regular screening for colon cancer to help detect and treat any abnormal growths or tumors in the colon.

There are several types of skin neoplasms, including:

1. Basal cell carcinoma (BCC): This is the most common type of skin cancer, and it usually appears as a small, fleshy bump or a flat, scaly patch. BCC is highly treatable, but if left untreated, it can grow and invade surrounding tissue.
2. Squamous cell carcinoma (SCC): This type of skin cancer is less common than BCC but more aggressive. It typically appears as a firm, flat, or raised bump on sun-exposed areas. SCC can spread to other parts of the body if left untreated.
3. Melanoma: This is the most serious type of skin cancer, accounting for only 1% of all skin neoplasms but responsible for the majority of skin cancer deaths. Melanoma can appear as a new or changing mole, and it's essential to recognize the ABCDE signs (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving size, shape, or color) to detect it early.
4. Sebaceous gland carcinoma: This rare type of skin cancer originates in the oil-producing glands of the skin and can appear as a firm, painless nodule on the forehead, nose, or other oily areas.
5. Merkel cell carcinoma: This is a rare and aggressive skin cancer that typically appears as a firm, shiny bump on the skin. It's more common in older adults and those with a history of sun exposure.
6. Cutaneous lymphoma: This type of cancer affects the immune system and can appear as a rash, nodules, or tumors on the skin.
7. Kaposi sarcoma: This is a rare type of skin cancer that affects people with weakened immune systems, such as those with HIV/AIDS. It typically appears as a flat, red or purple lesion on the skin.

While skin cancers are generally curable when detected early, it's important to be aware of your skin and notice any changes or unusual spots, especially if you have a history of sun exposure or other risk factors. If you suspect anything suspicious, see a dermatologist for an evaluation and potential biopsy. Remember, prevention is key to avoiding the harmful effects of UV radiation and reducing your risk of developing skin cancer.

Liver neoplasms, also known as liver tumors or hepatic tumors, are abnormal growths of tissue in the liver. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant liver tumors can be primary, meaning they originate in the liver, or metastatic, meaning they spread to the liver from another part of the body.

There are several types of liver neoplasms, including:

1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and arises from the main cells of the liver (hepatocytes). HCC is often associated with cirrhosis and can be caused by viral hepatitis or alcohol abuse.
2. Cholangiocarcinoma: This type of cancer arises from the cells lining the bile ducts within the liver (cholangiocytes). Cholangiocarcinoma is rare and often diagnosed at an advanced stage.
3. Hemangiosarcoma: This is a rare type of cancer that originates in the blood vessels of the liver. It is most commonly seen in dogs but can also occur in humans.
4. Fibromas: These are benign tumors that arise from the connective tissue of the liver (fibrocytes). Fibromas are usually small and do not spread to other parts of the body.
5. Adenomas: These are benign tumors that arise from the glandular cells of the liver (hepatocytes). Adenomas are usually small and do not spread to other parts of the body.

The symptoms of liver neoplasms vary depending on their size, location, and whether they are benign or malignant. Common symptoms include abdominal pain, fatigue, weight loss, and jaundice (yellowing of the skin and eyes). Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and ultrasound, and a biopsy to confirm the presence of cancer cells.

Treatment options for liver neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery may be an option for some patients with small, localized tumors, while others may require chemotherapy or radiation therapy to shrink the tumor before surgery can be performed. In some cases, liver transplantation may be necessary.

Prognosis for liver neoplasms varies depending on the type and stage of the cancer. In general, early detection and treatment improve the prognosis, while advanced-stage disease is associated with a poorer prognosis.

1. Asbestosis: a lung disease caused by inhaling asbestos fibers.
2. Carpal tunnel syndrome: a nerve disorder caused by repetitive motion and pressure on the wrist.
3. Mesothelioma: a type of cancer caused by exposure to asbestos.
4. Pneumoconiosis: a lung disease caused by inhaling dust from mining or other heavy industries.
5. Repetitive strain injuries: injuries caused by repetitive motions, such as typing or using vibrating tools.
6. Skin conditions: such as skin irritation and dermatitis caused by exposure to chemicals or other substances in the workplace.
7. Hearing loss: caused by loud noises in the workplace.
8. Back injuries: caused by lifting, bending, or twisting.
9. Respiratory problems: such as asthma and other breathing difficulties caused by exposure to chemicals or dust in the workplace.
10. Cancer: caused by exposure to carcinogens such as radiation, certain chemicals, or heavy metals in the workplace.

Occupational diseases can be difficult to diagnose and treat, as they often develop gradually over time and may not be immediately attributed to the work environment. In some cases, these diseases may not appear until years after exposure has ended. It is important for workers to be aware of the potential health risks associated with their job and take steps to protect themselves, such as wearing protective gear, following safety protocols, and seeking regular medical check-ups. Employers also have a responsibility to provide a safe work environment and follow strict regulations to prevent the spread of occupational diseases.

Adenomas are caused by genetic mutations that occur in the DNA of the affected cells. These mutations can be inherited or acquired through exposure to environmental factors such as tobacco smoke, radiation, or certain chemicals.

The symptoms of an adenoma can vary depending on its location and size. In general, they may include abdominal pain, bleeding, or changes in bowel movements. If the adenoma becomes large enough, it can obstruct the normal functioning of the affected organ or cause a blockage that can lead to severe health complications.

Adenomas are usually diagnosed through endoscopy, which involves inserting a flexible tube with a camera into the affected organ to visualize the inside. Biopsies may also be taken to confirm the presence of cancerous cells.

Treatment for adenomas depends on their size, location, and severity. Small, non-pedunculated adenomas can often be removed during endoscopy through a procedure called endoscopic mucosal resection (EMR). Larger adenomas may require surgical resection, and in some cases, chemotherapy or radiation therapy may also be necessary.

In summary, adenoma is a type of benign tumor that can occur in glandular tissue throughout the body. While they are not cancerous, they have the potential to become malignant over time if left untreated. Therefore, it is important to seek medical attention if symptoms persist or worsen over time. Early detection and treatment can help prevent complications and improve outcomes for patients with adenomas.

There are different types of hyperplasia, depending on the location and cause of the condition. Some examples include:

1. Benign hyperplasia: This type of hyperplasia is non-cancerous and does not spread to other parts of the body. It can occur in various tissues and organs, such as the uterus (fibroids), breast tissue (fibrocystic changes), or prostate gland (benign prostatic hyperplasia).
2. Malignant hyperplasia: This type of hyperplasia is cancerous and can invade nearby tissues and organs, leading to serious health problems. Examples include skin cancer, breast cancer, and colon cancer.
3. Hyperplastic polyps: These are abnormal growths that occur in the gastrointestinal tract and can be precancerous.
4. Adenomatous hyperplasia: This type of hyperplasia is characterized by an increase in the number of glandular cells in a specific organ, such as the colon or breast. It can be a precursor to cancer.

The symptoms of hyperplasia depend on the location and severity of the condition. In general, they may include:

* Enlargement or swelling of the affected tissue or organ
* Pain or discomfort in the affected area
* Abnormal bleeding or discharge
* Changes in bowel or bladder habits
* Unexplained weight loss or gain

Hyperplasia is diagnosed through a combination of physical examination, imaging tests such as ultrasound or MRI, and biopsy. Treatment options depend on the underlying cause and severity of the condition, and may include medication, surgery, or other interventions.

Example sentences:

1. The patient developed a radiation-induced neoplasm in their chest after undergoing radiation therapy for breast cancer.
2. The risk of radiation-induced neoplasms increases with higher doses of radiation exposure, making it crucial to minimize exposure during medical procedures.
3. The oncologist monitored the patient's health closely after their radiation therapy to detect any signs of radiation-induced neoplasms.

Adenocarcinoma is a term used to describe a variety of different types of cancer that arise in glandular tissue, including:

1. Colorectal adenocarcinoma (cancer of the colon or rectum)
2. Breast adenocarcinoma (cancer of the breast)
3. Prostate adenocarcinoma (cancer of the prostate gland)
4. Pancreatic adenocarcinoma (cancer of the pancreas)
5. Lung adenocarcinoma (cancer of the lung)
6. Thyroid adenocarcinoma (cancer of the thyroid gland)
7. Skin adenocarcinoma (cancer of the skin)

The symptoms of adenocarcinoma depend on the location of the cancer and can include:

1. Blood in the stool or urine
2. Abdominal pain or discomfort
3. Changes in bowel habits
4. Unusual vaginal bleeding (in the case of endometrial adenocarcinoma)
5. A lump or thickening in the breast or elsewhere
6. Weight loss
7. Fatigue
8. Coughing up blood (in the case of lung adenocarcinoma)

The diagnosis of adenocarcinoma is typically made through a combination of imaging tests, such as CT scans, MRI scans, and PET scans, and a biopsy, which involves removing a sample of tissue from the affected area and examining it under a microscope for cancer cells.

Treatment options for adenocarcinoma depend on the location of the cancer and can include:

1. Surgery to remove the tumor
2. Chemotherapy, which involves using drugs to kill cancer cells
3. Radiation therapy, which involves using high-energy X-rays or other particles to kill cancer cells
4. Targeted therapy, which involves using drugs that target specific molecules on cancer cells to kill them
5. Immunotherapy, which involves using drugs that stimulate the immune system to fight cancer cells.

The prognosis for adenocarcinoma is generally good if the cancer is detected and treated early, but it can be more challenging to treat if the cancer has spread to other parts of the body.

SCC typically appears as a firm, flat, or raised bump on the skin, and may be pink, red, or scaly. The cancer cells are usually well-differentiated, meaning they resemble normal squamous cells, but they can grow rapidly and invade surrounding tissues if left untreated.

SCC is more common in fair-skinned individuals and those who spend a lot of time in the sun, as UV radiation can damage the skin cells and increase the risk of cancer. The cancer can also spread to other parts of the body, such as lymph nodes or organs, and can be life-threatening if not treated promptly and effectively.

Treatment for SCC usually involves surgery to remove the cancerous tissue, and may also include radiation therapy or chemotherapy to kill any remaining cancer cells. Early detection and treatment are important to improve outcomes for patients with SCC.

Explanation: Genetic predisposition to disease is influenced by multiple factors, including the presence of inherited genetic mutations or variations, environmental factors, and lifestyle choices. The likelihood of developing a particular disease can be increased by inherited genetic mutations that affect the functioning of specific genes or biological pathways. For example, inherited mutations in the BRCA1 and BRCA2 genes increase the risk of developing breast and ovarian cancer.

The expression of genetic predisposition to disease can vary widely, and not all individuals with a genetic predisposition will develop the disease. Additionally, many factors can influence the likelihood of developing a particular disease, such as environmental exposures, lifestyle choices, and other health conditions.

Inheritance patterns: Genetic predisposition to disease can be inherited in an autosomal dominant, autosomal recessive, or multifactorial pattern, depending on the specific disease and the genetic mutations involved. Autosomal dominant inheritance means that a single copy of the mutated gene is enough to cause the disease, while autosomal recessive inheritance requires two copies of the mutated gene. Multifactorial inheritance involves multiple genes and environmental factors contributing to the development of the disease.

Examples of diseases with a known genetic predisposition:

1. Huntington's disease: An autosomal dominant disorder caused by an expansion of a CAG repeat in the Huntingtin gene, leading to progressive neurodegeneration and cognitive decline.
2. Cystic fibrosis: An autosomal recessive disorder caused by mutations in the CFTR gene, leading to respiratory and digestive problems.
3. BRCA1/2-related breast and ovarian cancer: An inherited increased risk of developing breast and ovarian cancer due to mutations in the BRCA1 or BRCA2 genes.
4. Sickle cell anemia: An autosomal recessive disorder caused by a point mutation in the HBB gene, leading to defective hemoglobin production and red blood cell sickling.
5. Type 1 diabetes: An autoimmune disease caused by a combination of genetic and environmental factors, including multiple genes in the HLA complex.

Understanding the genetic basis of disease can help with early detection, prevention, and treatment. For example, genetic testing can identify individuals who are at risk for certain diseases, allowing for earlier intervention and preventive measures. Additionally, understanding the genetic basis of a disease can inform the development of targeted therapies and personalized medicine."

There are several types of disease susceptibility, including:

1. Genetic predisposition: This refers to the inherent tendency of an individual to develop a particular disease due to their genetic makeup. For example, some families may have a higher risk of developing certain diseases such as cancer or heart disease due to inherited genetic mutations.
2. Environmental susceptibility: This refers to the increased risk of developing a disease due to exposure to environmental factors such as pollutants, toxins, or infectious agents. For example, someone who lives in an area with high levels of air pollution may be more susceptible to developing respiratory problems.
3. Lifestyle susceptibility: This refers to the increased risk of developing a disease due to unhealthy lifestyle choices such as smoking, lack of exercise, or poor diet. For example, someone who smokes and is overweight may be more susceptible to developing heart disease or lung cancer.
4. Immune system susceptibility: This refers to the increased risk of developing a disease due to an impaired immune system. For example, people with autoimmune disorders such as HIV/AIDS or rheumatoid arthritis may be more susceptible to opportunistic infections.

Understanding disease susceptibility can help healthcare providers identify individuals who are at risk of developing certain diseases and provide preventive measures or early intervention to reduce the risk of disease progression. Additionally, genetic testing can help identify individuals with a high risk of developing certain diseases, allowing for earlier diagnosis and treatment.

In summary, disease susceptibility refers to the predisposition of an individual to develop a particular disease or condition due to various factors such as genetics, environment, lifestyle choices, and immune system function. Understanding disease susceptibility can help healthcare providers identify individuals at risk and provide appropriate preventive measures or early intervention to reduce the risk of disease progression.

Types of Intestinal Neoplasms:

1. Adenomas: These are benign tumors that grow on the inner lining of the intestine. They can become malignant over time if left untreated.
2. Carcinomas: These are malignant tumors that develop in the inner lining of the intestine. They can be subdivided into several types, including colon cancer and rectal cancer.
3. Lymphoma: This is a type of cancer that affects the immune system and can occur in the intestines.
4. Leiomyosarcomas: These are rare malignant tumors that develop in the smooth muscle layers of the intestine.

Causes and Risk Factors:

The exact cause of intestinal neoplasms is not known, but several factors can increase the risk of developing these growths. These include:

1. Age: The risk of developing intestinal neoplasms increases with age.
2. Family history: Having a family history of colon cancer or other intestinal neoplasms can increase the risk of developing these growths.
3. Inflammatory bowel disease: People with inflammatory bowel diseases, such as ulcerative colitis and Crohn's disease, are at higher risk of developing intestinal neoplasms.
4. Genetic mutations: Certain genetic mutations can increase the risk of developing intestinal neoplasms.
5. Diet and lifestyle factors: A diet high in fat and low in fiber, as well as lack of physical activity, may increase the risk of developing intestinal neoplasms.

Symptoms:

Intestinal neoplasms can cause a variety of symptoms, including:

1. Abdominal pain or discomfort
2. Changes in bowel habits, such as diarrhea or constipation
3. Blood in the stool
4. Weight loss
5. Fatigue
6. Loss of appetite

Diagnosis:

To diagnose intestinal neoplasms, a doctor may perform several tests, including:

1. Colonoscopy: A colonoscope is inserted through the rectum and into the colon to visualize the inside of the colon and detect any abnormal growths.
2. Biopsy: A small sample of tissue is removed from the colon and examined under a microscope for cancer cells.
3. Imaging tests: Such as X-rays, CT scans, or MRI scans to look for any abnormalities in the colon.
4. Blood tests: To check for certain substances in the blood that are associated with intestinal neoplasms.

Treatment:

The treatment of intestinal neoplasms depends on the type and location of the growth, as well as the stage of the cancer. Treatment options may include:

1. Surgery: To remove the tumor and any affected tissue.
2. Chemotherapy: To kill any remaining cancer cells with drugs.
3. Radiation therapy: To kill cancer cells with high-energy X-rays or other forms of radiation.
4. Targeted therapy: To use drugs that target specific molecules on cancer cells to kill them.
5. Immunotherapy: To use drugs that stimulate the immune system to fight cancer cells.

Prognosis:

The prognosis for intestinal neoplasms depends on several factors, including the type and stage of the cancer, the location of the growth, and the effectiveness of treatment. In general, early detection and treatment improve the prognosis, while later-stage cancers have a poorer prognosis.

Complications:

Intestinal neoplasms can cause several complications, including:

1. Obstruction: The tumor can block the normal flow of food through the intestine, leading to abdominal pain and other symptoms.
2. Bleeding: The tumor can cause bleeding in the intestine, which can lead to anemia and other complications.
3. Perforation: The tumor can create a hole in the wall of the intestine, leading to peritonitis (inflammation of the lining of the abdomen) and other complications.
4. Metastasis: The cancer cells can spread to other parts of the body, such as the liver or lungs, and cause further complications.
5. Malnutrition: The tumor can make it difficult for the body to absorb nutrients, leading to malnutrition and other health problems.

Prevention:

There is no sure way to prevent intestinal neoplasms, but there are several steps that may help reduce the risk of developing these types of cancer. These include:

1. Avoiding known risk factors: Avoiding known risk factors such as smoking, excessive alcohol consumption, and a diet high in processed meat can help reduce the risk of developing intestinal neoplasms.
2. Maintaining a healthy diet: Eating a balanced diet that is high in fruits, vegetables, and whole grains can help keep the intestines healthy and may reduce the risk of cancer.
3. Exercise regularly: Regular exercise can help maintain a healthy weight, improve digestion, and may reduce the risk of developing intestinal neoplasms.
4. Managing chronic conditions: Managing chronic conditions such as inflammatory bowel disease, diabetes, and obesity can help reduce the risk of developing intestinal neoplasms.
5. Screening tests: Regular screening tests such as colonoscopy, CT scan, or barium enema can help detect precancerous polyps or early-stage cancer, allowing for early treatment and prevention of advanced disease.

Early detection and diagnosis are crucial for effective treatment and survival rates for intestinal neoplasms. If you have any of the risk factors or symptoms mentioned above, it is essential to consult a doctor as soon as possible. A thorough examination and diagnostic tests can help determine the cause of your symptoms and recommend appropriate treatment.

Nose neoplasms refer to any type of abnormal growth or tumor that develops in the nose or nasal passages. These tumors can be benign (non-cancerous) or malignant (cancerous), and they can affect people of all ages.

Types of Nose Neoplasms[2]

There are several types of nose neoplasms, including:

1. Nasal polyps: These are benign growths that can occur in the nasal passages and are usually associated with allergies or chronic sinus infections.
2. Nasal carcinoma: This is a type of cancer that affects the nasal passages and can be either benign or malignant.
3. Esthesioneuroblastoma: This is a rare type of cancer that occurs in the nasal passages and is usually found in children.
4. Adenocarcinoma: This is a type of cancer that affects the glandular tissue in the nose and can be either benign or malignant.
5. Squamous cell carcinoma: This is a type of cancer that affects the squamous cells in the skin and mucous membranes of the nose.

Symptoms of Nose Neoplasms[3]

The symptoms of nose neoplasms can vary depending on the type and location of the tumor. Some common symptoms include:

1. Nasal congestion or blockage
2. Nasal discharge or bleeding
3. Loss of sense of smell or taste
4. Headaches
5. Sinus infections or other respiratory problems
6. Swelling or lumps in the nose or face
7. Difficulty breathing through the nose

Diagnosis and Treatment of Nose Neoplasms[4]

The diagnosis of nose neoplasms typically involves a combination of physical examination, imaging tests (such as CT scans or MRI), and biopsies. Treatment depends on the type and location of the tumor, and may involve surgery, radiation therapy, chemotherapy, or a combination of these. Some common treatment options include:

1. Surgical excision: This involves removing the tumor and any affected tissue through a surgical procedure.
2. Radiation therapy: This involves using high-energy beams to kill cancer cells.
3. Chemotherapy: This involves using drugs to kill cancer cells.
4. Laser therapy: This involves using a laser to remove or destroy the tumor.
5. Cryotherapy: This involves using extreme cold to destroy the tumor.

Prognosis and Follow-Up Care[5]

The prognosis for nose neoplasms depends on the type and location of the tumor, as well as the stage of the cancer. In general, early detection and treatment improve the chances of a successful outcome. Follow-up care is important to monitor the patient's condition and detect any recurrences or complications. Some common follow-up procedures include:

1. Regular check-ups with an otolaryngologist (ENT specialist)
2. Imaging tests (such as CT scans or MRI) to monitor the tumor and detect any recurrences
3. Biopsies to evaluate any changes in the tumor
4. Treatment of any complications that may arise, such as bleeding or infection.

Lifestyle Changes and Home Remedies[6]

There are several lifestyle changes and home remedies that can help improve the symptoms and quality of life for patients with nose neoplasms. These include:

1. Maintaining good hygiene, such as regularly washing the hands and avoiding close contact with others.
2. Avoiding smoking and other tobacco products, which can exacerbate the symptoms of nose cancer.
3. Using saline nasal sprays or drops to keep the nasal passages moist and reduce congestion.
4. Applying warm compresses to the affected area to help reduce swelling and ease pain.
5. Using over-the-counter pain medications, such as acetaminophen or ibuprofen, to manage symptoms.
6. Avoiding blowing the nose, which can dislodge the tumor and cause bleeding.
7. Avoiding exposure to pollutants and allergens that can irritate the nasal passages.
8. Using a humidifier to add moisture to the air and relieve dryness and congestion in the nasal passages.
9. Practicing good sleep hygiene, such as avoiding caffeine and electronic screens before bedtime and creating a relaxing sleep environment.
10. Managing stress through relaxation techniques, such as meditation or deep breathing exercises.

Nose neoplasms can have a significant impact on a person's quality of life, but with proper diagnosis and treatment, many patients can experience improved symptoms and outcomes. It is important for patients to work closely with their healthcare providers to develop a personalized treatment plan that addresses their specific needs and goals. Additionally, lifestyle changes and home remedies can help improve symptoms and quality of life for patients with nose neoplasms.

The presence of chromosome-defective micronuclei in cells can be an indication of genetic damage and may be used as a diagnostic marker for certain diseases or conditions, such as cancer or exposure to toxic substances. The frequency and distribution of these structures within a cell population can also provide information about the type and severity of genetic damage present.

In contrast to other types of micronuclei, which are typically smaller and less complex, chromosome-defective micronuclei are larger and more irregular in shape, and may contain fragmented or abnormal chromatin material. They can also be distinguished from other types of micronuclei by their specific staining properties and the presence of certain structural features, such as the presence of nucleoli or the absence of a membrane boundary.

Overall, the study of chromosome-defective micronuclei is an important tool for understanding the mechanisms of genetic damage and disease, and may have practical applications in fields such as cancer diagnosis and environmental health assessment.

Types of mouth neoplasms include:

1. Oral squamous cell carcinoma (OSCC): This is the most common type of mouth cancer, accounting for about 90% of all cases. It usually occurs on the tongue, lips, or floor of the mouth.
2. Verrucous carcinoma: This type of cancer is slow-growing and typically affects the gums or the outer surface of the tongue.
3. Adenoid cystic carcinoma: This type of cancer is rare and usually affects the salivary glands. It can infiltrate surrounding tissues and cause significant destruction of nearby structures.
4. Mucoepidermoid carcinoma: This type of cancer is relatively rare and occurs most commonly on the tongue or the floor of the mouth. It can be benign or malignant, and its behavior varies depending on the type.
5. Melanotic neuroectodermal tumor: This is a rare type of cancer that affects the melanocytes (pigment-producing cells) in the mouth. It typically occurs in the tongue or the lips.

Symptoms of mouth neoplasms can include:

* A sore or ulcer that does not heal
* A lump or mass in the mouth
* Bleeding or pain in the mouth
* Difficulty swallowing or speaking
* Numbness or tingling in the mouth

Diagnosis of mouth neoplasms typically involves a combination of physical examination, imaging studies (such as X-rays or CT scans), and biopsy. Treatment options vary depending on the type and severity of the cancer, but may include surgery, radiation therapy, chemotherapy, or a combination of these. Early detection and treatment are important for improving outcomes in patients with mouth neoplasms.

There are several types of chromosome aberrations, including:

1. Chromosomal deletions: Loss of a portion of a chromosome.
2. Chromosomal duplications: Extra copies of a chromosome or a portion of a chromosome.
3. Chromosomal translocations: A change in the position of a chromosome or a portion of a chromosome.
4. Chromosomal inversions: A reversal of a segment of a chromosome.
5. Chromosomal amplifications: An increase in the number of copies of a particular chromosome or gene.

Chromosome aberrations can be detected through various techniques, such as karyotyping, fluorescence in situ hybridization (FISH), or array comparative genomic hybridization (aCGH). These tests can help identify changes in the chromosomal makeup of cells and provide information about the underlying genetic causes of disease.

Chromosome aberrations are associated with a wide range of diseases, including:

1. Cancer: Chromosome abnormalities are common in cancer cells and can contribute to the development and progression of cancer.
2. Birth defects: Many birth defects are caused by chromosome abnormalities, such as Down syndrome (trisomy 21), which is caused by an extra copy of chromosome 21.
3. Neurological disorders: Chromosome aberrations have been linked to various neurological disorders, including autism and intellectual disability.
4. Immunodeficiency diseases: Some immunodeficiency diseases, such as X-linked severe combined immunodeficiency (SCID), are caused by chromosome abnormalities.
5. Infectious diseases: Chromosome aberrations can increase the risk of infection with certain viruses, such as human immunodeficiency virus (HIV).
6. Ageing: Chromosome aberrations have been linked to the ageing process and may contribute to the development of age-related diseases.
7. Radiation exposure: Exposure to radiation can cause chromosome abnormalities, which can increase the risk of cancer and other diseases.
8. Genetic disorders: Many genetic disorders are caused by chromosome aberrations, such as Turner syndrome (45,X), which is caused by a missing X chromosome.
9. Rare diseases: Chromosome aberrations can cause rare diseases, such as Klinefelter syndrome (47,XXY), which is caused by an extra copy of the X chromosome.
10. Infertility: Chromosome abnormalities can contribute to infertility in both men and women.

Understanding the causes and consequences of chromosome aberrations is important for developing effective treatments and improving human health.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

Anatomy12

Organisms11

Diseases29

Chemicals and Drugs133

Analytical, Diagnostic and Therapeutic Techniques and Equipment17

Psychiatry and Psychology1

Phenomena and Processes27

Disciplines and Occupations1

Anthropology, Education, Sociology and Social Phenomena1

Technology, Industry, Agriculture5

Information Science1

Health Care13

Environmental factors as regulators and effectors of multistep carcinogenesis. (1/593)

Heterocyclic aromatic amines induce DNA strand breaks and cell transformation. (2/593)

Decreased expression of glutathione S-transferase M1 in HPV16-transfected human cervical keratinocytes in culture. (3/593)

Histopathology and gene expression changes in rat liver during feeding of fumonisin B1, a carcinogenic mycotoxin produced by Fusarium moniliforme. (4/593)

Differential protection against benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide-induced DNA damage in HepG2 cells stably transfected with allelic variants of pi class human glutathione S-transferase. (5/593)

Metabolic proficiency and benzo[a]pyrene DNA adduct formation in APCMin mouse adenomas and uninvolved mucosa. (6/593)

Cytosine methylation in a CpG sequence leads to enhanced reactivity with Benzo[a]pyrene diol epoxide that correlates with a conformational change. (7/593)

Mutagenic activation of environmental carcinogens by microsomes of gastric mucosa with intestinal metaplasia. (8/593)

Carcinogens

Nitrosamines

2-Acetylaminofluorene

Benzo(a)pyrene

Mutagens

Benzopyrenes

DNA Adducts

Carcinogenicity Tests

Acetoxyacetylaminofluorene

9,10-Dimethyl-1,2-benzanthracene

Mutagenicity Tests

Methylnitrosourea

Cocarcinogenesis

Aminobiphenyl Compounds

4-Nitroquinoline-1-oxide

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide

Biotransformation

Benz(a)Anthracenes

Rats, Inbred F344

Methylnitronitrosoguanidine

Neoplasms, Experimental

Polycyclic Compounds

Dimethylnitrosamine

Methyldimethylaminoazobenzene

p-Dimethylaminoazobenzene

Fluorenes

Liver Neoplasms, Experimental

Aflatoxin B1

Hydroxyacetylaminofluorene

Chrysenes

Nitroquinolines

Diethylnitrosamine

Methylcholanthrene

Dimethylhydrazines

Cell Transformation, Neoplastic

Glutathione Transferase

Anticarcinogenic Agents

Precancerous Conditions

Dihydroxydihydrobenzopyrenes

Aflatoxins

DNA

Liver

Urethane

Polycyclic Hydrocarbons, Aromatic

Lung Neoplasms

1,2-Dimethylhydrazine

Azoxymethane

Arylamine N-Acetyltransferase

Benzidines

Cytochrome P-450 CYP1A1

DNA Damage

Metabolic Detoxication, Drug

Neoplasms

Safrole

Ethylene Dibromide

Mammary Neoplasms, Experimental

Smoking

Methylazoxymethanol Acetate

Methylhydrazines

Cytochrome P-450 CYP1A2

Cytochrome P-450 Enzyme System

Papilloma

Acrylonitrile

Aryl Hydrocarbon Hydroxylases

Occupational Exposure

Environmental Exposure

Mesocricetus

Isothiocyanates

Amines

Azo Compounds

Alkylating Agents

Vinyl Chloride

Dose-Response Relationship, Drug

Chromium

Glucuronates

Urinary Bladder Neoplasms

Deoxyguanosine

Nitrosourea Compounds

Chromates

Propiolactone