Alkylating agents. Medical search

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 class of drugs that differs from other alkylating agents used clinically in that they are monofunctional and thus unable to cross-link cellular macromolecules. Among their common properties are a requirement for metabolic activation to intermediates with antitumor efficacy and the presence in their chemical structures of N-methyl groups, that after metabolism, can covalently modify cellular DNA. The precise mechanisms by which each of these drugs acts to kill tumor cells are not completely understood. (From AMA, Drug Evaluations Annual, 1994, p2026)

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.

An enzyme that transfers methyl groups from O(6)-methylguanine, and other methylated moieties of DNA, to a cysteine residue in itself, thus repairing alkylated DNA in a single-step reaction. EC 2.1.1.63.

A nitrosoguanidine derivative with potent mutagenic and carcinogenic properties.

An alkylating agent in cancer therapy that may also act as a mutagen by interfering with and causing damage to DNA.

A biologic alkylating agent that exerts its cytotoxic effects by forming DNA ADDUCTS and DNA interstrand crosslinks, thereby inhibiting rapidly proliferating cells. The hydrochloride is an antineoplastic agent used to treat HODGKIN DISEASE and LYMPHOMA.

A cell-cycle phase nonspecific alkylating antineoplastic agent. It is used in the treatment of brain tumors and various other malignant neoplasms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p462) This substance may reasonably be anticipated to be a carcinogen according to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (From Merck Index, 11th ed)

A nitrogen mustard alkylating agent used as antineoplastic for chronic lymphocytic leukemia, Hodgkin's disease, and others. Although it is less toxic than most other nitrogen mustards, it has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (Merck Index, 11th ed)

An antineoplastic agent with alkylating properties. It also acts as a mutagen by damaging DNA and is used experimentally for that effect.

A group of alkylating agents derived from mustard gas, with the sulfur replaced by nitrogen. They were formerly used as toxicants and vesicants, but now function as antineoplastic agents. These compounds are also powerful mutagens, teratogens, immunosuppressants, and carcinogens.

An antineoplastic agent. It has significant activity against melanomas. (from Martindale, The Extra Pharmacopoeia, 31st ed, p564)

An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - MELPHALAN, the racemic mixture - MERPHALAN, and the dextro isomer - MEDPHALAN; toxic to bone marrow, but little vesicant action; potential carcinogen.

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.

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.

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

Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the LIVER to form the active aldophosphamide. It has been used in the treatment of LYMPHOMA and LEUKEMIA. Its side effect, ALOPECIA, has been used for defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer.

Organic esters of sulfuric acid.

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

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 very toxic alkylating antineoplastic agent also used as an insect sterilant. It causes skin, gastrointestinal, CNS, and bone marrow damage. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), thiotepa may reasonably be anticipated to be a carcinogen (Merck Index, 11th ed).

A subclass of enzymes of the transferase class that catalyze the transfer of a methyl group from one compound to another. (Dorland, 28th ed) EC 2.1.1.

Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.

Alkylating antineoplastic agent used mainly for ovarian tumors. It is toxic to skin, gastrointestinal tract, bone marrow and kidneys.

A group of nitrogen mustard compounds which are substituted with a phosphoramide group or its derivatives. They are usually cytotoxic and used as antineoplastic agents.

Severe irritant and vesicant of skin, eyes, and lungs. It may cause blindness and lethal lung edema and was formerly used as a war gas. The substance has been proposed as a cytostatic and for treatment of psoriasis. It has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP-85-002, 1985) (Merck, 11th ed).

A group of methylazirinopyrroloindolediones obtained from certain Streptomyces strains. They are very toxic antibiotics used as ANTINEOPLASTIC AGENTS in some solid tumors. PORFIROMYCIN and MITOMYCIN are the most useful members of the group.

Saturated azacyclopropane compounds. They include compounds with substitutions on CARBON or NITROGEN atoms.

Substances that inhibit or prevent the proliferation of NEOPLASMS.

A nitroimidazole that sensitizes hypoxic tumor cells that are normally resistant to radiation therapy.

An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.

The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.

A family of DNA repair enzymes that recognize damaged nucleotide bases and remove them by hydrolyzing the N-glycosidic bond that attaches them to the sugar backbone of the DNA molecule. The process called BASE EXCISION REPAIR can be completed by a DNA-(APURINIC OR APYRIMIDINIC SITE) LYASE which excises the remaining RIBOSE sugar from the DNA.

Enzymes that are part of the restriction-modification systems. They are responsible for producing a species-characteristic methylation pattern, on either adenine or cytosine residues, in a specific short base sequence in the host cell's own DNA. This methylated sequence will occur many times in the host-cell DNA and remain intact for the lifetime of the cell. Any DNA from another species which gains entry into a living cell and lacks the characteristic methylation pattern will be recognized by the restriction endonucleases of similar specificity and destroyed by cleavage. Most have been studied in bacterial systems, but a few have been found in eukaryotic organisms.

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

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 sulfhydryl reagent that is widely used in experimental biochemical studies.

Enzymes that are involved in the reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule, which contained damaged regions.

Polymers where the main polymer chain comprises recurring amide groups. These compounds are generally formed from combinations of diamines, diacids, and amino acids and yield fibers, sheeting, or extruded forms used in textiles, gels, filters, sutures, contact lenses, and other biomaterials.

Abnormal growths of tissue that follow a previous neoplasm but are not metastases of the latter. The second neoplasm may have the same or different histological type and can occur in the same or different organs as the previous neoplasm but in all cases arises from an independent oncogenic event. The development of the second neoplasm may or may not be related to the treatment for the previous neoplasm since genetic risk or predisposing factors may actually be the cause.

An alkylating agent of value against both hematologic malignancies and solid tumors.

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

Antineoplastic agent especially effective against malignant brain tumors. The resistance which brain tumor cells acquire to the initial effectiveness of this drug can be partially overcome by the simultaneous use of membrane-modifying agents such as reserpine, calcium antagonists such as nicardipine or verapamil, or the calmodulin inhibitor, trifluoperazine. The drug has also been used in combination with other antineoplastic agents or with radiotherapy for the treatment of various neoplasms.

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

The action of a drug in promoting or enhancing the effectiveness of another drug.

Toxic antibiotic of the mitomycin group, obtained from MITOMYCIN and also from Streptomyces ardus and other species. It is proposed as an antineoplastic agent, with some antibiotic properties.

Organic salts or esters of methanesulfonic acid.

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

Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.

Nitrogen mustard analog of quinacrine used primarily as a stain in the studies of chromosomes and chromatin. Fluoresces by reaction with nucleic acids in chromosomes.

An oral anticoagulant that interferes with the metabolism of vitamin K. It is also used in biochemical experiments as an inhibitor of reductases.

An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle.

Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)

The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.

Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.

A class of enzymes involved in the hydrolysis of the N-glycosidic bond of nitrogen-linked sugars.

A synthetic amino acid that depletes glutathione by irreversibly inhibiting gamma-glutamylcysteine synthetase. Inhibition of this enzyme is a critical step in glutathione biosynthesis. It has been shown to inhibit the proliferative response in human T-lymphocytes and inhibit macrophage activation. (J Biol Chem 1995;270(33):1945-7)

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

Leukemia produced by exposure to IONIZING RADIATION or NON-IONIZING RADIATION.

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.

An experimental lymphocytic leukemia of mice.

An alkylating sulfhydryl reagent. Its actions are similar to those of iodoacetate.

Methods of investigating the effectiveness of anticancer cytotoxic drugs and biologic inhibitors. These include in vitro cell-kill models and cytostatic dye exclusion tests as well as in vivo measurement of tumor growth parameters in laboratory animals.

Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.

Six-carbon alicyclic hydrocarbons which contain one or more double bonds in the ring. The cyclohexadienes are not aromatic, in contrast to BENZOQUINONES which are sometimes called 2,5-cyclohexadiene-1,4-diones.

Enzymes that catalyze the transfer of multiple ADP-RIBOSE groups from nicotinamide-adenine dinucleotide (NAD) onto protein targets, thus building up a linear or branched homopolymer of repeating ADP-ribose units i.e., POLY ADENOSINE DIPHOSPHATE RIBOSE.

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 genus of the family Muridae consisting of eleven species. C. migratorius, the grey or Armenian hamster, and C. griseus, the Chinese hamster, are the two species used in biomedical research.

A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.

Established cell cultures that have the potential to propagate indefinitely.

A polynucleotide formed from the ADP-RIBOSE moiety of nicotinamide-adenine dinucleotide (NAD) by POLY(ADP-RIBOSE) POLYMERASES.

Reagents with two reactive groups, usually at opposite ends of the molecule, that are capable of reacting with and thereby forming bridges between side chains of amino acids in proteins; the locations of naturally reactive areas within proteins can thereby be identified; may also be used for other macromolecules, like glycoproteins, nucleic acids, or other.

An alkylating agent having a selective immunosuppressive effect on BONE MARROW. It has been used in the palliative treatment of chronic myeloid leukemia (MYELOID LEUKEMIA, CHRONIC), but although symptomatic relief is provided, no permanent remission is brought about. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), busulfan is listed as a known carcinogen.

The use of IONIZING RADIATION to treat malignant NEOPLASMS and some benign conditions.

DNA present in neoplastic tissue.

A DNA repair enzyme that catalyses the excision of ribose residues at apurinic and apyrimidinic DNA sites that can result from the action of DNA GLYCOSYLASES. The enzyme catalyzes a beta-elimination reaction in which the C-O-P bond 3' to the apurinic or apyrimidinic site in DNA is broken, leaving a 3'-terminal unsaturated sugar and a product with a terminal 5'-phosphate. This enzyme was previously listed under EC 3.1.25.2.

A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides.

The rate dynamics in chemical or physical systems.

A lymphoproliferative disorder characterized by pleomorphic B-LYMPHOCYTES including PLASMA CELLS, with increased levels of monoclonal serum IMMUNOGLOBULIN M. There is lymphoplasmacytic cells infiltration into bone marrow and often other tissues, also known as lymphoplasmacytic lymphoma. Clinical features include ANEMIA; HEMORRHAGES; and hyperviscosity.

A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.

A basic polypeptide isolated from Streptomyces netropsis. It is cytotoxic and its strong, specific binding to A-T areas of DNA is useful to genetics research.

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.

Compounds containing the -SH radical.

The treatment of a disease or condition by several different means simultaneously or sequentially. Chemoimmunotherapy, RADIOIMMUNOTHERAPY, chemoradiotherapy, cryochemotherapy, and SALVAGE THERAPY are seen most frequently, but their combinations with each other and surgery are also used.

4-Methyl derivative of LOMUSTINE; (CCNU). An antineoplastic agent which functions as an alkylating agent.

Clonal hematopoietic stem cell disorders characterized by dysplasia in one or more hematopoietic cell lineages. They predominantly affect patients over 60, are considered preleukemic conditions, and have high probability of transformation into ACUTE MYELOID LEUKEMIA.

The presence of an uncomplimentary base in double-stranded DNA caused by spontaneous deamination of cytosine or adenine, mismatching during homologous recombination, or errors in DNA replication. Multiple, sequential base pair mismatches lead to formation of heteroduplex DNA; (NUCLEIC ACID HETERODUPLEXES).

Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.

An antibiotic compound derived from Streptomyces niveus. It has a chemical structure similar to coumarin. Novobiocin binds to DNA gyrase, and blocks adenosine triphosphatase (ATPase) activity. (From Reynolds, Martindale The Extra Pharmacopoeia, 30th ed, p189)

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

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.

Alkylating antineoplastic toxic to bone marrow; used in breast cancer, also in combination with other drugs.

Positional isomer of CYCLOPHOSPHAMIDE which is active as an alkylating agent and an immunosuppressive agent.

Materials that add an electron to an element or compound, that is, decrease the positiveness of its valence. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)

An experimental lymphocytic leukemia originally induced in DBA/2 mice by painting with methylcholanthrene.

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.

Oligopeptide antibiotics from Streptomyces distallicus. Their binding to DNA inhibits synthesis of nucleic acids.

An antitumor alkaloid isolated from VINCA ROSEA. (Merck, 11th ed.)

Compounds that inhibit the activity of DNA TOPOISOMERASES.

Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.

Hydrolysate of DNA in which purine bases have been removed.

A lignan (LIGNANS) found in PODOPHYLLIN resin from the roots of PODOPHYLLUM plants. It is a potent spindle poison, toxic if taken internally, and has been used as a cathartic. It is very irritating to skin and mucous membranes, has keratolytic actions, has been used to treat warts and keratoses, and may have antineoplastic properties, as do some of its congeners and derivatives.

Alkylating anti-neoplastic agent.

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

Compounds that inhibit the activity of DNA TOPOISOMERASE II. Included in this category are a variety of ANTINEOPLASTIC AGENTS which target the eukaryotic form of topoisomerase II and ANTIBACTERIAL AGENTS which target the prokaryotic form of topoisomerase II.

A chlorinated epoxy compound used as an industrial solvent. It is a strong skin irritant and carcinogen.

CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.

Chemicals that are used to cause the disturbance, disease, or death of humans during WARFARE.

A transplantable carcinoma of the rat that originally appeared spontaneously in the mammary gland of a pregnant albino rat, and which now resembles a carcinoma in young transplants and a sarcoma in older transplants. (Stedman, 25th ed)

An enzyme which catalyzes the endonucleolytic cleavage of phosphodiester bonds at purinic or apyrimidinic sites (AP-sites) to produce 5'-Phosphooligonucleotide end products. The enzyme prefers single-stranded DNA (ssDNA) and was formerly classified as EC 3.1.4.30.

Enzymes that catalyze the cleavage of a carbon-oxygen bond by means other than hydrolysis or oxidation. EC 4.2.

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

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.

A group of indole-indoline dimers which are ALKALOIDS obtained from the VINCA genus of plants. They inhibit polymerization of TUBULIN into MICROTUBULES thus blocking spindle formation and arresting cells in METAPHASE. They are some of the most useful ANTINEOPLASTIC AGENTS.

A cell line derived from cultured tumor cells.

A thiol-containing non-essential amino acid that is oxidized to form CYSTINE.

A sarcoma derived from deep fibrous tissue, characterized by bundles of immature proliferating fibroblasts with variable collagen formation, which tends to invade locally and metastasize by the bloodstream. (Stedman, 25th ed)

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.

A nitroimidazole that sensitizes normally radio-resistant hypoxic cells to radiation. It may also be directly cytotoxic to hypoxic cells and has been proposed as an antineoplastic.

A cytologic technique for measuring the functional capacity of tumor stem cells by assaying their activity. It is used primarily for the in vitro testing of antineoplastic agents.

A nucleoside antibiotic isolated from Streptomyces antibioticus. It has some antineoplastic properties and has broad spectrum activity against DNA viruses in cell cultures and significant antiviral activity against infections caused by a variety of viruses such as the herpes viruses, the VACCINIA VIRUS and varicella zoster virus.

One of the SCHISTOSOMICIDES, it has been replaced largely by HYCANTHONE and more recently PRAZIQUANTEL. (From Martindale The Extrapharmacopoeia, 30th ed., p46)

The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells.

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.

Abnormal number or structure of chromosomes. Chromosome aberrations may result in CHROMOSOME DISORDERS.

A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)

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

Congenital disorder affecting all bone marrow elements, resulting in ANEMIA; LEUKOPENIA; and THROMBOPENIA, and associated with cardiac, renal, and limb malformations as well as dermal pigmentary changes. Spontaneous CHROMOSOME BREAKAGE is a feature of this disease along with predisposition to LEUKEMIA. There are at least 7 complementation groups in Fanconi anemia: FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, and FANCL. (from Online Mendelian Inheritance in Man, http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=227650, August 20, 2004)

A chronic leukemia characterized by abnormal B-lymphocytes and often generalized lymphadenopathy. In patients presenting predominately with blood and bone marrow involvement it is called chronic lymphocytic leukemia (CLL); in those predominately with enlarged lymph nodes it is called small lymphocytic lymphoma. These terms represent spectrums of the same disease.

Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (MYELOID PROGENITOR CELLS) in the bone marrow and other sites.

A malignancy of mature PLASMA CELLS engaging in monoclonal immunoglobulin production. It is characterized by hyperglobulinemia, excess Bence-Jones proteins (free monoclonal IMMUNOGLOBULIN LIGHT CHAINS) in the urine, skeletal destruction, bone pain, and fractures. Other features include ANEMIA; HYPERCALCEMIA; and RENAL INSUFFICIENCY.

A malignant disease characterized by progressive enlargement of the lymph nodes, spleen, and general lymphoid tissue. In the classical variant, giant usually multinucleate Hodgkin's and REED-STERNBERG CELLS are present; in the nodular lymphocyte predominant variant, lymphocytic and histiocytic cells are seen.

Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.

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.

Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.

Activation of c-Jun N-terminal kinase 1 by UV irradiation is inhibited by wortmannin without affecting c-iun expression. (1/1003)

Activation of c-Jun N-terminal kinases (JNKs)/stress-activated protein kinases is an early response of cells upon exposure to DNA-damaging agents. JNK-mediated phosphorylation of c-Jun is currently understood to stimulate the transactivating potency of AP-1 (e.g., c-Jun/c-Fos; c-Jun/ATF-2), thereby increasing the expression of AP-1 target genes. Here we show that stimulation of JNK1 activity is not a general early response of cells exposed to genotoxic agents. Treatment of NIH 3T3 cells with UV light (UV-C) as well as with methyl methanesulfonate (MMS) caused activation of JNK1 and an increase in c-Jun protein and AP-1 binding activity, whereas antineoplastic drugs such as mafosfamide, mitomycin C, N-hydroxyethyl-N-chloroethylnitrosourea, and treosulfan did not elicit this response. The phosphatidylinositol 3-kinase inhibitor wortmannin specifically blocked the UV-stimulated activation of JNK1 but did not affect UV-driven activation of extracellular regulated kinase 2 (ERK2). To investigate the significance of JNK1 for transactivation of c-jun, we analyzed the effect of UV irradiation on c-jun expression under conditions of wortmannin-mediated inhibition of UV-induced stimulation of JNK1. Neither the UV-induced increase in c-jun mRNA, c-Jun protein, and AP-1 binding nor the activation of the collagenase and c-jun promoters was affected by wortmannin. In contrast, the mitogen-activated protein kinase/ERK kinase inhibitor PD98056, which blocked ERK2 but not JNK1 activation by UV irradiation, impaired UV-driven c-Jun protein induction and AP-1 binding. Based on the data, we suggest that JNK1 stimulation is not essential for transactivation of c-jun after UV exposure, whereas activation of ERK2 is required for UV-induced signaling leading to elevated c-jun expression. (+info)

The Saccharomyces cerevisiae ETH1 gene, an inducible homolog of exonuclease III that provides resistance to DNA-damaging agents and limits spontaneous mutagenesis. (2/1003)

The recently sequenced Saccharomyces cerevisiae genome was searched for a gene with homology to the gene encoding the major human AP endonuclease, a component of the highly conserved DNA base excision repair pathway. An open reading frame was found to encode a putative protein (34% identical to the Schizosaccharomyces pombe eth1(+) [open reading frame SPBC3D6.10] gene product) with a 347-residue segment homologous to the exonuclease III family of AP endonucleases. Synthesis of mRNA from ETH1 in wild-type cells was induced sixfold relative to that in untreated cells after exposure to the alkylating agent methyl methanesulfonate (MMS). To investigate the function of ETH1, deletions of the open reading frame were made in a wild-type strain and a strain deficient in the known yeast AP endonuclease encoded by APN1. eth1 strains were not more sensitive to killing by MMS, hydrogen peroxide, or phleomycin D1, whereas apn1 strains were approximately 3-fold more sensitive to MMS and approximately 10-fold more sensitive to hydrogen peroxide than was the wild type. Double-mutant strains (apn1 eth1) were approximately 15-fold more sensitive to MMS and approximately 2- to 3-fold more sensitive to hydrogen peroxide and phleomycin D1 than were apn1 strains. Elimination of ETH1 in apn1 strains also increased spontaneous mutation rates 9- or 31-fold compared to the wild type as determined by reversion to adenine or lysine prototrophy, respectively. Transformation of apn1 eth1 cells with an expression vector containing ETH1 reversed the hypersensitivity to MMS and limited the rate of spontaneous mutagenesis. Expression of ETH1 in a dut-1 xthA3 Escherichia coli strain demonstrated that the gene product functionally complements the missing AP endonuclease activity. Thus, in apn1 cells where the major AP endonuclease activity is missing, ETH1 offers an alternate capacity for repair of spontaneous or induced damage to DNA that is normally repaired by Apn1 protein. (+info)

Mismatch repair and differential sensitivity of mouse and human cells to methylating agents. (3/1003)

The long-patch mismatch repair pathway contributes to the cytotoxic effect of methylating agents and loss of this pathway confers tolerance to DNA methylation damage. Two methylation-tolerant mouse cell lines were identified and were shown to be defective in the MSH2 protein by in vitro mismatch repair assay. A normal copy of the human MSH2 gene, introduced by transfer of human chromosome 2, reversed the methylation tolerance. These mismatch repair defective mouse cells together with a fibroblast cell line derived from an MSH2-/- mouse, were all as resistant to N-methyl-N-nitrosourea as repair-defective human cells. Although long-patch mismatch repair-defective human cells were 50- to 100-fold more resistant to methylating agents than repair-proficient cells, loss of the same pathway from mouse cells conferred only a 3-fold increase. This discrepancy was accounted for by the intrinsic N-methyl-N-nitrosourea resistance of normal or transformed mouse cells compared with human cells. The >20-fold differential resistance between mouse and human cells could not be explained by the levels of either DNA methylation damage or the repair enzyme O6-methylguanine-DNA methyltransferase. The resistance of mouse cells to N-methyl-N-nitrosourea was selective and no cross-resistance to unrelated DNA damaging agents was observed. Pathways of apoptosis were apparently intact and functional after exposure to either N-methyl-N-nitrosourea or ultraviolet light. Extracts of mouse cells were found to perform 2-fold less long-patch mismatch repair. The reduced level of mismatch repair may contribute to their lack of sensitivity to DNA methylation damage. (+info)

Tightly regulated and inducible expression of rabbit CYP2E1 using a tetracycline-controlled expression system. (4/1003)

A tetracycline (Tc)-controlled gene expression system that quantitatively controls gene expression in eukaryotic cells () was used to express cytochrome P-450 2E1 (CYP2E1) in HeLa cells in culture. The rabbit CYP2E1 cDNA was subcloned into the Tc-controlled expression vector (pUHD10-3) and transfected into a HeLa cell line constitutively expressing the Tc-controlled transactivator, a positive regulator of expression in the absence of Tc. The expression of CYP2E1 was tightly regulated. There was a time-dependent induction of CYP2E1 after removal of Tc. In the absence of Tc, the enzyme was induced more than 100-fold and expressed about 18 pmol of CYP2E1/mg microsomal protein. At maximal levels of expression the enzyme catalyzed the formation of 158 pmol 6-hydroxychlorzoxazone/min/mg total cellular protein. In addition, the level of the enzyme could be modulated by the concentration of Tc in the media. In the absence of Tc, exposure of cells to N-nitrosodimethylamine caused a significant dose-dependent decrease in cell viability. In contrast, menadione, a redox cycling toxicant, was less toxic to the cells after induction of CYP2E1 when compared with noninduced cells. Pulse-chase studies conducted 72 h after removal of Tc indicated a rapid turnover of CYP2E1 with a half-life of 3.9 h. Addition of the ligand, 4-methylpyrazole, and the suicide substrate, 1-aminobenzotrizole, decreased the degradation of CYP2E1. This cell line offers a useful system to examine the role of CYP2E1 in the cytotoxicity of xenobiotics and to investigate post-translational regulation of the enzyme. (+info)

Cells deficient in DNA polymerase beta are hypersensitive to alkylating agent-induced apoptosis and chromosomal breakage. (5/1003)

DNA polymerase beta (beta-pol), which is involved in base excision repair, was investigated for its role in protection of cells against various genotoxic agents and cytostatic drugs using beta-pol knockout mouse fibroblasts. We show that cells lacking beta-pol are highly sensitive to induction of apoptosis and chromosomal breakage by methylating agents, such as N-methyl-N'-nitro-N-nitrosoguanidine and methyl methanesulfonate and the cross-linking antineoplastic drugs mitomycin C and mafosfamide. The cross-sensitivity between the agents observed suggests that beta-pol is involved in repair not only of DNA methylation lesions but also of other kinds of DNA damage induced by various cytostatic drugs. Cells deficient in beta-pol were not hypersensitive to cisplatin, melphalan, benzo(a)pyrene diol epoxide, chloroethylnitrosourea, or UV light. Because both established and primary beta-pol knockout fibroblasts displayed the hypersensitive phenotype, which, moreover, was complemented by transfection with a beta-pol expression vector, the alkylating agent hypersensitivity can clearly be attributed to the beta-pol deficiency. The results demonstrate that beta-pol-driven base excision repair is highly important for protection of cells against cell killing due to apoptosis and induced chromosomal breakage and suggest that incompletely repaired DNA damage causes chromosomal changes and may act as a trigger of DNA damage-induced apoptosis. (+info)

Molecular analysis of mutants obtained by treatment with alkylating agents in a quadruplicated white-ivory strain of Drosophila melanogaster. (6/1003)

The use of a white-ivory (wi) strain of Drosophila melanogaster carrying four copies of this allele, (wi)4, has proved to be useful in detecting somatic mutation in genotoxicity testing. Nevertheless, until now very little information exists about the nature of the genetic effects detected in such a strain. This work presents molecular data on the changes that have taken place in different germinal mutants obtained after treatment with alkylating agents. Three different phenotypes were obtained: wild-type red eyes, dark red eyes and eyes lighter than (wi)4. Our results show that, in at least one of the four copies of the allele, the wild-type red eye phenotypes are due to a precise excision of the 2.96 kb duplicated region characteristic of the wi allele. These data agree with previous results obtained in a strain carrying only a single copy of the wi allele. The dark red eye mutants analysed seemed to be generated as a cluster and all proved to be caused by deletions at the 3'-end of the duplicated wi region in two of the copies of the (wi)4 genome. Finally, the light eye mutants (obtained at high frequencies) failed to show alterations at the molecular level, although we cannot discard the possibility that they might have originated by the loss of some of the wi copies of the (wi)4 strain. (+info)

Alterations in Bacillus subtilis transforming DNA induced by beta-propiolactone and 1,3-propane sultone, two mutagenic and carcinogenic alkylating agents. (7/1003)

Transforming DNA was exposed to either beta-propiolactone or 1,3-propane sultone and then used for transformation of competent bacteria to nutritional independence from tyrosine and tryptophan (linked markers) and leucine (an unlinked marker). The ability to transform was progressively lost by the DNA during incubation with either of these two chemicals. For all three markers the inactivation curve was biphasic, with a short period of rapid inactivation followed by one characterized by a much slower rate. The overall rate of inactivation was different for all three markers and presumably was related to the size of the marker. The decrease in the transforming activity was in part due to the slower rate of penetration of alkylated DNA through the cellular membrane and its inability to enter the recipient bacteria. This decrease in the rate of cellular uptake, even for DNA eventually destined to enter the cell, began almost immediately after its exposure to the chemical and ended up with an almost complete lack of recognition of the heavily alkylated DNA by the specific surface receptors of competent cells. Such DNA attached to sites on the surface of competent bacteria which were different from receptors specific for the untreated nucleic acid. This attachment was not followed by uptake of the altered DNA. Presence of albumin during the incubation with a carcinogen further increased the degree of inactivation, indicating that the artificial nucleoproteins produced under such conditions were less efficient in the transformation assay than was the naked DNA. Cotransfomration of close markers progressively decreased, beginning immediately after the start of incubation of DNA with the chemicals. Extensively alkylated DNA fractionated by sedimentation through sucrose density gradients showed a peculiar distribution of cotransforming activity for such markers; namely, molecules larger than the bulk of DNA ("megamolecules") showed less ability to transform the second marker than did some of the apparently smaller molecules which sedimented more slowly through the gradient. An increase in cotransformation of distant markers was evident in DNA molecules after a short exposure to an alkylating agent, but cotransformation of such markers was absent in DNA treated for longer periods. The observed changes in the transforming and cotransforming activities of the alkylated DNA can be explained by what is known about the physicochemistry of such DNA and in particular about the propensity of the alkylated and broken molecules to form complexes with themselves and with other macromolecules. (+info)

The role of thiotepa in allogeneic bone marrow transplantation for genetic diseases. (8/1003)

Graft-versus-host disease (GVHD), graft rejection, disease recurrence and long-term toxicity remain significant obstacles to successful allogeneic bone marrow transplantation (BMT) in children with genetic diseases. In an attempt to improve results, we used a preparative regimen consisting of three alkylating agents, busulfan (BU), thiotepa (TTP) and cyclophosphamide (CY), for T cell-depleted allogeneic bone marrow transplantation instead of the conventional BU-CY protocol. The effect of this intensified regimen was investigated in 26 consecutive children with genetic diseases who underwent T cell-depleted BMT from HLA-identical siblings. Sixteen patients were males and 10 females, of median age 5 (0.2-14) years. The diseases included beta-thalassemia major, osteopetrosis, severe combined immunodeficiency, Wiskott-Aldrich syndrome, familial agranulocytosis, congenital idiopathic hemolytic anemia (CIHA), Gaucher's disease, Niemann-Pick disease, Hurler's syndrome, and adrenoleukodystrophy. The conditioning regimen consisted of BU 4 mg/kg x 4 days (-8 to -5), TTP 5 mg/kg x 2 days (-4 and -3), and CY 60 mg/kg x 2 days (-2 and -1). Engraftment was as expected, with WBC >1.0 x 10(9)/l at day +19 (10-33), ANC >0.5 x 10(9)/l at day +22 (10-56) and platelets >25 x 10(9)/l at day +32 (18-131). Transplant-related mortality was 19%. Overall survival and disease-free survival (DFS) at 60 months follow-up were both 77%. Our results with the BU-TTP-CY regimen followed by T cell-depleted BMT in genetic diseases may provide a basis for prospective comparison with the standard conditioning regimen of BU-CY in the management of children suffering from these conditions. (+info)

Previous articleNeoplastic Cells
Next articleNephrocalcinosis

The symptoms of Sarcoma, Yoshida can vary depending on the location of the tumor, but may include pain, swelling, and limited mobility in the affected limb. The diagnosis of this condition is based on a combination of imaging studies such as CT or MRI scans, and a biopsy to confirm the presence of cancer cells.

Treatment for Sarcoma, Yoshida usually involves a combination of surgery, chemotherapy, and radiation therapy. The prognosis for this condition is generally poor, with a five-year survival rate of around 30%. However, early detection and aggressive treatment can improve outcomes.

There are several types of gliomas, including:

1. Astrocytoma: This is the most common type of glioma, accounting for about 50% of all cases. It arises from the star-shaped cells called astrocytes that provide support and nutrients to the brain's nerve cells.
2. Oligodendroglioma: This type of glioma originates from the oligodendrocytes, which are responsible for producing the fatty substance called myelin that insulates the nerve fibers.
3. Glioblastoma (GBM): This is the most aggressive and malignant type of glioma, accounting for about 70% of all cases. It is fast-growing and often spreads to other parts of the brain.
4. Brain stem glioma: This type of glioma arises in the brain stem, which is responsible for controlling many of the body's vital functions such as breathing, heart rate, and blood pressure.

The symptoms of glioma depend on the location and size of the tumor. Common symptoms include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory, or speech.

Gliomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and tissue biopsy to confirm the presence of cancer cells. Treatment options for glioma depend on the type and location of the tumor, as well as the patient's overall health. Surgery is often the first line of treatment to remove as much of the tumor as possible, followed by radiation therapy and/or chemotherapy to kill any remaining cancer cells.

The prognosis for glioma patients varies depending on the type and location of the tumor, as well as the patient's overall health. In general, the prognosis is better for patients with slow-growing, low-grade tumors, while those with fast-growing, high-grade tumors have a poorer prognosis. Overall, the 5-year survival rate for glioma patients is around 30-40%.

Brain neoplasms can arise from various types of cells in the brain, including glial cells (such as astrocytes and oligodendrocytes), neurons, and vascular tissues. The symptoms of brain neoplasms vary depending on their size, location, and type, but may include headaches, seizures, weakness or numbness in the limbs, and changes in personality or cognitive function.

There are several different types of brain neoplasms, including:

1. Meningiomas: These are benign tumors that arise from the meninges, the thin layers of tissue that cover the brain and spinal cord.
2. Gliomas: These are malignant tumors that arise from glial cells in the brain. The most common type of glioma is a glioblastoma, which is aggressive and hard to treat.
3. Pineal parenchymal tumors: These are rare tumors that arise in the pineal gland, a small endocrine gland in the brain.
4. Craniopharyngiomas: These are benign tumors that arise from the epithelial cells of the pituitary gland and the hypothalamus.
5. Medulloblastomas: These are malignant tumors that arise in the cerebellum, specifically in the medulla oblongata. They are most common in children.
6. Acoustic neurinomas: These are benign tumors that arise on the nerve that connects the inner ear to the brain.
7. Oligodendrogliomas: These are malignant tumors that arise from oligodendrocytes, the cells that produce the fatty substance called myelin that insulates nerve fibers.
8. Lymphomas: These are cancers of the immune system that can arise in the brain and spinal cord. The most common type of lymphoma in the CNS is primary central nervous system (CNS) lymphoma, which is usually a type of B-cell non-Hodgkin lymphoma.
9. Metastatic tumors: These are tumors that have spread to the brain from another part of the body. The most common types of metastatic tumors in the CNS are breast cancer, lung cancer, and melanoma.

These are just a few examples of the many types of brain and spinal cord tumors that can occur. Each type of tumor has its own unique characteristics, such as its location, size, growth rate, and biological behavior. These factors can help doctors determine the best course of treatment for each patient.

Radiation-induced leukemia is a rare but potentially fatal condition that occurs when a person is exposed to high levels of ionizing radiation, such as from nuclear fallout or radiation therapy. The radiation damages the DNA in the stem cells of the bone marrow, leading to mutations that can cause the development of cancer.

There are two main types of radiation-induced leukemia: acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). AML is the more common type and typically occurs within 1-5 years after exposure to high levels of radiation. CML can take up to 10 years or more to develop.

Symptoms of radiation-induced leukemia can include fatigue, fever, night sweats, weight loss, and easy bruising or bleeding. Treatment typically involves chemotherapy and/or bone marrow transplantation. The prognosis for radiation-induced leukemia is generally poor, with a 5-year survival rate of less than 50%.

Prevention is key to avoiding radiation-induced leukemia. People who work with or are exposed to high levels of radiation, such as nuclear power plant workers, should take precautions to minimize their exposure and undergo regular medical checkups to monitor their health. Additionally, people who have undergone radiation therapy for cancer should be closely monitored by their healthcare providers for any signs of leukemia or other radiation-related side effects.

The Leukemia L5178 cell line has been used in numerous studies to investigate the molecular mechanisms underlying cancer development and progression. For example, researchers have used these cells to study the role of specific genes and proteins in tumorigenesis, as well as the effects of environmental factors such as radiation and chemical carcinogens on cancer development.

In addition to its use in basic research, the Leukemia L5178 cell line has also been used as a model system for testing the efficacy of new anti-cancer drugs. These cells are often implanted into mice and then treated with different drug regimens to assess their ability to inhibit tumor growth and induce apoptosis (programmed cell death).

Overall, the Leukemia L5178 cell line is a valuable tool for cancer researchers, providing a reliable and well-characterized model system for studying various aspects of cancer biology. Its use has contributed significantly to our understanding of the molecular mechanisms underlying cancer development and progression, and has helped to identify potential therapeutic targets for the treatment of this disease.

Glioblastomas are highly malignant tumors that can grow rapidly and infiltrate surrounding brain tissue, making them difficult to remove surgically. They often recur after treatment and are usually fatal within a few years of diagnosis.

The symptoms of glioblastoma can vary depending on the location and size of the tumor but may include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory or cognitive function.

Glioblastomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and a biopsy to confirm the presence of cancerous cells. Treatment typically involves surgery to remove as much of the tumor as possible, followed by radiation therapy and chemotherapy to slow the growth of any remaining cancerous cells.

Prognosis for glioblastoma is generally poor, with a five-year survival rate of around 5% for newly diagnosed patients. However, the prognosis can vary depending on factors such as the location and size of the tumor, the patient's age and overall health, and the effectiveness of treatment.

The disease is named after the Swedish physician Jan G. Waldenström, who first described it in 1944. It is also known as lymphoplasmacytic lymphoma or IgM multoculullarity.

The exact cause of Waldenström macroglobulinemia is not known, but it is believed to be linked to genetic mutations that occur in the plasma cells. The condition usually affects older adults and is more common in males than females.

Symptoms of Waldenström macroglobulinemia can include:

* Fatigue
* Weight loss
* Enlargement of the liver and spleen
* Swelling in the legs, ankles, and hands
* Pain in the bones or joints
* Increased risk of infections
* Numbness or tingling in the hands and feet

The diagnosis of Waldenström macroglobulinemia is based on a combination of physical examination, blood tests, and imaging studies. Treatment options include chemotherapy, immunomodulatory drugs, and stem cell transplantation. The prognosis for the disease varies depending on the severity of the symptoms and the response to treatment.

Overall, Waldenström macroglobulinemia is a rare and complex condition that requires careful management by a team of healthcare professionals. With appropriate treatment, many patients with this condition can experience long-term remission and improved quality of life.

There are several subtypes of MDS, each with distinct clinical features and prognosis. The most common subtype is refractory anemia with excess blasts (RAEB), followed by chronic myelomonocytic leukemia (CMMoL) and acute myeloid leukemia (AML).

The exact cause of MDS is not fully understood, but it is believed to result from a combination of genetic mutations and environmental factors. Risk factors for developing MDS include exposure to certain chemicals or radiation, age over 60, and a history of previous cancer treatment.

Symptoms of MDS can vary depending on the specific subtype and severity of the disorder, but may include fatigue, weakness, shortness of breath, infection, bleeding, and easy bruising. Diagnosis is typically made through a combination of physical examination, medical history, blood tests, and bone marrow biopsy.

Treatment for MDS depends on the specific subtype and severity of the disorder, as well as the patient's overall health and preferences. Options may include supportive care, such as blood transfusions and antibiotics, or more intensive therapies like chemotherapy, bone marrow transplantation, or gene therapy.

Overall, myelodysplastic syndromes are a complex and heterogeneous group of disorders that can have a significant impact on quality of life and survival. Ongoing research is focused on improving diagnostic accuracy, developing more effective treatments, and exploring novel therapeutic approaches to improve outcomes for patients with MDS.

In the medical field, Leukemia P388 is defined as a subline of leukemia cells that exhibits a specific set of genetic alterations and characteristics, including the ability to grow and proliferate in culture and in vivo, resistance to certain drugs and therapies, and the presence of specific markers and mutations.

Leukemia P388 is commonly used in research to study the biology of leukemia and to develop new treatments for this disease. It is also sometimes used as a model to study other types of cancer, such as lymphoma and solid tumors.

Overall, Leukemia P388 is an important tool in the study of cancer biology and is used to advance our understanding of the disease and to develop new treatments for patients with leukemia and other types of cancer.

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.

Without more information about the context in which this term is being used, it is difficult to provide a clear definition or interpretation of its meaning. However, based on the name "Walker" and the fact that it is followed by a number (256), it is possible that this term may refer to a specific type of cancer or tumor that has been identified in a patient with the last name Walker.

It's important to note that the diagnosis and treatment of cancer can be complex and highly individualized, and any medical information or terminology should only be interpreted and applied by qualified healthcare professionals who have access to the relevant clinical context and patient information.

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.

The exact cause of fibrosarcoma is not known, but it is believed to be linked to genetic mutations that occur during a person's lifetime. Some risk factors for developing fibrosarcoma include previous radiation exposure, chronic inflammation, and certain inherited conditions such as neurofibromatosis type 1 (NF1).

The symptoms of fibrosarcoma can vary depending on the location and size of the tumor. In some cases, there may be no symptoms until the tumor has grown to a significant size. Common symptoms include pain, swelling, and limited mobility in the affected limb. If the tumor is near a nerve, it can also cause numbness or tingling sensations in the affected area.

Diagnosis of fibrosarcoma typically involves a combination of imaging tests such as X-rays, CT scans, and MRI scans, as well as a biopsy to confirm the presence of cancer cells. Treatment options for fibrosarcoma may include surgery, radiation therapy, and chemotherapy, depending on the size and location of the tumor, as well as the patient's overall health.

Prognosis for fibrosarcoma is generally good if the tumor is caught early and treated aggressively. However, if the cancer has spread to other parts of the body (metastasized), the prognosis is generally poorer. In some cases, the cancer can recur after treatment, so it is important for patients to follow their doctor's recommendations for regular check-ups and follow-up testing.

Overall, fibrosarcoma is a rare and aggressive form of cancer that can be challenging to diagnose and treat. However, with early detection and appropriate treatment, many people with this condition can achieve long-term survival and a good quality of life.

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.

There are several different types of leukemia, including:

1. Acute Lymphoblastic Leukemia (ALL): This is the most common type of leukemia in children, but it can also occur in adults. It is characterized by an overproduction of immature white blood cells called lymphoblasts.
2. Acute Myeloid Leukemia (AML): This type of leukemia affects the bone marrow's ability to produce red blood cells, platelets, and other white blood cells. It can occur at any age but is most common in adults.
3. Chronic Lymphocytic Leukemia (CLL): This type of leukemia affects older adults and is characterized by the slow growth of abnormal white blood cells called lymphocytes.
4. Chronic Myeloid Leukemia (CML): This type of leukemia is caused by a genetic mutation in a gene called BCR-ABL. It can occur at any age but is most common in adults.
5. Hairy Cell Leukemia: This is a rare type of leukemia that affects older adults and is characterized by the presence of abnormal white blood cells called hairy cells.
6. Myelodysplastic Syndrome (MDS): This is a group of disorders that occur when the bone marrow is unable to produce healthy blood cells. It can lead to leukemia if left untreated.

Treatment for leukemia depends on the type and severity of the disease, but may include chemotherapy, radiation therapy, targeted therapy, or stem cell transplantation.

There are currently no cures for Fanconi anemia, but bone marrow transplantation and other supportive therapies can help manage some of the symptoms and improve quality of life. Research into the genetics and molecular biology of Fanconi anemia is ongoing to better understand the disorder and develop new treatments.

Some of the common symptoms of Fanconi anemia include short stature, limb deformities, hearing loss, vision problems, and an increased risk of infections and cancer. Children with Fanconi anemia may also experience developmental delays, learning disabilities, and social and emotional challenges.

The diagnosis of Fanconi anemia is typically made based on a combination of clinical findings, laboratory tests, and genetic analysis. Treatment options for Fanconi anemia depend on the severity of the disorder and may include bone marrow transplantation, blood transfusions, antibiotics, and other supportive therapies.

Fanconi anemia is a rare disorder that affects approximately 1 in 160,000 births worldwide. It is more common in certain populations, such as Ashkenazi Jews and individuals of Spanish descent. Fanconi anemia can be inherited in an autosomal recessive pattern, meaning that a child must inherit two copies of the mutated gene (one from each parent) to develop the disorder.

Overall, Fanconi anemia is a complex and rare genetic disorder that requires specialized medical care and ongoing research to better understand its causes and develop effective treatments. With appropriate management and supportive therapies, individuals with Fanconi anemia can lead fulfilling lives despite the challenges associated with the disorder.

White blood cells are an important part of the immune system, and they help to fight off infections and diseases. A low number of white blood cells can make a person more susceptible to infections and other health problems.

There are several different types of leukopenia, including:

* Severe congenital neutropenia: This is a rare genetic disorder that causes a severe decrease in the number of neutrophils, a type of white blood cell.
* Chronic granulomatous disease: This is a genetic disorder that affects the production of white blood cells and can cause recurring infections.
* Autoimmune disorders: These are conditions where the immune system mistakenly attacks its own cells, including white blood cells. Examples include lupus and rheumatoid arthritis.
* Bone marrow failure: This is a condition where the bone marrow does not produce enough white blood cells, red blood cells, or platelets.

Symptoms of leukopenia can include recurring infections, fever, fatigue, and weight loss. Treatment depends on the underlying cause of the condition and may include antibiotics, immunoglobulin replacement therapy, or bone marrow transplantation.

In LLCB, the B cells undergo a mutation that causes them to become cancerous and multiply rapidly. This can lead to an overproduction of these cells in the bone marrow, causing the bone marrow to become crowded and unable to produce healthy red blood cells, platelets, and white blood cells.

LLCB is typically a slow-growing cancer, and it can take years for symptoms to develop. However, as the cancer progresses, it can lead to a range of symptoms including fatigue, weakness, weight loss, fever, night sweats, and swollen lymph nodes.

LLCB is typically diagnosed through a combination of physical examination, blood tests, bone marrow biopsy, and imaging studies such as X-rays or CT scans. Treatment options for LLCB include chemotherapy, radiation therapy, and in some cases, stem cell transplantation.

Overall, while LLCB is a serious condition, it is typically slow-growing and can be managed with appropriate treatment. With current treatments, many people with LLCB can achieve long-term remission and a good quality of life.

Myeloid leukemia can be classified into several subtypes based on the type of cell involved and the degree of maturity of the abnormal cells. The most common types of myeloid leukemia include:

1. Acute Myeloid Leukemia (AML): This is the most aggressive form of myeloid leukemia, characterized by a rapid progression of immature cells that do not mature or differentiate into normal cells. AML can be further divided into several subtypes based on the presence of certain genetic mutations or chromosomal abnormalities.
2. Chronic Myeloid Leukemia (CML): This is a slower-growing form of myeloid leukemia, characterized by the presence of a genetic abnormality known as the Philadelphia chromosome. CML is typically treated with targeted therapies or bone marrow transplantation.
3. Myelodysplastic Syndrome (MDS): This is a group of disorders characterized by the impaired development of immature blood cells in the bone marrow. MDS can progress to AML if left untreated.
4. Chronic Myelomonocytic Leukemia (CMML): This is a rare form of myeloid leukemia that is characterized by the accumulation of immature monocytes in the blood and bone marrow. CMML can be treated with chemotherapy or bone marrow transplantation.

The symptoms of myeloid leukemia can vary depending on the subtype and severity of the disease. Common symptoms include fatigue, weakness, fever, night sweats, and weight loss. Diagnosis is typically made through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment options for myeloid leukemia can include chemotherapy, targeted therapies, bone marrow transplantation, and supportive care to manage symptoms and prevent complications. The prognosis for myeloid leukemia varies depending on the subtype of the disease and the patient's overall health. With current treatments, many patients with myeloid leukemia can achieve long-term remission or even be cured.

Multiple myeloma is the second most common type of hematologic cancer after non-Hodgkin's lymphoma, accounting for approximately 1% of all cancer deaths worldwide. It is more common in older adults, with most patients being diagnosed over the age of 65.

The exact cause of multiple myeloma is not known, but it is believed to be linked to genetic mutations that occur in the plasma cells. There are several risk factors that have been associated with an increased risk of developing multiple myeloma, including:

1. Family history: Having a family history of multiple myeloma or other plasma cell disorders increases the risk of developing the disease.
2. Age: The risk of developing multiple myeloma increases with age, with most patients being diagnosed over the age of 65.
3. Race: African Americans are at higher risk of developing multiple myeloma than other races.
4. Obesity: Being overweight or obese may increase the risk of developing multiple myeloma.
5. Exposure to certain chemicals: Exposure to certain chemicals such as pesticides, solvents, and heavy metals has been linked to an increased risk of developing multiple myeloma.

The symptoms of multiple myeloma can vary depending on the severity of the disease and the organs affected. Common symptoms include:

1. Bone pain: Pain in the bones, particularly in the spine, ribs, or long bones, is a common symptom of multiple myeloma.
2. Fatigue: Feeling tired or weak is another common symptom of the disease.
3. Infections: Patients with multiple myeloma may be more susceptible to infections due to the impaired functioning of their immune system.
4. Bone fractures: Weakened bones can lead to an increased risk of fractures, particularly in the spine, hips, or ribs.
5. Kidney problems: Multiple myeloma can cause damage to the kidneys, leading to problems such as kidney failure or proteinuria (excess protein in the urine).
6. Anemia: A low red blood cell count can cause anemia, which can lead to fatigue, weakness, and shortness of breath.
7. Increased calcium levels: High levels of calcium in the blood can cause symptoms such as nausea, vomiting, constipation, and confusion.
8. Neurological problems: Multiple myeloma can cause neurological problems such as headaches, numbness or tingling in the arms and legs, and difficulty with coordination and balance.

The diagnosis of multiple myeloma typically involves a combination of physical examination, medical history, and laboratory tests. These may include:

1. Complete blood count (CBC): A CBC can help identify abnormalities in the numbers and characteristics of different types of blood cells, including red blood cells, white blood cells, and platelets.
2. Serum protein electrophoresis (SPEP): This test measures the levels of different proteins in the blood, including immunoglobulins (antibodies) and abnormal proteins produced by myeloma cells.
3. Urine protein electrophoresis (UPEP): This test measures the levels of different proteins in the urine.
4. Immunofixation: This test is used to identify the type of antibody produced by myeloma cells and to rule out other conditions that may cause similar symptoms.
5. Bone marrow biopsy: A bone marrow biopsy involves removing a sample of tissue from the bone marrow for examination under a microscope. This can help confirm the diagnosis of multiple myeloma and determine the extent of the disease.
6. Imaging tests: Imaging tests such as X-rays, CT scans, or MRI scans may be used to assess the extent of bone damage or other complications of multiple myeloma.
7. Genetic testing: Genetic testing may be used to identify specific genetic abnormalities that are associated with multiple myeloma and to monitor the response of the disease to treatment.

It's important to note that not all patients with MGUS or smoldering myeloma will develop multiple myeloma, and some patients with multiple myeloma may not have any symptoms at all. However, if you are experiencing any of the symptoms listed above or have a family history of multiple myeloma, it's important to talk to your doctor about your risk and any tests that may be appropriate for you.

Hodgkin Disease can spread to other parts of the body through the lymphatic system, and it can affect people of all ages, although it is most common in young adults and teenagers. The symptoms of Hodgkin Disease can vary depending on the stage of the disease, but they may include swollen lymph nodes, fever, night sweats, fatigue, weight loss, and itching.

There are several types of Hodgkin Disease, including:

* Classical Hodgkin Disease: This is the most common type of Hodgkin Disease and is characterized by the presence of Reed-Sternberg cells.
* Nodular Lymphocytic predominant Hodgkin Disease: This type of Hodgkin Disease is characterized by the presence of nodules in the lymph nodes.
* Mixed Cellularity Hodgkin Disease: This type of Hodgkin Disease is characterized by a mixture of Reed-Sternberg cells and other immune cells.

Hodgkin Disease is usually diagnosed with a biopsy, which involves removing a sample of tissue from the affected lymph node or other area and examining it under a microscope for cancer cells. Treatment for Hodgkin Disease typically involves chemotherapy, radiation therapy, or a combination of both. In some cases, bone marrow or stem cell transplantation may be necessary.

The prognosis for Hodgkin Disease is generally good, especially if the disease is detected and treated early. According to the American Cancer Society, the 5-year survival rate for people with Hodgkin Disease is about 85%. However, the disease can sometimes recur after treatment, and the long-term effects of radiation therapy and chemotherapy can include infertility, heart problems, and an increased risk of secondary cancers.

Hodgkin Disease is a rare form of cancer that affects the immune system. It is most commonly diagnosed in young adults and is usually treatable with chemotherapy or radiation therapy. However, the disease can sometimes recur after treatment, and the long-term effects of treatment can include infertility, heart problems, and an increased risk of secondary cancers.

... alkylating agents are classified under L01A. Many of the agents are known as "classical alkylating agents". These include true ... An alkylating antineoplastic agent is an alkylating agent used in cancer treatment that attaches an alkyl group (CnH2n+1) to ... Most of the alkylating agents are also carcinogenic. Before their use in chemotherapy, alkylating agents were better known for ... University of Nebraska page on alkylating agent drugs Alkylating+antineoplastic+agents at the US National Library of Medicine ...

https://en.wikipedia.org/wiki/Alkylating_antineoplastic_agent

Gate, Laurent; Tew, Kenneth D. (2011). "Alkylating Agents". Cancer Management in Man: Chemotherapy, Biological Therapy, ... EMP is a dual cytostatic and hence chemotherapeutic agent and a hormonal anticancer agent of the estrogen type. It is a prodrug ... and hence was thought to be an alkylating antineoplastic agent. However, subsequent research has found that EMP is devoid of ... or other more marked toxicity associated with such agents. In contrast to most other cytostatic agents, which often cause ...

https://en.wikipedia.org/wiki/Estramustine_phosphate

Scholar E (2007). "Alkylating Agents". XPharm: The Comprehensive Pharmacology Reference: 1-4. doi:10.1016/B978-008055232- ... The common property of alkylating agents, including semustine, is their capacity to become very strong electrophiles through ... a drug family consisting of alkylating anti-tumour agents that can be employed for treatment of human cancer. CENU's exert ... Alkylating antineoplastic agents, IARC Group 1 carcinogens, Nitrosamines, Nitrosoureas, Organochlorides, Withdrawn drugs, ...

https://en.wikipedia.org/wiki/Semustine

Trifluoroiodomethane, an alkylating agent. Pentafluoroethyl iodide, an alkylating agent. Perfluorooctyl bromide, or perflubron ...

https://en.wikipedia.org/wiki/Perfluorinated_compound

It is an alkylating agent. 2-Chloromethylpyridine is a precursor to pyridine-containing ligands. 2-Chloromethylpyridine is an ... Alkylating agents, Organochlorides, 2-Pyridyl compounds, IARC Group 1 carcinogens). ...

https://en.wikipedia.org/wiki/2-Chloromethylpyridine

Strong alkylating agents are required. Metal organic frameworks, porous, three-dimensional coordination polymers, are often ... Related to these synthetic chelating agents are the amino acids, which form large families of amino acid complexes. Two amino ...

https://en.wikipedia.org/wiki/Transition_metal_carboxylate_complex

It is an alkylating agent. It can react with DNA to form intrastrand crosslinks. Huang CH, Kuo HS, Liu JW, Lin YL (June 2009 ... Alkylating antineoplastic agents, 1,4-Benzoquinones, All stub articles, Antineoplastic and immunomodulating drug stubs). ...

https://en.wikipedia.org/wiki/Triaziquone

Alkylating agents such as cyclophosphamide and cisplatin, as well as intercalating agent such as daunorubicin and doxorubicin ... Alkylating agents such as ethylnitrosourea. The compounds transfer methyl or ethyl group to bases or the backbone phosphate ... Other alkylating agents include mustard gas and vinyl chloride. Aromatic amines and amides have been associated with ... 2016). "Contributions of DNA repair and damage response pathways to the non-linear genotoxic responses of alkylating agents". ...

https://en.wikipedia.org/wiki/Mutagen

... an alkylating antineoplastic agent; Hydroxydaunorubicin, also known as doxorubicin: an anthracycline antibiotic that is able to ...

https://en.wikipedia.org/wiki/EPOCH_(chemotherapy)

They are strong alkylating agents. Aside from the BF− 4 salt, many related derivatives are available. Triethyloxonium ... Triethyloxonium tetrafluoroborate is a strong alkylating agent, although the hazards are diminished because it is non-volatile ...

https://en.wikipedia.org/wiki/Triethyloxonium_tetrafluoroborate

α-haloketones are alkylating agents. Prominent α-haloketones include phenacyl bromide and chloroacetone. The general structure ... Illustrative of their alkylating activity are reactions with potassium iodide in acetone, chloroacetone reacts faster than 1- ... HX Specialized sources of electrophilic halogenating agents include N-Bromosuccinimide and 1,3-dibromo-5,5-dimethylhydantoin ( ...

https://en.wikipedia.org/wiki/Alpha-Haloketone

The original reaction formed the alkylating agent using an alkene in the presence of a strong acid. The Ritter reaction ... Fernholz, H.; Schmidt, H. J. (1969). "Tert-Butyl Acetate as Alkylating Agent". Angewandte Chemie International Edition in ... Ritter reaction is a chemical reaction that transforms a nitrile into an N-alkyl amide using various electrophilic alkylating ...

https://en.wikipedia.org/wiki/Ritter_reaction

Siddik ZH (2005). "Mechanisms of Action of Cancer Chemotherapeutic Agents: DNA-Interactive Alkylating Agents and Antitumour ... chemotherapeutic agents or alkylating agents) as part of a standardized chemotherapy regimen. Chemotherapy may be given with a ... there are now many types of alkylating agents in use. They are so named because of their ability to alkylate many molecules, ... Alkylating agents will work at any point in the cell cycle and thus are known as cell cycle-independent drugs. For this reason ...

https://en.wikipedia.org/wiki/Chemotherapy

Alkylating agents (e.g., N-ethyl-N-nitrosourea (ENU). These agents can mutate both replicating and non-replicating DNA. In ... Agents that form DNA adducts (e.g., ochratoxin A) DNA intercalating agents (e.g., ethidium bromide) DNA crosslinkers Oxidative ...

https://en.wikipedia.org/wiki/Mutation

... is an alkylating agent. With dimethylsulfide, it reacts to give the sulfonium salt: HCCCH2Br + S(CH3)2 → [ ... Propargyl bromide is a lachrymator and an alkylating agent. Propargyl Propargyl chloride Propargyl alcohol Allyl bromide Record ... HCCCH2S(CH3)2]Br It also alkylates even weakly basic amines such as aniline. Aldehydes react with propargyl bromide in a ...

https://en.wikipedia.org/wiki/Propargyl_bromide

... is an alkylating agent. Indicative of its high reactivity (relative to alkyl chlorides), benzyl chloride reacts ... Lachrymatory agents, IARC Group 2A carcinogens, Benzyl compounds). ...

https://en.wikipedia.org/wiki/Benzyl_chloride

It is an alkylating antineoplastic agent. Dibrospidium chloride and related compounds were developed in Russia in the 1980s. It ... Alkylating antineoplastic agents, Quaternary ammonium compounds, Spiro compounds, Nitrogen heterocycles, Organobromides, ... 1983). "New antitumor agent - Spirobromin". Pharmaceutical Chemistry Journal. 17 (5): 375-377. doi:10.1007/BF00765650. S2CID ...

https://en.wikipedia.org/wiki/Dibrospidium_chloride

... is an alkylating agent; it has irritating, sensitizing and narcotic effects. Chronic exposure to ethylene oxide ... Ethylene oxide is used as a sterilizing agent, disinfecting agent and fumigant as a mixture with carbon dioxide (8.5-80% of ... the reducing agent is actually titanium dichloride, formed by the reaction between LiAlH4 and TiCl3) and of iron(III) chloride ...

https://en.wikipedia.org/wiki/Ethylene_oxide

It is incompatible with acids, bases, oxidizing agents, and reducing agents. Methyl bromoacetate is an alkylating agent. It has ... It reacts with conjugated base and produce alkylated carbene complexes. Methyl bromoacetate can be toxic by ingestion and ... been used to alkylate phenol and amino groups. Moreover, it can be used to make vitamins and pharmaceutical drugs. It is ... Alkylating agents, Lachrymatory agents). ...

https://en.wikipedia.org/wiki/Methyl_2-bromoacetate

Because HN1 is an alkylating agent, it damages DNA, causes immunosuppression, and causes injury to areas that come into contact ... HN1 is also an alkylating agent. Nitrogen mustards react via an initial cyclization to the corresponding aziridinium salt. The ... HN1 was developed in the 1920s and 1930s to remove warts and later as a military agent. Because of the latter use, it is a ... If HN1 has been ingested, emetics (agents that induce vomiting) and gastric lavage are contraindicated, and nothing should be ...

https://en.wikipedia.org/wiki/HN1_(nitrogen_mustard)

... an alkylating antineoplastic agent; (P)rednisone or (P)rednisolone - a glucocorticoid hormone that has the ability to cause ... an alkylating antineoplastic agent; (E)toposide - a topoisomerase inhibitor from the epipodophyllotoxin group; (P)rocarbazine ...

https://en.wikipedia.org/wiki/CEPP

As alkylating agents, haloalkanes are potential carcinogens. The more reactive members of this large class of compounds ... Many are alkylating agents, with primary haloalkanes and those containing heavier halogens being the most active (fluoroalkanes ... do not act as alkylating agents under normal conditions). The ozone-depleting abilities of the CFCs arises from the ... In the presence of a base, haloalkanes alkylate alcohols, amines, and thiols to obtain ethers, N-substituted amines, and ...

https://en.wikipedia.org/wiki/Haloalkane

Treatment with alkylating agents gives organic polysulfides. In one commercial application, it is used to produce the cross- ... linking agent bis(triethoxysilylpropyl)tetrasulfide: Na2S4 + 2 ClC3H6Si(OEt)3 → S4[C3H6Si(OEt)3]2 + 2 NaCl Sometimes as a ...

https://en.wikipedia.org/wiki/Sodium_tetrasulfide

These compounds are potentially dangerous alkylating agents. Dialkylsulfates do not occur in nature. Several classes of sulfate ...

https://en.wikipedia.org/wiki/Organosulfate

... (INN) is a nitrosourea alkylating agent. It is used to treat malignant brain tumors and has proven to be rather ... Alkylating antineoplastic agents, Nitrosamines, Nitrosoureas, Organochlorides, Pyrimidines, Ureas, Chloroethyl compounds, All ...

https://en.wikipedia.org/wiki/Nimustine

Kang SI, Spears CP (January 1990). "Structure-activity studies on organoselenium alkylating agents". Journal of Pharmaceutical ... however it is still a potent alkylating agent and has potential uses in chemotherapy. Diethyl selenide O-Mustard Sesquimustard ... Alkylating agents, Chloroethyl compounds, Mustard compounds, Organoselenium compounds, All stub articles, Chemistry stubs). ... Selenium mustard is somewhat less toxic than its relatives and has not been used as a chemical warfare agent, ...

https://en.wikipedia.org/wiki/Selenium_mustard

It is used as an alkylating agent. In organic synthesis, it is used for introducing the methoxymethyl (MOM) protecting group, ... Alkylating agents, Protecting groups, Organochlorides, Ethers, IARC Group 1 carcinogens). ... It also finds application as a chloromethylating agent in some variants of the Blanc chloromethylation. A convenient synthesis ...

https://en.wikipedia.org/wiki/Chloromethyl_methyl_ether

Traditionally, the alkylating agents are alkyl halides. Many alkylating agents can be used instead of alkyl halides. For ... For the intermolecular case, the reaction is limited to tertiary alkylating agents, some secondary alkylating agents (ones for ... In commercial applications, the alkylating agents are generally alkenes. Protonation of alkenes generates carbocations, the ... or alkylating agents that yield stabilized carbocations (e.g., benzylic or allylic ones). In the case of primary alkyl halides ...

https://en.wikipedia.org/wiki/Friedel–Crafts_reaction

... they were the first chemotherapeutic agents for treatment of cancer. Nitrogen mustards are nonspecific DNA alkylating agents. ... Brookes P, Lawley PD (September 1961). "The reaction of mono- and di-functional alkylating agents with nucleic acids". Biochem ... Note that the alkylating damage itself is not cytotoxic and does not directly cause cell death. Nitrogen mustards are powerful ... This aziridinium group then alkylates DNA once it is attacked by the N-7 nucleophilic center on the guanine base. A second ...

https://en.wikipedia.org/wiki/Nitrogen_mustard

SAM is a weak DNA-alkylating agent. Another reported side effect of SAM is insomnia; therefore, the supplement is often taken ...

https://en.wikipedia.org/wiki/S-Adenosyl_methionine

In a one-pot reaction, 1,2,4,5-tetrabromobenzene reacts with 4-hydroxybenzaldehyde, the alkylating agent 1-bromopentane, the ...

https://en.wikipedia.org/wiki/1,2,4,5-Tetrabromobenzene

ISBN 978-3-642-99941-3. De Winter MS, Siegman CM, Szpilfogel SA (1959). "17-alkylated-3-deoxo-19-nor-testosterone". Chem. Ind ... Kanimoto Y, Okada K (November 1991). "[Antiandrogen therapy of benign prostatic hyperplasia--review of the agents evaluation of ... Morton IK, Hall JM (6 December 2012). Concise Dictionary of Pharmacological Agents: Properties and Synonyms. Springer Science ... The preventive effect of indeloxazine hydrochloride to the sexual dysfunction caused by anti-androgenergic agent (allylestrenol ...

https://en.wikipedia.org/wiki/Allylestrenol

It has been investigated as a metabolic poison and an anticancer agent. Like other α-bromoketones, it is a strong alkylating ... Alkylating agents, Propionic acids, Organobromides, Alpha-keto acids). ... Anti-Cancer Agent Taken from Labside to Bedside: Introduction to a Special Issue". J. Bioenerg. Biomembr. 44 (1): 1-6. doi: ... agent. The pyruvate transporter system can be used to deliver bromopyruvate inside trypanosomal cells. Once intracellular, the ...

https://en.wikipedia.org/wiki/Bromopyruvic_acid

Derivatives of cyclo(L-His-L-Pro) have been studied extensively to develop therapeutic agents for neurodegeneration. These ... The diketopiperazine obtains from glycylserine is a reagent for the preparation of C-alkylated derivatives of glycine. This ... For this application, the diketopiperazine is O-alkylated with concomitant N-deprotonation to give what is called the ... Wirth, Thomas (1997). "New Strategies toα-Alkylatedα-Amino Acids". Angewandte Chemie International Edition in English. 36 (3): ...

https://en.wikipedia.org/wiki/2,5-Diketopiperazine

... "mTOR target NDRG1 confers MGMT-dependent resistance to alkylating chemotherapy". Proc. Natl. Acad. Sci. U.S.A. 111 (1): 409-14 ... that the ability of skin fibroblasts of seven mammalian species to perform DNA repair after exposure to a DNA damaging agent ... for maturation of prelamin A show increased DNA damage and chromosome aberrations and are more sensitive to DNA damaging agents ...

https://en.wikipedia.org/wiki/DNA_damage_theory_of_aging

... the IARC Working Group took into consideration that aziridine is a direct-acting alkylating agent, which is mutagenic in a wide ... Mapp CE (2001). "Agents, old and new, causing occupational asthma". Occup. Environ. Med. 58 (5): 354-60. doi:10.1136/oem.58.5. ... Ismail, Fyaz M.D.; Levitsky, Dmitri O.; Dembitsky, Valery M. (2009). "Aziridine alkaloids as potential therapeutic agents". ...

https://en.wikipedia.org/wiki/Aziridines

... is an enzyme induced by treatment of bacterial cells with alkylating agents that mainly cause methylation damage. This ... Ada enzyme has two active sites, one for the alkylated guanines and thymines and the other for alkylated phosphotriesters. Ogt ... "Regulation and expression of adaptive response to alkylating agents". Annu Rev Biochem. 57 (1): 133-57. doi:10.1146/annurev.bi. ... McCarthy TV, Lindahl T (1985). "Methyl phosphotriesters in alkylated DNA are repaired by the Ada regulatory protein of E. coli ...

https://en.wikipedia.org/wiki/Ada_(protein)

The dialkylmagnesium compounds are potent alkylating agents and are popular in the synthesis of organometallic compounds. W. ...

https://en.wikipedia.org/wiki/Schlenk_equilibrium

... which are divided into broad categories such as alkylating agents and antimetabolites. Traditional chemotherapeutic agents act ... Hormones are important agents in sex-related cancers, such as cancer of the breast, endometrium, prostate, ovary and testis and ... Radiation is a more potent source of cancer when combined with other cancer-causing agents, such as radon plus tobacco smoke. ... Pagano JS, Blaser M, Buendia MA, Damania B, Khalili K, Raab-Traub N, Roizman B (December 2004). "Infectious agents and cancer: ...

https://en.wikipedia.org/wiki/Cancer

Copper-free click chemistry is being explored for use in synthesizing PET imaging agents which must be made quickly with high ... This cycloaddition between a nitrone and a cyclooctyne forms N-alkylated isoxazolines. The reaction rate is enhanced by water ... is in biological imaging in live cells or animals using an azide-tagged biomolecule and a cyclooctyne bearing an imaging agent ...

https://en.wikipedia.org/wiki/Bioorthogonal_chemistry

... in DNA to itself to fight against mutagenesis and the buildup of toxic compounds that result from alkylating agents. Therefore ... traditional chemotherapy agents, and epigenetic drugs. Human cancer is generally characterized by hypermethylation of specific ...

https://en.wikipedia.org/wiki/Pharmacoepigenetics

O6-BG was used clinically in combination with the alkylating agent temozolomide for glioblastoma, however the combination was ... It is an antineoplastic agent. It exerts its effect by acting as a suicide inhibitor of the enzyme O6-alkylguanine-DNA ...

https://en.wikipedia.org/wiki/O6-Benzylguanine

Borch, R. F.; Bernstein, M. D.; Durst H. D. (1971). "Cyanohydridoborate anion as a selective reducing agent". J. Am. Chem. Soc ... materials due to the high propensity of amines to overalkylate.Reductive amination is a more common and effective alkylating ...

https://en.wikipedia.org/wiki/Aza-Cope_rearrangement

The alkylating agent affects more the upper parts of the respiratory tract, and only intensely exposed victims showed signs ... Sulfur mustard is a vesicant alkylating agent with strong cytotoxic, mutagenic, and carcinogenic properties. After exposure, ... followed by death allowing for evaluation of novel cytoprotective agents. Potential tissue reparative agents can be evaluated ... Other inhaled agents may be directly toxic (e.g. cyanide, carbon monoxide), or cause harm simply by displacing oxygen and ...

https://en.wikipedia.org/wiki/Acute_inhalation_injury

The aromatic ring in 6 is activated at positions ortho to the hydroxyl group, and is alkylated by 5, an alkylating agent. The ... Photosensitizing agents, Furanocoumarins, DNA intercalaters, Plant toxins). ...

https://en.wikipedia.org/wiki/Psoralen

Alkylating agents, Organobromides, Lactams, Hydrazides). ... it alkylates thiol groups, displacing the bromine and adding ... Its alkylating properties are comparable to iodoacetamide. Bromobimane is prepared from 3,4-dimethyl-2-pyrazolin-5-one (a ...

https://en.wikipedia.org/wiki/Bromobimane

It is used as a long chain alkylating agent to improve the lipophilicity and hydrophobicity of organic molecules for biological ...

https://en.wikipedia.org/wiki/1-Bromododecane

Alkylated naphthalenes (AN) Silicate esters Ionic fluids Multiply alkylated cyclopentanes (MAC) PTFE: polytetrafluoroethylene ( ... Anti-sticking agents differ from lubricants in that they are designed to reduce the inherently adhesive qualities of a given ... Anti-foaming agents are typically silicone compounds which increase surface tension in order to discourage foam formation. ... These agents are often sulfur compounds, such as dithiophosphates. Friction modifiers reduce friction and wear, particularly in ...

https://en.wikipedia.org/wiki/Lubricant

... which are in contrast to the fused amidine bases DBN or DBU not alkylated. A modification of the Koenigs-Knorr reaction for ... a very electron-rich alkene and a strong reducing agent, available from tris(dimethylamino)methane by pyrolysis or from ... "The use of sodium hydride as a reducing agent in nitrogen-containing solvents I. The reduction of chlorosilanes in ...

https://en.wikipedia.org/wiki/Tetramethylurea

Since α,β-unsaturated compounds are electrophiles and alkylating agents, many α,β-unsaturated carbonyl compounds are toxic. The ... The enolate product can either be trapped or alkylated. By using "masked functionality", it is possible to produce enolates ...

https://en.wikipedia.org/wiki/Α,β-Unsaturated_carbonyl_compound

Combinations of fludarabine with alkylating agents (cyclophosphamide) produce higher response rates and longer progression-free ... Alkylating agents approved for CLL include bendamustine and cyclophosphamide. Targeted therapy attacks cancer cells at a ... Exposure to Agent Orange increases the risk of CLL, and exposure to hepatitis C virus may increase the risk. There is no clear ... Exposure to Agent Orange, certain insecticides, sun exposure, exposure to hepatitis C virus, and common infections are also ...

https://en.wikipedia.org/wiki/Chronic_lymphocytic_leukemia

Alkylating agents, Alpha-1 blockers, Alpha-2 blockers, IARC Group 2B carcinogens, Irreversible antagonists, Organochlorides, ... Kjaergaard N, Kjaergaard B, Lauritsen JG (June 1988). "Prazosin, an adrenergic blocking agent inadequate as male contraceptive ...

https://en.wikipedia.org/wiki/Phenoxybenzamine

Animal studies and anecdotal reports show that BDB is a slightly more potent serotonin releasing agent than its methylated ... ", "Methyl-J"). However, it is more commonly known as a metabolite of the N-alkylated analogues MBDB and ... Serotonin-norepinephrine-dopamine releasing agents, Entactogens and empathogens). ...

https://en.wikipedia.org/wiki/1,3-Benzodioxolylbutanamine

... to methylating agents in bacteria is known as the adaptive response and confers a level of resistance to alkylating agents upon ... Several agents reported to have anti-aging properties have been shown to attenuate constitutive level of mTOR signaling, an ... Moreover, DNA damaging agents can damage other biomolecules such as proteins, carbohydrates, lipids, and RNA. The accumulation ... Halicka HD, Zhao H, Li J, Lee YS, Hsieh TC, Wu JM, Darzynkiewicz Z (December 2012). "Potential anti-aging agents suppress the ...

https://en.wikipedia.org/wiki/DNA_repair

It is a toxic compound, because, like many alkyl halides, it is an alkylating agent. It reacts with cysteine residues in ... Its toxicity correlates to its ability as an alkylating agent, which will modify cysteine residues in proteins. Monohaloacetic ...

https://en.wikipedia.org/wiki/Iodoacetic_acid

... a platinum-based antineoplastic agent, also an alkylating antineoplastic agent. ESHAP--an effective chemotherapy regimen in ...

https://en.wikipedia.org/wiki/ESHAP

Cyclophosphamide, an alkylating agent that cross-links DNA and is used to treat both cancer and autoimmune diseases, has ...

https://en.wikipedia.org/wiki/Anti-NMDA_receptor_encephalitis

Chemotherapy (especially alkylating agents) can affect a female's ovaries, causing them to stop releasing eggs and estrogen, ...

https://en.wikipedia.org/wiki/Cancer_in_adolescents_and_young_adults

Typical of activated esters, 1,3-propane sultone is an alkylating agent. 1,3-Propane sultone is toxic, carcinogenic, mutagenic ...

https://en.wikipedia.org/wiki/1,3-Propane_sultone

Alkylating agents substitute alkyl groups for hydrogen atoms on DNA, resulting in the formation of cross links within the DNA ... Alkylating agents are a class of antineoplastic or anticancer drugs which act by inhibiting the transcription of DNA into RNA ... Alkylating Agents No authors listed In: LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. ... Alkylating agents are a class of antineoplastic or anticancer drugs which act by inhibiting the transcription of DNA into RNA ...

https://pubmed.ncbi.nlm.nih.gov/31643188

Alkylating agents substitute alkyl groups for hydrogen atoms on DNA, resulting in the formation of cross links within the DNA ... This action occurs in all cells, but alkylating agents have their primary effect on rapidly dividing cells which do not have ... The alkylating agents are generally separated into six classes: ... accounts for the common side effects of the alkylating agents: ... Alkylating agents are a class of antineoplastic or anticancer drugs which act by inhibiting the transcription of DNA into RNA ...

https://www.ncbi.nlm.nih.gov/books/NBK547849/

This is consistent with our in vivo finding that the nimustine MTD, among several alkylating agents, is most effective in ... This can be achieved with selected alkylating agents such as nimustine. ... and bifunctional alkylating agents in a genetically engineered mouse model for BRCA1/p53-mutant breast cancer. Due to the large ... Intriguingly, these cells are more sensitive to the DNA crosslinking agent nimustine resulting in an increased number of ...

https://www.garvan.org.au/research/publications/14288

Alkylating agents. Alkylating agents act directly on cell DNA. They damage DNA to prevent cells from multiplying. ... Combination therapy can also include immunotherapy or targeted agents. *Adjuvant chemotherapy: A person will receive adjuvant ... Antineoplastic agents. (2021). https://www.ncbi.nlm.nih.gov/books/NBK548022/. *. Chemotherapy. (n.d.). https://training.seer. ... Antineoplastic agents. (2017). https://www.cdc.gov/niosh/topics/hazdrug/antineoplastic.html. ...

https://www.medicalnewstoday.com/articles/antineoplastic-chemotherapy

Alkylating agents are one of the oldest classes of anticancer medicine with a wide variety of molecular actions and thus the ... Bendamustine as a model for the activity of alkylating agents. Future Oncology, 4 (3). pp. 323-332. ISSN 1479-6694 ...

http://sro.sussex.ac.uk/id/eprint/55186/

for patients who are resistant to alkylating agents, a nucleoside analog plus rituximab will be effective in 30-40% of cases. ... The largest experience is in combining rituximab with alkylating agents or nucleoside analogs. Rituximab can be also combined ... Rituximab in combination with alkylating agents. In a prospective randomized trial the, German Low-Grade Lymphoma Group could ... Front-line treatments options include alkylating agents, nucleoside analogs, bortezomib (added in the Newport consensus) and ...

https://www.nature.com/articles/leu201336?error=cookies_not_supported&code=339b92c6-8ab1-4108-b93c-dc949309b335

Some aromatic amines, hydrazine and related substances, N-nitroso compounds and miscellaneous alkylating agents / this ... Carcinogenicity of alkylating cytostatic drugs : proceedings of a symposium organized by IARC and the German Cancer Research ...

https://kohahq.searo.who.int/cgi-bin/koha/opac-search.pl?q=su:%7BAlkylating%20agents%7D

Alkylating Agents Alkylating agents are chemotherapy drugs that work by keeping cancer cells from multiplying. These drugs ... Most alkylating agents are used to treat leukemia, lymphoma, Hodgkins disease, multiple myeloma, sarcoma, and cancers of the ... Nitrosoureas are the only type of alkylating agent that can cross the blood-brain barrier and travel to the brain. They are ...

https://www.health.com/chemotherapy-7489350

Alkylating agents. *Antimetabolites. *Radiation. *Tumor necrosis factor (TNF) inhibitors. *High-dose corticosteroids (≥2 mg/kg ...

https://www.cdc.gov/smallpox/clinicians/vaccination-contraindications1.html

Alkylating Agents. Molecular Mechanisms of Pharmacological Action. Immunosuppressive Agents. Immunologic Factors. Physiological ... Participants may not be receiving any other investigational agents, or concurrent biological, chemotherapy, or radiation ...

https://clinicaltrials.gov/ct2/show/NCT02500849

Drug class: alkylating agents. Carmustine systemic is used in the treatment of:. *Brain Tumor ...

https://www.drugs.com/ingredient/carmustine.html

Immunosuppressive Agents. Immunologic Factors. Physiological Effects of Drugs. Alkylating Agents. Antineoplastic Agents, ... Antineoplastic Agents. Molecular Mechanisms of Pharmacological Action. ...

https://www.clinicaltrials.gov/show/NCT00408447

Alkylating Agents * Antioxidants * Insulin * Iodoacetates * Ketone Bodies * Reactive Oxygen Species * Thiobarbituric Acid ...

https://pubmed.ncbi.nlm.nih.gov/18339375/

Medications for cancer (Alkylating Agents). Alpha-lipoic acid is an antioxidant. There is some concern that antioxidants might ... Doggrell, S. A. Alpha-lipoic acid, an anti-obesity agent? Expert.Opin.Investig.Drugs 2004;13:1641-1643. View abstract. ... Antioxidant agents are effective in inducing lymphocyte progression through cell cycle in advanced cancer patients: assessment ... standard hydration therapy during a coronary angiography doesnt seem to prevent kidney damage caused by contrast agents. ...

https://medlineplus.gov/druginfo/natural/767.html

T1 - Leukemia risk following Hodgkins disease: relation to cumulative dose of alkylating agents, treatment with teniposide ... title = "Leukemia risk following Hodgkins disease: relation to cumulative dose of alkylating agents, treatment with teniposide ... Leukemia risk following Hodgkins disease: relation to cumulative dose of alkylating agents, treatment with teniposide ... Leukemia risk following Hodgkins disease: relation to cumulative dose of alkylating agents, treatment with teniposide ...

https://research.vumc.nl/en/publications/leukemia-risk-following-hodgkins-disease-relation-to-cumulative-d

Antineoplastics, Alkylating. Class Summary. Alkylating agents bind with DNA and interfere with cell growth and differentiation. ... This agent interferes with the inflammatory response by decreasing bone marrow response through the interference of DNA cross- ... Angiotensin-converting enzyme inhibitors should be used with caution, because these agents may increase serum potassium levels ... Methylprednisolone is used to treat pulmonary hemorrhage and rapidly progressive glomerulonephritis (RPGN). This agent ...

https://emedicine.medscape.com/article/1001872-medication

Alkylating agents: These medicines prevent cells from reproducing by damaging their DNA in every stage of the cell cycle. This ...

https://www.uhc.com/health-and-wellness/health-topics/cancer/chemotherapy-and-side-effects

Alkylating agent (%). 92. 90. Thalidomide/lenalidomide (%). 40. 43. Stem cell transplantation (%). 57. 54. ... In a pooled analysis of Trials 1-3, the response rate for all patients refractory to paclitaxel and platinum agents was 13.8% ( ... Retrospective efficacy analyses were performed in two trials that had subsets of patients who received single-agent doxorubicin ... The following tables present adverse reactions from clinical trials of single-agent doxorubicin hydrochloride liposomal ...

https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=15a84bd6-b565-4722-bb92-e4c919620a90&version=2

... agent T (a closely related vesicant with a lower freezing point). Sulfur mustards evaporate slowly. They are very sparingly ... Sulfur mustards are vesicants and alkylating agents. They are colorless when pure but are typically a yellow to brown oily ... Sulfur mustards are alkylating agents that may cause bone marrow suppression and neurologic and gastrointestinal toxicity. ... Sulfur Mustard Agent HT. CAS# Sulfur Mustard Agent H or HD 505-60-2, Sulfur Mustard Agent HT 6392-89-8. UN# Sulfur Mustard ...

https://wwwn.cdc.gov/TSP/MMG/MMGDetails.aspx?mmgid=924&toxid=191

Patients must have received rituximab and an alkylating agent. Baseline patient characteristics are summarized in Table 5. The ... bulking agent). Citric acid anhydrous acts as a buffering agent and may be used together with sodium hydroxide for pH ... Administer ALIQOPA as a single agent, following reconstitution and dilution. Mix only with sterile 0.9% Sodium Chloride ...

https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ade50241-2c10-4038-b4e9-72f6bf905f03&audience=consumer

I am looking foralkylating agent. I am looking forsugars. I am looking foramyloid. ...

https://www.centerwatch.com/clinical-trials/listings/search/?q=ocular+disease&page=6

Bromoethane, chloroethane and ethylene oxide are mutagenic alkylating agents. Bromoethane is a chemical in the class of ... Bromoethane has limited commercial use as an ethylating agent in organic syntheses, for ethylation of gasoline, and has been ... halogenated alkanes, which encompasses a wide range of industrial and pharmaceutical agents. Haloalkanes are highly lipophilic ...

https://www.niehs.nih.gov/research/atniehs/labs/mtb/comp_path/studies/effects/index.cfm

Like many alkylating agents, thiotepa has been reported to be carcinogenic when administered to laboratory animals [see ... TEPADINA (thiotepa) is an alkylating agent. TEPADINA (thiotepa) for injection is supplied as a non-pyrogenic, sterile ... TEPADINA (thiotepa) is an alkylating drug indicated: (1). *To reduce the risk of graft rejection when used in conjunction with ... Thiotepa is a cytotoxic agent of the polyfunctional type, related chemically and pharmacologically to the nitrogen mustard. The ...

https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=559e353c-2dc0-16ba-e054-00144ff8d46c&audience=consumer

Alkylating Agent Nitrogen Mustard. Oral. Nov. 23, 2022 In Use. 49884-0128-91. 49884-0128 Everolimus. Everolimus. 10.0 mg/1. ... Alkylating Agent Nitrogen Mustard. Oral. Nov. 23, 2022 In Use. 65219-0550-01. 65219-0550 Pralatrexate. Pralatrexate. 20.0 mg/mL ... Alkylating Agent/ Mitomycin. Intravenous. Nov. 22, 2022 In Use. 43598-0171-11. 43598-0171 Thiotepa. Thiotepa. 100.0 mg/1. ... Alkylating Agent Nitrogen Mustard. Intravenous. Dec. 7, 2022 In Use. 71335-2181-01. 71335-2181 Megestrol Acetate. Megestrol ...

https://seer.cancer.gov/oncologytoolbox/canmed/ndconc/?paginate_by=50&s=-discontinued&p=183

Streptozocin is classified as an alkylating agent. Alkylating agents are most active in the resting phase of the cell. These ... This medication is classified as an "alkylating agent." (For more detail, see "How this drug works" section below). ... There are several types of alkylating agents.. *Mustard gas derivatives: Mechlorethamine, Cyclophosphamide, Chlorambucil, ...

https://chemocare.com/chemotherapy/drug-info/Streptozocin.aspx

This mechanism of toxicity is also responsible for the ability of some alkylating agents to perform as anti-cancer drugs in the form of alkylating antineoplastic agents , and also as chemical weapons such as mustard gas . (wikidoc.org)

Alkylating agents are chemotherapy drugs that work by keeping cancer cells from multiplying. (health.com)
Multiple chemotherapeutic agents are active against non-Hodgkin lymphoma (NHL) and can be used alone or in combination, depending on the histology and stage of the disease and whether the patient can tolerate chemotherapy. (medscape.com)
This agent can be used alone but is mostly used as a component of multiple combination chemotherapy regimens. (medscape.com)

Alkylating agents are a class of antineoplastic or anticancer drugs which act by inhibiting the transcription of DNA into RNA and thereby stopping the protein synthesis. (nih.gov)
Review Therapeutic journery of nitrogen mustard as alkylating anticancer agents: Historic to future perspectives. (nih.gov)
Alkylating agents are one of the oldest classes of anticancer medicine with a wide variety of molecular actions and thus the potential for broad utility. (sussex.ac.uk)
10. Anticancer activities of alkylating pyrrole-imidazole polyamides with specific sequence recognition. (nih.gov)

Nitrogen mustards are vesicants and alkylating agents. (cdc.gov)

Alkylating agents substitute alkyl groups for hydrogen atoms on DNA, resulting in the formation of cross links within the DNA chain and thereby resulting in cytotoxic, mutagenic, and carcinogenic effects. (nih.gov)
Mutagenic damage to mammalian cells by therapeutic alkylating agents. (nih.gov)
AB is an alkylating agent, which is reported to be mutagenic in the Ames/Salmonella assay and is shown to bind to DNA. (nih.gov)
Bromoethane, chloroethane and ethylene oxide are mutagenic alkylating agents. (nih.gov)

The toxicity, carcinogenity, and paradoxically, cancer cell-killing abilities of different DNA alkylating agents are an example. (wikidoc.org)

Experimental Design: We studied responses to various mono- and bifunctional alkylating agents in a genetically engineered mouse model for BRCA1/p53-mutant breast cancer. (garvan.org.au)
Busulfan is a bifunctional alkylating agent. (pediatriconcall.com)

Carcinogenicity of alkylating cytostatic drugs : proceedings of a symposium organized by IARC and the German Cancer Research Centre, held at the German Cancer Research Centre, Heidelberg, Federal Republic of Germany, 25-27 November 1985 / editors, D. Schmähl & J. M. Kaldor. (who.int)

Alkylating agents are widely used in chemistry because the alkyl group is probably the most common group encountered in organic molecules. (wikidoc.org)
In the presence of catalysts , they also alkylate alkyl and aryl halides, as exemplified by Suzuki couplings . (wikidoc.org)
Electrophilic alkylating agents deliver the equivalent of an alkyl cation . (wikidoc.org)
Examples include the use of alkyl halides with a Lewis acid catalyst to alkylate aromatic substrates in Friedel-Crafts reactions. (wikidoc.org)
The electrophilic alkylating agents are commonly of concern as alkylating antineoplastic agent that attaches an alkyl group to DNA . (wikidoc.org)

Several alkylating agents have also been implicated in causing rare cases of idiosyncratic, clinically apparent acute liver injury which is typically cholestatic and best described for temozolomide, cyclophosphamide and chlorambucil, perhaps because these agents are most frequently used and can be given orally over a prolonged period. (nih.gov)
Chlorambucil alkylates and cross-links strands of DNA, inhibiting DNA replication and RNA transcription. (medscape.com)

Alkylating agents impair cell function by forming covalent bonds with DNA, ribonucleic acid (RNA), and proteins. (medscape.com)

Examples of alkylating agents include Temodar (temozolomide), Myleran (busulfan), and cyclophosphamide. (health.com)

Nitrosoureas are the only type of alkylating agent that can cross the blood-brain barrier and travel to the brain. (health.com)

When inhaled, these agents may cause systemic effects. (cdc.gov)

As a validation of the approach, we show that the AZL protein, HedH4, associated with biosynthesis of the alkylating agent hedamycin, excises hedamycin-DNA adducts with exquisite specificity and provides resistance to the natural product in cells. (nih.gov)

Some aromatic amines, hydrazine and related substances, N-nitroso compounds and miscellaneous alkylating agents / this publication represents the views of the IARC Working Group on the Evaluation of the Carcinogenic Risk of Chemicals to Man, which met in Lyon, 18-25 June 1973. (who.int)

Procarbazine is an atypical alkylating agent that inhibits RNA, DNA and protein synthesis. (wedgewoodpharmacy.com)

As an alkylating agent, the mechanism of action of the active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells. (medscape.com)

These agents are characterized by their ability to bind covalently to nucleophilic sites in proteins and DNA. (cdc.gov)

Electrophilic compounds may alkylate different nucleophiles in the body. (wikidoc.org)
nitroheterocyclic compounds, and cytotoxic agents. (nih.gov)

The mainstay of treatment for granulomatosis with polyangiitis (GPA) is a combination of corticosteroids and cytotoxic agents. (medscape.com)

1. Synthesis and biological properties of highly sequence-specific-alkylating N-methylpyrrole-N-methylimidazole polyamide conjugates. (nih.gov)
7. Synthesis and biological properties of sequence-specific DNA-alkylating pyrrole-imidazole polyamides. (nih.gov)

Bromoethane has limited commercial use as an ethylating agent in organic syntheses, for ethylation of gasoline, and has been formerly used as an anesthetic. (nih.gov)
Alkylate is a premium gasoline blending stock because it has exceptional antiknock properties and is clean burning. (wikidoc.org)

Bromoethane is a chemical in the class of halogenated alkanes, which encompasses a wide range of industrial and pharmaceutical agents. (nih.gov)
Alkylating agents, either direct-acting or generated in vivo, form an important class of environmental mutagens and carcinogens. (cdc.gov)

This is consistent with our in vivo finding that the nimustine MTD, among several alkylating agents, is most effective in eradicating Brca1-mutated mouse mammary tumors. (garvan.org.au)

8. Synthesis and evaluation of sequence-specific DNA alkylating agents: effect of alkylation subunits. (nih.gov)
12. Evaluation of alkylating pyrrole-imidazole polyamide conjugates by a novel method for high-throughput sequencer. (nih.gov)

This medication is classified as an "alkylating agent. (chemocare.com)
These agents are also used as adjunctive antiemetic agents, to decrease vasogenic edema associated with tumors, and as prophylactic medication to prevent hypersensitivity reactions associated with some chemotherapeutic drugs. (medscape.com)

This action occurs in all cells, but alkylating agents have their primary effect on rapidly dividing cells which do not have time for DNA repair. (nih.gov)
Intriguingly, these cells are more sensitive to the DNA crosslinking agent nimustine resulting in an increased number of multinucleated cells that lack clonogenicity. (garvan.org.au)

Combination therapy can also include immunotherapy or targeted agents. (medicalnewstoday.com)

Ocular exposure to these agents may cause incapacitating damage to the cornea and conjunctiva. (cdc.gov)

Taking alpha-lipoic acid by mouth with or without standard hydration therapy during a coronary angiography doesn't seem to prevent kidney damage caused by contrast agents. (medlineplus.gov)

The specific objectives of the project are the design, synthesis, and testing of non-steroidal and non-hormonal male contraceptive agents that inhibit testicular sperm development, post-testicular sperm maturation, and epididymal function. (nih.gov)

HT is a mixture of 60% HD and 40% agent T (a closely related vesicant with a lower freezing point). (cdc.gov)
In a standard oil refinery process, isobutane is alkylated with low-molecular-weight alkenes (primarily a mixture of propylene and butylene ) in the presence of a strong acid catalyst , either sulfuric acid or hydrofluoric acid . (wikidoc.org)
The product is called alkylate and is composed of a mixture of high- octane , branched-chain paraffinic hydrocarbons (mostly isopentane and isooctane ). (wikidoc.org)

This agent may be preferable for elderly patients with serious comorbid medical problems who require treatment for lymphoma. (medscape.com)

Sulfur mustards were first developed in the early-to-mid-1800s and were introduced as chemical warfare agents in 1917 during World War I. They have been used extensively in chemical warfare and remain a major threat. (cdc.gov)
Destruction of U.S. stockpiles of chemical agents, including sulfur mustards, was mandated by the Chemical Weapons Convention to take place before April 2007. (cdc.gov)

9. Molecular design of sequence specific DNA alkylating agents. (nih.gov)

Alkylating agents are often very toxic, due to their ability to alkylate DNA. (wikidoc.org)

Most agents have been shown to cause transient serum aminotransferase elevations in a proportion of patients. (nih.gov)

14. Targeting specific gene by alkylating pyrrole-imidazole polyamides. (nih.gov)
These agents are not cell cycle phase-specific and are used for hematologic and nonhematologic malignancies. (medscape.com)

The alkylating agents all have major toxicities, but the predominant toxicities are to the bone marrow and gastrointestinal tract. (nih.gov)

trouvera une liste plus complète de références, ainsi int/immunization/documents/positionpapers/ que des résumés dans http://www.who.int/immuni- en/index.html. (who.int)
zation/documents/positionpapers/en/index.html. (who.int)

Anatomy5

Organisms3

Diseases23

Chemicals and Drugs88

Analytical, Diagnostic and Therapeutic Techniques and Equipment9

Phenomena and Processes18

Technology, Industry, Agriculture2

Information Science2

Health Care1

Activation of c-Jun N-terminal kinase 1 by UV irradiation is inhibited by wortmannin without affecting c-iun expression. (1/1003)

The Saccharomyces cerevisiae ETH1 gene, an inducible homolog of exonuclease III that provides resistance to DNA-damaging agents and limits spontaneous mutagenesis. (2/1003)

Mismatch repair and differential sensitivity of mouse and human cells to methylating agents. (3/1003)

Tightly regulated and inducible expression of rabbit CYP2E1 using a tetracycline-controlled expression system. (4/1003)

Cells deficient in DNA polymerase beta are hypersensitive to alkylating agent-induced apoptosis and chromosomal breakage. (5/1003)

Molecular analysis of mutants obtained by treatment with alkylating agents in a quadruplicated white-ivory strain of Drosophila melanogaster. (6/1003)

Alterations in Bacillus subtilis transforming DNA induced by beta-propiolactone and 1,3-propane sultone, two mutagenic and carcinogenic alkylating agents. (7/1003)

The role of thiotepa in allogeneic bone marrow transplantation for genetic diseases. (8/1003)

Alkylating Agents

Antineoplastic Agents, Alkylating

Alkylation

O(6)-Methylguanine-DNA Methyltransferase

Methylnitronitrosoguanidine

Methyl Methanesulfonate

Mechlorethamine

Carmustine

Chlorambucil

Ethyl Methanesulfonate

Nitrogen Mustard Compounds

Dacarbazine

Melphalan

DNA Repair

DNA Damage

Methylnitrosourea

Guanine

Cyclophosphamide

Sulfuric Acid Esters

Ethylnitrosourea

Mutagens

Thiotepa

Nitrosourea Compounds

Methyltransferases

Drug Resistance

Triaziquone

Phosphoramide Mustards

Mustard Gas

Mitomycins

Aziridines

Antineoplastic Agents

Etanidazole

Mitomycin

Cell Survival

DNA Glycosylases

DNA Modification Methylases

Propiolactone

DNA

Ethylmaleimide

DNA Repair Enzymes

Nylons

Neoplasms, Second Primary

Lomustine

Dose-Response Relationship, Drug

Nimustine

DNA Adducts

Drug Synergism

Sarcoma, Yoshida

Porfiromycin

Methionine Sulfoximine

Mesylates

Cricetinae

Drug Resistance, Neoplasm

Quinacrine Mustard

Dicumarol

Cisplatin

Glioma

Antineoplastic Combined Chemotherapy Protocols

Brain Neoplasms

N-Glycosyl Hydrolases

Buthionine Sulfoximine

4-Nitroquinoline-1-oxide

Leukemia, Radiation-Induced

Leukemia L1210

Mutation

Leukemia L5178

Iodoacetamide

Drug Screening Assays, Antitumor

Tumor Cells, Cultured

Cyclohexenes

Poly(ADP-ribose) Polymerases

Carcinogens

Cricetulus

Glioblastoma

Cell Line

Poly Adenosine Diphosphate Ribose

Cross-Linking Reagents

Busulfan

Radiotherapy

DNA, Neoplasm