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
Cyclophosphamide
Mutagens
Thiotepa
Methyltransferases
Drug Resistance
Triaziquone
Phosphoramide Mustards
Mustard Gas
Mitomycins
Aziridines
Etanidazole
Mitomycin
Cell Survival
DNA Glycosylases
DNA Modification Methylases
Propiolactone
DNA
DNA Repair Enzymes
Nylons
Neoplasms, Second Primary
Dose-Response Relationship, Drug
Nimustine
DNA Adducts
Porfiromycin
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
Mutation
Drug Screening Assays, Antitumor
Tumor Cells, Cultured
Cyclohexenes
Poly(ADP-ribose) Polymerases
Carcinogens
Cricetulus
Glioblastoma
Poly Adenosine Diphosphate Ribose
Cross-Linking Reagents
Busulfan
DNA-(Apurinic or Apyrimidinic Site) Lyase
Glutathione
Waldenstrom Macroglobulinemia
Escherichia coli
Netropsin
Ultraviolet Rays
Combined Modality Therapy
Semustine
Myelodysplastic Syndromes
Base Pair Mismatch
Doxorubicin
Novobiocin
Mutagenicity Tests
Epoxy Compounds
Mitolactol
Ifosfamide
Reducing Agents
Leukemia P388
Neoplasms
Distamycins
Molecular Sequence Data
Podophyllotoxin
Base Sequence
Topoisomerase II Inhibitors
Epichlorohydrin
CHO Cells
Chemical Warfare Agents
Carcinoma 256, Walker
Deoxyribonuclease IV (Phage T4-Induced)
Carbon-Oxygen Lyases
Neoplasms, Experimental
Glutathione Transferase
Vinca Alkaloids
Fibrosarcoma
Biotransformation
Misonidazole
Tumor Stem Cell Assay
Vidarabine
Lucanthone
Bone Marrow
Sister Chromatid Exchange
Chromosome Aberrations
Leukemia
Fanconi Anemia
Leukemia, Lymphocytic, Chronic, B-Cell
Leukemia, Myeloid
Multiple Myeloma
Hodgkin Disease
Drug Administration Schedule
Comet Assay
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
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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 antineoplastic agent
Estramustine phosphate
Semustine
Perfluorinated compound
2-Chloromethylpyridine
Transition metal carboxylate complex
Triaziquone
Mutagen
EPOCH (chemotherapy)
Triethyloxonium tetrafluoroborate
Alpha-Haloketone
Ritter reaction
Chemotherapy
Mutation
Propargyl bromide
Benzyl chloride
Dibrospidium chloride
Ethylene oxide
Methyl 2-bromoacetate
HN1 (nitrogen mustard)
CEPP
Haloalkane
Sodium tetrasulfide
Organosulfate
Nimustine
Selenium mustard
Chloromethyl methyl ether
Friedel-Crafts reaction
Nitrogen mustard
S-Adenosyl methionine
1,2,4,5-Tetrabromobenzene
Allylestrenol
Bromopyruvic acid
2,5-Diketopiperazine
DNA damage theory of aging
Aziridines
Ada (protein)
Schlenk equilibrium
Cancer
Bioorthogonal chemistry
Pharmacoepigenetics
O6-Benzylguanine
Aza-Cope rearrangement
Acute inhalation injury
Psoralen
Bromobimane
1-Bromododecane
Lubricant
Tetramethylurea
Α,β-Unsaturated carbonyl compound
Chronic lymphocytic leukemia
Phenoxybenzamine
1,3-Benzodioxolylbutanamine
DNA repair
Iodoacetic acid
ESHAP
Anti-NMDA receptor encephalitis
Cancer in adolescents and young adults
1,3-Propane sultone
Alkylating Agents - PubMed
Alkylating Agents - LiverTox - NCBI Bookshelf
Selected alkylating agents can overcome drug tolerance of G0-like tumor cells and eradicate BRCA1-deficient mammary tumors in...
Antineoplastic drugs and chemotherapy: Types and side effects
Bendamustine as a model for the activity of alkylating agents : Sussex Research Online
How to manage Waldenstrom's macroglobulinemia | Leukemia
Results of search for 'su:{Alkylating agents}'
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WHO HQ Library catalog
Chemotherapy: Purpose, Preparation, Risks, and Results
Contraindications to Vaccination | Smallpox | CDC
Safety Study of Zinc Finger Nuclease CCR5-modified Hematopoietic Stem/Progenitor Cells in HIV-1 Infected Patients - Full Text...
Carmustine - brand name list from Drugs.com
Current version of study NCT00408447 on ClinicalTrials.gov
Antioxidant capacity contributes to protection of ketone bodies against oxidative damage induced during hypoglycemic conditions
Alpha-Lipoic Acid: MedlinePlus Supplements
Leukemia risk following Hodgkin's disease: relation to cumulative dose of alkylating agents, treatment with teniposide...
Pediatric Anti-GBM Disease (Goodpasture Syndrome) Medication: Corticosteroids, Antineoplastics, Alkylating, Monoclonal...
Chemotherapy and side effects | UnitedHealthcare
DailyMed - DOXORUBICIN HYDROCHLORIDE injectable, liposomal
Blister Agents: Sulfur Mustard Agent H/HD, Sulfur Mustard Agent HT | Medical Management Guidelines | Toxic Substance Portal |...
DailyMed - ALIQOPA- copanlisib injection, powder, lyophilized, for solution
ocular disease Clinical Research Trials | CenterWatch
Effects of Bromoethane in the Uterus of Ovariectomized B6C3F1 Mice - Molecular Pathogenesis Group
DailyMed - TEPADINA- thiotepa injection, powder, for solution
CanMED: NDC
Streptozocin - Chemotherapy Drugs - Chemocare
Antineoplastic Agents1
- 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)
Chemotherapy3
- 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)
Anticancer4
- 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)
Nitrogen1
- Nitrogen mustards are vesicants and alkylating agents. (cdc.gov)
Mutagenic4
- 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)
Toxicity1
- The toxicity, carcinogenity, and paradoxically, cancer cell-killing abilities of different DNA alkylating agents are an example. (wikidoc.org)
Bifunctional2
- 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)
Carcinogenicity1
- 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)
Alkyl5
- 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)
Chlorambucil2
- 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)
Covalent1
- Alkylating agents impair cell function by forming covalent bonds with DNA, ribonucleic acid (RNA), and proteins. (medscape.com)
Busulfan1
- Examples of alkylating agents include Temodar (temozolomide), Myleran (busulfan), and cyclophosphamide. (health.com)
Cross the blood-brain b1
- Nitrosoureas are the only type of alkylating agent that can cross the blood-brain barrier and travel to the brain. (health.com)
Systemic1
- When inhaled, these agents may cause systemic effects. (cdc.gov)
Adducts1
- 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)
Substances1
- 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)
Procarbazine1
- Procarbazine is an atypical alkylating agent that inhibits RNA, DNA and protein synthesis. (wedgewoodpharmacy.com)
Mechanism1
- 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)
Proteins1
- These agents are characterized by their ability to bind covalently to nucleophilic sites in proteins and DNA. (cdc.gov)
Compounds2
- Electrophilic compounds may alkylate different nucleophiles in the body. (wikidoc.org)
- nitroheterocyclic compounds, and cytotoxic agents. (nih.gov)
Cytotoxic agents1
- The mainstay of treatment for granulomatosis with polyangiitis (GPA) is a combination of corticosteroids and cytotoxic agents. (medscape.com)
Biological2
Gasoline2
- 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)
Class2
Vivo1
- 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)
Evaluation2
Medication2
- 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)
Cells2
- 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)
Include1
- Combination therapy can also include immunotherapy or targeted agents. (medicalnewstoday.com)
Exposure1
- Ocular exposure to these agents may cause incapacitating damage to the cornea and conjunctiva. (cdc.gov)
Therapy1
- 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)
Function1
- 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)
Mixture3
- 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)
Treatment1
- This agent may be preferable for elderly patients with serious comorbid medical problems who require treatment for lymphoma. (medscape.com)
Chemical2
- 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)
Design1
- 9. Molecular design of sequence specific DNA alkylating agents. (nih.gov)
Ability1
- Alkylating agents are often very toxic, due to their ability to alkylate DNA. (wikidoc.org)
Patients1
- Most agents have been shown to cause transient serum aminotransferase elevations in a proportion of patients. (nih.gov)
Specific2
- 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)
Major1
- The alkylating agents all have major toxicities, but the predominant toxicities are to the bone marrow and gastrointestinal tract. (nih.gov)