Dictionaries as Topic
Terminology as Topic
Cluster Analysis
A set of statistical methods used to group variables or observations into strongly inter-related subgroups. In epidemiology, it may be used to analyze a closely grouped series of events or cases of disease or other health-related phenomenon with well-defined distribution patterns in relation to time or place or both.
Cell Aggregation
Aerosols
Immunohistochemistry
Multigene Family
A set of genes descended by duplication and variation from some ancestral gene. Such genes may be clustered together on the same chromosome or dispersed on different chromosomes. Examples of multigene families include those that encode the hemoglobins, immunoglobulins, histocompatibility antigens, actins, tubulins, keratins, collagens, heat shock proteins, salivary glue proteins, chorion proteins, cuticle proteins, yolk proteins, and phaseolins, as well as histones, ribosomal RNA, and transfer RNA genes. The latter three are examples of reiterated genes, where hundreds of identical genes are present in a tandem array. (King & Stanfield, A Dictionary of Genetics, 4th ed)
Islets of Langerhans Transplantation
PubMed
A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.
Alcohol Dehydrogenase
Publishing
MEDLINE
Serial Publications
Vaccines
Abortion, Spontaneous
Pregnancy
Vaccines, Inactivated
Viral Vaccines
Cyclofenil
Benz(a)Anthracenes
Fluorine
Papilloma
Benzopyrenes
American Cancer Society
National Institutes of Health (U.S.)
National Institute of Environmental Health Sciences (U.S.)
Component of the NATIONAL INSTITUTES OF HEALTH. It conducts and supports basic and applied research to reduce the burden of human illness and dysfunction from environmental causes by, defining how environmental exposures, genetic susceptibility, and age interact to affect an individual's health. It was established in 1969.
Environmental Health
Toxicology
Carcinogenicity Tests
Tests to experimentally measure the tumor-producing/cancer cell-producing potency of an agent by administering the agent (e.g., benzanthracenes) and observing the quantity of tumors or the cell transformation developed over a given period of time. The carcinogenicity value is usually measured as milligrams of agent administered per tumor developed. Though this test differs from the DNA-repair and bacterial microsome MUTAGENICITY TESTS, researchers often attempt to correlate the finding of carcinogenicity values and mutagenicity values.
Databases, Factual
Extensive collections, reputedly complete, of facts and data garnered from material of a specialized subject area and made available for analysis and application. The collection can be automated by various contemporary methods for retrieval. The concept should be differentiated from DATABASES, BIBLIOGRAPHIC which is restricted to collections of bibliographic references.
Internet
Research
Critical and exhaustive investigation or experimentation, having for its aim the discovery of new facts and their correct interpretation, the revision of accepted conclusions, theories, or laws in the light of newly discovered facts, or the practical application of such new or revised conclusions, theories, or laws. (Webster, 3d ed)
Software
Gene Library
Databases, Protein
Algorithms
Toxicogenetics
Caenorhabditis elegans
Caenorhabditis elegans Proteins
Metals
High-Throughput Screening Assays
Effect of magnetic field exposure on anchorage-independent growth of a promoter-sensitive mouse epidermal cell line (JB6). (1/596)
The anchorage-independent growth of mouse epidermal cells (JB6) exposed to 60-Hz magnetic fields (MF) was investigated. Promotion-responsive JB6 cells were suspended in agar (10(4)cells/plate) and exposed continuously to 0.10 or 0.96 mT, 60-Hz magnetic fields for 10-14 days, with or without concurrent treatment with the tumor promoter tetradecanoylphorbol acetate (TPA). Exposures to MF were conducted in a manner such that the experimenter was blind to the treatment group of the cells. At the end of the exposure period, the anchorage-independent growth of JB6 cells on soft agar was examined by counting the number of colonies larger than 60 microm (minimum of 60 cells). The use of a combined treatment of the cells with both MF and TPA was to provide an internal positive control to estimate the success of the assay and to allow evaluation of co-promotion. Statistical analysis was performed by a randomized block design analysis of variance to examine both the effect of TPA treatment (alone and in combination with MF exposure) and the effect of intra-assay variability. Transformation frequency of JB6 cells displayed a dose-dependent response to increasing concentrations of TPA. Coexposure of cells to both TPA and 0.10 or 0.96 mT, 60-Hz MF did not result in any differences in transformation frequency for any TPA concentrations tested (0-1 ng/ml). These data indicate that exposure to a 0.10 or 0.96 mT, 60-Hz MF does not act as a promoter or co-promoter in promotion-sensitive JB6 cell anchorage-independent growth. (+info)Possible carcinogenic effects of X-rays in a transgenerational study with CBA mice. (2/596)
A lifetime experiment using 4279 CBA/J mice was carried out to investigate whether the pre-conceptual exposure of sperm cells to X-ray radiation or urethane would result in an increased cancer risk in the untreated progeny, and/or increased susceptibility to cancer following exposure to a promoting agent. The study consisted of four main groups, namely a control group (saline), a urethane group (1 mg/g body wt) and two X-ray radiation groups (1 Gy, 2 Gy). At 1, 3 and 9 weeks after treatment, the males of these four parental groups were mated with untreated virgin females. The offspring of each parental group was divided into two subgroups: one received s.c. urethane (0.1 mg/g body wt once) as a promoter, the other saline, at the age of 6 weeks. All animals were evaluated for the occurrence of tumours. K-ras oncogene and p53 tumour suppressor gene mutations were investigated in frozen lung tumour samples. The female offspring of male parents exposed to X-rays 1 week before their mating showed a trend towards a higher tumour incidence of the haematopoietic system than the F1 controls. In addition, a higher percentage of bronchioloalveolar adenocarcinomas in male offspring born to irradiated paternals mated 1 week after X-ray treatment points to a plausible increased sensitivity of post-meiotic germ cell stages towards transgenerational carcinogenic effects. On the other hand, no increased tumour incidence and malignancy were observed in the offspring born to irradiated paternals mated 3 and 9 weeks after X-ray treatment. Paternal urethane treatment 1, 3 and 9 weeks prior to conception did not result in significantly altered incidence or malignancy of tumours of the lung, liver and haematopoietic tissue in the offspring. K-ras mutations increased during tumour progression from bronchioloalveolar hyperplasia to adenoma. Codon 61 K-ras mutations were more frequent in lung tumours of urethane-promoted progeny from irradiated parents than from control parents. P53 mutations were absent from these lung alterations. (+info)Potency of dietary indole-3-carbinol as a promoter of aflatoxin B1-initiated hepatocarcinogenesis: results from a 9000 animal tumor study. (3/596)
Indole-3-carbinol (I3C), a metabolite of glucobrassicin found in cruciferous vegetables, is documented as acting as a modulator of carcinogenesis and, depending on timing and dose of administration, it may promote hepatocarcinogenesis in some animal models. In this study we demonstrate that, when given post-initiation, dietary I3C promotes aflatoxin B1 (AFB1)-induced hepatocarcinogenesis in the rainbow trout model at levels as low as 500 p.p.m. Trout embryos (approximately 9000) were initiated with 0, 25, 50, 100, 175 or 250 p.p.b. AFB1 by a 30 min immersion. Experimental diets containing 0, 250, 500, 750, 1000 or 1250 p.p.m. I3C were administered starting at 3 months and fish were sampled for liver tumors at 11-13 months. Promotion at the level of tumor incidence was statistically significant for all dietary levels, except 250 p.p.m. Relative potency for promotion markedly increased at dietary levels >750 p.p.m. We propose that more than one mechanism could be involved in promotion and that both estrogenic and Ah receptor-mediated pathways could be active. The estrogenicity of I3C, measured as its ability to induce vitellogenin (an estrogen biomarker in oviparous vertebrates) was evident at the lowest dietary level (250 p.p.m.), whereas CYPIA (a P450 isozyme induced through the Ah receptor pathway) was not induced until dietary levels of 1000 p.p.m. Therefore, at lower dietary levels, promotion by I3C in this model could be explained by estrogenic activities of I3C acid derivatives, as it is known that estrogens promote hepatocarcinogenesis in trout. Much stronger promotion was observed at high dietary I3C levels (1000 and 1250 p.p.m.), at which levels both CYP1A and vitellogenin were induced. (+info)Environmental factors as regulators and effectors of multistep carcinogenesis. (4/596)
This review highlights current knowledge of environmental factors in carcinogenesis and their cellular targets. The hypothesis that environmental factors influence carcinogenesis is widely supported by both epidemiological and experimental studies. The fact that only a small fraction of cancers can be attributed to germline mutations in cancer-related genes further buttresses the importance of environmental factors in carcinogenesis. Furthermore, penetrance of germline mutations may be modified by either environmental or other genetic factors. Examples of environmental factors that have been associated with increased cancer risk in the human population include chemical and physical mutagens (e.g. cigarette smoke, heterocyclic amines, asbestos and UV irradiation), infection by certain viral or bacterial pathogens, and dietary non-genotoxic constituents (e.g. macro- and micronutrients). Among molecular targets of environmental influences on carcinogenesis are somatic mutation (genetic change) and aberrant DNA methylation (epigenetic change) at the genomic level and post-translational modifications at the protein level. At both levels, changes elicited affect either the stability or the activity of key regulatory proteins, including oncoproteins and tumor suppressor proteins. Together, via multiple genetic and epigenetic lesions, environmental factors modulate important changes in the pathway of cellular carcinogenesis. (+info)A comparison of the effects of dietary cellulose and fermentable galacto-oligosaccharide, in a rat model of colorectal carcinogenesis: fermentable fibre confers greater protection than non-fermentable fibre in both high and low fat backgrounds. (5/596)
The objective of this experiment was to compare the effects of diets with either a non-fermentable fibre source (cellulose) or a fermentable fibre source [galacto-oligosaccharide (GOS)], combined with different levels of dietary fat, on the development of colorectal cancer. Male Wistar rats were fed AIN76-based diets with either a low or high level of cellulose, or a low or high level of GOS, for 9 months. The fat content of the diets was low, medium or high. All rats were treated with 1,2-dimethylhydrazine to induce colorectal tumours. Generally, the tumour incidence increased with increasing fat content in the diet. Despite marked faeces bulking, dietary cellulose either had no effect or an enhancing effect on the formation of colorectal tumours in general, although the development of carcinomas was decreased. GOS appeared to be highly protective against the development of colorectal tumours, as was demonstrated by an inhibitory effect on tumour incidence, multiplicity and size, regardless of the fat content of the diet. Neither fibre source influenced the bromodeoxyuridine labelling index determined in colon crypts or tumours. In animals fed high-GOS diets, the caecal content was significantly increased in weight and significantly decreased in pH. It was concluded that tumorigenesis was enhanced by increased fat content of the diet, and that the diets containing fermentable GOS conferred a greater protection against colorectal cancer than did the diets containing non-fermentable cellulose. (+info)Helicobacter pylori infection enhances glandular stomach carcinogenesis in Mongolian gerbils treated with chemical carcinogens. (6/596)
Helicobacter pylori (Hp) is thought to be a stomach carcinogen from epidemiological findings. To determine the effects of infection with the bacteria on experimental carcinogenesis, a study of the glandular stomach of Mongolian gerbils (MGs) was performed. Male MGs were treated with N-methyl-N'-nitro-N-nitrosoguanidine followed by inoculation with Hp or infected with Hp followed by N-methyl-N'-nitro-N-nitrosoguanidine administration. Animals were killed at week 50, and their excised stomachs underwent microbiological and histopathological examinations. In addition, a serological investigation was performed. The incidences of adenocarcinomas were significantly higher in animals treated with 60 or 300 p.p.m. N-methyl-N'-nitro-N-nitrosoguanidine for 10 weeks followed by Hp inoculation or Hp followed by 20 p.p.m. N-methyl-N'-nitro-N-nitrosoguanidine for 30 weeks than in the respective controls. Moreover, tumour-bearing animals had higher titres of anti-Hp antibodies than tumour-free animals. Of interest was the finding that a dose of 100 p.p.m. N-methyl-N'-nitro-N-nitrosoguanidine given to infected gerbils eradicated the Hp in about half the animals, with a concomitant reduction in the promoting effect. No tumours were found in animals infected with Hp without N-methyl-N'-nitro-N-nitrosoguanidine or non-treated gerbils. Hp infection enhances glandular stomach carcinogenesis in MGs treated with N-methyl-N'-nitro-N-nitrosoguanidine. Animals with high titres of anti-Hp antibodies are at greatest risk of developing neoplasms. (+info)Lack of effect of a 60 Hz magnetic field on biomarkers of tumor promotion in the skin of SENCAR mice. (7/596)
It has been proposed that extremely low frequency magnetic fields may enhance tumorigenesis through a co-promotional mechanism. This hypothesis has been further tested using the two-stage model of mouse skin carcinogenesis, i.e. 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced promotion of skin carcinogenesis in mice initiated by a single subcarcinogenic dose of 7,12-dimethylbenz[a]anthracene. Experimentation utilized three different doses of TPA within its dose-response range (0.85, 1.70 or 3.40 nmol) and examined the following early biomarkers of tumor promotion after 1, 2 and 5 weeks of promotion: increases in epidermal thickness and the labeling index of epidermal cells, induction of epidermal ornithine decarboxylase activity and down-regulation of epidermal protein kinase C activity. Mice exposed to a 60 Hz magnetic field having a flux density of 2 mT for 6 h/day for 5 days/week were compared with mice exposed to an ambient magnetic field. Within the sensitivity limits of the biomarker methodology and the exposure parameters employed, no consistent, statistically significant effects indicative of promotion or co-promotion by the magnetic field were demonstrated. (+info)Promoting effects of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone on rat glandular stomach carcinogenesis initiated with N-methyl-N'-nitro-N-nitrosoguanidine. (8/596)
The modifying effects of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX), a mutagenic by-product in chlorinated water, on the development of glandular stomach cancers were investigated in Wistar rats. A total of 120 males, 6 weeks of age, were divided into six groups. After initiation with 100 ppm N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) solution and 5% NaCl diet for 8 weeks, 30 rats each in groups 1-3 were given MX in the drinking water at concentrations of 30, 10, or 0 ppm for the following 57 weeks. Ten animals each in groups 4-6 were administered the MX without prior carcinogen exposure. There were no statistical significant differences in final body weights between the groups. The incidences and multiplicities of adenocarcinomas in the glandular stomachs were significantly higher (P < 0.05) in the initiated 30 ppm MX group than those in the MNNG/NaCl group. The incidences of atypical hyperplasias in the glandular stomachs were also significantly increased (P < 0.05 or 0.01) by the MX treatments. With their multiplicity, the effects were clearly dose dependent. Interestingly, the 30 ppm MX alone itself induced atypical hyperplasias in the pylorus, although the incidences and severity were low. Moreover, MX showed a tendency to enhance the development of intrahepatic cholangiocellular tumors and thyroid follicular cell tumors in the MNNG-treated animals. The results of the present study thus indicate that MX exerts promoting effects when given during the postinitiation phase of two-stage glandular stomach carcinogenesis in rats. (+info)
Cocarcinogenic effects of alcohol in hepatocarcinogenesis | Gut
13 letter words that begin with Co in the enable uncensored word list.
Cocarcinogenesis | definition of cocarcinogenesis by Medical dictionary
Cocarcinogenic Effect of Capsaicin Involves Activation of EGFR Signaling but Not TRPV1 | Cancer Research
Differential gene expression during multistage carcinogenesis....
Reactive oxygen species (ROS) in multistage carcinogenesis<...
Arans Fotos - Galeria de Fotos CochesRc @ CochesRc, coches radiocontrol gasolina y electricos, coches rc.
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Cocarcinogenic effects of alcohol in hepatocarcinogenesis | Gut
Improved two-stage model averaging for high-dimensional linear regression, with application to Riboflavin data analysis | BMC...
eKVV: Mathematik / Promotion - Vorlesungsverzeichnis (Universität Bielefeld)
NIOSHTIC-2 Publications Search - 00168044 - The role of the lung in stomach carcinogenesis: a revision of the Meyer hypothesis.
The Risk Assessment Information System
Sodium Saccharin
Colorado Breath: Healthy Links
Take The Challenge | The Power To Change Is Within You | Dena Warfield
Medeniyet Med J: 33 (2)
Chinese Manufacturer 4-6 Mesh, 5-8 Mesh, 20-40 Mesh Sodium Saccharin - China Sodium Saccharin, Food Grade Sodium Saccharin
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Tea, instant, sweetened with sodium saccharin, lemon-flavored, prepared - nutrtion information: calories, carbohydrates,...
Jams and preserves, dietetic (with sodium saccharin), any flavor Nutrition
Re: Yang, J. and Duerksen-Hughes, P. (1998) A new approach to identifying genotoxic carcinogens: p53 induction as an indicator...
Benalmádena, Spain Events | Eventbrite
Molecular Carcinogenesis
Promotion | Price | Printed | Baskent Promotion | Promotion Products | 0312 436 4265
Phorbol ester tumor promoters and the anti-tumor-promoter dexamethasone share a molecular target: modulation of the...
China Food Additive Sodium Saccharin 99% - China Sodium Saccharin, Saccharin
The EPA National Library Catalog | EPA National Library Network | US EPA
Multistage carcinogenesis and the incidence of thyroid cancer in the US by sex, race, stage and histology | BMC Public Health |...
Analysis of two inbred strains of mice derived from the SENCAR stock with different susceptibility to skin tumor progression. :...
FORECASTING VALUE-AT-RISK WITH TWO-STEP METHOD: GARCH-EXPONENTIATED ODD LOG-LOGISTIC NORMAL MODEL | AVESİS
Carcinogenic Effects of Immunosuppressive Drugs in Man | SpringerLink
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Physical Carcinogenesis: Radiation-History and Sources | SpringerLink
EMF-Portal | Gene expression profiling of human endothelial cells exposed to 50-Hz magnetic fields fails to produce regulated...
SAS Training in Deutschland -- Establishing Causal Inferences: Propensity Score Matching, Heckmans Two-Stage Model,...
SAS Training in Italia -- Establishing Causal Inferences: Propensity Score Matching, Heckmans Two-Stage Model, Interrupted...
EMF-Portal | Psychological effects of chronic exposure to 50 Hz magnetic fields in humans living near extra-high-voltage...
Determination of isamoxole (N-butyl-N-(4-methyloxazol-2-yl)-2-methylpropanamide, LRCL 3950) in plasma by selected ion...
Chemoprevention of urinary bladder carcinogenesis by flavokawain A - Xiaolin Zi
Calories in 4 tbsps of Tea (Lemon Flavored, Instant Powder, Decaffeinated, with Sodium Saccharin) and Nutrition Facts
Investigations of Nitric Oxide Formation Through the Use of Barium Additive and Two-Stage Model - SAE International
Cytological changes during chemical carcinogenesis in mouse epithelium by Harry L. Malech
China Big discounting Sodium Saccharin Granule - Enhance immunity L-alanine CAS 56-41-7 White crystal - Huanhao Manufacturers...
Collaboration of RON and Epidermal Growth Factor Receptor in Human Bladder Carcinogenesis<...
Topical retinoic acid reduces skin papilloma formation but resistant papillomas are at high risk for malignant conversion<...
Blocking Transforming Growth Factor β Signaling in Transgenic Epidermis Accelerates Chemical Carcinogenesis | Cancer Research
Are There Thresholds for Non-genotoxic and Genotoxic Carcinogens?
SODIUM SACCHARIN | LOREAL
Chemical Carcinogenesis | Casarett & Doulls Essentials of Toxicology, 3e | AccessPharmacy | McGraw-Hill Medical
NEW AGGREGATE AND SOURCE SPECIFIC PORK IMPORT DEMAND ELASTICITY FOR JAPAN: IMPLICATIONS TO U.S. EXPORTS - AgEcon Search
JWH-073 3-HYDROXYBUTYL METABOLITE (INDOLE-D5, 98%) 100 UG/ML IN METHANOL - Creative Proteomics
Chromosomal approaches to oncogenes and oncogenesis
Anthracene
Carcinogenesis • Dr. Denis Slinkin
Mutagenesis
Salnikow K, Zhitkovich (January 2008). "Genetic and epigenetic mechanisms in metal carcinogenesis and cocarcinogenesis: nickel ...
Hexavalent chromium
Salnikow, K.; Zhitkovich, A. (2008). "Genetic and Epigenetic Mechanisms in Metal Carcinogenesis and Cocarcinogenesis: Nickel, ...
Co-carcinogen
Liu, S. (2005). Effects of arsenic on DNA repair and cell checkpoints involvement in arsenic co-mutagenesis and co-carcinogenesis ...
List of MeSH codes (C23)
... cocarcinogenesis MeSH C23.550.727.645 - neoplasm invasiveness MeSH C23.550.727.645.500 - leukemic infiltration MeSH C23.550. ...
TNO Repository search for: subject:'Cocarcinogenesis'
Chemistry · 1,2-Dimethylhydrazine · Animals · Bile Acids and Salts · Carcinogens · Cecum · Cellulose · Cocarcinogenesis · ... Tissue damage and nutritional factors in experimental respiratory tract (co-)carcinogenesis article. 1983 ... Nutrition · Animals · Anticarcinogenic Agents · Azaserine · Body Weight · Carcinogens · Cell Division · Cocarcinogenesis · ... Cocarcinogenesis · Female · Flour · Hyperplasia · Male · Pancreas · Pancreatic Ducts · Pancreatic Neoplasms · Poultry · Random ...
Cocarcinogenesis | definition of cocarcinogenesis by Medical dictionary
What is cocarcinogenesis? Meaning of cocarcinogenesis medical term. What does cocarcinogenesis mean? ... Looking for online definition of cocarcinogenesis in the Medical Dictionary? cocarcinogenesis explanation free. ... cocarcinogenesis. cocarcinogenesis. [ko-kahr″sĭ-no-jen´ĕ-sis] the development, according to one theory, of cancer only in ... cocarcinogenesis. /co·car·ci·no·gen·e·sis/ (ko-kahr″sĭ-no-jen´ĕ-sis) the development, according to one theory, of cancer only ...
Ozone Carcinogenesis and Co-Carcinogenesis and its Prevention | Springer for Research & Development
Cocarcinogenesis | Profiles RNS
"Cocarcinogenesis" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... This graph shows the total number of publications written about "Cocarcinogenesis" by people in this website by year, and ... Below are the most recent publications written about "Cocarcinogenesis" by people in Profiles. ... whether "Cocarcinogenesis" was a major or minor topic of these publications. To see the data from this visualization as text, ...
Liver as a Model System for Analyzing Mechanisms of Tumor Initiation and Promotion | SpringerLink
Nonclinical Safety Assessment: A Guide to International Pharmaceutical Regulations | Drug Discovery & Development |...
Spontaneous and nitrosourea-induced primary tumors of the central nervous system in Fischer 344 rats chronically exposed to 836...
We have tested an 836.55 MHz field with North American Digital Cellular (NADC) modulation in a 2-year animal bioassay that included fetal exposure. In offspring of pregnant Fischer 344 rats, we tested both spontaneous tumorigenicity and the incidence of induced central nervous system (CNS) tumors af …
Inhibition of soybean lipoxygenase and mouse skin tumor promotion by onion and garlic components
Onion and garlic essential oils were previously shown to inhibit mouse skin tumor promotion, as were the enzymes, lipoxygenase, and cyclooxygenase. In the present study, the inhibition of soybean lipoxygenase (EC 1.13.11.12) by onion and garlic components and related compounds was investigated. The …
NewGeneris: A European Study on Maternal Diet during Pregnancy and Child Health | Cancer Epidemiology, Biomarkers & Prevention
A method for parametric estimation of the number and size distribution of cell clusters from observations in a section plane.
Food and cancer.
Gastrointestinal alcohol dehydrogenase. - PubMed - NCBI
611. Tocopherol, alpha- (WHO Food Additives Series 21)
CDC Allegedly falsified reports ignoring up to 3587 miscarriages from H1N1 Vaccine, page 1
NIOSHTIC-2 Publications Search - 00177552 - Information Profile. Sodium Azide.
Hexavalent chromium - Wikipedia
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Mouse skin tumor-initiating activity of 5-, 7-, and 12-methyl- and fluorine-substituted benz[a]anthracenes. | CureHunter
Frederick Beland | FDA
A case of Bowen's disease and small-cell lung carcinoma: long-term consequences of chronic arsenic exposure in Chinese...
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Frontiers | Genome-Wide Analyses of Metal Responsive Genes in Caenorhabditis elegans | Genetics
Mutagenesis - Wikipedia
NICKEL: Overview, Uses, Side Effects, Precautions, Interactions, Dosing and Reviews
Human mesothelial cells are unusually susceptible to simian virus 40-mediated transformation and asbestos cocarcinogenicity |...
Ethanol-related2
- Possible role of acetaldehyde in ethanol-related rectal cocarcinogenesis in the rat. (thefreedictionary.com)
- In conclusion, because of the oncofetal phenotype of H, B, and Le(b) antigens, their reappearance in the distal colon may serve as a cytochemical marker for early recognition of epithelial changes of the colon in ethanol-related cocarcinogenesis before more overt manifestations of neoplasia. (augmentin2020.site)
Tumor2
- The coke oven sample was approximately 12 times as active as the roofing tar sample as a tumor promoter in mouse skin initiated with benzo(a)pyrene (B(a)P). Cocarcinogenesis was studied in SENCAR mice by using the tumor co-initiation protocol. (epa.gov)
- The resultant comprehensive data clearly illustrate established pathways of cancer induction involving carcinogen exposure, metabolic activation, DNA adduct formation, and consequent mutation of critical genes along with the exacerbating influences of inflammation, cocarcinogenesis, and tumor promotion. (aacrjournals.org)
Arsenic2
- Salnikow K, Zhitkovich A (2008) Genetic and epigenetic mechanisms in metal carcinogenesis and cocarcinogenesis: nickel, arsenic, and chromium. (springer.com)
- Florea A, Yamoah EN, Dopp E. Intracellular Calcium Disturbances Induced by Arsenic and Its Methylated Derivatives in Relation to Genomic Damage and Apoptosis Induction. (aaem.pl)
Neoplasia1
- The cocarcinogenesis studies using IR chrysotile asbestos and 1,2-dimethylhydrazine dihydrochloride were considered inadequate because there was no increase in intestinal neoplasia in the DMH group. (nih.gov)
Acetaldehyde1
- Acetaldehyde seems to be involved in ethanol-associated cocarcinogenesis. (nih.gov)
Gastrointestinal1
- The metabolism of retinol and the generation of retinoic acid is a function of class I and class IV ADH, and its inhibition by alcohol may lead to an alteration of epithelial cell differentiation and cell growth and may also be involved in ethanol-associated gastrointestinal cocarcinogenesis. (nih.gov)
Exposure2
- Due to the constantly increasing hazard of styrene exposure and possible cocarcinogenesis in digestive tract with bilious acids, an experimental model of chronic exposure of stomach mucosa to styrene oxide [SO] with accompanying bilious reflux has been elaborated. (medscimonit.com)
- Data on the cocarcinogenesis of certain Sorbitan Esters were positive, but only with high exposure levels and a high frequency of exposure, and the results lacked a dose-response. (cosmeticsinfo.org)
Descriptor1
- Cocarcinogenesis" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
Mechanisms1
- however, several indirect cocarcinogenesis mechanisms have been proposed. (thefreedictionary.com)
Environmental1
- 2007a), and cocarcinogenesis with other environmental toxicants (Rossman et al. (thefreedictionary.com)
Year1
- This graph shows the total number of publications written about "Cocarcinogenesis" by people in this website by year, and whether "Cocarcinogenesis" was a major or minor topic of these publications. (umassmed.edu)