Vermont Mesothelioma Fact Sheet
While mesothelioma is a problem in all states, the specific incident rate for Vermont is 0.9 / 100,000. This is below the average rate of 1.1 / 100,000. Click on the tabs below to find mesothelioma and asbestos research in VT, recent VT mesothelioma-related court cases, mesothelioma specialists in VT and potential asbestos hotspots in Vermont.
Vermont Mesothelioma Info
By clicking on the above tabs, you will find information on mesothelioma specific to the state of Vermont
Vermont Research and Clinical Trials
This is a partial list of scientific or medical grants in your state for research into mesothelioma and related illnesses.
Vermont Doctors and Hospitals
This is a partial list of hospitals and physicians that reportedly treat mesothelioma patients in your state.
Vermont Cases
This is a partial list of relevant court cases on mesothelioma in your state.
Disclaimer: Inclusion on this directory does not constitute endorsement by Cancer Monthly, Inc. All physicians who appear in this section do so based on their own expression of interest in the fields of mesothelioma treatment. Cancer Monthly, Inc. has not verified the competence, professional credentials, business practices or validity of the expressed interests of these physicians. Cancer Monthly makes no recommendation of any physician on this list and makes no suggestion that any such physician will cure or prevent any disease. Those consulting a physician on this list should approach the consultation exactly as they would with any other unknown physician.
This is a partial list of scientific or medical grants in your state for research into mesothelioma and related illnesses.
Vermont Doctors and Hospitals
This is a partial list of hospitals and physicians that reportedly treat mesothelioma patients in your state.
Vermont Cases
This is a partial list of relevant court cases on mesothelioma in your state.
Disclaimer: Inclusion on this directory does not constitute endorsement by Cancer Monthly, Inc. All physicians who appear in this section do so based on their own expression of interest in the fields of mesothelioma treatment. Cancer Monthly, Inc. has not verified the competence, professional credentials, business practices or validity of the expressed interests of these physicians. Cancer Monthly makes no recommendation of any physician on this list and makes no suggestion that any such physician will cure or prevent any disease. Those consulting a physician on this list should approach the consultation exactly as they would with any other unknown physician.
Hospitals and Cancer Centers
Veterans Affairs Medical Center-White River Junction
250 N. Main St.
White River Junction , VT
802.295.9363
Veterans Affairs Medical Center-White River Junction
250 N. Main St.
White River Junction , VT
802.295.9363
| City | Site |
|
No information available |
Research
Ramos, Maria E. Role Of Fra-1 In Mesothelioma
Grant: 1K01CA104159-01
Grant: 1K01CA104159-01
Abstract: DESCRIPTION (provided by applicant): Mesothelioma, an aggressive malignancy associated with occupational exposure to asbestos and more recently linked to Simian Virus 40 (SV40) is a fatal tumor resistant to therapy. The incidence of mesothelioma is predicted to rise in the next decades, creating a pressing need for new therapeutic strategies. Efforts to elucidate the molecular events that drive tumor promotion and progression in mesothelioma have revealed a relationship between Activator Protein-1 (AP-1), increased expression of Fra-1 in AP-1 complexes and morphologic transformation of mesothelial cells. Pathogenic fibers, including certain families of asbestos fibers and/or SV40, activate the mitogen-activated protein kinase (MAPK) cascade; an event that precedes increases in steady-state mRNA levels of AP-1 (fos/jun) family members. The study of the molecular events that lead to Fra-1 expression, and the discovery of target genes of Fra-1 is a novel approach to establish possible molecular targets for mesothelioma treatment and to establish the role of these molecular events in carcinogenesis. In this proposal, it is hypothesized that asbestos and/or SV40-induced Fra-1 and expression of target genes is linked to mesothelial cell proliferation, transformation and malignancy. In Specific Aim 1, genes involved in tumorigenesis that are regulated by Fra-1 will be determined in human mesotheliomas using microarray techniques. In Specific Aim 2, novel Fra-1 target promoters will be assessed in human mesothelioma cells by chromatin immunoprecipitation techniques. In Specific Aim 3, the effect of modulating Fra-1 and selected genes in proliferation, morphological transformation and tumorigenesis will be studied in normal and asbestos-exposed isolated rat mesothelial (RPM) cells, a mesothelial cell line isolated from a rat chronically exposed to asbestos in vivo and rat and human mesothelioma cells. This proposal will provide the basis for the candidate's training and career in cancer research. It will also provide information on the role of Fra-1 in functional outcomes linked to fiber- and SV40-induced carcinogenesis, allowing future development of possible therapeutic strategies in mesothelioma. The long-term goal of this research plan is to understand the molecular mechanisms governing mesothelial cell tumorigenesis.
Tags: Carcinogenesis, Fos Protein, Gene Expression, Mesothelioma, Neoplasm /cancer Genetics, Neoplastic Transformation, Protooncogene Asbestos, Cell Proliferation, Environment Related Neoplasm /cancer, Epithelium, Genetic Promoter Element, Lung Neoplasm, Mitogen Activated Protein Kinase, Molecular Oncology, Molecular Pathology, Occupational Disease /disorder, Simian Virus 40, Virus Related Neoplasm /cancer Animal Tissue, Cell Line, Chromatin Immunoprecipitation, Human Tissue, Laboratory Mouse, Microarray Technology, Tissue /cell Culture
Tags: Carcinogenesis, Fos Protein, Gene Expression, Mesothelioma, Neoplasm /cancer Genetics, Neoplastic Transformation, Protooncogene Asbestos, Cell Proliferation, Environment Related Neoplasm /cancer, Epithelium, Genetic Promoter Element, Lung Neoplasm, Mitogen Activated Protein Kinase, Molecular Oncology, Molecular Pathology, Occupational Disease /disorder, Simian Virus 40, Virus Related Neoplasm /cancer Animal Tissue, Cell Line, Chromatin Immunoprecipitation, Human Tissue, Laboratory Mouse, Microarray Technology, Tissue /cell Culture
- Followup Grant: 5K01CA104159-02
- Followup Grant: 5K01CA104159-03
- Followup Grant: 5K01CA104159-04
- Followup Grant: 5K01CA104159-05
Mossman, Brooke T. Erk Pathways In Pathogenesis Of Mesothelioma
Grant: 1P01CA114047-01A10002
Grant: 1P01CA114047-01A10002
Abstract: Extracellular signal regulated kinases, ERK1/2 and ERK5, are activated by asbestos fibers in mesothelial
and airway epithelial cells and play critical roles in cell survival. ERK1/2-dependent Fra-1 expression is also
linked causally to morphologic transformation of rat mesothelial cells and expression of genes (c-met, cd44)
stimulating cell proliferation and migration. We hypothesize that activation of ERK1/2 and ERK5 signaling
pathways occur by carcinogenic fibers (asbestos, erionite) in the pathogenesis of human malignant
mesothelioma (MM) and are potentiated by SV40 in a co-carcinogenic manner. Recent exciting data also
suggest that these survival pathways are activated in MMs after exposure to chemotherapeutic drugs and
can be manipulated to achieve increased cell killing. Thus, we also hypothesize that ERK1/2 and ERK5
pathways contribute, alone or cooperatively, to MM cell survival after chemotherapy. In Aim 1, we will test
crocidolite and chrysotile asbestos, well-characterized Turkish erionite (see Project 1), and their nonfibrous
analogs, alone and with co-exposures to SV40 to determine if ERK1/2, and ERK5 activity, fos/jun family
members, and AP-1 transactivation correlate with patterns of transformation and carcinogenicity as
determined in the in vitro/in vivo models developed by Dr. Carbone (Core C). In Aim 2, we will use a panel
of SV40+ and - MMs from Core B to determine the effects of dominant negative constructs and small hairpin
(sh) RNA interference (RNAi) vectors targeting ERK1/2 and ERK5 on parameters of in vitro cell
transformation and survival after treatment with Carmustine (BCNU). In collaboration with Dr. Testa (Project
3) we will also determine if the AKT survival pathway is modified in these studies. In Aim 3, a mouse
orthotopic model will be used to determine if SV40+ and - MMs stably transfected with shMEKI, shERKS or
both constructs before intrapleural injection and administration of Carmustine, have altered growth and
metastases. Identifying the pathways of cell survival in the pathogenesis of MMs is highly significant for
prevention and treatment of these devastating tumors. This Program Project allows our previous
mechanistic studies in rodent mesothelioma models to be validated in human mesotheliomas and provides
us with expertise on virology and MM pathology (Dr. Carbone), AKT survival pathways (Dr. Testa) and use
of normal human mesothelial and MM cells (Dr. Pass).
Tags: Asbestos, Cocarcinogen, Environment Related Neoplasm /cancer, Enzyme Activity, Enzyme Mechanism, Mesothelioma, Mitogen Activated Protein Kinase, Silicate, Simian Virus 40, Virus Related Neoplasm /cancer Antineoplastic, Carcinogen, Carmustine, Cell Proliferation, Gene Environment Interaction, Gene Expression, Neoplastic Transformation Athymic Mouse, Genetically Modified Animal, Human Tissue, Xenotransplantation
Tags: Asbestos, Cocarcinogen, Environment Related Neoplasm /cancer, Enzyme Activity, Enzyme Mechanism, Mesothelioma, Mitogen Activated Protein Kinase, Silicate, Simian Virus 40, Virus Related Neoplasm /cancer Antineoplastic, Carcinogen, Carmustine, Cell Proliferation, Gene Environment Interaction, Gene Expression, Neoplastic Transformation Athymic Mouse, Genetically Modified Animal, Human Tissue, Xenotransplantation
- Followup Grant: 5P01CA114047-020002
- Followup Grant: 5P01CA114047-030002
- Followup Grant: 5P01CA114047-040002
Craighead, John E. Experimental Asbestos-induced Mesothelioma
Grant: 2R01CA036993-04
Grant: 2R01CA036993-04
Abstract: Malignant mesotheliomas in man are associated with asbestos
exposure. Although customarily rare, these tumors are dramatically
increasing in prevalence in our population. Rats inoculated by the
intrapleural and intraperitoneal routes with asbestos of several
different types develop lesions which strikingly resemble the human
cancers after latency periods of 6 to 24 months. In work supported
by this grant, we characterized these lesions and initiated studies
to elucidate the pathogenesis of the neoplasm. The proposed
research will attempt to develop a model of carcinogenesis
originating in the granuloma which forms in and around the
accumulations of asbestos that develop after thoracic inoculation
of asbestos. Attempts will be made to determine whether or not
asbestos-laden macrophages generate oxygen metabolites and damage
the chromosomes or the mitotic spindle as a result. Efforts will
be made to demonstrate the release of growth factors elicited by
the macrophages of the granuloma and their effect on presumptive
progenitor cells of the mesothelioma. The outcome of these studies
will support or refute the hypothesis that pro-growth substances
stimulate their replication in the course of multistage
carcinogenesis. Additional work will attempt to demonstrate the
presence of premalignant and malignant cells in the reactive tissue
mass which forms in and around granulomas in the cavities of
animals. Finally, efforts will be made to determine the possible
role of proto-oncogenes in the genesis of the tumors and the
utility of these genes as markers for identifying transformation
of the mesothelial cell or its precursor. These studies are
designed to elucidate mechanisms of carcinogenesis for this unique
and poorly understood tumor, based on the notion that its
pathogenesis may be an example of foreign body carcinogenesis.
Tags: Animals, Chordates, Mammals, Rodents, Myomorpha, Rats (laboratory), Models, Design And Development Of Models, Models, Disease Models, Neoplasms Of Body Cavities, Mesothelioma, Neoplasms, Environment-induced (ecologic), Neoplastic Transformation, Carcinogenesis, Chemical, Silicates, Asbestos Blood And Re System, Macrophages, Growth Factors (incl. Anabolics), Neoplasms Characteristics, Cellular Level Studies, Neoplasms Classification And Staging, Neoplasms Genetics, Neoplasms Of Body Cavities, Peritoneal And Retroperitoneal, Neoplasms Related Interest, Preneoplastic Conditions, Neoplasms Resources, Registries, Neoplasms, Chemical Induced, Neoplastic Growth, Latent Cancer, Occupational Health And Safety, Occupational Diseases, Oxides, Superoxide, Histopathology, Neoplastic Growth Genetics, Karyotypes, Histochemistry And Cytochemistry, Neoplasms Transplantation, Tissue (cell) Culture, Clone Cells, Growth Media
Tags: Animals, Chordates, Mammals, Rodents, Myomorpha, Rats (laboratory), Models, Design And Development Of Models, Models, Disease Models, Neoplasms Of Body Cavities, Mesothelioma, Neoplasms, Environment-induced (ecologic), Neoplastic Transformation, Carcinogenesis, Chemical, Silicates, Asbestos Blood And Re System, Macrophages, Growth Factors (incl. Anabolics), Neoplasms Characteristics, Cellular Level Studies, Neoplasms Classification And Staging, Neoplasms Genetics, Neoplasms Of Body Cavities, Peritoneal And Retroperitoneal, Neoplasms Related Interest, Preneoplastic Conditions, Neoplasms Resources, Registries, Neoplasms, Chemical Induced, Neoplastic Growth, Latent Cancer, Occupational Health And Safety, Occupational Diseases, Oxides, Superoxide, Histopathology, Neoplastic Growth Genetics, Karyotypes, Histochemistry And Cytochemistry, Neoplasms Transplantation, Tissue (cell) Culture, Clone Cells, Growth Media
- Followup Grant: 5R01CA036993-05
- Followup Grant: 5R01CA036993-06
- Followup Grant: 5R01CA036993-07
- Followup Grant: 5R01CA036993-08
- Followup Grant: 1R01CA036993-01
- Followup Grant: 5R01CA036993-02
- Followup Grant: 5R01CA036993-03
Mossman, Brooke T. Oxygen Radicals In Mineral Damage/tumor Promotion
Grant: 2R01CA033501-04
Grant: 2R01CA033501-04
Abstract: Bronchogenic carcinoma is the leading cause of cancer deaths in man. Both
epidemiologic and experimental studies suggest the importance of asbestos
and other minerals as cofactors in the development of this neoplasm and
mesothelioma, a tumor occurring rarely in the general population but
frequently in asbestos workers. Over the previous period of funding, the
principal investigator has documented in tracheal bronchial epithelial
cells exposed to asbestos a constellation of promoter-like effects
resembling the actions of phorbol esters on target cells. These include
initial cell damage, inflammatory changes and regenerative hyperplasia and
metaplasia. In recent studies, the prevention of asbestos-associated
cytotoxicity has been accomplished using scavengers of superoxide (02) and
the hydroxyl (OH.) radical. This project is designed to test the
hypothesis that active oxygen species play a role in asbestos-induced cell
damage and promotion in target cells, i.e. those giving rise to
bronchogenic carcinoma and mesothelioma. Specifically, we will address the
questions: 1) Do specific scavengers of oxygen free radicals prevent
asbestos induced damage to mesothelial cells? 2) Do mesothelial and
epithelial cell types contain various scavenger enzymes (SOD, catalase,
glutathione peroxidase) and is the activity of endogenous SOD altered after
exposure of cells to asbestos? 3) Can administration of exogenous
scavengers of oxygen free radicals prevent fiber-associated hyperplasis,
squamous metaplasia and inflammation in tracheal (and mesothelial) organ
cultures and grafts? 4) Does asbestos cause release of OH., H202 and 02
from both epithelial and mesothelial cells? and 5) is actual fiber-cell
contact necessary for generation of oxygen free radicals? The importance
of mineral chemistry, size and shape in the causation of biological
responses will be addressed by using two types of asbestos (crocidolite and
chrysotile) in comparison with their nonfibrous analogs (riebeckite and
antigorite, respectively). Sized preparations (i.e. long (greater than
10Mu) vs short (less than 2Mu) of chrysotile also will be assessed. In
addition glass particles will be included in experiments as an example of
an amorphous, non-carcinogenic dust.
Elucidation of the properties of minerals which are important in tumor
promotion is intrinsic to understanding the process of multi-stage
carcinogenesis in lung. The results of this proposal will provide a
mechanistic framework for preventive and therapeutic approaches using
scavengers of oxygen free radicals in man.
Tags: Chemical Pathology Study Section, Chemicals (general), Minerals (general), Electronic Spectra, Free Radicals, Neoplasms Of Body Cavities, Mesothelioma, Neoplasms Of Respiratory System, Lung Neoplasms, Bronchogenic Carcinoma, Neoplasms, Environment Induced (ecologic) (general), Neoplastic Transformation, Carcinogenesis, Chemical, Neoplastic Transformation, Carcinogens, Cocarcinogens, Neoplastic Transformation, Carcinogens, Tumor Promoters, Silicates, Asbestos Amines, Polyamines, Cell Components, Cell Membrane, Decarboxylases, Ornithine Decarboxylase, Diseases, Pathologic Processes, Inflammation, Enzyme Mechanisms, Growth Abnormal, Hyperplasia (general), Growth Abnormal, Metaplasia, Growth Factors (incl. Anabolics), Transforming Growth Factors, Iron Oxides, Membrane Surface (biological) Activity (general), Neoplasms Of Respiratory System, Tracheal Neoplasms, Oxidoreductases, Superoxide Dismutase, Physical Properties, Particles, Respiratory System, Epithelium, Silicates, Glass, Cell Growth Regulation Cyclics, Carbopolycyclics, Benzopyrenes, Mammals, Rodents, Myomorpha, Hamsters, Mammals, Rodents, Myomorpha, Rats (laboratory), Radioautography, Radiotracers, Tissue (cell) Culture, Clone Cells, Tissue (cell) Culture, Organ Culture, Bioassay
Tags: Chemical Pathology Study Section, Chemicals (general), Minerals (general), Electronic Spectra, Free Radicals, Neoplasms Of Body Cavities, Mesothelioma, Neoplasms Of Respiratory System, Lung Neoplasms, Bronchogenic Carcinoma, Neoplasms, Environment Induced (ecologic) (general), Neoplastic Transformation, Carcinogenesis, Chemical, Neoplastic Transformation, Carcinogens, Cocarcinogens, Neoplastic Transformation, Carcinogens, Tumor Promoters, Silicates, Asbestos Amines, Polyamines, Cell Components, Cell Membrane, Decarboxylases, Ornithine Decarboxylase, Diseases, Pathologic Processes, Inflammation, Enzyme Mechanisms, Growth Abnormal, Hyperplasia (general), Growth Abnormal, Metaplasia, Growth Factors (incl. Anabolics), Transforming Growth Factors, Iron Oxides, Membrane Surface (biological) Activity (general), Neoplasms Of Respiratory System, Tracheal Neoplasms, Oxidoreductases, Superoxide Dismutase, Physical Properties, Particles, Respiratory System, Epithelium, Silicates, Glass, Cell Growth Regulation Cyclics, Carbopolycyclics, Benzopyrenes, Mammals, Rodents, Myomorpha, Hamsters, Mammals, Rodents, Myomorpha, Rats (laboratory), Radioautography, Radiotracers, Tissue (cell) Culture, Clone Cells, Tissue (cell) Culture, Organ Culture, Bioassay
- Followup Grant: 5R01CA033501-05
- Followup Grant: 5R01CA033501-06
Landry, Christopher Improving The Transfer Of Erk Sirna Constructs Using Nanoporous Silica
Grant: 1R41CA126155-01A1
Grant: 1R41CA126155-01A1
Abstract:
DESCRIPTION (provided by applicant): Our research is focused on the potential of acid-prepared mesoporous silica (APMS) as a delivery agent for siRNA constructs to inhibit the ERK1/2 and ERK5 pathways in the treatment of human malignant mesothelioma (MM). These pathways are critical to MM cell proliferation and chemoresistance. Our initial research suggests that APMS will be significantly more effective as a vehicle for uptake and delivery of siRNA constructs into the thoracic cavity than current alternatives. Prior research shows that modified APMS effectively transfers DNA plasmids to epithelial and mesothelioma cells in vitro. APMS itself is not toxic to cells in vitro or after injection intranasally or intrathoracically into mice. The external surface of APMS can be modified for cell specific targeting and maximal uptake. The proposed research as three main goals: (1) engineer APMS for maximum and selective uptake by human MM cells in vitro; (2) study the kinetics of uptake of shRNA constructs into APMS; and (3) use shRNA-loaded APMS to block ERK1/2 and ERK5 pathways. Assuming the Phase I in vitro research validates our hypothesis that shRNA-loaded APMS both improves the uptake of the constructs to MM cells and significantly increases the interference of the constructs with the ERK1/2 and ERK5 pathways, our Phase II research will involve the in vitro functional effects of shRNA-loaded constructs in human MM and in vivo work with a mouse xenograft model. In addition, we plan to expand our research to other shRNA constructs that block other signaling pathways. Since a universal obstacle to all siRNA therapeutics is the delivery of the molecules into the cells, APMS offers the potential of revolutionizing the clinical opportunity for siRNA. Our primary focus is on the cancer drug market, a $36.9B in 2004.
Tags: There Are No Thesaurus Terms On File For This Project.
Tags: There Are No Thesaurus Terms On File For This Project.
- Followup Grant: 5R41CA126155-02
Effects Of Mineral Dusts On Cells
Grant:
Grant:
Abstract:
Tritton, Thomas R. Membrane Targets In Cancer Chemotherapy
Grant: 2R01CA044729-04
Grant: 2R01CA044729-04
Abstract: The objective of this research is to test the hypothesis that the plasma
membrane may represent a sensitive site for anticancer drug action. The
work focuses on adriamycin and related anthracyclines. Damage to nuclear
DNA has been considered to be a primary target for adriamycin action, but
there is also a large body of evidence suggesting that the structure and
functions of biological membranes are also sensitive to adriamycin
disruption. This laboratory has shown that adriamycin immobilized on large
polymers can be actively cytoxic under conditions where it does not enter
the cell and bind to DNA, but only accesses the cell surface. Experiments
are proposed to put this finding to a practical test by using the
immobilized drug as a direct therapeutic agent in animals. The polymer
bound drug will be used as an intracavitary agent to treat ovarian
epithelial malignancies, mesothelioma, and ascites tumors. Preliminary
results show that immobilization retains the anticancer activity of
adriamycin, and intraperitoneal administration lacks significant toxic side
effects. The second major aim of this research is to study the role of
phosphatidyl inositol (PI) turnover in mediating the cytotoxic action of
free adriamycin. Drug treatment enhances PI turnover, leading to the
generation of two second messengers- inositol trisphosphate (Ip3) and
diacylglycerol (DG). The function of Ip3 is to mobilize intracellular free
Ca++, but these processes appear to be decoupled in the presence of
adriamycin. The other messenger, DG, activates protein kinase C (PKC). The
activity of this enzyme appears to be linked to the induction of adriamycin
cytotoxicity, so experiments are proposed to determine the role of the
following properties in drug mechanism: (1) cofactor requirements, (2)
translocation between cytoplasm and membrane, (3) isozyme distribution, (4)
phosphorylation of topoisomerase II and other substrates. These experiments
will provide a detailed understanding of how the PI/PKC signal transduction
pathway functions to mediate the cytotoxic cascade induced by adriamycin.
Tags: Antibiotics, Anthracyclines, Adriamycin, Cell Components, Cell Membrane, Drugs, Pharmacology, Biochemical, Neoplasms Pharmacology, Neoplastic Therapy, Cancer Chemotherapy, Receptors, Drug Receptors Antibiotics, Anthracyclines, Biological Signal Transduction, Second Messengers, Drugs Synthesis, Design And Production, Lipids, Glycerides, Diglycerides, Diacylglycerol, Neoplasms Of Body Cavities, Mesothelioma, Neoplasms Of Reproductive System Female, Ovary Neoplasms, Neoplasms, Ascites Tumors, Nucleic Acids, Dna, Phospholipids, Phosphoglycerides, Phosphoinositides, Phosphotransferases-atp, Protein Kinases, Protein Kinase C, Sugar Alcohols, Hexitols, Inositol Phosphates, Toxicology, Cytotoxicity Animals, Chordates, Mammals, Rodents, Myomorpha, Mice (laboratory), Animals, Chordates, Mammals, Rodents, Myomorpha, Rats (laboratory), Chemistry, Analytical Methods, Spectrometry, Fluorescence, Immunological Tests And Immunoassay, Immunoblotting, Physical Separation, Electrophoresis, Gel, Radioautography
Tags: Antibiotics, Anthracyclines, Adriamycin, Cell Components, Cell Membrane, Drugs, Pharmacology, Biochemical, Neoplasms Pharmacology, Neoplastic Therapy, Cancer Chemotherapy, Receptors, Drug Receptors Antibiotics, Anthracyclines, Biological Signal Transduction, Second Messengers, Drugs Synthesis, Design And Production, Lipids, Glycerides, Diglycerides, Diacylglycerol, Neoplasms Of Body Cavities, Mesothelioma, Neoplasms Of Reproductive System Female, Ovary Neoplasms, Neoplasms, Ascites Tumors, Nucleic Acids, Dna, Phospholipids, Phosphoglycerides, Phosphoinositides, Phosphotransferases-atp, Protein Kinases, Protein Kinase C, Sugar Alcohols, Hexitols, Inositol Phosphates, Toxicology, Cytotoxicity Animals, Chordates, Mammals, Rodents, Myomorpha, Mice (laboratory), Animals, Chordates, Mammals, Rodents, Myomorpha, Rats (laboratory), Chemistry, Analytical Methods, Spectrometry, Fluorescence, Immunological Tests And Immunoassay, Immunoblotting, Physical Separation, Electrophoresis, Gel, Radioautography
- Followup Grant: 5R01CA044729-05
- Followup Grant: 5R01CA044729-06
Durand, David B. Malignant Mesothelioma: Growth & Differentiation Pathways
Grant: 2S07RR005429-300190
Grant: 2S07RR005429-300190
Abstract: There is no text on file for this abstract.
Tags: There Are No Thesaurus Terms On File For This Project.
Tags: There Are No Thesaurus Terms On File For This Project.
Mossman, Brooke T. Mechanisms Of Cell Replication In Asbestos Cancers
Grant: 1R01ES006499-01
Grant: 1R01ES006499-01
Abstract: This project will focus on the molecular mechanisms by which crocidolite
and chrysotile asbestos induce proliferation of rodent pleural
mesothelial (RPM) and tracheobronchial epithelial (HTE) cells, the
progenitor cells of mesotheliomas and bronchogenic carcinomas. Since
increased cell proliferation is causally related and/or contributory to
many cancers, we hypothesize that asbestos fibers provide a persistent
mitogenic stimulus necessary for tumor development as is suggested by the
persistent induction of c-fos and c-jun protooncogenes by asbestos. To
determine if crocidolite and chrysotile induce proliferation by similar
or unique processes in various cell types, we will examine the mechanisms
of activation of c-fos and c-jun gene expression using inhibitors of
protein kinase C (PKC) and ADP-ribose transferase. Scavengers of active
oxygen species (AOS) and iron-chelated fibers will be used to test the
hypothesis that asbestos-associated induction of c-fos and c-jun may be
mediated by AOS. Moreover, comparative experiments using nonasbestos
fibers [refractory ceramic (RCF) and glass (MMVF-10)] of similar
dimension to asbestos, sized long (>10 microm) vs. short (
Tags: Asbestos, Cell Cycle, Chemical Carcinogen, Chemical Carcinogenesis, Mutagen Acetylcysteine, Antioxidant, Bronchogenic Carcinoma, Ceramic, Free Radical Scavenger, Gene Induction /repression, Glass, Hydrogen Peroxide, Mesothelioma, Neoplasm /cancer Genetics, Neoplastic Transformation, Phorbol, Protooncogene, Respiratory Epithelium, Transcription Factor Carcinogen Testing, Immunocytochemistry, Laboratory Rat, Mutagen Testing, Tissue /cell Culture
Tags: Asbestos, Cell Cycle, Chemical Carcinogen, Chemical Carcinogenesis, Mutagen Acetylcysteine, Antioxidant, Bronchogenic Carcinoma, Ceramic, Free Radical Scavenger, Gene Induction /repression, Glass, Hydrogen Peroxide, Mesothelioma, Neoplasm /cancer Genetics, Neoplastic Transformation, Phorbol, Protooncogene, Respiratory Epithelium, Transcription Factor Carcinogen Testing, Immunocytochemistry, Laboratory Rat, Mutagen Testing, Tissue /cell Culture
- Followup Grant: 5R01ES006499-02
- Followup Grant: 5R01ES006499-03
- Followup Grant: 5R01ES006499-05
Timblin, Cynthia R. Molecular And Cellular Response To Carcinogenic Fibers
Grant: 1R55CA080131-01A1
Grant: 1R55CA080131-01A1
Abstract: There is no text on file for this abstract.
Tags: Asbestos, Carcinogen, Cell Transformation, Cellular Oncology, Molecular Oncology, Physical /chemical Interaction, Protooncogene, Stress Protein Cell Proliferation, Environment Related Neoplasm /cancer, Gene Expression, Gene Mutation, Mesothelioma, Neoplastic Transformation, Oncoprotein, Programmed Cell Death, Protein Structure /function, Transcription Factor, Tumor Progression Flow Cytometry, Gel Mobility Shift Assay, Laboratory Rat
Tags: Asbestos, Carcinogen, Cell Transformation, Cellular Oncology, Molecular Oncology, Physical /chemical Interaction, Protooncogene, Stress Protein Cell Proliferation, Environment Related Neoplasm /cancer, Gene Expression, Gene Mutation, Mesothelioma, Neoplastic Transformation, Oncoprotein, Programmed Cell Death, Protein Structure /function, Transcription Factor, Tumor Progression Flow Cytometry, Gel Mobility Shift Assay, Laboratory Rat
Clinical Trials
Active, not recruiting Dasatinib in Treating Patients With Previously Treated Malignant Mesothelioma
Condition: Malignant Mesothelioma
Intervention: Drug: dasatinib; Other: immunoenzyme technique; Other: immunohistochemistry staining method; Other: laboratory biomarker analysis
More Information
Intervention: Drug: dasatinib; Other: immunoenzyme technique; Other: immunohistochemistry staining method; Other: laboratory biomarker analysis
More Information