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Mesothelioma in Vermont
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.
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.
[doptab title=”Treatment and Research”]
[dopaccordion title=”Ramos, Maria E. Role Of Fra-1 In Mesothelioma
Grant: 1K01CA104159-01″ icon=27 activeicon=28]
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
- Followup Grant: 5K01CA104159-02
- Followup Grant: 5K01CA104159-03
- Followup Grant: 5K01CA104159-04
- Followup Grant: 5K01CA104159-05
[dopaccordion title=”Mossman, Brooke T. Erk Pathways In Pathogenesis Of Mesothelioma
Grant: 1P01CA114047-01A10002″ icon=27 activeicon=28]
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
- Followup Grant: 5P01CA114047-020002
- Followup Grant: 5P01CA114047-030002
- Followup Grant: 5P01CA114047-040002
[dopaccordion title=”Craighead, John E. Experimental Asbestos-induced Mesothelioma
Grant: 2R01CA036993-04″ icon=27 activeicon=28]
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
- 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
[dopaccordion title=”Mossman, Brooke T. Oxygen Radicals In Mineral Damage/tumor Promotion
Grant: 2R01CA033501-04″ icon=27 activeicon=28]
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
- Followup Grant: 5R01CA033501-05
- Followup Grant: 5R01CA033501-06
[dopaccordion title=”Landry, Christopher Improving The Transfer Of Erk Sirna Constructs Using Nanoporous Silica
Grant: 1R41CA126155-01A1″ icon=27 activeicon=28]
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.
- Followup Grant: 5R41CA126155-02
[dopaccordion title=”Effects Of Mineral Dusts On Cells
Grant:” icon=27 activeicon=28]
[dopaccordion title=”Tritton, Thomas R. Membrane Targets In Cancer Chemotherapy
Grant: 2R01CA044729-04″ icon=27 activeicon=28]
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
- Followup Grant: 5R01CA044729-05
- Followup Grant: 5R01CA044729-06
[dopaccordion title=”Durand, David B. Malignant Mesothelioma: Growth & Differentiation Pathways
Grant: 2S07RR005429-300190″ icon=27 activeicon=28]
Abstract: There is no text on file for this abstract.
Tags: There Are No Thesaurus Terms On File For This Project.
[dopaccordion title=”Mossman, Brooke T. Mechanisms Of Cell Replication In Asbestos Cancers
Grant: 1R01ES006499-01″ icon=27 activeicon=28]
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
- Followup Grant: 5R01ES006499-02
- Followup Grant: 5R01ES006499-03
- Followup Grant: 5R01ES006499-05
[dopaccordion title=”Timblin, Cynthia R. Molecular And Cellular Response To Carcinogenic Fibers
Grant: 1R55CA080131-01A1″ icon=27 activeicon=28]
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
[dopaccordion title=”Active, not recruiting Capecitabine in Treating Patients With Malignant Mesothelioma” icon=27 activeicon=28]
Condition: Malignant Mesothelioma
[dopaccordion title=”Completed Gefitinib in Treating Patients With Malignant Mesothelioma” icon=27 activeicon=28]
Condition: Malignant Mesothelioma
Intervention: Drug: gefitinib
[dopaccordion title=”Active, not recruiting PTK787/ZK 222584 in Treating Patients With Unresectable Malignant Mesothelioma” icon=27 activeicon=28]
Condition: Malignant Mesothelioma
Intervention: Drug: vatalanib
[dopaccordion title=”Active, not recruiting Dasatinib in Treating Patients With Previously Treated Malignant Mesothelioma” icon=27 activeicon=28]
Condition: Malignant Mesothelioma
Intervention: Drug: dasatinib; Other: immunoenzyme technique; Other: immunohistochemistry staining method; Other: laboratory biomarker analysis
[dopaccordion title=”Active, not recruiting Sorafenib in Treating Patients With Malignant Mesothelioma” icon=27 activeicon=28]
Condition: Malignant Mesothelioma
Intervention: Drug: sorafenib tosylate
[dopaccordion title=”Recruiting Collecting Tumor Samples From Patients With Gynecological Tumors” icon=27 activeicon=28]
Intervention: Other: biologic sample preservation procedure
[doptab title=”Doctors and Hospital”]
Hospitals and Cancer Centers
Veterans Affairs Medical Center-White River Junction
250 N. Main St.
White River Junction , VT
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