Surviving Mesothelioma / Mesothelioma in Hawaii
Mesothelioma in Hawaii
Hawaii Mesothelioma Info
By clicking on the above tabs, you will find information on mesothelioma specific to the state of Hawaii
Hawaii Research and Clinical Trials
This is a partial list of scientific or medical grants in your state for research into mesothelioma and related illnesses.
Hawaii 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.
Abstract:DESCRIPTION (provided by applicant): Simian virus 40 (SV40 is a DNA virus which specifically induces mesotheliomas, ependymomas, sarcomas and osteosarcomas in rodents. These same tumor types contain SV40 sequences in humans, but the role of SV40 in human carcinogenesis is unknown. We are investigating if SV40 contributes to the development of human mesothelioma, a very aggressive tumor of the pleura whose incidence continues to increase. Mesothelioma is strongly associated with asbestos exposure, but only 5-10 percent of workers exposed to high levels of asbestos develop this tumor, and about 20 percent of mesotheliomas patients have not been exposed to asbestos. It would be very important to find the co-factor/s that render some workers more susceptible to asbestos or that cause mesothelioma in individuals who have not been exposed to asbestos. We propose to investigate the mechanisms that make mesothelial cells very susceptible to SV40-mediated transformation, and their possible relevance to human malignant mesothelioma. During the previous grant period, we established the possible biological significance of SV40 when present in some human mesotheliomas, and the utility of an in vitro SV40-human mesothelial cell system for studying this association. We propose to build on these studies to identify: 1) the natural history of SV40 infection in humans, 2) the mechanisms that cause the frequent immortalization of mesothelial cells following infection with SV40, 3) the mechanisms which may account for the presence of the more rapidly replicating non-archetypal SV40 in mesotheliomas, compared to the less rapidly replicating archetypal SV40 in ependymomas and bone tumors, and whether these mechanisms are related to oncogenesis.
Tags:Mesothelioma, Neoplastic Transformation, Simian Virus 40, Viral Carcinogenesis, Virus Genetics Athymic Mouse, Human Tissue, Neoplasm /cancer Transplantation, Nucleic Acid Sequence, Tissue /cell Culture
Abstract: DESCRIPTION (provided by applicant): Our hypothesis is that asbestos and SV40 are co-carcinogens in causing malignant mesothelioma (MM). This hypothesis is based on in vitro experiments using human mesothelial cells (HM) and in vivo experiments in hamsters. We found that neither asbestos nor SV40 small t antigen mutants could cause HM malignant transformation. However, when HM were exposed to both asbestos and SV40 small t mutants, malignant transformation and focus formation occurred. Moreover, preliminary results demonstrated a potent co-carcinogenic effect in hamsters coinjected with SV40 small t mutant intracardially and with asbestos intrapleurally and intraperitoneally. Our findings suggest that individuals exposed to both asbestos and SV40 are at increased risk of developing mesothelioma. Here we want to study the mechanisms of co-carcinogenesis. We propose to conduct these studies in human and in hamster mesothelial cells in tissue culture, and in hamster and human mesothelioma biopsies. In Aim 1 we will determine the biological effect of TNF-alpha, PDGF and TGF- beta in SV40-asbestos co-carcinogenesis in HM in tissue culture. In preliminary results we found that our mesothelial cells express receptors for these cytokines. We also found that TNF-alpha expression and receptor are induced in HM following asbestos exposure or SV40 infection. HM exposure to TNF-alpha induced NF-kbeta activation which plays an important role in oncogenesis. In parallel we are studying the effect of SV40 and asbestos on the Ras-ERK pathways and AP-1 induction, because we found that both, SV40 and asbestos induce ERK1/2 and downstream effectors in HM in tissue culture. Our hypothesis is that all these mechanisms are inter-related and we will study the biological significance of these mechanisms in SV40-asbestos co-carcinogenesis. In Aim 2A, the same cytokines and gene pathways studied in Aim 1, will be investigated in frozen specimens from MM we induced in hamster with asbestos, SV40, and SV40 small t mutant plus asbestos, and the results compared. By comparing the in vitro data (aim I), with those produced in an experimental MM model (Aim 2A) in which exposure, was under our control, we will identify among many possible candidate gene pathways, those that are most relevant to MM pathogenesis and to SV40-asbestos pathogenesis and co-carcinogenesis. The results will be validated by studying the same cytokines and gene pathways identified in vitro (Aim 1) and in hamster MM (aim 2A) in a unique collection of 38 frozen MM biopsies and matching lung tissue (Aim 2B). In these 38 samples we have determined SV40 status and type and amount of asbestos exposure. Finally, in Aim 3 we will attempt to establish an SV40-asbestos mouse tumor model, similar to the one we established in hasmters. The availability of a mouse model would be ideal for future mechanistic and experimental therapeutic approaches because of the large number of mouse reagents (monoclonals, transgenic mice, knock-out mice, etc.). It is anticipated that the results of the experimens proposed in this application will provide information to design novel preventive and therapeutic approaches for MM.
Tags: Asbestos, Chemical Carcinogenesis, Cocarcinogen, Mesothelioma, Simian Virus 40, Viral Carcinogenesis Cytokine Receptor, Disease /disorder Model, Guanine Nucleotide Binding Protein, Mitogen Activated Protein Kinase, Nuclear Factor Kappa Beta, Platelet Derived Growth Factor, Protooncogene, Transforming Growth Factor, Tumor Necrosis Factor Alpha Genetically Modified Animal, Hamster, Human Tissue, Laboratory Mouse, Tissue /cell Culture
- Followup Grant: 5R01CA106567-04
- Followup Grant: 5R01CA106567-05
- Followup Grant: 5R01CA106567-06
Abstract:DESCRIPTION (provided by applicant): Asbestos is the most important cause of malignant mesothelioma (MM.) in the industrialized world. Because less than 5% of heavily exposed asbestos workers develop MM, additional factors are suspected to render certain individuals more susceptible to asbestos carcinogenicity. Cigarette smoke has been ruled out as a co-factor in MM. Instead, both genetic predisposition and simian virus 40 infections (SV40) have been linked to MM pathogenesis. The central hypothesis of this Program Project is that MM is a malignancy that is mainly caused by asbestos or related fibers (erionite), and that genetic predisposition and SV40 infection make certain individuals more susceptible to asbestos or erionite carcinogenesis. In Project 1, a team of investigators with different expertise led by Dr. Carbone, will try to identify the gene/s that predispose to MM in three villages of Cappadocia, Turkey, where 50% of total deaths are caused by MM. The interaction among genetic predisposition and erionite, a fiber related to crocidolite asbestos which is present in these villages, will also be investigated. Our hypothesis is that this MM-gene/s that is mutated in these Cappadocian families is targeted by asbestos, and possibly by SV40, in sporadic MM in the USA. In Project 2, Dr. Mossman will study if SV40 infection interferes with the mechanisms of asbestos carcinogenesis that she has elucidated throughout the years (ERK pathway and AP-1 activation). In Project 3, Dr. Testa will study how asbestos and SV40 influence the AKT pathway and tumor suppressors (NF-2, p16 and p19) that his work indicates play an important role in MM pathogenesis. Together, these results will provide information on the pathogenesis of MM and on the factors that make certain individuals more susceptible to asbestos/erionite carcinogenesis. This information should allow us to design novel and specific preventive/therapeutic approaches for MM patients. The information developed in this Program Project has general relevance to environmental carcinogenesis because the results will address the hypothesis that genetics and viruses influence the carcinogenesis of mineral fibers. Our multidisciplinary team bridges basic science and clinical expertise. Therefore, our team is perfectly placed to capitalize on the pathogenic information that we will develop during the 5 years of this PO-1 and to take this information to the patient’s bed, or preferably, to use this information to reduce the number of those who would become patients.
Tags: Asbestos, Environment Related Neoplasm /cancer, Gene Environment Interaction, Mesothelioma, Simian Virus 40 Clinical Research
- Followup Grant: 5P01CA114047-02
- Followup Grant: 5P01CA114047-03
- Followup Grant: 5P01CA114047-020001
- Followup Grant: 5P01CA114047-030001
Abstract:Core C is a new core in our submission that offers much needed expertise in pathology and virology to Projects 2 and 3 and to Core B. The services, expertise and reagents provided by this core helps Projects 2 and 3 and Core B to address criticisms and concerns that were raised by the review panel. Moreover, this core provides some key services and reagents originally provided by former project 2 that has been deleted in this resubmission. This core will 1). provide diagnostic pathology for the identification of hamster, mouse and human malignant mesotheliomas (MM) and derived cell lines; 2). provide virology expertise and reagents to Projects 2 and 3; 3). Characterize primary human mesothelial cell cultures and obtain primary hamster mesothelial cell cultures; 4). provide human cell lines transformed by SV40, SV40 small tag mutants and asbestos – alone or in combination; 5). provide hamster MM and derived cell lines induced by crocidolite asbestos, SV40, SV40 small tag mutant plus crocidolite; 6). produce and provide similar in vitro and vivo models using chrysotile asbestos; 7). using immunohistochemistry, in situ hibridization and laser capture microdisection followed by Real Time and RT – PCR analyze gene pathways studied in Project 2 and 3 in animal and human MM tumors induced by SV40 alone, SV40 small tag mutant plus crocidolite or chrysotile, or by crocidolite or chrysotile alone; 8). provide independent SV40 testing of human MM biopsies using immunoprecipitation, Western blotting and immunohistochemistry.
Tags: Animal Care, Asbestos, Biomedical Facility, Environment Related Neoplasm /cancer, Gene Environment Interaction, Histopathology, Mesothelioma, Simian Virus 40 Neoplasm /cancer Genetics, Oncogenic Virus Genetically Modified Animal, Hamster, Human Tissue, Immunocytochemistry, In Situ Hybridization, Laboratory Mouse, Laser Capture Microdissection, Western Blotting
- Followup Grant: 5P01CA114047-039002
Condition: Malignant Mesothelioma
Intervention: Drug: erlotinib hydrochloride
Condition: Malignant Mesothelioma
Intervention: Drug: cisplatin; Drug: gemcitabine hydrochloride
Hospitals and Cancer Centers
We do not have any doctors or cancer centers for this state at the moment.
State v. Wakisaka
NO. 25348 , SUPREME COURT OF HAWAI’I, October 23, 2003, Decided