California Mesothelioma Information

California

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California Mesothelioma Info

By clicking on the above tabs, you will find information on mesothelioma specific to the state of California

California Research and Clinical Trials

This is a partial list of scientific or medical grants in your state for research into mesothelioma and related illnesses.

California Doctors and Hospitals

This is a partial list of hospitals and physicians that reportedly treat mesothelioma patients in your state.

California 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.

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Research

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[dopaccordion title=”He, Jiang Targeted Liposomal Radiotherapy Of Malignant Mesothelioma Grant: 1R01CA135358-01″ icon=27 activeicon=28]

Abstract: DESCRIPTION (provided by applicant): Mesothelioma, a malignancy associated with occupational exposure to asbestos is a devastating disease without attractive therapies. For decades, asbestos was used heavily in construction, industry, the Navy, even household products and appliances, and is still present in many homes, schools, and office buildings. The disease can arise from small exposures, and even as much as 50 years later. As a result, each year 3,000 Americans and many thousands more worldwide develop mesothelioma, and millions of us are at risk, creating a pressing need for new therapeutic strategies. Since mesothelioma is generally a regional disease within the pleura and peritoneum, aggressive surgery can resect most of solid viable tumor. However, microscopic residues and recurrence, especially in the peritoneal mesothelioma because of the complexity of the space and fragility of the organs, are increasingly recognized as major problems. Highly selective tumor location and targeting are needed. Our long term goal is to develop effective radioimmunotherapy (RIT) for human cancers by marrying radiotherapy with nanotechnology. The objective of this application is to engineer nano liposome as the dose delivery media to carry high payload of radionuclides for specific targeting of the methothelioma tumor cells by intraperitoneal administration. To accomplish, the first Aim is to identify optimal scFv antibodies targeting to malignant mesothelioma from a panel of 15 antibodies we have recently discovered. The native antibodies will be labeled with 99mTc for in vitro and in vivo evaluation of targeting. The remaining best 5 will be conjugated to nanosized liposome for further characterization in vitro and in vivo of the performance of these nanoparticle radioimmunoconjugates. The results will guide changes to the synthesis parameters in order to produce antibody liposome conjugates with promising properties for in vivo application. The second aim will focus on the 177Lu labeling of the nanosized liposome conjugated with optimal antibody (177Lu-LP-scFv) to achieve high specific activity and characterize the targeting capability, stability and radiolysis in vitro. In vivo localization and biodistribution will be evaluated and optimized in animals bearing malignant peritoneal mesothelioma. In Aim 3, the biodistribution and treatment efficacy of the best 177Lu-LP-scFv will then be evaluated in mice with malignant peritoneal mesothelioma xenografts. A variety of dosing schemes will also be tested. Execution of this project will provide effective and safe radioimmunotherapy of this aggressive disease. The novel antibody identified from in vivo screening will also have great potential to translate into specific marker for malignant mesothelioma and targeting vector for other targeted modality therapy. Additionally, the modular approach inherent in the nanoliposome simultalously loaded with targeting vector and high payload of cytotoxic agent holds promise as of potential template for multimodality intracavity locoregional therapies (e.g. photodynamic-radiotherapy) for malignant mesothelioma and other human cancers. PUBLIC HEALTH RELEVANCE: Malignant mesothelioma is a neoplasm of the mesothelial lining of the pleural or peritoneal cavity linked to prior exposure to asbestos. For decades, asbestos was used heavily in construction, industry, the Navy, even household products and appliances, and is still present in many homes, schools, and office buildings. The disease can arise from small exposures, and even as much as 50 years later with reported median survivals of only 18 to 24 months after diagnosis. As a result, each year more than 3,000 Americans and many thousands more worldwide develop mesothelioma, millions of us are at risk and projections suggest that the incidence will continue to rise, creating a pressing need for new therapeutic strategies. This project addresses key challenges of radioimmunotherapy (RIT) for the treatment of malignant mesothelioma. The goal for the study is to use nano liposome as the dose delivery media to carry high payload of radionuclides for specific targeting of the methothelioma tumor cells. If successfully completed, this novel method will create far-reaching applications in RIT, particularly for high-potent treatments of malignant mesothelioma.

Tags: There Are No Thesaurus Terms On File For This Project.

  • Followup Grant:5R01CA135358-02

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[dopaccordion title=”Jablons, David M. The Wnt Pathway In Malignant Mesothelioma Grant: 1R01CA093708-01A3″ icon=27 activeicon=28]

Abstract: DESCRIPTION (provided by applicant): The long-term objective for this proposal is the elucidation of molecular mechanisms for the wingless-type (Wnt)/beta-catenin signaling pathway in malignant mesothelioma (MM) and the development of molecular therapies for this malignancy. Mesothelioma is a relatively uncommon but inexorably fatal tumor, affecting about 3000 new patients in the United States annually. Despite advances in cancer treatment, the medium survival rate remains low and most patients die within two years after diagnosis. The pathogenesis of mesothelioma remains poorly understood and the molecular mechanism by which mesothelial cells undergo neoplastic transformation is largely unknown. For this proposal, we will test the hypothesis that aberrant activation of Wnt signaling pathway plays important roles in malignant mesothelioma. Preliminary data from our laboratory showed that the Wnt signaling pathway is activated in MM as evidenced by increased cytosolic/nuclear beta-catenin, and c-Myc, the two downstream target genes, downregulation of the potential endogenous inhibitor secreted frizzled related protein (SFRP2), and an increased phosphorylation of the Wnt pathway mediator dishevelled protein (Dvl-3). These observations have not been described previously nor elucidated in MM. The specific Aims for this application are 1) to confirm that Wnt signaling pathway is activated in mesothelioma in a large number of primary tumor samples: 2) to investigate molecular mechanisms of Wnt signaling activation in mesothelioma. initially by examining the role of SFRP2 and Dvl-3; 3) to investigate whether a Wnt-1 signaling is a survival factor, thus inhibits apoptosis, in mesothelioma using an anti-Wnt-1 ligand monoclonal antibody and siRNA; and 4) to develop molecular therapies by targeting the Wnt-1 ligand with monoclonal antibody in vivo. Recent information about the Wnt signaling pathway reveals its vital importance in both embryogenesis and oncogenesis. Our study aims to reveals its role in malignant mesothelioma, and to add significantly to the emerging knowledge about the Wnt pathway in cancer in general.

Tags: Cadherin, Gene Expression, Mesothelioma, Molecular Oncology, Neoplastic Process, Oncoprotein, Protooncogene Dna Methylation, Apoptosis, Monoclonal Antibody, Neoplasm /cancer Genetics, Neoplasm /cancer Immunotherapy, Protein Protein Interaction, Transcription Factor Athymic Mouse, Cell Line, Clinical Research, Human Tissue, Immunocytochemistry, In Situ Hybridization, Neoplasm /cancer Transplantation, Small Interfering Rna, Transfection, Xenotransplantation

  • Followup Grant:5R01CA093708-02
  • Followup Grant:5R01CA093708-03
  • Followup Grant:R01CA093708-04

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[dopaccordion title=”Schenker, Marc B. Environmental Asbestos And Mesothelioma In California Grant: 1R03CA081615-01″ icon=27 activeicon=28]

Abstract:This study will examine whether environmental asbestos deposits in California are associated with increased rates of mesothelioma, a rare cancer of the pleura and peritoneum that occurs almost solely as a result of asbestos exposure. The project brings together a multidisciplinary team to address geologic occurrence of asbestos in California, potential human exposure based on population patterns and known occupational exposures, and epidemiologic characteristics of disease in the state. The study will provide the ability to assess age-, race- and sex- adjusted mesothelioma rates in relation to asbestiform type and location as determined by geographic mapping. Previous epidemiological studies of asbestos-induced malignancy have focused primarily on occupation asbestos exposures. Studies in other countries have documented mesotheliomas due to environmental asbestos exposure, but there has been little research on this in the U.S. Information on mesothelioma cases from 1988-96 will be obtained from the California Cancer Registry, which maintains a database of all cancer cases in the state. The analysis will examine the distribution of age-, sex- and race-adjusted county-specific mesothelioma rates to assess whether populations in counties with large concentrations of environmental asbestos have a higher rate of mesothelioma than populations in counties with little or no endogenous asbestos. The location and distribution of amphibole and serpentine asbestos deposits in California will be determined by a review of existing geological surveys and publications, along with case studies of the occurrence of tremolite asbestos. This information will be combined with measures of human interaction with environmental asbestos, such as development, mining, and population density, to determine potential human exposure to environmental asbestos by county. Lastly, this project will plan a case-control study to more rigorously test the hypothesis that mesothelioma in California is independently associated with environmental asbestos exposure. The proposed project will be the first study to test the association of environmental asbestos and adjusted county- specific rates of mesothelioma. It is particularly strengthened by a comprehensive analysis of environmental tremolite and asbestos in California to be conducted by Dr. Howard Day, Department of Geology, UC Davis. This study is particularly important and timely because of the increasing population in the state living in asbestos-containing areas. California represents a unique location for these studies because of the statewide tumor registry, the largest tumor registry in the world.

Tags:Asbestos, Disease /disorder Etiology, Environment Related Neoplasm /cancer, Geographic Site, Mesothelioma, Neoplasm /cancer Epidemiology, Soil Environmental Contamination, Environmental Health, Human Population Density, Human Population Distribution, Human Population Study, Soil Sampling Clinical Research, Human Data

  • Followup Grant: 5R03CA081615-02
  • Followup Grant:5R03CA081615-03

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[dopaccordion title=”Broaddus, V Courtney. Amplification Of Trail-induced Apoptosis In Mesothelioma Grant: 1R01CA095671-01A1″ icon=27 activeicon=28]

Abstract: DESCRIPTION (provided by applicant): Activation of death receptors offers a possible mechanism of bypassing sites of resistance and engaging the caspase machinery of apoptosis directly Death receptor pathways also cooperate in unknown ways with other signals to amplify apoptosis. For several highly resistant mesothelioma lines, including M28, the TNF-related apoptosis inducing ligand (TRAIL) induces apoptosis, an apoptosis greatly amplified by concurrent treatment either with chemotherapeutic agents, such as etoposide, or with proteasome inhibitors In our proposal, the mechanism(s) by which TRAIL-induced apoptosis can be amplified and the relevance of these findings to in vivo models of mesothelioma will be explored. First, specific pathways by which etoposide amplifies TRAIL-induced apoptosis will be investigated, with particular attention to the role of mitochondria, by blocking mitochondrial pathways with overexpression of Bcl-XL or dominant negative caspase 9, by testing mitochondrial sensitivity to the death receptor signal tBid, and by analysis of mitochondrial BH3-containing proteins. The possible role of the stress activated pathway, JNK/SAPK, will be examined in M28 cells with stable blockade with dominant negative JNK1 and/or JNK2 or with stimulation of JNK by MEKK4 Secondly, the mechanism(s) by which proteasome inhibitors amplify TRAIL-induced apoptosis will be investigated Proteasome inhibitors, unlike chemotherapeutic agents, increase expression of the TRAIL receptor, DR5. This suggests a novel role for the proteasome in the degradation and regulation of expression of a death receptor. The role of the proteasome in DR5 degradation, the specificity for DR5 and the contribution of increased DR5 to the amplified apoptosis will be determined. Finally, the in vitro findings will be tested lot their relevance to in vivo mesothelioma models In nude mice with subcutaneous tumors of M28 cells, systemic TRAIL and either chemotherapy, proteasome inhibitors or both given systemically will be assessed for effects on tumor size, apoptotic index and expression of the DR5 receptor In human mesothelioma tumors from individual patients studied as tumor fragment spheroids, response to TRAIL and/or etoposide, proteasome inhibitors or both will also be determined Understanding the mechanisms of amplification of TRAIL-induced apoptosis can provide insight into the means by which malignant cells evade apoptosis and ways to bypass those sites of resistance and thereby improve treatment strategies

Tags: Apoptosis, Cytokine Receptor, Etoposide, Mesothelioma, Neoplastic Growth, Proteasome, Receptor Expression Bcl2 Gene /protein, Jun Kinase, Antineoplastic, Mitochondria, Neoplasm /cancer Pharmacology, Pharmacokinetics, Protease Inhibitor, Tumor Necrosis Factor Alpha Athymic Mouse, Cell Line, Clinical Research, Human Tissue

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[dopaccordion title=”Broaddus, V Courtney. Amplification Of Trial-indcued Apoptosis In Mesothelioma Grant: 5R01CA095671-02″ icon=27 activeicon=28]

Abstract:DESCRIPTION (provided by applicant): Activation of death receptors offers a possible mechanism of bypassing sites of resistance and engaging the caspase machinery of apoptosis directly Death receptor pathways also cooperate in unknown ways with other signals to amplify apoptosis. For several highly resistant mesothelioma lines, including M28, the TNF-related apoptosis inducing ligand (TRAIL) induces apoptosis, an apoptosis greatly amplified by concurrent treatment either with chemotherapeutic agents, such as etoposide, or with proteasome inhibitors In our proposal, the mechanism(s) by which TRAIL-induced apoptosis can be amplified and the relevance of these findings to in vivo models of mesothelioma will be explored. First, specific pathways by which etoposide amplifies TRAIL-induced apoptosis will be investigated, with particular attention to the role of mitochondria, by blocking mitochondrial pathways with overexpression of Bcl-XL or dominant negative caspase 9, by testing mitochondrial sensitivity to the death receptor signal tBid, and by analysis of mitochondrial BH3-containing proteins. The possible role of the stress activated pathway, JNK/SAPK, will be examined in M28 cells with stable blockade with dominant negative JNK1 and/or JNK2 or with stimulation of JNK by MEKK4 Secondly, the mechanism(s) by which proteasome inhibitors amplify TRAIL-induced apoptosis will be investigated Proteasome inhibitors, unlike chemotherapeutic agents, increase expression of the TRAIL receptor, DR5. This suggests a novel role for the proteasome in the degradation and regulation of expression of a death receptor. The role of the proteasome in DR5 degradation, the specificity for DR5 and the contribution of increased DR5 to the amplified apoptosis will be determined. Finally, the in vitro findings will be tested lot their relevance to in vivo mesothelioma models In nude mice with subcutaneous tumors of M28 cells, systemic TRAIL and either chemotherapy, proteasome inhibitors or both given systemically will be assessed for effects on tumor size, apoptotic index and expression of the DR5 receptor In human mesothelioma tumors from individual patients studied as tumor fragment spheroids, response to TRAIL and/or etoposide, proteasome inhibitors or both will also be determined Understanding the mechanisms of amplification of TRAIL-induced apoptosis can provide insight into the means by which malignant cells evade apoptosis and ways to bypass those sites of resistance and thereby improve treatment strategies

Tags: Apoptosis, Cytokine Receptor, Etoposide, Mesothelioma, Neoplastic Growth, Proteasome, Receptor Expression Bcl2 Gene /protein, Jun Kinase, Antineoplastic, Mitochondria, Neoplasm /cancer Pharmacology, Pharmacokinetics, Protease Inhibitor, Tumor Necrosis Factor Alpha Athymic Mouse, Cell Line, Clinical Research, Human Tissue

  • Followup Grant:5R01CA095671-03
  • Followup Grant:5R01CA095671-04

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[dopaccordion title=”Broaddus, V Courtney. Protective Role Of Apoptosis In Asbestos Pleural Injury Grant: 1R01ES008985-01″ icon=27 activeicon=28]

Abstract: DESCRIPTION: Pleural mesothelial cells, the progenitor of the asbestos-induced tumor mesothelioma, undergo apoptosis when exposed to asbestos. Important mechanisms may include oxygen radical generation, DNA damage and fiber internalization. Because an inability to undergo apoptosis may allow cells with DNA damage to survive, a loss of apoptosis may be a major step in the multistep process leading to neoplasia. Therefore, mechanisms promoting or inhibiting apoptosis may play a dynamic process determining whether the toxic effects of asbestos eventually result in neoplasia. We propose to investigate the role of apoptosis in the pathology of asbestos to the mesothelial cells and pleura. Initially, Dr. Broaddus aims to delineate the major mechanisms inducing asbestos-induced apoptosis in both rabbit and human pleural mesothelial cells and rabbit pleura. By measures of DNA damage, oxidant stress and stress-related signaling (ceramide, jun kinase, MAP kinase) in vitro and in vivo, she propose to show the pathways essential to mesothelial apoptosis. Then, she will determine the mechanisms by which certain signals, namely those initiated by vitronectin receptors, inhibit asbestos-induced apoptosis. Using vitronectin-coated particles or anti-integrin antibodies to activate the integrins, she will confirm the role of vitronectin receptors as anti-apoptotic, and identify whether the integrins are altering the balance of the apoptotic pathways such as ceramide and JNK with proliferative pathways such as MAP kinase. In in vivo studies in rabbits after activation or inhibition of vitronectin receptors or in genetically-engineered mice without vitronectin or vitronectin receptors, she will learn the importance of this anti-apoptotic effect in vivo. Finally, she intends to use inhibitors of asbestos-induced apoptosis (anti-oxidant B-carotene, inhibition of PARP, vitronectin-coated beads) to determine whether longterm inhibition of apoptosis will lead to accumulation of DNA damage in asbestos-exposed mesothelial cells. We will assess chronically asbestos-exposed cells for the presence of DNA structural damage by the presence of micronuclei and for changes in gene copy number using comparative genomic hybridization. From these studies, Dr. Broaddus will proceed to long term studies in genetically-engineered mice without vitronectin, the B5 subunit of a major vitronectin receptor, or p53 to confirm that this inhibition of apoptosis leads to an increased sensitivity to asbestos-induced abnormalities, including mesothelioma. These studies should provide important information about the mechanisms by which asbestos induces apoptosis in mesothelial cells and the role of asbestos-induced apoptosis in asbestos-induced pathology.

Tags: Asbestos, Biological Signal Transduction, Cell Growth Regulation, Mesothelioma, Pleural Cavity, Programmed Cell Death, Vitronectin Dna Damage, Antioxidant, Ceramide, Chemical Carcinogenesis, Free Radical Oxygen, Mitogen Activated Protein Kinase, Oxidative Stress, Receptor Expression Comparative Genomic Hybridization, Human Tissue, Laboratory Mouse, Laboratory Rabbit, Tissue /cell Culture, Transgenic Animal, Western Blotting

  • Followup Grant:5R01ES008985-02
  • Followup Grant:5R01ES008985-03
  • Followup Grant:5R01ES008985-04
  • Followup Grant:3R01ES008985-04S1
  • Followup Grant:5R01ES008985-05

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[dopaccordion title=”Markman, Maurice Intracavitary Cisplatin With Thiosulfate For Malignant Mesothelioma Grant: 5M01RR000827-100237″ icon=27 activeicon=28]

Abstract: There is no text on file for this abstract.

Tags: Drugs, Pharmacology, Bioavailability, Metals, Heavy Metals, Platinum (compounds), Cis Platinum Compounds, Neoplasms Of Body Cavities, Mesothelioma, Neoplastic Therapy, Cancer Chemotherapy, Sulfates, Thiosulfates Drugs Screening Human, Clinical

  • Followup Grant: 2M01RR000827-110237

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[dopaccordion title=”Balmes, John R. Caret–the Carotene And Retinol Efficacy Trial Grant: 2U01CA047989-06″ icon=27 activeicon=28]

Abstract:This chemoprevention trial tests the efficacy of retinol and beta- carotene in preventing lung cancer in two related high-risk populations: (a) heavy smokers recruited from insurance-based sources, and (b) current and former workers with heavy occupational asbestos exposure recruited from workers’ compensation and employment-based sources. The double-blind two-arm randomized protocol compares placebos with a daily combination of 30 mg beta- carotene plus 25,000 IU retinol. We will recruit eligible asbestos-exposed subjects from the San Francisco/Oakland area. We will participate in implementing a cost-effective, well-integrated, multi-clinic strategy, with the Seattle-based coordinating center for project management and data analysis. During the first 3 years of the new grant period (1988-91) we will recruit and enroll 800 subjects randomized according to the multi center protocol. We will provide all necessary data to evaluate accrual, coordination, and costs in geographically-dispersed clinic sites to generate best estimates of the remaining needs for the full-scale enrollment and follow-up. Current assumptions and projections indicate that the full-scale Efficacy Trial will be capable of detecting significant reductions in lung cancer incidence in the high-risk groups combined, and in either subgroup alone, with 13,000 smokers and 4000 asbestos-exposed subjects.

Tags: All Trans Retinol, Asbestos, Cancer Risk, Carotene, Chemoprevention, Lung Neoplasm, Nutrition Aspect Of Cancer, Tobacco Abuse Chemical Carcinogenesis, Clinical Trial, Combination Chemotherapy, Cooperative Study, Environment Related Neoplasm /cancer, Health Care Cost /financing, Longitudinal Human Study, Mesothelioma, Occupational Hazard, Prognosis, Work Site Computer Data Analysis, Dosage, Human Middle Age (45-64), Human Subject, Nutrition Related Tag, Spirometry

  • Followup Grant:5U01CA047989-07
  • Followup Grant:2U01CA052596-05

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[dopaccordion title=”Lipsett, James A. Southeastern Cancer Study Group Cooperative Trials Grant: 5U10CA030247-02″ icon=27 activeicon=28]

Abstract:The city of Hope will participate in the Southeastern Cancer Study Group (SEG) clinical investigation trials. Dr. Presant will provide leadership for the Melanoma-Sarcoma Committee which he chairs. SEG members at City of Hope will provide input into pilot protocol development, group-wide phase II and phase III protocol development, pharmacology trials, nursing protocols, data management committee acitivities. In addition, SEG members will participate heavily in the areas of chemotherapy, and moderately in the areas of surgery, immunotherapy, radiation therapy, and pathology. By participation of City of Hope in SEG activities, the quality of SEG protocols will be improved, and the rate to completion of better quality protocols will be increased. Research results will be communicated to the scientific community by presentations at national meetings and publication of ideas in peer-reviewed journals.

Tags: Cancer Clinical Investigation Review Committee, Neoplasms Immunization (immunotherapy), Neoplasms Surgery, Neoplastic Therapy, Cancer Chemotherapy, Neoplastic Therapy, Cancer Radiotherapy Neoplasms Of Body Cavities, Mesothelioma, Neoplasms, Sarcoma, Pigment Cell Neoplasms, Melanoma, Therapy Evaluation, Cooperative Study Human, Clinical

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[dopaccordion title=”Sikic, Branimir I. Gene Expression Profiling Of Unknown Primary Cancers Grant: 1R33CA089830-01″ icon=27 activeicon=28]

Abstract: DESCRIPTION: (Applicant’s Description) Cancers of unknown primary site are a diagnostic and therapeutic dilemma in oncology. Information from DNA micro array technologies on the gene expression profile of cancers has led to the hypothesis that there are diagnostic sets of genes which can resolve the origin of unknown primary cancers (UPC) with a high degree of confidence. The purpose of this project is to test this hypothesis, by both retrospective and prospective analysis of cases of UPC from Stanford Medical Center and the Sarah Cannon Cancer Center, in the context of a rapidly evolving database of site-specific clusters of gene expression. Specific Aims are: (1) Definition of the gene expression profile of known human cancers. We now have extensive information on the profiles of lymphomas, leukemia, and carcinomas of the breast, prostate, lung, ovary, and liver. Additional tumors to be accrued from our tumor bank and ongoing sample acquisitions include sarcomas, germ cell cancers, melanomas, mesotheliomas, and carcinomas of the colon, stomach, pancreas, bladder, and kidney. (2) Determination of the diagnostic cluster of gene expression for each of the above tumor types. We anticipate that several hundred genes may differentiate one from the others of these known tumors. (3) Acquisition, gene expression profiling, and diagnostic classification of unknown primary cancer specimens. This aim will involve a close collaboration with the world’s leading center for the clinical evaluation of unknown primary cancers, the Sarah Cannon Cancer Center in Nashville. (4) Evaluation of a panel of histospecific antisera for diagnostic utility with UPC specimens. This aim will utilize retrospective archived specimens as well as prospectively acquired samples from this project. (5) Identification of specific or clustered gene expression associated with known prognostic factors, response to therapies, and survival of patients with UPC.

Tags: Diagnosis Design /evaluation, Gene Expression, Neoplasm /cancer, Neoplasm /cancer Diagnosis, Neoplasm /cancer Genetics Antitumor Antibody, Bladder Neoplasm, Colon Neoplasm, Germ Cell Neoplasm, Kidney Neoplasm, Melanoma, Mesothelioma, Neoplasm /cancer Classification /staging, Neoplasm /cancer Immunology, Pancreas Neoplasm, Prognosis, Sarcoma, Stomach Neoplasm Clinical Research, Human Genetic Material Tag, Human Subject, Microarray Technology

  • Followup Grant:5R33CA089830-02
  • Followup Grant:5R33CA089830-03

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[dopaccordion title=”Valanis, Barbara G. Caret–study Center
Grant: 2U01CA048203-06″ icon=27 activeicon=28]

Abstract:CARET is an ongoing double-blind lung cancer chemoprevention trial of the efficacy and safety of the combination of 30 mg beta-carotene and 25,000 IU retinyl palmitate daily in two high-risk populations: (a) male and female current and former smokers recruited primarily from insurance-based sources, and (b) males with extensive occupational asbestos exposure recruited primarily from employment-based sources. We have documented successful recruitment, excellent compliance, and minimal side effects in over 15,000 participants randomized thus far at six study centers. Through 30 April, 1993, CARET has randomized 4,000 asbestos-exposed workers, exceeding accrual goals at all five CARET asbestos centers, and 11,105 heavy smokers. Seattle and Portland have exceeded their heavy smoker goals, and Irvine is on track to achieve its goal in July 1994. During the final five-year period, CARET will focus on retention, adherence to protocol, ascertainment of endpoints, monitoring of key design parameters, closeout of the trial, and analysis and publication. Projections indicate that with 14,240 smokers and 4,010 asbestos-exposed participants and 114,100 person-years of follow-up through February 1998, CARET will be capable of detecting a 23% reduction in lung cancer incidence in the two high-risk populations combined, and 27%, 49%, 32%, and 35% reductions in the smokers, female smokers, male smokers, and asbestos-exposed subgroups, respectively. The Portland Study Center will conduct follow-up activities with 4,200 participants randomized into the heavy smoker cohort, 280 participants randomized into the asbestos-exposed worker cohort, and 32 Vanguard transfer participants. High adherence and retention and complete ascertainment of endpoints and other data will be primary goals. Clinical, data management, and follow-up activities include annual and semiannual clinic visits; routine telephone interviews; symptom, adherence, ancillary variables, and study endpoint documentation and reporting; quality assurance of data collection; and other tasks according to the established CARET protocol and procedures. The investigators will collaborate with the Coordinating Center and other Study Centers on the analyses and publication of data.

Tags:Asbestos, Cancer Prevention, Carotene, Chemoprevention, Drug Screening /evaluation, Human Therapy Evaluation, Lung Neoplasm, Nutrition Aspect Of Cancer, Tobacco Abuse Cancer Risk, Carcinogenesis Inhibitor, Chemical Carcinogen, Clinical Trial, Cooperative Study, Female, Interview, Longitudinal Human Study, Male, Mesothelioma, Occupational Hazard, Sex Difference, Therapy Compliance Human Subject, Nutrition Related Tag, Spirometry

  • Followup Grant:5U01CA048203-07

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Clinical Trials

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[dopaccordion title=”Completed PXD101 as Second-Line Therapy in Treating Patients With Malignant Mesothelioma of the Chest That Cannot Be Removed By Surgery” icon=27 activeicon=28]

Condition: Malignant Mesothelioma
Intervention: Drug: belinostat; Genetic: reverse transcriptase-polymerase chain reaction; Other: laboratory biomarker analysis
More Information

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[dopaccordion title=”Recruiting AZD2171 in Treating Patients With Malignant Mesothelioma That Cannot Be Removed By Surgery” icon=27 activeicon=28]

Condition: Malignant Mesothelioma
Intervention:Drug: cediranib maleate; Other: laboratory biomarker analysis
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[dopaccordion title=”Withdrawn A Study of VEGF-Antisense Oligonucleotide in Combination With Pemetrexed and Cisplatin for the Treatment of Advanced Malignant Mesothelioma” icon=27 activeicon=28]

Condition: Mesothelioma
Intervention:Drug: VEGF-Antisense Oligonucleotide , Pemetrexed, Cisplatin
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[dopaccordion title=”Completed Gefitinib in Treating Patients With Malignant Mesothelioma” icon=27 activeicon=28]

Condition: Malignant Mesothelioma
Intervention:Drug: gefitinib
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[dopaccordion title=”Completed Erlotinib in Treating Patients With Malignant Mesothelioma of the Lung” icon=27 activeicon=28]

Condition: Malignant Mesothelioma
Intervention:Drug: erlotinib hydrochloride
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[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
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[dopaccordion title=”Active, not recruiting Gemcitabine Plus Cisplatin in Treating Patients With Malignant Mesothelioma of the Pleura That Cannot Be Removed by Surgery” icon=27 activeicon=28]

Condition: Malignant Mesothelioma
Intervention: Drug: cisplatin; Drug: gemcitabine hydrochloride
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[dopaccordion title=”Active, not recruiting Capecitabine in Treating Patients With Malignant Mesothelioma” icon=27 activeicon=28]

Condition: Malignant Mesothelioma
Intervention:Drug: capecitabine
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[dopaccordion title=”Active, not recruiting AZD2171 in Treating Patients With Malignant Pleural Mesothelioma That Cannot Be Removed By Surgery” icon=27 activeicon=28]

Condition: Malignant Mesothelioma
Intervention:Drug: cediranib maleate
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[dopaccordion title=”Active, not recruiting Combination Chemotherapy With or Without Bevacizumab in Treating Patients With Malignant Mesothelioma” icon=27 activeicon=28]

Condition: Malignant Mesothelioma
Intervention:Biological: bevacizumab; Drug: cisplatin; Drug: gemcitabine hydrochloride
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[dopaccordion title=”Recruiting An Efficacy Study of MORAb-009 in Subjects With Pleural Mesothelioma” icon=27 activeicon=28]

Condition: Malignant Pleural Mesothelioma
Intervention:Drug: MORAb-009 by IV on Days 1 and 8 every 21 days for 6 cycles.
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[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
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[dopaccordion title=”Active, not recruiting Sorafenib in Treating Patients With Malignant Mesothelioma” icon=27 activeicon=28]

Condition: Malignant Mesothelioma
Intervention:Drug: sorafenib tosylate
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[dopaccordion title=”Active, not recruiting Alanosine in Treating Patients With Cancer” icon=27 activeicon=28]

Condition: Lung Cancer; Malignant Mesothelioma; Pancreatic Cancer; Sarcoma
Intervention:Drug: L-alanosine
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[dopaccordion title=”Recruiting Study of CBP501 + Pemetrexed + Cisplatin in Patients With Solid Tumors (Phase I) and Patients With Malignant Pleural Mesothelioma (Phase II)” icon=27 activeicon=28]

Condition: Malignant Pleural Mesothelioma; MPM; Solid Tumors
Intervention:Drug: pemetrexed, cisplatin and CBP501; Drug: pemetrexed and cisplatin
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[dopaccordion title=”Active, not recruiting High-Dose Megestrol in Treating Patients With Metastatic Breast Cancer, Endometrial Cancer, or Mesothelioma” icon=27 activeicon=28]

Condition: Breast Cancer; Endometrial Cancer; Malignant Mesothelioma
Intervention:Drug: megestrol acetate
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[dopaccordion title=”Completed Completed” icon=27 activeicon=28]

Condition:
Intervention:
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[dopaccordion title=”Phase II Trial of Neo-Adjuvant Pemetrexed Plus Cisplatin Followed by Surgery and Radiation for Pleural Mesothelioma” icon=27 activeicon=28]

Condition:Pleural Neoplasms
Intervention:Drug: pemetrexed; Drug: cisplatin
More Information

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[dopaccordion title=”Terminated CryoSpray Ablation(tm)in Malignant Airway Disease to Determine Safety, and Tissue Effect in the Lung (ICE the MAD)” icon=27 activeicon=28]

Condition: Lung Cancer; Mesothelioma; Malignant Airway Obstruction
Intervention:Device: CryoSpray Ablation (TM) System
More Information

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[dopaccordion title=”Completed Cyclophosphamide Plus Vaccine Therapy in Treating Patients With Advanced Cancer” icon=27 activeicon=28]

Condition: Breast Cancer; Colorectal Cancer; Kidney Cancer; Lung Cancer; Malignant Mesothelioma; Pancreatic Cancer
Intervention:Biological: allogeneic tumor cell vaccine; Biological: autologous tumor cell vaccine; Biological: recombinant interferon alfa; Biological: recombinant interferon gamma; Biological: sargramostim; Drug: cyclophosphamide
More Information

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[dopaccordion title=”Active, not recruiting Radiofrequency Ablation in Treating Patients With Refractory or Advanced Lung Cancer” icon=27 activeicon=28]

Condition: Lung Cancer; Malignant Mesothelioma; Metastatic Cancer; Thymoma and Thymic Carcinoma
Intervention:Procedure: radiofrequency ablation
More Information

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[/doptab]
[doptab title=”Doctors and Hospital”]

Hospitals and Cancer Centers

Cedars-Sinai Medical Center

8700 Beverly Blvd.
Los Angeles, CA
310.423.5874

City of Hope Comprehensive Cancer Center

City of Hope Comprehensive Cancer Center
Duarte, CA
626-256-4673

Physicians

Dr. Robert Cameron
P. O. Box 951741
Los Angeles, California 90095-1741
(310) 794.7333
rcameron@mednet.ucla.edu

Dr. David Jablons
UCSF Mt. Zion Medical Center
2330 Post St., Suite 420
San Francisco, CA 94115
(415) 885-3882

Dr. Theirry Jahan
2356 Sutter, 7th FL
San Francisco, CA 94115
(415) 567-5581

[/doptab]
[doptab title=”Cases”]

Kinsman v. Unocal Corp.

S118561 , SUPREME COURT OF CALIFORNIA, December 19, 2005, Filed

Hamilton v. Asbestos Corp.

No. S069596. , SUPREME COURT OF CALIFORNIA , May 15, 2000, Decided

Chevron U.S.A., Inc. v. Workers’ Comp. Appeals Bd.

No. S059214. , SUPREME COURT OF CALIFORNIA, January 25, 1999, Decided

Oxford v. Foster Wheeler LLC

A121577, COURT OF APPEAL OF CALIFORNIA, FIRST APPELLATE DISTRICT, DIVISION ONE, September 9, 2009, Filed

Taylor v. Elliott Turbomachinery Co., Inc.

A116816, A117648, COURT OF APPEAL OF CALIFORNIA, FIRST APPELLATE DISTRICT, DIVISION FIVE, February 25, 2009, Filed

Garza v. Asbestos Corp., Ltd.

A116523, A119262, COURT OF APPEAL OF CALIFORNIA, FIRST APPELLATE DISTRICT, DIVISION THREE, March 28, 2008, Filed

McCann v. Foster Wheeler

B189898, COURT OF APPEAL OF CALIFORNIA, SECOND APPELLATE DISTRICT, DIVISION EIGHT, February 28, 2008, Filed

Whitlock v. Foster Wheeler, LLC

A117221, COURT OF APPEAL OF CALIFORNIA, FIRST APPELLATE DISTRICT, DIVISION THREE, February 15, 2008, Filed

Boeken v. Philip Morris USA, Inc.

B198220, COURT OF APPEAL OF CALIFORNIA, SECOND APPELLATE DISTRICT, DIVISION FIVE, February 11, 2008, Filed

[/doptab]
[doptab title=”Lawyers”]
[/doptab]
[/doptabs]

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