Rhode Island Mesothelioma Fact Sheet

While mesothelioma is a problem in all states, the specific incident rate for Rhode Island is 1.2 / 100,000. This is above the average rate of 1.1 / 100,000. Click on the tabs below to find mesothelioma and asbestos research in RI, recent RI mesothelioma-related court cases, mesothelioma specialists in RI and potential asbestos hot spots in Rhode Island.

[doptab title=”Overview”]

Rhode Island Mesothelioma Info

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

Rhode Island Research and Clinical Trials

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

Rhode Island Doctors and Hospitals

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

Rhode Island 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.

[doptab title=”Treatment and Research”]


[dopaccordion title=”Kelsey, Karl T. The Epidemiology Of Molecular Alterations In Mesothelioma
Grant: 1R01CA126939-01A1″ icon=27 activeicon=28]

Abstract:DESCRIPTION (provided by applicant): Exposure to asbestos has long been associated with pleural mesothelioma. The mode of action of asbestos in inducing mesothelioma, however, remains to be completely described, and relatively little is known about the association of epigenetic inactivation of tumor suppressor genes with carcinogenic exposures. Asbestos is not a direct-acting mutagen, but is carcinogenic; as such, it is also known to persist in the lungs of exposed individuals. Our preliminary data has demonstrated that asbestos fiber burden is significantly associated with the number of tumor suppressor genes inactivated by epigenetic silencing and DNA methylation. We propose to expand this research by taking advantage of the newly developed International Mesothelioma Program (IMP) at the Brigham and Women’s Hospital (BWH), where novel surgical treatment protocols have made possible for the first time investigation of tumor tissue from individuals with mesothelioma. We propose to test hypotheses positing that epigenetic inactivation of tumor suppressor genes, measured by assessing the DNA methylation profile, is associated with asbestos fiber type and burden. Further, we will test the hypothesis that the SV40 virus is involved in mesothelioma using a novel artifact resistant approach, and investigate the role of miRNAs in mesothelioma, asking if this might be a novel biomarker for this disease. Finally, we will test the hypothesis that survival in mesothelioma is associated with the individual molecular profile of the tumor. Our data will also be pooled with the expression profile data being generated at the BWH as part of the IMP, giving rise to a very rich repository of global genomic data for the exploratory analysis of the systems biology of malignant mesothelioma. In sum, we propose to continue to enroll and study patients referred to the BWH for new surgical treatments of this often fatal cancer. We will study the molecular character of their tumors, proposing that the character of the lesions in the tumor is associated with the nature of their asbestos exposure and well as with their response to treatment. Mesothelioma is a most often fatal cancer caused by asbestos exposure. We propose to study novel mechanisms of asbestos action in the body (including the inactivation and silencing of genes by induction of altered chromosome conformations), associating these with quantitative measures of asbestos exposure. This may help to explain, for example, why even small exposures (“doses”) of asbestos pose a fatal cancer risk.

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

  • Followup Grant: 5R01CA126939-02

[dopaccordion title=”Kane, Agnes B. Pathogenesis Of Mesenchymal Tumors Induced By Asbestos
Grant: 2R01ES003721-09A1″ icon=27 activeicon=28]

Abstract:DESCRIPTION (Adapted from the investigator’s abstract): Exposure to asbestos fibers causes diffuse malignant mesothelioma arising from the pleural, pericardial, or peritoneal linings.The ultimate objective of this research is to identify the cellular and molecular events in the development and progression of malignant mesotheliomas induced by asbestos fibers. The proposed experiments will focus on the role of the TGF-beta growth stimulatory pathway and alterations in the p53 tumor suppressor gene during the preneoplastic and neoplastic stages in a murine model system of asbestos tumorigenesis. It is hypothesized that constitutive activation of the TGF- alpha growth stimulatory pathway is an early step in the development of malignant mesotheliomas, followed by alterations in the p53 tumor suppressor gene during progression from focal to invasive growth. The role of the TGF-alpha growth regulatory pathway in the development of malignant mesothelioma will be assessed in vivo and in vitro. MT42 transgenic mice will be used to test whether overexpression of TGF-alpha accelerates the development of malignant mesotheliomas induced by weekly intraperitoneal injections of asbestos fibers. The correlation between overexpression of TGF- alpha, its receptor (EGF-R), cell proliferation, and specific histopathologic stages in the development of malignant mesothelioma will be assessed. A critical evaluation of the role of TGF-alpha expression during the preneoplastic and neoplastic stages in the development of these tumors will be assessed directly by transfection of sense or antisense TGF-alpha vectors in vitro. The effects of increased or decreased TGF-alpha expression on growth of these transfected cell lines will be determined in vitro and in vivo. p53- deficient mice will be used to determine whether heterozygosity at this gene locus accelerates progression from focal to invasive malignant mesotheliomas. Man-made mineral fibers have been developed and used commercially as asbestos fiber substitutes. Few of these materials have been tested for carcinogenicity because lifetime rodent inhalation studies are technically difficult and expensive. These new transgenic mouse model systems may provide a more rapid, cost-effective screening assay for potentially carcinogenic man- made fibers.

Tags: Asbestos, Chemical Carcinogenesis, Mesothelioma, Molecular Oncology, Tumor Progression Chemical Related Neoplasm /cancer, Disease Model, Environment Related Neoplasm /cancer, Model Design /development, Toxicant Screening, Transforming Growth Factor, Tumor Suppressor Gene Laboratory Mouse, Tissue /cell Culture, Transfection

  • Followup Grant: 5R01ES003721-10
  • Followup Grant: 2R01ES003721-12
  • Followup Grant: 5R01ES003721-13
  • Followup Grant: 5R01ES003721-14
  • Followup Grant: 5R01ES003721-15
  • Followup Grant: 1R01ES003721-01
  • Followup Grant: 5R01ES003721-02
  • Followup Grant: 5R01ES003721-03
  • Followup Grant: 2R01ES003721-04
  • Followup Grant: 5R01ES003721-05
  • Followup Grant: 5R01ES003721-06
  • Followup Grant: 5R01ES003721-07

[dopaccordion title=”Kane, Agnes B. Pathogenesis Of Mesenchymal Tumors Induced By Asbestos
Grant: 2R01ES003721-16A1″ icon=27 activeicon=28]

Abstract: DESCRIPTION (provided by applicant): Asbestos fibers persist in the lungs and cause chronic inflammation, pulmonary and pleural fibrosis, lung cancer, and malignant mesothelioma after latent periods of 20-40 years. Recent experimental evidence based on animal models using genetically engineered mice have provided new insight about the mechanistic links between chronic inflammation, fibrosis, and cancer. Recruitment and activation of inflammatory cells in response to biopersistent fibers is accompanied by release of reactive oxygen species leading to oxidant stress, DNA damage, and mutations. Inflammatory cells can release cytokines and growth factors that stimulate stromal remodeling and angiogenesis. It is hypothesized that reciprocal activation of tumor and stromal cells results in local release of matrix metalloproteinases that facilitate growth and invasion of diffuse malignant mesothelioma. In vitro, ex vivo, and in vivo assays using well characterized, transplantable murine mesothelial cell lines will be used to test this hypothesis. The specific aims of the proposed research are: 1) To determine whether induction of matrix metalloproteinases in murine peritoneal macrophages is correlated with exposure to biopersistent, carcinogenic fibers; 2) To assess the contribution of macrophages to growth and invasion of neoplastic mesothelial cells in vivo; 3) To determine whether asbestos-activated macrophages stimulate invasion of preneoplastic and neoplastic mesothelial cells; 4) To determine whether overexpression of MMP9 leads to autonomous invasion of neoplastic mesothelial cells; and 5) To assess the contribution of stromal macrophages to growth and invasion of human neoplastic mesothelial cells. Newly developed technologies including laser capture microdissection and quantitative analysis of gene expression provide powerful tools for this experimental approach. Pharmacologic modulation of persistent inflammation triggered by biopersistent, carcinogenic fibers may provide a new strategy to prevent progression of malignant mesothelioma in exposed populations.

Tags: Asbestos, Chemical Carcinogenesis, Chemical Related Neoplasm /cancer, Environment Related Neoplasm /cancer, Mesothelioma Cytokine, Extracellular Matrix, Gene Expression, Inflammation, Lung Neoplasm, Macrophage, Mesenchymoma, Neoplasm /cancer Invasiveness Enzyme Linked Immunosorbent Assay, Histopathology, Laboratory Mouse, Laser Capture Microdissection, Polymerase Chain Reaction, Tissue /cell Culture, Transgenic Animal

  • Followup Grant: 5R01ES003721-17
  • Followup Grant: 5R01ES003721-18
  • Followup Grant: 5R01ES003721-19

[dopaccordion title=”Kane, Agnes B. Pleural Dosimetry And Biomarkers Of Response To Fibers
Grant: 1R01ES005712-01A1″ icon=27 activeicon=28]

Abstract: Occupational exposure to asbestos fibers is associated with an increased risk of developing mesotheliomas, malignant tumors arising from the pleural or peritoneal linings. Widespread use of asbestos in the past raises public concern that environmental exposure may also produce mesotheliomas. Assessment of the risk of developing malignant mesothelioma after exposure to asbestos or other fibers is difficult because the minimum dose of fibers required to produce these tumors is unknown. Current rodent models of mesothelioma are unsatisfactory because they use extremely high doses of fibers delivered directly by intraperitoneal or intrapleural injection instead of inhalation. The objective of the proposed research is to develop a new animal model to determine the biologic effective dose of crocidolite asbestos fibers required to initiate the development of mesotheliomas. Fiber dosimetry will be expressed as the total number of fibers that deposit and persist in the pleural lining using tissue digestion, transmission electron microscopy, and video-enhanced differential interference contrast light microscopy to visualize fibers in potential target cell populations (Specific Aim #1). Two responses of potential target cells will be validated as specific and sensitive biologic markers of response to asbestos fibers deposited in the pleura. First, molecular markers for chromosomal damage induced by asbestos fibers will be developed using biotinylated DNA probes and in-situ hybridization. A mouse centromeric DNA probe will be used to detect chromosomal aneuploidy and structural aberrations. Loss of heterozygosity at the p53 tumor suppressor gene locus will be visualized by indirect immunofluorescence on metaphase spreads and interphase nuclei (Specific Aim #2). Second, quantitative markers of mesothelial cell injury and proliferation will be developed using morphometry (Specific Aim #3). Fiber dosimetry and biologic markers of response will be compared following intrapleural injection and inhalation of crocidolite asbestos fibers. These experiments will assess whether there is a correlation between the number of fibers deposited in the pleura, their persistence, and the number of population doubling times before the histologic appearance of malignant mesothelioma (Specific Aims #4 and 5). Ultimately, this new model could be used to extrapolate dose-response relationships to human exposure to asbestos and man-made mineral fibers in order to assess more accurately the risk of developing malignant mesotheliomas.

Tags: Asbestos, Biomarker, Cancer Risk, Pleural Cavity Chromosome Aberration, Disease Model, Environment Related Neoplasm /cancer, Genetic Marker, Model Design /development, Molecular Oncology, Neoplasm /cancer Genetics Histopathology, Immunofluorescence Technique, In Situ Hybridization, Inhalation Drug Administration, Injection, Laboratory Mouse, Nucleic Acid Probe, Transmission Electron Microscopy, Tumor Suppressor Gene

  • Followup Grant: 5R01ES005712-02
  • Followup Grant: 5R01ES005712-03

[dopaccordion title=”Chu, Ming-yu Growth And Sensitivity Of Human Tumor Cells
Grant: 5P01CA020892-060021″ icon=27 activeicon=28]


Tags: Drugs, Pharmacology, Biochemical, Neoplastic Therapy, Antineoplastic Agents, Antileukemic, Neoplastic Therapy, Cancer Chemotherapy, Neoplastic Growth Alkaloids, Vincristine, Antibiotics, Anthracyclines, Adriamycin, Azo Compounds, Hydrazines, Procarbazine, Drugs Resistance, Genetic Disorders, Chromosome Abnormalities, Genetics, Cytogenetics, Haloalkylamines, Bcnu, Haloalkylamines, Cyclophosphamide, Models, Biological, Molecules, Macromolecules, Neoplasms Characteristics, Cellular Level Studies (general), Neoplasms Of Blood And Re System, Leukemia Acute, Neoplasms Of Blood And Re System, Lymphoma, Neoplasms Of Body Cavities, Mesothelioma, Neoplasms Of Pancreas, Neoplasms Of Respiratory System, Lung Neoplasms, Therapy Evaluation, Triazine Nucleosides, Azauracil Nucleosides, 6-azauridine Communicable Disease Control, Laminar Flow System, Human, Clinical, Human, Tissues, Fluids Etc. From Non-related Sources Outside Immediate Project, Mammals, Rodents, Myomorpha, Athymic Mice (nude), Radioautography, Radiotracers, Tissue (cell) Culture, Clone Cells

  • Followup Grant: 2P01CA020892-070021
  • Followup Grant: 5P01CA020892-080021
  • Followup Grant: 5P01CA020892-090021
  • Followup Grant: 2P01CA020892-100021

[dopaccordion title=”Chu, Ming-yu W. Chemotherapy Response Of Human Solid Tumor Xenografts
Grant: 5R01CA025631-03″ icon=27 activeicon=28]

Abstract: Seven cancer cell strains and 5 sublines of pancreatic carcinoma have been successfully grown in culture. Drug sensitivity studies have been carried out using pancreatic carcinoma (Dangeraux) and lung mesothelioma, VAMT-1. Of all single agents studied, vincristine exhibited the highest inhibitory activity against Dangeraux. This correlates with the in vivo results using the subrenal capsule assay. Two chemotherapeutic combinations, 2′-deoxycoformycin (DCF) plus 8-azaadenosine (8-Aza-Ado) or formycin and 3-deazauridine (3-DAU) plus Ara-C, have been established. In culture, DCF pretreatment for 15 minutes greatly potentiates 8-Aza-Ado or formycin activity against Dangeraux. 3-DAU pretreatment for 2 hours increases inhibitory activity of Ara-C 35 fold. The in vivo studies using ATS-mouse xenografts showed that DCF one hour pretreatment, followed by 8-Aza-Ado significantly reduced the tumor weight to 20 percent of the untreated control while 8-Aza-Ado alone had very little effect. However, DCF in combination with formycin was not as effective. Of nine single agents studied in vitro, vincristine was the most effective against VAMT-1. However, 5-fluorouridine-diphosphate-diglyceride exhibited the highest inhibitory activity among the 5-fluorouracil derivatives (5-FU, 5-FUR, 5-FUdR). 5′-Deoxy- 5 fluorouridine (5′-deoxy-5-FUR) had no activity at all. Since 5′-deoxy-5’FUR cannot be phosphorylated, it appears to indicate that VAMT-1 is deficient in nucleoside phosphorylase which liberates 5-FU from the analog and is phosphorylated via PRPP with the formation of 5-FUMP.

Tags: Experimental Therapeutics Study Section, Neoplasms Pharmacology, Neoplastic Therapy, Cancer Chemotherapy, Therapy Evaluation Drugs Adverse Effects, Drugs Hypersensitivity, Drugs Resistance, Immunity, Immunosuppression, Models, Biological, Neoplasms Of Gastrointestinal System, Colon Growths, Neoplasms Of Gastrointestinal System, Rectum Growths, Neoplasms Of Reproductive System, Breast Neoplasms, Neoplasms Of Respiratory System, Lung Neoplasms, Neoplasms Transplantation, Neoplasms, Carcinoma, Tissue (cell) Culture, Cell Culture Collections Banks And Registries Human, Tissues, Fluids Etc. From Non-related Sources Outside Immediate Project, Mammals, Rodents, Myomorpha, Mice (laboratory)



Clinical Trials

[dopaccordion title=”Completed Gefitinib in Treating Patients With Malignant Mesothelioma” icon=27 activeicon=28]

Condition: Malignant Mesothelioma

Intervention:Drug: gefitinib

More Information

[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 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=”Recruiting Collecting Tumor Samples From Patients With Gynecological Tumors” icon=27 activeicon=28]

Condition: Cancer
Intervention: Other: biologic sample preservation procedure
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[doptab title=”Doctors and Hospital”]

Hospitals and Cancer Centers


David Ettensohn, M.D.
Pulmonary Medicine
109 Beechwood Ave.
Pawtucket, RI

David Kern, M.D.
Memorial Hospital of RI
Occupational Health Clinic
111 Brewster St.
Pawtucket, RI 02860

John Pella, M.D.
St. Joseph Hospital
Pulmonary Fatima Unit
200 High Service Ave.
North Providence, RI 02904

S.T. Sambandan, M.D.
1180 Hope St.
Bristol, RI

Anthony Testa M.D.
100 Highland Ave.
Providence, RI 02904

[doptab title=”Cases”]

Sargent v. Sargent

Benoit v. A.W. Smith Corp.

Clayton v. Am. Biltrate

Dyer v. Aurora Pump Co.
C.A. No.: PC/07-2062, SUPERIOR COURT OF RHODE ISLAND, PROVIDENCE, March 26, 2008, Filed

LaPointe v. 3M Co.
C.A. No. PC 06-2418, SUPERIOR COURT OF RHODE ISLAND, PROVIDENCE, March 25, 2008, Filed

LaPointe v. 3M Co.
C.A. No. PC 06-2418, SUPERIOR COURT OF RHODE ISLAND, PROVIDENCE, March 25, 2008, Filed

Plympton v. Am. Std. (Inc.)
C.A. No. PC 05-1534, SUPERIOR COURT OF RHODE ISLAND, PROVIDENCE, February 6, 2008, Filed

Quackenbos v. Am. Optical Corp.
C.A. No. PC 04-6504, SUPERIOR COURT OF RHODE ISLAND, PROVIDENCE, January 17, 2008, Filed

LaPointe v. 3m Co.
C.A. No. PC 06-2418, SUPERIOR COURT OF RHODE ISLAND, PROVIDENCE, November 5, 2007, Filed

LaPointe v. 3M Co.
C.A. No. PC 06-2418, SUPERIOR COURT OF RHODE ISLAND, PROVIDENCE, November 5, 2007, Filed

[doptab title=”Lawyers”]

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