Mesothelioma in Nebraska

While mesothelioma is a problem in all states, the specific incident rate for Nebraska is 1 / 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 NE, recent NE mesothelioma-related court cases, mesothelioma specialists in NE and potential asbestos hotspots in Nebraska.

Nebraska Mesothelioma Info

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

Nebraska Research and Clinical Trials

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

Nebraska Doctors and Hospitals

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

Nebraska 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.


Abstract: DESCRIPTION: (Adapted from investigator’s abstract) The Wilms’ tumor suppressor gene, wt1, encodes a zinc finger transcription factor, WT1. A number of mutations to the wt1 gene have been identified in subsets of Wilms tumor, mesothelioma, ovarian tumor and acute myeloid leukemia, suggesting that dysfunction of WT1 may be important in many tumors. However, effectively nothing is known about the endogenous genes regulated by WT1, and thus the signaling pathways triggered by WT1 and how mutated WT1 influences these pathways to result in Wilms’ tumor remain to be discovered. The long-term objective of the investigator’s research is to characterize the normal functions of WT1 during development and the dysfunctions of mutated WT1 that lead to the genesis of Wilms’ tumor. The investigators recently cloned a gene whose expression is over tenfold greater in cells expressing WT1 than in cells with undetectable levels of WT1. The gene was identified as retinoblastoma (Rb) suppressor associated protein (AP) (RbAp46), a nuclear protein that physically interacts with Rb. The investigators have recently cloned and expressed the full-length cDNA of RbAp46, and analyzed its effect on tumor cells. Remarkably, expression of exogenous RbAp46 suppressed growth in four out of four tumor cell lines, suggesting that RbAp46 itself has growth inhibitory activity. The investigators now plan to establish the positive correlation between the levels of WT1 and RbAp46 expression in different tumor cells and in mouse tissues from different stages of development using Northern and in situ hybridization analysis. They plan to analyze the promoter region of RbAp46 to determine whether WT1 directly regulates the expression of RbAp46. They plan to explore the possible roles of RbAp46 as a mediator of WT1 function by expressing exogenous RbAp46 or by down-regulating RbAp46 in cells. The investigators plan to probe the mechanisms by which RbAp46 functions as a growth inhibitor by analyzing its impact on the cell cycle and its influence on the ras signaling pathway. The investigators plan to perform structure and function analysis to identify the domain(s) of RbAp46 required for its function. The investigators plan to identify the proteins which interact with RbAp46 by co-immunoprecipitation and an in vivo GST capture assay and, if necessary, by a yeast two-hybrid strategy. It is hoped that these studies will lay the foundation of therapeutic intervention for the Wilms’ tumor and other tumors as well.

Tags: Wilms’ Tumor, Cell Growth Regulation, Gene Expression, Neoplasm /cancer Genetics, Retinoblastoma Protein, Transcription Factor, Tumor Suppressor Gene, Tumor Suppressor Protein Cell Differentiation, Developmental Genetics, Gene Interaction, Genetic Promoter Element, Growth Inhibitor, Neoplastic Transformation, Protein Structure Function, Regulatory Gene 3t3 Cell, Athymic Mouse, Cell Line, Immunoprecipitation, In Situ Hybridization, Neoplastic Cell, Northern Blotting

Clinical Trials

Condition: Malignant Mesothelioma
Intervention: Drug: pazopanib hydrochloride; Other: laboratory biomarker analysis
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Condition: Malignant Mesothelioma
Intervention: Drug: gefitinib
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Condition: Malignant Mesothelioma
Intervention: Drug: capecitabine
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Condition: Malignant Mesothelioma
Intervention: Drug: vatalanib
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Condition: Malignant Mesothelioma
Intervention: Drug: doxorubicin hydrochloride; Drug: ranpirnase
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Condition: Malignant Mesothelioma
Intervention: Drug: dasatinib;
Other: immunoenzyme technique; Other: immunohistochemistry staining method; Other: laboratory biomarker analysis
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Condition: Malignant Mesothelioma
Intervention: Drug: epirubicin hydrochloride; Drug: gemcitabine hydrochloride
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Condition: Tumor
Intervention: Drug: belinostat; Drug: 5-Fluorouracil (5-FU)
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Condition: Cancer
Intervention: Other: biologic sample preservation procedure
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Hospital and Cancer Centers

Creighton University Medical Center: Cancer Center-Suite 2321
601 N. 30th Street
Omaha, NE


Olivotto v. DeMarco Bros. Co.
No. S-05-1526., SUPREME COURT OF NEBRASKA, June 1, 2007, Filed

Morris v. Neb. Health Sys.
No. S-01-1194. , SUPREME COURT OF NEBRASKA, July 11, 2003, Filed


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