J Clin Oncol 2003, 21:473–482 PubMedCrossRef 31 Leibovich BC, Sh

J Clin Oncol 2003, 21:473–482.PubMedCrossRef 31. Leibovich BC, Sheinin Y, Lohse CM, Thompson RH, Cheville JC, Zavada J, Kwon ED: Carbonic anhydrase IX is not an independent predictor of outcome for patients with clear cell renal cell carcinoma.

J Clin Oncol 2007, 25:4757–4764.PubMedCrossRef 32. Liao SY, Aurelio ON, Jan K, Zavada J, Stanbridge EJ: Identification of the MN/CA9 protein as a reliable diagnostic biomarker of clear cell carcinoma of the kidney. Cancer Res 1997, GSK458 price 57:2827–2831.PubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions YW, RZ, DW and ZL carried out the experiments and data analyses. WS and CW collected the clinical samples and completed immunohistochemistry. Ralimetinib cell line YC and JJ drafted the manuscript. All authors read and approved the final manuscript.”
“Background Malignant mesothelioma is an aggressive, treatment-resistant tumor, arising from transformed mesothelial cells lining the pleura, peritoneum and pericardium. Athough relatively a rare disease, its incidence rate is increasing throughout the world [1, 2]. Its major risk factor is asbestos

exposure, besides it can also be caused by ionizing radiation, erionite exposure, chest injuries, and presumably SV40 virus [3]. Patients with malignant pleural mesothelioma (MPM) usually present with shortness of breath and chest pain with pleural effusions. Patients are diagnosed with cytopathology of mesothelioma effusions or fine-needle aspirations, and histopathology is often required to establish the diagnosis [4]. Despite the current regimen of

surgical resection, chemotherapy, and radiation Vactosertib ic50 therapy until for treating MPM, the prognosis remains dismal, with median survival being 9–12 months from diagnosis [3]. Therefore developing new molecular targeted therapies may pose promise for this devastating illness. The pathogenic mechanisms underlying mesothelioma involve deregulation of multiple signaling pathways, including activation of multiple receptor tyrosine kinases such as the epidermal growth factor receptor (EGFR) family and MET, and subsequent deregulations of mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3K)-AKT signaling cascades, the TNF-α / NF-κB survival pathway, Wnt signaling, and loss of tumor suppressors such as Neurofibromatosis type 2(NF2), p16INK4A, and p14ARF[5]–[7]. Understanding mechanisms of the dysregulated signaling pathways allows strategies for development of targeted new therapies against this devastating disease. It has been recently reported that sonic hedgehog (Hh) signaling, another important pathway during development and tumorigenesis, is aberrantly activated in MPM, and inhibition of hedgehog signaling suppresses tumor growth [8]. Deregulated Hedgehog (Hh) pathway activation has been implicated in several human cancers including glioma, basal cell carcinoma, medulloblastoma, lung, breast, pancreatic and gastric cancers [9]–[14].

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