October 18th, 2008. Expression and Regulation of Epithelial Na+ Channels by Nucleotides in Pleural Mesothelial Cells
Furthermore, we found that both forskolin and cGMP increased the short-circuit currents in mouse pleural tissues. Taken together, our data demonstrate that the ENaC channels are biochemically and functionally expressed in human pleural mesothelial cells, and can be up-regulated by cAMP and cGMP.
September 5th, 2008. Systemic Treatments for Mesothelioma: Standard and Novel
These include drugs targeted against the epidermal growth factor, platelet-derived growth factor, vascular endothelial growth factor, src kinase, histone deacetylase, the proteasome, and mesothelin. Given the progress made in recent years, there is reason to believe that more effective treatments will continue to be developed.
September 4th, 2008. Protein kinase C beta in malignant pleural mesothelioma
Enzastaurin has preclinical activity against MPM, and exhibited synergism with cisplatin. PKC[beta] inhibition in MPM might be able to reduce the invasiveness of MPM by affecting cytoskeletal function.
August 14th, 2008. Enhanced antitumor therapy by inhibition of p21waf1 in human malignant mesothelioma
Conclusions: These results indicated that p21 might play an important role in chemosensitivity to anticancer agents, and the suppression of its expression might be a potential therapeutic target for MPM.
August 2nd, 2008. MET as a target for treatment of chest tumors
These drugs function at a variety of steps within the HGF-MET pathway, including MET expression at the RNA or protein level, the ligand-receptor interaction, and tyrosine kinase function. This paper will review the structure, function, mechanisms of tumorigenesis, and potential for therapeutic inhibition of the MET receptor in lung cancer and mesothelioma.
June 27th, 2008. The tyrosine kinase inhibitor cediranib for non-small cell lung cancer and other thoracic malignancies
The NSCLC trials include patients with squamous cell histologic features and treated brain metastases, populations for which bevacizumab is currently not indicated. These trials will determine whether cediranib will join the growing armamentarium of therapeutic options for thoracic malignancies and broaden the number of patients with NSCLC who could potentially benefit from antiangiogenic therapy.
June 24th, 2008. Phosphorylation and localization of protein-zero related (PZR) in cultured endothelial cells
To see if tyrosine kinases other than Src are also capable of phosphorylating PZR, the authors cotransfected HEK293 cells with PZR and one of several tyrosine kinases and found that c-Src, c-Fyn, c-Lyn, Csk, and c-Abl, but not c-Fes, phosphorylated PZR and increased PZR/SHP-2 interaction. These results suggest that PZR is a cell adhesion protein that may be involved in SHP-2-dependent signaling at interendothelial cell contacts.
April 9th, 2008. Epidermal growth factor receptor gene mutation, amplification and protein expression in malignant pleural mesothelioma
In MPM, EGFR seems to play a role in a limited subset of patients. To identify possible candidates for EGFR tyrosine kinase in inhibitor therapy, the information on the EGFR gene status may be valuable.
In contrast, the selective EGFR tyrosine kinase inhibitor, gefitinib, had no effect against EHMES-10 cells both in vitro and in vivo. Our results suggest that using vandetanib to target RET-dependent tumor cell proliferation and survival and VEGFR-2-dependent tumor angiogenesis may be promising against MPM expressing RET oncogenic rearrangement and VEGF.
February 28th, 2008. Pleural mesothelioma: diagnostic problems and evaluation of prognostic factors
Conclusion: MPM is an increasing disaster in Egypt which is underestimated and neglected. A panel of immunohistochemical markers should be used for proper evaluation. p27 has proven to be a potential biologic prognostic marker for mesothelioma and more studies as regard its significance are recommended on a larger number.
January 29th, 2008. Imatinib mesylate enhances therapeutic effects of gemcitabine in human malignant mesothelioma xenografts
Conclusions: Imatinib mesylate enhances the therapeutic response to gemcitabine, in accordance with our previous in vitro data. These in vivo results validate imatinib mesylate and gemcitabine as a combination treatment of malignant mesothelioma, also in view of its known positive effects on tumor drug uptake. These evidences provide the rationale for the currently ongoing clinical trials.
November 28th, 2007. Molecular genetics and mechanisms of apoptosis in carcinomas of the lung and pleura: Therapeutic targets
Stem cell therapy and gene replacement offer the prospect of novel approaches that are likely in the near future to play a definitive role in the treatment of advanced lung cancer. Furthermore, with their apparent minimal toxicity to normal tissues, the newer molecular targets represent attractive investigational directions for innovative cancer therapies.
November 23rd, 2007. Survivin is highly expressed and promotes cell survival in malignant peritoneal mesothelioma
Conclusion: Our results show for the first time that survivin, as well as other IAPs, is largely expressed in clinical MPMs and suggest that strategies aimed at down-regulating survivin may provide a novel approach for the treatment of the malignancy.
October 24th, 2007. Receptor EphA2 activation with ephrinA1 suppresses growth of malignant mesothelioma (MM)
Ligand activated and ephrinA1 vector (pcDNA/EFNA1) transfected MMC demonstrated decreased clonal growth in 3-D matrigels when compared to resting MMC. These studies suggest that EphA2 activation by its ligand ephrinA1 transmits intracellular signals from cell membrane to nucleus via ERK1/2 signaling cascade and inhibits MM growth.
September 18th, 2007. HGF Mediates Cell Proliferation of Human Mesothelioma Cells Through a PI3K/MEK5/Fra-1 Pathway
HGF also caused increased MM cell viability and proliferating cell nuclear antigen (PCNA) expression that were abolished by knockdown of MEK5 or Fra-1. Data suggest that HGF-induced effects in the some MM cells are mediated via activation of a novel PI3K/ERK5/Fra-1 feedback pathway that might explain tumor-specific effects of c-Met inhibitors on MM and other tumors.
September 7th, 2007. Ras Pathway Activation in Malignant Mesothelioma
Conclusions: These experiments provide a rationale for targeting Ras and associated signaling pathways in mesothelioma and also suggest cap-dependent translation as one mechanism by which Ras induces proliferation in this disease.
August 22nd, 2007. Phase II testing of sunitinib: the National Cancer Institute of Canada Clinical Trials Group IND Program Trials IND.182-185
Because angiogenesis is necessary for the growth and metastasis of solid tumours, and vegf is believed to have a pivotal role in that process, sunitinib treatment may have broad-spectrum clinical utility. In the present article, we discuss the biologic and clinical rationales that have recently led the Investigational New Drug Program of the National Cancer Institute of Canada Clinical Trials Group to initiate four phase ii trials testing this agent in the following four different tumour types: relapsed diffuse large cell lymphoma, malignant pleural mesothelioma, locally advanced or metastatic cervical cancer and recurrent epithelial ovarian, fallopian tube, or primary peritoneal carcinoma.
02). Activated c-Src may play a role in survival, metastasis, and invasion of MPM, and targeting c-Src may be an important therapeutic strategy.
June 15th, 2007. Phase II study of erlotinib in patients with malignant pleural mesothelioma: a Southwest Oncology Group Study
Conclusion: Single-agent erlotinib was not effective in MPM, despite high expression of EGFR. Activation of the ERK and phosphatidylinositol 3-kinase/Akt downstream pathways are possible resistance mechanisms to EGFR TKI. The activated phosphatidylinositol 3-kinase/Akt pathway is a potential therapeutic target for MPM.
Thus, SM16 shows potent activity against established AB12 malignant mesothelioma tumors using an immune-mediated mechanism and can significantly prevent tumor recurrence after resection of bulky AB12 malignant mesothelioma tumors. These data suggest that ALK5 inhibitors, such as SM16, offer significant potential for the treatment of malignant mesothelioma and possibly other cancers.
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