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Journal Articles on Mesothelioma: Cancer Information for Patients and Families

Journal Articles on Mesothelioma: 'New & Novel' Category


New & Novel news feed.

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.

June 24th, 2008. Measles virus induces oncolysis of mesothelioma cells and allows dendritic cells to cross-prime tumor-specific CD8 response

Priming of autologous T cells by DCs loaded with MV-infected MPM cells led to a significant proliferation of tumor-specific CD8 T cells. Altogether, these data strongly support the potential of oncolytic MV as an efficient therapeutic agent for mesothelioma cancer.

June 4th, 2008. Malignant mesothelioma 2008

Novel therapies including intrapleural chemotherapy, photodynamic therapy and hyperthermic perfusion have also been used with some success. Finally there are several attempts at immunomodulating and targeted treatments, which are in phase I/II trials.

May 31st, 2008. mTOR Mediates Survival Signals in Malignant Mesothelioma Grown as Tumor Fragment Spheroids

We propose that mTOR mediates survival signals in many mesothelioma tumors. Inhibition of mTOR may provide a non-toxic adjunct to therapy directed against malignant mesothelioma, especially in those with high baseline expression of p-S6K.

May 24th, 2008. Effects of Piroxicam and Cisplatin on mesothelioma cells growth and viability

In particular, the two drugs in NCI cell line had a synergistic effect on apoptosis, probably through activation of caspase 8 and caspase 9, while the most evident targets among the cell cycle regulators were cyclin D1 and p21waf1. These results suggest that the association of piroxicam and CDDP specifically triggers cell cycle regulation and apoptosis in different mesothelioma cell lines and may hold promise in the treatment of mesothelioma.

May 21st, 2008. Human Tumor-Derived Exosomes Down-Modulate NKG2D Expression

This hyporesponsiveness was evident even in the presence of IL-15, a strong inducer of NKG2D. Our data show that NKG2D is a likely physiological target for exosome-mediated immune evasion in cancer.

May 14th, 2008. Molecular targets and targeted therapies for malignant mesothelioma

Alternative approaches are based on inhibitors of the ubiquitin-proteasome pathway and of histone deacetylases which, notwithstanding the functional divergence of the corresponding targets, share the ability to determine a wide modulation of the cancer cell phenotype that can lead to cell cycle arrest, apoptosis and sensitization to different antineoplastic treatments. A recombinant immunotoxin targeted to the membrane antigen mesothelin is an additional agent whose activity is being evaluated in mesothelioma patients.

May 6th, 2008. Overexpression and altered glycosylation of MUC1 in malignant mesothelioma

CA15-3 in effusions could differentiate malignant from benign effusions but were not specific for mesothelioma. Thus, as in other cancers, alterations in MUC1 biology occur in mesothelioma and these results suggest that specific MUC1 characteristics may be useful for mesothelioma diagnosis and should also be investigated as a potential therapeutic target.

April 22nd, 2008. Increased exosome production from tumour cell cultures using the Integra CELLine Culture System

This simple culture system is a cost effective, useful method for significantly increasing the quantity of exosomes available from cultured cells, without detrimental effects. This tool should prove advantageous in future studies of exosome-immune modulation in cancer and other settings.

April 21st, 2008. Genetic susceptibility to malignant pleural mesothelioma and other asbestos-associated diseases

Major limitations in the study design, including the small size of study groups, affected the reliability of these studies. Technical improvements such as the use of high-throughput techniques will help to identify molecular pathways regulated by candidate genes.

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.

April 9th, 2008. ANTI-ADHESION Evolves To a Promising Therapeutic Concept in Oncology

ANTI-ADHESION strategies include targeting of surface antigens, inhibition of cell adhesion associated pathways, inhibition of CAM-DR, and targeted drug delivery. As ANTI-ADHESION is based on general characteristics of cancer cells independent of specific disease entities or treatment modalities, it may become a successful, low-toxic and broadly applicable concept in cancer treatment.

April 4th, 2008. Inhibition of both mesothelioma cell growth and Cdk4 activity following treatment with a TATp16INK4a peptide

Conclusion: Therapeutic strategies which introduce either TATp16INK4a peptide, or small molecule mimetic, could be an effective strategy for mesothelioma treatment.

April 2nd, 2008. Response to the methylation inhibitor dihydro-5-azacytidine in mesothelioma is not associated with methylation of p16INK4a: results of cancer and leukemia group B 159904

Conclusions: There was no significant correlation between the presence of p16INK4a methylation and response to DHAC therapy or overall survival.

April 1st, 2008. Targeting tumor-associated macrophages in an orthotopic murine model of diffuse malignant mesothelioma

injection. These reductions in tumor burden are statistically significant and identify TAMs as an important host-derived cell that contributes to growth, invasion, and metastasis in diffuse malignant peritoneal mesothelioma.

March 29th, 2008. Cytotoxic activities of nucleoside and nucleobase analog drugs in malignant mesothelioma: Characterization of a novel nucleobase transport activity

A novel combination of gemcitabine and fludarabine or cladribine had synergistic cytotoxic activity against the least sensitive mesothelioma cell line. These drug combinations merit further evaluation as effective therapeutic regimens in patients with aggressive mesothelioma.

March 28th, 2008. Novel dual targeting strategy with vandetanib induces tumor cell apoptosis and inhibits angiogenesis in malignant pleural mesothelioma cells expressing RET oncogenic rearrangement

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.

March 26th, 2008. Toxin of Staphylococcus aureus overcomes acquired cisplatin-resistance in malignant mesothelioma cells

A low-toxic concentration of alpha-toxin re-sensitized cisplatin P31res cytotoxicity by apoptosis-induced through the mitochondrial pathway without detectable activation of common up-stream apoptosis signaling proteins. The toxin/drug combination should be tested for cisplatin-resistant mesothelioma treatment.

March 25th, 2008. Bcl-xL antisense oligonucleotide and cisplatin combination therapy extends survival in SCID mice with established mesothelioma xenografts

ASO 15999 induced reduction of Bcl-xL is effective in slowing the progression of human mesothelioma cell lines both in vitro and in vivo. More notably, the combination of Bcl-xL ASO and cisplatin extends survival in an orthotopic tumor xenograft model.

March 15th, 2008. mTOR contributes to the acquired apoptotic resistance of human mesothelioma multicellular spheroids

In sum, mTOR and S6K contribute to the apoptotic resistance of mesothelioma cells in 3D, not in 2D, cultures. The 3D model may reflect a more clinically relevant in vitro setting in which mTOR exhibits anti-apoptotic properties.