December 26th, 2005. EGFR overexpression in malignant pleural mesothelioma An immunohistochemical and molecular study with clinico-pathological correlations
This study documents EGFR overexpression in MPM at the protein and the transcriptional levels; it proposes a reliable method for EGFR expression evaluation in MPM. EGFR levels are not associated with clinico-pathological features of patients, including survival.
December 14th, 2005. Mesothelioma: advances in chemotherapy
Some preliminary data from studies of second line chemotherapy is also available. Finally studies of targeted therapies such as anti-EGFR, anti VEGF and anti PDGF are underway but have not as yet demonstrated major therapeutic benefit.
December 2nd, 2005. Interleukin-2 for the treatment of solid tumors other than melanoma and renal cell carcinoma
The activity of IL-2 in monotherapy or in association with immunotherapy is clinically relevant in hepatocarcinoma, mesothelioma and in malignant overflows as palliative treatment. Randomized trials would be required in order to be able to draw conclusions about its indication in other tumors.
November 21st, 2005. Perspective on the development of new agents in thoracic cancers
Inhibitors of the epidermal growth factor receptor (EGFR) are one of many promising targeted therapies for non-small-cell lung cancer (NSCLC). By utilizing agents that specifically target the biochemical and molecular changes underlying cancer, it is possible to envision a future in which combinations of therapies treat cancer on multiple fronts, significantly enhancing tumor responses and improving survival beyond current expectations.
August 5th, 2005. Receptor tyrosine kinase and phosphoinositide-3 kinase signaling in malignant mesothelioma
Conclusion: In malignant mesothelioma constitutive activation of phosphoinositide-3 kinase/Akt results in cellular survival and contributes to the malignant phenotype. We have demonstrated that epidermal growth factor receptor inhibition leads to apoptotic cell death through downregulation of phosphoinositide-3 kinase signaling in mesothelioma cell lines, whereas insulin-like growth factor receptor inhibition leads to apoptosis independent of phosphoinositide-3 kinase. Epidermal growth factor receptor, insulin-like growth factor receptor, and phosphoinositide-3 kinase inhibition might be clinically relevant in malignant mesothelioma.
July 13th, 2005. Therapeutic Targeting of Multiple Signaling Pathways in Malignant Pleural Mesothelioma
Our findings suggest that ErbB1 alone is a therapeutic target for the minority of mesotheliomas and that combining ErbB1 inhibitors with signal transduction inhibitors in mesothelioma will enhance their effectiveness. Furthermore, combinations of growth factor and signal transduction inhibitors may be needed to inhibit the growth of the majority of MPM cell lines, and therefore patients with MPM.
May 1st, 2005. Therapeutic options in malignant pleural mesothelioma
Radiotherapy may be applied in case of local tumour growth. The individual therapeutic decision will depend on tumour stage, concomitant diseases, performance status, and on the patient's preference.
Conclusions: Epidermal growth factor receptor tyrosine kinase inhibitor PD153035 significantly inhibited motility and invasion in malignant pleural mesothelioma cells in vitro, regardless of their epidermal growth factor receptor expression levels. Inhibition of epidermal growth factor receptor-dependent signaling might be a useful strategy to diminish malignant pleural mesothelioma recurrence after aggressive cytoreductive surgery.
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