Origin of Connective Tissue Type Mesotheliomas from Multipotential Spindle Cells

Origin of Connective Tissue Type Mesotheliomas from Multipotential Spindle Cells

Another interesting study is called, "Pleural mesothelioma of connective tissue type, localized fibrous tumour of the pleura, and reactive submesothelial hyperplasia. An immunohistochemical comparison" by Moutaiz Al-Izzi, Nicola P. Thurlow, Professor Bryan Corrin - The Journal of Pathology Volume 158, Issue 1, pages 4144, May 1989. Here is an excerpt: "Abstract - Ten diffuse pleural mesotheliomas of connective tissue type have been compared with 14 examples of pleural granulation tissue and 7 localized fibrous tumours of the pleura, using immunohistochemistry to identify cytokeralins oflow and high molecular weight and vimentin. Low molecular weight cytokeratin and vimentin were both delected in 8 of the 10 mesotheliomas and in 12 of the 14 reactive iesions. High molecular weight cylokeratin was rarely detected in either lesion. The seven localized fibrous tumours of the pleura were all positive for virnentin and negative for both cytokeratins. These findings support an origin of connective tissue type mesotheliomas from multipotential submesothelial spindle cells and of localized fibrous tumours of the pleura from either conventional fibroblasts or resting submesothelial spindle cells. Antibodies to cytokeratin help distinguish these two neoplasms but provide no assistance in the more difficult diagnostic problem of distinguishing mesotheliomas of connective tissue type from pleural reactions characterized by abundant granulation tissue."

Another interesting study is called, "Final analysis of a multi-center, double-blind, placebo-controlled, randomized phase II trial of gemcitabine/cisplatin (GC) plus bevacizumab (B) or placebo (P) in patients (pts) with malignant mesothelioma (MM)" -

Journal of Clinical Oncology, 2007 ASCO Annual Meeting Proceedings (Post-Meeting edition). Vol 25, No 18S (June 20 Supplement), 2007: 7526 by T. Karrison, H. L. Kindler, D. R. Gandara, C. Lu, T. L. Guterz, K. Nichols, H. Chen, W. M. Stadler and E. E. Vokes - University of Chicago Medical Center, Chicago, IL; UC Davis Cancer Center, Sacramento, CA; MD Anderson Cancer Center, Houston, TX; CTEP National Cancer Institute, Rockville, MD. Here is an excerpt: "Background: In phase II trials in MM, GC on a 21-day (D) schedule has response rates of 16%26% and median overall survival (OS) of 9.613 months (mo). Since VEGF has a key role in MM biology, we added anti-VEGF antibody B to GC in a multi-center, double- blind, placebo-controlled randomized phase II trial. Methods: Eligible pts had unresectable MM; no prior chemotherapy; PS 01; no thrombosis, bleeding, or major vessel invasion. Primary endpoint: progression-free survival (PFS). Statistics: 90% power to detect HR 0.57. Stratification: PS (0/1), histology (epithelial/other). G 1,250 mg/m2 D 1, 8 Q21D, C 75 mg/m2 D1 Q21D, and B 15 mg/kg or P D1 Q21D was given x 6 cycles, then B or P Q21D until progression. Baseline plasma VEGF was measured. 115 pts enrolled 12/01- 07/05 at 11 sites, 108 (GCB/GCP) 53/55 were evaluable. Male 74%/84%; median age 62/65 (range 4478/2084); PS 1 55%/47%; epithelial 74%/67%; pleural 93%/91%; thrombocytosis 40%/40%. Results: Cycles: total 458/424, median 7/6, range 142/239. Statistically significantly different (SSD) toxicity (p

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