Origin of Connective Tissue Type Mesotheliomas from Multipotential Spindle Cells
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Home Page > Health > Cancer > Origin of Connective Tissue Type Mesotheliomas from Multipotential Spindle Cells
Origin of Connective Tissue Type Mesotheliomas from Multipotential Spindle Cells
Posted: Oct 24, 2010 |Comments: 0
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Origin of Connective Tissue Type Mesotheliomas from Multipotential Spindle Cells
By: Montwrobleski77
About the Author
Monty Wrobleski is the author of this article. For more information please click on the following links
(ArticlesBase SC #3536196)
Article Source: http://www.articlesbase.com/ – 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 41–44, 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 9.6–13 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 0–1; 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 44–78/20–84); PS 1 55%/47%; epithelial 74%/67%; pleural 93%/91%; thrombocytosis 40%/40%. Results: Cycles: total 458/424, median 7/6, range 1–42/2–39. Statistically significantly different (SSD) toxicity (p <0.05), any grade: alopecia 60%/38%; epistaxis 62%/24%; hypertension 45%/22%; non-neutropenic infection 15%/4%; proteinuria 62%/47%; stomatitis 23%/7%. There were no SSD toxicities = grade 3. Median PFS 6.9/6.0 mo (HR 0.93, p=0.88). Median OS 15.6/14.7 mo (p=0.91). 1-year survival 59%/57%. Partial response 25%/22%; stable disease 51%/60%. Median VEGF (N=56) 131/154 pg/ml (range 31–1760/5–1786). Higher VEGF was associated with shorter PFS (p=0.02) and OS (p=0.0066). In pts with VEGF = the median, PFS (p=0.043) and OS (p=0.028) were significantly greater for GCB than GCP; in high VEGF strata this was not SSD. Conclusion: Adding B to GC in MM pts does not yield statistically significant differences in PFS, OS, response, or grade toxicity. GCB-treated pts with low VEGF levels had longer PFS and OS. Supported by NCI grant N01-CM-17102.”
Another interesting study is called, “Technique for external beam treatment for Mesothelioma” by G.J. Kutcher, PH.D., C. Kestler, R.T., D. Greenblatt, M.D., H. Brenner, M.D., B.S. Hilaris, M.D., D. Nori, M.D. – Volume 13, Issue 11, Pages 1747-1752 (November 1987). Here is an excerpt: “Abtract – A combined photon-electron beam treatment for diffuse pleural mesothelioma is discussed in this paper. The technique consists of parallel opposed 10 MV X rays prescribed to 4250 cGy using customized blocks to shield the lung. The pleura is then boosted with electrons to a dose of 3600 cGy. The combination yields a TDF of 74 ret to the pleura. As discussed in an earlier paper, this treatment method when combined with subtotal pleurectomy and I-125 implantation leads to improved survivals with minimal complications. The details of this 3-dimensional radiation treatment method were not described in detail. To improve target coverage and local control, the technique has been modified. CT is now used along with simulation plane films to define the entire pleural surface. The target volume has also been extended from the dome to the base of this diaphragm. These changes have led to improved pleural dose distributions; by blocking the liver or stomach, and boosting the crus of the diaphragm with electrons, there is little added morbidity. As is demonstrated by dose volume histograms, we have been able to deliver 4250 cGy 10% to most of the pleura with ; of the lung parenchyma receiving less than 2100 cGy.”
Another interesting study is called, “Laparoscopy: An important tool in the staging of malignant pleural Mesothelioma” by Kevin C. Conlon, Valerie W. Rusch and Susan Gillern – Annals of Surgical Oncology Volume 3, Number 5, 489-494, DOI: 10.1007 — Here is an excerpt: “Abstract – Background: The current standard for the noninvasive staging of patients with malignant pleural mesothelioma is computed tomography (CT). However, CT often cannot determine whether a tumor is unresectable because of direct extension through the diaphragm to the peritoneal cavity. The aim of this prospective study was to determine whether laparoscopy detected transdiaphragmatic tumor extension when CT findings were equivocal.
Methods: From June 1993 to July 1994, 12 of 36 patients considered for possible thoracotomy and surgical resection had equivocal CT findings of diaphragmatic invasion. All underwent laparoscopy using a multiport technique with diaphragmatic and peritoneal biopsies.
Results: The mean operative time was 83 min. There were no perioperative complications. The median hospital stay was 1 day. Six patients had biopsy-proven transdiaphragmatic extension, or peritoneal studding of tumor. The other six patients subsequently underwent thoracotomy: three had a complete resection, and three had unresectable tumor due to chest wall (N=2) or mediastinal (N=1) invasion. In no case was transdiaphragmatic extension of a tumor seen.
Conclusions: This preliminary experience demonstrates that laparoscopy is a safe and accurate method for detecting transdiaphragmatic tumor extension when CT fails to do so. Laparoscopy should be considered a standard part of prethoracotomy staging in this subset of patients.”
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(ArticlesBase SC #3536196)
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About the Author:
Monty Wrobleski is the author of this article. For more information please click on the following links
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