Seminars in Oncology - Volume 29, Concern 1, Pages 62-69 (February 2002) by Paul Baas
Here is an excerpt: "Abstract - It has been a challenge to discover helpful chemotherapeutic remedies for . Over the last numerous decades a lot of single-drug and combination regimens have been examined, but no normal treatment with chemotherapy alone has emerged. Probable explanations for this lack of good results are the heterogeneity in between the distinctive subclasses and the difficulties experienced in determining responses on computed tomographic (CT) scan. This evaluation will present the outcomes of most chemotherapy trials. An attempt is also been created to overcome the challenge of identifying the overall response rate by presenting the median survival time. Other varieties of response evaluation and guidelines for patient choice are warranted to appropriately compare chemotherapeutic treatments. Semin Oncol 29:62-69.
A further interesting study is called, "Intrapleural Production of Interleukin 6 for the duration of Mesothelioma and Its Modulation by γ-Interferon Treatment" by Gianpaola Monti, Marie-Claude Jaurand, Isabelle Monnet, Pascale Chretien, Laure Saint-Etienne, Lin Zeng, Alain Portier, Philippe Devillier, Pierre Galanaud, Jean Bignon, and Dominique Emilie - Cancer Res August 15, 1994 54 4419. Here is an excerpt: "Abstract - In vivo production of monokines was analyzed in 17 human malignant pleural . High concentrations of interleukin 6 (IL-6) were detected in pleural effusions, contrasting with low levels of IL-1β and tumor necrosis factor α. This production arose from malignant cells, as shown by immunochemical analysis of pleural cells and by production of IL-6 by mesothelial cell lines. Intrapleural administration of recombinant human γ-interferon to six patients led to a marked decrease in intrapleural IL-6 concentrations in all circumstances. This therapy was connected with in situ activation of macrophages and cytotoxic T-lymphocytes, as indicated by increased intrapleural neopterin and soluble CD8 concentrations. In vitro γ-interferon had no impact on the production of IL-6 by mesothelial cell lines but decreased the growth of three of 6 mesothelioma cell lines. These results indicate that systemic manifestations of malignant mesothelioma, including fever, cachexia, and thrombocytosis may possibly be related to the production of IL-6 by malignant cells, and that nearby γ-interferon infusion could decrease this production by stimulating antitumoral immunity and/or by directly decreasing the proliferation of malignant cells."
One other intriguing study is called, "Lengthy-term survival in the role of radiotherapy and combined modality therapy" by Gilbert S. Lederman MD, Abram Recht MD, Terence Herman MD, Robert Osteen MD, Joseph Corson MD, Karen H. Antman MD – Cancer Volume 59, Issue 11, pages 1882–1886, 1 June 1987. Here is an excerpt: "Abstract - Ten patients with peritoneal mesothelioma had been treated at the Joint Center for Radiation Therapy among 1968 and 1985. Six of the ten patients remained no cost of disease at 19+ to 78+ months after diagnosis. The six patients received sequential surgical debulking, combination chemotherapy, and entire-abdomen irradiation. 4 patients not treated with this multimodality approach died with illness. This approach could possibly have an impact on the natural course of peritoneal mesothelioma, and warrants further study."
A further intriguing study is known as, "Somatic genetic alterations in human malignant mesothelioma (assessment)." By Lee WC, Testa JR. - Department of Medical Oncology, Fox Chase Cancer Center, Philadelphia, PA 19111, USA. Int J Oncol. 1999 Jan14(1):181-8. Here is an excerpt: "Abstract - A evaluation of cytogenetic and molecular genetic findings in human malignant mesotheliomas (MMs) is presented. The complex profile of somatic genetic changes characteristic of MMs implicates a multistep process of tumorigenesis in this malignancy. In particular, the occurrence of several, recurrent cytogenetic deletions in MMs suggests that loss and/or inactivation of tumor suppressor genes (TSGs) are critical to the development and progression of such tumors. Karyotypic and comparative genomic hybridization analyses of MMs have demonstrated frequent deletions of specific regions within chromosome arms 1p, 3p, 6q, 9p, 15q and 22q, and subsequent loss of heterozygosity (LOH) studies have documented high frequencies of allelic loss from every of these chromosomal websites. Positional candidate gene approaches have identified TSGs within two of these regions, i.e., p16/CDKN2A at 9p21 and NF2 at 22q12, which are frequently altered in MMs. Homozygous deletions appear to be the significant mechanism affecting p16/CDKN2A, whereas inactivating mutations coupled with allelic loss occur at the NF2 locus. High density LOH analyses have pinpointed minimal regions of deletion in 1p, 3p, 6q, and 15q and are expected to facilitate efforts to identify putative TSGs at these locations which contribute to the pathogenesis of MMs."
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