Another interesting study is called, "Diagnostic tools for differentiating between pleural mesothelioma and lung adenocarcinoma in paraffin embedded tissue. Part I: immunohistochemical findings" by H. Moch, M. Oberholzer, P. Dalquen, W. Wegmann and F. Gudat - Virchows Archiv - Volume 423, Number 1, 19-27, DOI: Here is an excerpt: "Abstract - Specimens of 27 histologically definite mesotheliomas and 34 proven adenocarcinomas were examined with a panel of 14 antibodies: pan-epithelial antibody Lu-5, anti-keratin-18, anti-keratin-7, Ber-EP4, anti-Leu-M1, HEA-125, anti-carcino-embryonic antigen (CEA), anti-blood group-related antigens (anti-BGR A, B, H), B 72.3, anti-placental alkaline phosphatase (PLAP), anti-vimentin and BMA-120 used to determine their value in the differentiation between pleural mesothelioma and lung adenocarcinoma. Lu-5, anti-cytokeratin-7 and -18, B 72.3 and PLAP reacted in a high percentage of cases with both mesothelioma and adenocarcinoma. Anti-CEA and anti-Leu-Ml did not react with any of the 27 mesotheliomas tested but showed a reaction in 75% (anti-CEA) and 66% (anti-Leu-M1) of the lung adenocarcinomas. Seventeen percent of the adenocarcinomas and 96% of the mesotheliomas showed a positive reaction with anti-vimentin. Ber-EP4 was demonstrated in all lung adenocarcinomas, but only in 2 mesotheliomas in a focal manner (7%). HEA-125 and anti-BGR A, B, H reacted with 83% (HEA-125) and 75% (anti-BGR A, B, H) of the lung adenocarcinomas. The statistical parameters, sensitivity and efficiency were estimated and a normogram for judging the diagnostic power of a single antibody for the differential diagnosis of mesothelioma versus adenocarcinoma was developed. According to this, Ber-EP4, HEA-125, anti-BGR A, B, H and anti-CEA were, in descending order, the most powerful discriminatory antibodies."
Another interesting study is called, "Altered CD3 chain and cytokine gene expression in tumor infiltrating T lymphocytes during the development of Mesothelioma" - Cancer Letters Volume 103, Issue 1, 15 May 1996, Pages 1-9 by Andrew G. Jarnicki, David R. Fitzpatrick, Bruce W. S. Robinson and Helle Bielefeldt-Ohmannc Here is an excerpt: "Abstract - The mechanisms whereby tumors escape immunosurveillance remain poorly understood. De-activation or deviation of T lymphocyte responses may occur following exposure to tumor-associated or -derived signals. In the present study it is demonstrated that during development of syngeneic malignant mesothelioma in mice, the relative CD3, CD3 and CD3/ mRNA levels expressed by tumor infiltrating lymphocytes (TIL) decrease, while CD3 mRNA levels remain relatively constant. Expression of IFN mRNA by TIL decreased during tumor development, while IL-2 mRNA levels showed slight increases. IL-3 mRNA was not detected at any time during tumor development and IL-4 transcripts were only detected in the later stages of tumor development. In the spleens of tumor-bearing mice, IL-2 transcripts were detected throughout the time course from days 1 to 22(24), while IFN mRNA was only detected at early times from days 013. Previous work demonstrated a role for tumor cell-derived TGF in the immunobiology of mesothelioma. Here it is shown that the suppression of CD3-subunit expression by TIL was ameliorated in tumors where TGF-expression was reduced by inducible TGF-specific antisense-RNA, thus, suggesting that lymphocytes may become de-activated upon infiltration of the tumor micro-environment."
Another interesting study is called, "Control of cell cycle progression in human mesothelioma cells treated with gamma interferon" - Oncogene 2001, vol. 20, no9, pp. 1085-1093 Here is an excerpt: "Abstract - Recombinant human interferon gamma (r-hu-IFN) exerts both antitumoral activity in the early stages of human malignant mesothelioma and a cytostatic effect in human mesothelioma (HM) cell lines in vitro. The antiproliferative effect of interferons (IFNs) reported in a variety of cells has been attributed to several mechanisms. In order to progress in the understanding of HM cell growth modulation by r-hu-IFN, modifications of cell cycle progression and expression of key cell cycle regulator proteins in response to r-hu-IFN were examined. Nine HM cell lines were studied, including one resistant to the antiproliferative effect of r-hu-IFN. Except in the resistant cell line r-hu-IFN produced an arrest in the G1 and G2-M phases of the cell cycle, associated with a reduction in both cyclin A and cyclin dependent kinase inhibitors (CDKIs) expression. Moreover cyclin B1/cdc2 activity was decreased. The present study provides the first evidence of a G2-arrest in r-hu-IFN-treated HM cell lines and indicates that HM cell lines, despite their tumorigenic origin still support cell cycle control. The cell cycle arrest induced by r-hu-IFN seems to depend on cyclin regulation through p21WAF1/CIP1- and p27Kip1-independent mechanisms and is not directly related to the induced DNA damage."
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