Mechanisms Whereby Mesothelioma Tumors Escape Immunosurveillance
Mechanisms Whereby Mesothelioma Tumors Escape Immunosurveillance
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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