However, the presence of SV40 DNA sequences is not sufficient to account for its possible role in tumor development because the viral proteins must be expressed and ultimately impair the function of relevant cell proteins, such as p53 and pRb. In this study we investigated SV40 large T antigen (SV40 Tag) protein expression in mesothelioma cell lines, established in our laboratory, by Western blotting, immunoprecipitation, and immunocytochemistry using Tag-specific mouse monoclonal antibodies (mAbs) Ab-1 (or Pab 419).
By Western blotting of cell extracts, none of the mesothelioma cell lines expressed detectable amounts of SV40 Tag. However, we found that Ab-1 as well as Pab-101, another SV 40 Tag-specific mAb, may generate false-positive signals due to the fact that both antibody preparations are contaminated by a protein of similar size (90 kD) as SV40 Tag and react with the various secondary horseradish peroxidase- conjugated antimouse immunoglobulin Gs tested. The present study suggests that immunodetection of SV40 Tag protein may be puzzling because this contaminating Taglike protein may bind to particular cell structures, thereby generating false-positive signals.”
Another study is called, “Pseudomesotheliomatous angiosarcoma: a pleuropulmonary lesion simulating malignant pleural Mesothelioma” by G. Falconieri, R. Bussani1, M. Mirra, M. Zanella – Histopathology Volume 30, Issue 5, pages 419–424, May 1997.
Here is an excerpt: “We report two cases of autopsy confirmed angiosarcoma in adult males, presenting as diffuse pleuropulmonary tumours and simulating malignant mesothelioma. Both the lesions grew along the serosal surfaces and were characterized by variably thick rinds of tissue encasing the lung.
The pulmonary parenchyma showed diffuse, dark red, subpleural consolidations and multiple cavitations. Histologically, the lesions were composed by atypical spindle and polygonal, epithelioid cells showing rudimentary vascular differentiation and exhibiting strong positivity for factor VIII, CD31, CD34 and vimentin.
We conclude that angiosarcoma may present with preponderant or exclusive involvement of pleura and peripheral lung and that it should be added to the list of tumours capable of simulating malignant mesothelioma.”
Another study is called, “D2-40: A Reliable Marker in the Diagnosis of Pleural Mesothelioma” by Annette M. Müllera, Folker E. Frankeb, Klaus-Michael Müllera - Institute of Pathology, BG Clinics ‘Bergmannsheil’, Ruhr University Bochum, Bochum, and Justus Liebig University, Giessen, Germany - Pathobiology 2006;73:50-54.
Here is an excerpt: “Abstract - Objective: Malignant mesotheliomas of the pleura, peritoneum and pericardium can easily be confused with either metastatic adenocarcinomas or reactive pleural lesions. D2-40, a monoclonal antibody used as a marker for seminomatous germ cell tumours and lymphatic endothelial cells, was recently described in mesothelial cells and type I but not type II pneumocytes.
Method: The immunoreactivities of D2-40 in 76 lung carcinomas of different histological types (adenocarcinomas, squamous cell, small cell, and bronchioloalveolar carcinomas) were compared with those of 36 pleural epithelioid and sarcomatoid mesotheliomas and 5 specimens of chronic pleuritis.
Results: While all 18 analysed epithelioid mesotheliomas displayed a strong membranous immunostaining, 18 sarcomatoid mesotheliomas showed no, or a merely faint, cytoplasmic signal, comparable with fibroblasts in chronic pleuritis. Out of all analysed lung carcinomas, 49 showed no immunoreactivity for D2-40 (64%), while the other 27 (36%) showed a focal weak to moderate and only cytoplasmic signal.
Conclusions: We regard D2-40 as a valid marker in the differential diagnosis of epithelioid mesotheliomas versus pulmonary adenocarcinomas. However, this marker may not properly label sarcomatoid mesotheliomas or distinguish them from reactive pleural lesions.”
We all owe a debt of gratitude to these fine researchers. If you found any of these excerpts interesting, please read the studies in their entirety.
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