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Should cytology be an acceptable means of diagnosing malignant mesothelioma?

The confidence with which one can make a cytological diagnosis of malignant mesothelioma has been a controversial topic for many years, with many opponents and a number of persistent advocates. The literature is extensive and is well referenced in the comprehensive article in this issue by Davidson and some years ago by Whitaker in this journal. A range of well-recognized situations can lead to reactive mesothelial cell proliferations or other types of cancer cells closely resembling malignant mesothelioma in cytological preparations. This is the main reason why the definitive diagnosis is usually based upon histology, which has the additional advantage of being able to confirm tissue invasion. Most agree, however, that it is possible at least to suspect the diagnosis on the basis of the findings in a fluid sample. This is important not only for allowing appropriate management to be instituted for treatment of the condition, when a cytological diagnosis is supported by clinical and radiological appearances, but also because cytology may be the only source of pathological material available for diagnosis in those who develop mesothelioma as a result of occupational exposure to asbestos and are pursuing compensation via a medicolegal route. The current British Thoracic Society guidelines on the management of pleural effusion and malignant mesothelioma, the European Respiratory Society ⁄ European Society of Thoracic Surgeons task force, the International Mesothelioma Interest Group and the American Thoracic Society all acknowledge a role for cytology in the diagnosis of malignant mesothelioma but they tend to favour a tissue diagnosis for ultimate confirmation. Part of the problem is the lack of a marker or markers specific for malignant mesothelioma and, particularly, to distinguish reactive from malignant mesothelium when the mesothelial phenotype is established. One might have imagined that molecular dissection of this tumour would have detected a marker by now that could reliably differentiate between mesothelioma and other tumours, especially metastatic adenocarcinoma, but, to date, this is not the case. Furthermore, a marker that could reliably and consistently differentiate between reactive and neoplastic mesothelial cells would also be an enormous benefit to the diagnostic pathologist, although there are some non-specific antibodies in current use. There are of course existing markers that can be used to characterize a serosal malignancy but no single marker is entirely specific for malignant mesothelioma or its mimics and patterns of results are generally described. These are thoroughly reviewed by Dr Davidson in his review article, with a suggested panel that can be applied in this situation at the present moment. As other primary serous tumours and metastatic tumours to the serosal surfaces will require a completely different approach to therapy and, when appropriate, different chemotherapeutic agents, it is essential to establish a robust diagnosis prior to initiating treatment. Often it is possible to confirm a diagnosis of metastatic adenocarcinoma and exclude mesothelioma on cytology with the aid of immunohistochemistry including CEA, BerEP4 and TTF1 but the problem is more complicated for peritoneal tumours in women, where the intriguing entity, primary serous adenocarcinoma, is a particularly troublesome mimic of peritoneal malignant mesothelioma in both morphological and immunohistochemical terms. There is such a marked degree of overlap clinically, radiologically and pathologically between advanced serous adenocarcinomas in the abdomen and intra-abdominal mesothelioma that some have proposed the term peritoneal surface malignancy . In addition, primary peritoneal serous carcinomas are essentially identical to ovarian and other gynaecological serous tumours and can only be differentiated from them by their anatomical location. The common features shared by peritoneal mesothelioma and the serous carcinomas also raise several interesting questions in terms of histogenesis and phenotype, which inevitably provoke exploration. These questions include the possibility that these tumours arise from a similar (or even identical) cell type, whether it is possible to see primary peritoneal serous carcinomas in men and whether serous adenocarcinomas can occur at sites other than the peritoneum. Interestingly, we have fairly recently seen a female patient who presented with a malignant pleural effusion that proved to be an adenocarcinoma on cytology and subsequent histology with the immunophenotype of a serous carcinoma. We debated at the time whether this could be a primary pleural serous adenocarcinoma (which to the best of the author s knowledge does not appear to have been described previously in the literature as all such tumours are assumed to be metastatic). In fact this lady re-presented nearly 2 years later with a high-grade serous adenocarcinoma of the endometrium, which, in retrospect, was considered to be the source of the pleural metastases. This case highlights two other critical points in differentiating between these tumours. First, the results of all pathological investigations require close clinical and radiological correlation before arriving at a