Japanese researchers have recently investigated the mechanisms of the mesothelin gene that result in malignant mesothelioma. The study is published in the journal Human Pathology.
Mesothelioma is a rare cancer almost entirely caused by exposure to asbestos. Since there is no cure for this disease, the life expectancy for most mesothelioma patients ranges between four and 18 months after the exact diagnosis of mesothelioma is known. Although there is no cure to date, some patients with early diagnosis of mesothelioma may be given a combination of aggressive therapy, such as surgery, chemotherapy and radiation. Combination therapy, known as multimodality therapy, currently has the best chance of extending patient life.
The study authors explain, 'Gene methylation leads to the development of malignant tumors in some tumors [malignant mesothelioma] which are histologically divided into 3 subtypes, namely, epithelioid, sarcomatoid, and bipase type, and it shows that mesothelin expression is restricted to epithelioid and epithelioid bifase MM type (malignant mesothelioma). However, the regulatory mechanism of expression has not been clarified. '
A total of 118 lung specimens were studied, including 39 MM, 41 lung carcinomas, 26 nonneoplastic pulmonary lesions, and 12 samples of normal lung tissue. The specimens were tested for mesothelin expression through immunohistochemical assays, together with the methylation status of 20 mesothelin gene promoter sites.
The results show that mesothelin is expressed on the epithelioid subtype and epithelioid part of the bipase subtype. However, mesothelin expression is not found in either the sarcomatoid subtype or the sarcomatous part of the bifase type. Promotor gene mesothelin significantly hypomethylasi on malignant mesotehelioma specimen without subtype when compared with other lung lesions and samples of normal lung tissue.
The findings suggest that hypomethylation of the mesothelin gene promoter may be specifically associated with MM formation, regardless of expression status, and that the expression of the mesothelin protein is lost in the sarcomatoid type due to some posttranscriptional regulatory mechanism
Mesothelioma is a rare cancer almost entirely caused by exposure to asbestos. Since there is no cure for this disease, the life expectancy for most mesothelioma patients ranges between four and 18 months after the exact diagnosis of mesothelioma is known. Although there is no cure to date, some patients with early diagnosis of mesothelioma may be given a combination of aggressive therapy, such as surgery, chemotherapy and radiation. Combination therapy, known as multimodality therapy, currently has the best chance of extending patient life.
The study authors explain, 'Gene methylation leads to the development of malignant tumors in some tumors [malignant mesothelioma] which are histologically divided into 3 subtypes, namely, epithelioid, sarcomatoid, and bipase type, and it shows that mesothelin expression is restricted to epithelioid and epithelioid bifase MM type (malignant mesothelioma). However, the regulatory mechanism of expression has not been clarified. '
A total of 118 lung specimens were studied, including 39 MM, 41 lung carcinomas, 26 nonneoplastic pulmonary lesions, and 12 samples of normal lung tissue. The specimens were tested for mesothelin expression through immunohistochemical assays, together with the methylation status of 20 mesothelin gene promoter sites.
The results show that mesothelin is expressed on the epithelioid subtype and epithelioid part of the bipase subtype. However, mesothelin expression is not found in either the sarcomatoid subtype or the sarcomatous part of the bifase type. Promotor gene mesothelin significantly hypomethylasi on malignant mesotehelioma specimen without subtype when compared with other lung lesions and samples of normal lung tissue.
The findings suggest that hypomethylation of the mesothelin gene promoter may be specifically associated with MM formation, regardless of expression status, and that the expression of the mesothelin protein is lost in the sarcomatoid type due to some posttranscriptional regulatory mechanism
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