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Pleuropulmonary Meningothelial Proliferations: Evidence for a Common Histogenesis
Annikka Weissferdt1, Ximing Tang, Saul Suster
1Departments of *Pathology †Translational Molecular Pathology, MD Anderson Cancer Center, Houston, TX ‡Department of Pathology, Medical College of Wisconsin, Milwaukee, WI.
Abstract:
Primary pleuropulmonary meningothelial proliferations include minute pulmonary meningothelial-like nodules (MPMN) and pleural or pulmonary meningiomas (PPM). These lesions share histologic, ultrastructural, and immunohistochemical features with meningiomas of the central nervous system (CNS). Meningiomas of the CNS exhibit a number of genetic abnormalities, most commonly loss of the neurofibromatosis (NF) 2 gene on chromosome 22. The molecular changes of pleuropulmonary meningothelial proliferations, however, have only rarely been investigated. This study explores the status of the NF2 gene in pleuropulmonary meningothelial proliferations compared with CNS meningioma using interphase fluorescence in situ hybridization. Whole tissue sections of 9 pleuropulmonary meningothelial lesions (6 MPMNs and 3 PPMs) and 9 CNS meningiomas were analyzed by fluorescence in situ hybridization using a commercially available locus-specific probe for the NF2 region. Deletion of the NF2 gene was identified in 2 MPMNs, 1 PPM, and 4 CNS meningiomas. Chromosomal gains of 22q were noted in 2 cases of MPMN and 1 PPM. Our results indicate that pleuropulmonary meningothelial lesions share common genetic pathways with CNS meningiomas. In addition, they provide support for the hypothesis that MPMN and PPM are related lesions that may arise from the same precursor cell. As for CNS meningiomas, these mutational changes may provide additional targets for future personalized therapies.
Insights
Minute pulmonary meningothelial-like nodules (MPMN) and pleural or pulmonary meningiomas (PPM) share genetic similarities with central nervous system (CNS) meningiomas. These pleuropulmonary lesions also exhibit NF2 gene alterations, suggesting common origins and potential therapeutic targets.
Area of Science:
- Oncology
- Genetics
- Pathology
Background:
- Primary pleuropulmonary meningothelial proliferations, including minute pulmonary meningothelial-like nodules (MPMN) and pleural or pulmonary meningiomas (PPM), resemble central nervous system (CNS) meningiomas histologically.
- CNS meningiomas frequently harbor genetic abnormalities, particularly involving the neurofibromatosis type 2 (NF2) gene on chromosome 22.
- The molecular basis of pleuropulmonary meningothelial lesions remains largely unexplored.
Purpose of the Study:
- To investigate the status of the NF2 gene in pleuropulmonary meningothelial proliferations.
- To compare the genetic alterations in these lesions with those found in CNS meningiomas.
- To explore potential common molecular pathways and precursor cells for these related tumors.
Main Methods:
- Analysis of whole tissue sections from 9 pleuropulmonary meningothelial lesions (6 MPMNs, 3 PPMs) and 9 CNS meningiomas.
- Utilized interphase fluorescence in situ hybridization (FISH) with a locus-specific probe for the NF2 gene region on chromosome 22.
Main Results:
- NF2 gene deletion was detected in 2 MPMNs, 1 PPM, and 4 CNS meningiomas.
- Chromosomal gains at 22q were observed in 2 MPMNs and 1 PPM.
- These findings indicate shared genetic alterations between pleuropulmonary and CNS meningiomas.
Conclusions:
- Pleuropulmonary meningothelial lesions share common genetic pathways with CNS meningiomas.
- The results support the hypothesis that MPMN and PPM may originate from the same precursor cell.
- Identified genetic changes may offer targets for future personalized therapies in pleuropulmonary meningiomas.
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