Cytogenomic characterization of three murine malignant mesothelioma tumor cell lines
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RESEARCH
Cytogenomic characterization of three murine malignant mesothelioma tumor cell lines Eva Wahlbuhl1, Thomas Liehr1* , Martina Rincic2 and Shaymaa Azawi1
Abstract Background: Malignant mesothelioma (MM) is a rare aggressive cancer primary located in pleura and lung. MMs can be divided into biphasic, epithelioid and sarcomatoid subtypes. In majority of cases MMs are induced by asbestos fiber exposure. As latency period after asbestos exposure ranges between ~ 10 and 60 years MMs are mainly observed in elder people. Human MM, being a rare tumor type, lacks detailed cytogenetic data, while molecular genetic studies have been undertaken more frequently. However, murine MM cell lines are also regularly applied to get more insight into MM biology and to test new therapy strategies. Results: Here the murine MM cell lines AB1, AB22 and AC29 were studied by molecular cytogenetics and molecular karyotyping. Interestingly, yet there were no genetic or genomic studies undertaken for these already in 1992 estab‑ lished cell lines. The obtained data on genomic imbalances in these murine cell lines was translated into the human genome as previously reported based on human and murine genomic browsers. Conclusions: It turned out that all three cell lines showed high similarities in copy number variants as observed typically in human MM. Also, all three cell lines were most similar to human epithelioid MMs, and should be used as models therefore. Keywords: Murine multicolor banding (mcb), Array comparative genomic hybridization (aCGH), Malignant mesothelioma, Murine cell line, AB1, AB22, AC29 Background Malignant mesothelioma (MM) is a rare aggressive tumor-family of pleura and lung, with an incidence of about 0.002% [1, 2]. In most of the cases, MMs are located in pleural mesothelium, and only rarely in peritoneal cavities, tunica vaginalis or pericardium. MM can be specifically promoted by exposure to asbestos fibers [3, 4]. Besides working with asbestos, accordingly contaminated buildings provide an additional, often unrecognized problem, where affected person can undergo *Correspondence: [email protected]‑jena.de 1 Jena University Hospital, Institute of Human Genetics, Friedrich Schiller University, Am Klinikum 1, 07747 Jena, Germany Full list of author information is available at the end of the article
asbestos inhalation, ingestion, or less often, severe exposures via the skin [3, 5]. The latency periods for MM after asbestos exposure can range from 1 to 6 decades, and the median age of onset is 72 years [6]. Numerous genetic changes are involved in MM. These include numerical and structural chromosomal aberrations and molecular genetically detectable alterations in the cellular signal transduction pathways, among others caused by activation of oncogenes or loss of tumor suppressor genes [5]. In human the genes cyclin-dependent kinase inhibitor 2A (CDKN2A), neurofibromatosis type 2 (NF2), the breast cancer associated gene 1 (BRCA1) associated protein 1 (BAP1) and tumorsuppressorprotein 53 (TP53) g
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