Mesothelioma and homozygous deletions in cell lines
Another interesting study is called a "change of β-catenin Genetics gene (CTNNB1) in human lung cancer and Malignant Mesothelioma and identification of new 3 p 21.3 homozygous deletion "- Oncogene,2001,vol 20,No. 31,p. 4249-4257 according to Kiku Shigemitsu,Yoshitaka Sekido,Noriyasu ears,Shoichi Mori,Mitsuo Sato,. Yoshitsugu Horio,Yoshinori Hasegawa,Scott A. Bader,Adi F. Gazdar,John D. Minna,Toyoaki Hida,Hiromu Yoshioka,Munehisa Imaizumi,Yuichi Ueda,Masahide Takahashi,Kaoru Shimokata –Here's an excerpt:"Summary –β-catenin gene (CTNNB1) has been shown that genetically mutated in various cancers to identify people. if the β-catenin gene is responsible for oncogenesis in thoracic cancer,we examined mutations in 166 lung cancer (90 primary tumors and 76 cell lines),and blastoma 10 malignant mesotheliomas (two primary tumors and eight cell lines). Among lung cancers,43 small cell lung cancer (SCLC) and 123 cancers in non-small cell lung cancer (NSCLC),there are four changes in exon 3,which is the target region of the mutation to stabilize β-catenin. Primary adenocarcinoma had somatic mutation of C to G,leading to amino acid substitution of Ser Cys codon in the 37th Among the cell lines,SCLC NCI-H1092 had a mutation from A to G,resulting Asp to Gly substitution at codon 6,NSCLC HCC15 had a C to T mutation,leading to Ser Phe substitution at codon 45 and NSCLC NCI-H358 had a mutation A to G,leading to replacement Thr Ala codon in the 75th Blastoma also had a somatic mutation of C to G,leading to a Cys Ser substitution at codon 37th Of the 10 mesotheliomas,we identified homozygous deletions in cell lines NCI-H28. Cloning of fragment rearrangement NCI-H28 indicated that all exons except exon 1 of β-catenin gene is deleted and the deletion junction is 13 kilobytes current first exon In addition,Northern blot analysis of 26 lung cancer and Mesothelioma Cell Line RNAs detected eight ubiquitous expression of β-catenin messages except NCI-H28,although Western blot analysis showed that the relatively low amount protein products were expressed in some lung cancer cell lines. Our results suggest that β-catenin gene is often present in lung cancers and NCI-H28 homozygous deletion of β-catenin gene might indicate the possibility of a new cancer gene suppressor residing in this region at 3p21.3,where various types of human cancers frequently showed allelic loss. "
More interesting study called "Gene therapy of mesothelioma experiments using adenovirus vectors encoding HSVtk gene"in Esanda MC,van Someren GD,Vincent AJ,van Bekkum DW,Valerio D,Noteboom JL Bout .. –Gene here. . April 1997,4 (4):280-7 Here is a snippet:"Summary –replication-defective adenovirus vectors were generated in which the gene of interest (lacZ,luciferase or HSV-tk),directed by the adenovirus major late promoter (MLP) or the cytomegalovirus promoter human immediate early gene / enhancer (CMV). In vitro experiments in rats (II-45) and human (RME 25) mesothelioma cell lines showed that the CMV promoter was stronger than the MLP promoter expression levels of luciferase reporter gene and ganciclovir (GCV) efficiency kill the tk gene transfer. After administration of recombinant adenovirus IG.Ad.CMV.lacZ (Introgene IG) in the pleural cavity of Fischer rats with established Mesothelioma has a wide spread of infectious viral particles using the contents of the chest were found. However,the proportion relatively small tumor cells were transduced. However,inhibition of tumor growth was strong observed after treatment with recombinant adenovirus IG.Ad.CMV.TK GCV. Separate groups of rats inoculated on day 0 and 10 (5) II-45 cells in the pleural cavity,won 7 x 10 (9) infectious particles IG.Ad. CMV.TK day 1,day 2,day 4 or 8 days. One day after the virus,25 mg / kg GCV or PBS (control) was injected intraperitoneally (ip) twice daily. 15th day,all animals were killed. significant tumor regression,which corresponds to 5 log cell kill occurred in rats suggests bystander effect is impressive. In a survival study,animals were treated 9 days after inoculation of tumor cells from 10 (5) with IG.Ad.CMV.TK and within 14 days of GCV. Treatment of prolonged survival without symptoms 19 days in the control to 33 days in the treated group. These responses can be best explained by assuming that the continuation of TK expression in or around tumor tissue during treatment with GCV. Our results confirm and extend previous findings on the same model and demonstrate potential of herpes simplex virus thymidine kinase suicide gene therapy for local treatment of malignant mesothelioma. "
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