NDLI: Nontumorigenic squamous cell carcinoma line converted to tumorigenicity with methyl methanesulfonate without activation of HRAS or MYC.

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Nontumorigenic squamous cell carcinoma line converted to tumorigenicity with methyl methanesulfonate without activation of HRAS or MYC.

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Nontumorigenic squamous cell carcinoma line converted to tumorigenicity with methyl methanesulfonate without activation of HRAS or MYC.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Schuller, D. Shuler, C. Trewyn, R. W. Hollering, J. Kurian, P. Sital, N. Milo, G. E. Mannix, D. G. French, B. T. Noyes, I.
Description	Author Affiliation: Milo GE ( Department of Physiological Chemistry, Ohio State University, Columbus 43210.);
Abstract	Plasticity of human tumor populations could account for the reason why many tumorigenic human cell lines lose this feature when grown in culture. Methyl methanesulfonate (MMS) was used to convert premalignant squamous cell carcinoma (SCC) cell line SCC-83-01-82 to a malignant phenotype. The MMS-treated SCC-83-01-82 cells (MMS-SCC-83-01-82) produced progressively growing tumors in 5 of 11 splenectomized BALB/c nude mice within 3-5 months. A cell line, designated SCC-83-01-82 CA, was established in vitro from one of the mouse tumors and was repassaged successively. This SCC-83-01-82 CA cell line was aggressively tumorigenic. A tumor greater than or equal to 2.0 cm in size was present within a month, as opposed to the 3-5 months required for the tumors produced by the MMS-SCC-83-01-82 cells. Examination of frozen cross sections by in situ hybridization revealed that focal areas of the tumor produced by the MMS-SCC-83-01-82 cells expressed MYC and HRAS mRNA. However, by the third passage in vivo, the levels of expression of the corresponding genes in the mouse tumors were undetectable. Blot-hybridization analysis of the RNA from the MMS-SCC-83-01-82 cells and the subsequently derived tumors and cells did not indicate any consistent overexpression of MYC, HRAS, or KRAS. Restriction fragment length polymorphism analysis of both MYC and HRAS genes revealed neither rearrangement nor amplification of MYC nor point mutation in the 11th or 12th codon of HRAS. The data suggest that alterations in MYC and HRAS were not directly involved in either the initial transformation or MMS-induced tumorigenic conversion of the SCC-83-01-82 cell line. Persistence of tumorigenicity after reisolation of the MMS-converted premalignant SCC-83-01-82 cells did not disappear immediately following the treatment with MMS.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	4
Volume Number	87
Language	English
Publisher	National Academy of Sciences
Publisher Date	1990-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Transformation, Neoplastic Gene Expression Regulation, Neoplastic Genes, Ras Methyl Methanesulfonate Pharmacology Proto-Oncogene Proteins Genetics Proto-Oncogenes Tumor Cells, Cultured Drug Effects Animals Blotting, Southern Carcinoma, Squamous Cell Cell Line DNA, Neoplasm Isolation & Purification Gene Amplification Genotype Mice Mice, Nude Neoplasm Transplantation Nucleic Acid Hybridization Protein-Tyrosine Kinases Proto-Oncogene Proteins C-myc Transplantation, Heterologous Cytology Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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