This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Corominas, M. Articles by Pellicer, A. Search for Related Content PubMed PubMed Citation Articles by Corominas, M. Articles by Pellicer, A.

Differential Expression of the Normal and Mutated K-ras Alleles in Chemically Induced Thymic Lymphomas

Department of Pathology and Kaplan Cancer Center, New York University Medical Center, New York, New York 10016 [M. C., E. W. N., A. P.], and California Institute of Biological Research, La Jolla, California 92037 [M. P.]

The presence of point mutations in the K-ras gene was examined in murine thymic lymphomas induced by a single dose of N-methylnitrosourea by the RNase A mismatch cleavage method and by allelic-specific oligonucleotide hybridization of in vitro amplified DNA by polymerase chain reaction. The results show that the frequency of mutations is lower than that of tumors induced by multiple N-methylnitrosourea treatments. Four mutations identified were the aspartic acid at codon 12, a G:C to A:T transition in its second position. A G:C to T:A transversion in codon 146 was also found in one thymic lymphoma, changing the amino acid alanine to serine. The use of the RNase A assay allowed an estimation of the relative expression levels of both normal and mutant K-ras alleles. The results show that in approximately one half of the tumors the mutant allele is predominantly expressed, suggesting that the normal allele has been lost or that the mutant allele has been amplified relative to the normal. Altogether, these findings are consistent with ras mutations occurring in some instances during tumor development and with a ras effect being not strictly dominant but favoring selection for increasing levels of expression from the oncogenic allele.

¹ Present address: Division of Toxicology, Massachusetts Institute of Technology, Cambridge, MA 02139.

² To whom requests for reprints should be addressed, at Department of Pathology, New York University Medical Center, 550 First Avenue, New York, NY 10016.

Received 4/11/91. Accepted 7/19/91.

This article has been cited by other articles:

				X. O. Shu, J. P. Perentesis, W. Wen, J. D. Buckley, E. Boyle, J. A. Ross, and L. L. Robison Parental Exposure to Medications and Hydrocarbons and ras Mutations in Children with Acute Lymphoblastic Leukemia: A Report from the Children's Oncology Group Cancer Epidemiol. Biomarkers Prev., July 1, 2004; 13(7): 1230 - 1235. [Abstract] [Full Text] [PDF]

				R. Diaz, D. Ahn, L. Lopez-Barcons, M. Malumbres, I. Perez de Castro, J. Lue, N. Ferrer-Miralles, R. Mangues, J. Tsong, R. Garcia, et al. The N-ras Proto-oncogene Can Suppress the Malignant Phenotype in the Presence or Absence of Its Oncogene Cancer Res., August 1, 2002; 62(15): 4514 - 4518. [Abstract] [Full Text] [PDF]

				X. Qin, H. Zhou, L. Liu, and S. L. Gerson Transgenic expression of human MGMT blocks the hypersensitivity of PMS2-deficient mice to low dose MNU thymic lymphomagenesis Carcinogenesis, September 1, 1999; 20(9): 1667 - 1673. [Abstract] [Full Text] [PDF]