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Melanoma line LG2-MEL expresses several antigens recognized by autologous CTLs. One of them consists of a peptide derived from tyrosinase and presented by HLA-B*3503. We have identified another antigen of LG2-MEL as a peptide presented by HLA-B*4403 and resulting from a point mutation in gene OS-9. This gene is expressed in various normal tissues. It is located on chromosome 12 in the vicinity of the CDK4 locus and is frequently co-amplified with CDK4 in human sarcomas. The mutation, a C-to-T transition, changes a proline residue into a leucine at position 446 of the OS-9 protein. Mutated transcripts were found in all the melanoma sublines of LG2-MEL. None of the 184 tumor samples collected from other cancer patients expressed the mutated transcript, indicating that this is a rare mutational event. Interestingly, some of the melanoma sublines of LG2-MEL have lost the wild-type allele of gene OS-9. Those sublines appear to grow faster in vitro than the sublines that retained the wild-type allele, suggesting that this loss of heterozygosity may favor tumor progression. The mutation we have identified in gene OS-9 might therefore participate in the oncogenic process by affecting the function of this potential tumor-suppressor gene.

Type

Journal article

Journal

Cancer immunity

Publication Date

19/07/2002

Volume

2

Addresses

Laboratory of Experimental Surgery, Tour de Pathologie, Université de Liège, Liège, Belgium.

Keywords

T-Lymphocytes, Cytotoxic, COS Cells, Clone Cells, Tumor Cells, Cultured, Animals, Humans, Melanoma, Lectins, Neoplasm Proteins, DNA, Complementary, Antigens, Neoplasm, HLA-B Antigens, Cytotoxicity Tests, Immunologic, Amino Acid Sequence, Base Sequence, Point Mutation, Molecular Sequence Data, HLA-B44 Antigen