Aberration of oncogenes and tumor suppressor genes in hematopocetic tumors in animals

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To understand the molecular mechanism of tumorigenesis in hematopoetic malignancies, aberration of oncogenes and tumor suppressor genes were investigated in naturally ocurring lymphomas and leukemias in animals. On the nuclear oncogenes, aberrations of myc gene were observed in 4 feline cases and 1 canine case. In 2 of the 4 feline cases, transduction of c-myc gene by feline leukemia virus (FeLV) was found. Investigation of the integration region revealed a 8-kb common integration region in 8 feline cases with lymphomas. Since this common integration region (fit-1) was located on the feline B2 chromosome and different from known oncogenes and common integration regions, the fit-1 region was considered to include an new oncogene. On the other hand, we cloned a feline p53 tumor suppressor gene cDNA containing its whole coding sequence. This cDNA clone was shown to code 386 amino acids and showed 82.1% and 74.9% amino acid sequence identities with human and mouse p53 genes, respectively. PCR-SSCP (single strand conformation polymorphism) analysis indicated abnormal bands in 2 feline cases of lymphoma. Nucleotide sequence determination revealed point mutations substituting amino acids in the conserved regions of III and IV.Furthermore, a study on the rearrangement of T-cell receptor and immunoglobulin genes in canine and feline lymphoid tumors disclosed the clonality, differentiation stage and their relation with aberrations of oncogenes and tumor suppressor genes. It is conceivable that the present studies have provided many useful findings for understanding the molecular tumorigenesis mechanism of hematopoietic tumors.