Fig. 1.
Fig. 1. Overview of the strategy used to target the BCR-ABL mRNA by RNase P. (A) The translocation t(9:22)(q34;11) in Ph1+-leukemia. / The BCR-ABL oncogene is created by the translocation of sequences from the ABL gene on chromosome 9 to the BCRgene on chromosome 22. The same cytogenetic aberration can generate alternative chimeric mRNA and proteins, depending on the precise breakpoint within the BCR gene.BCR-ABLp190 and p210 oncogenes contain identical ABL-derived sequences but differ in the number of BCR nucleotides. (B) Nucleotide sequences of the fusion point between BCR and ABL sequences inBCR-ABLp190 andBCR-ABLp210 cDNA. The chimeric molecules generated by the recurrent chromosomal rearrangements represent ideal therapeutic targets because they are unique to the disease state. (C) Inhibition of the tumor-specific product by the specific cleavage of the tumor-specific BCR-ABLp190 andBCR-ABLp210 products by RNase P.

Overview of the strategy used to target the BCR-ABL mRNA by RNase P. (A) The translocation t(9:22)(q34;11) in Ph1+-leukemia.

The BCR-ABL oncogene is created by the translocation of sequences from the ABL gene on chromosome 9 to the BCRgene on chromosome 22. The same cytogenetic aberration can generate alternative chimeric mRNA and proteins, depending on the precise breakpoint within the BCR gene.BCR-ABLp190 and p210 oncogenes contain identical ABL-derived sequences but differ in the number of BCR nucleotides. (B) Nucleotide sequences of the fusion point between BCR and ABL sequences inBCR-ABLp190 andBCR-ABLp210 cDNA. The chimeric molecules generated by the recurrent chromosomal rearrangements represent ideal therapeutic targets because they are unique to the disease state. (C) Inhibition of the tumor-specific product by the specific cleavage of the tumor-specific BCR-ABLp190 andBCR-ABLp210 products by RNase P.

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