Selective inhibition of leukemia cell proliferation by BCR-ABL antisense oligodeoxynucleotides.

By C. Szczylik, T. Skorski, N. Nicolaides, L. Manzella, L. Malaguarnera, D. Venturelli, A. Gewirtz, B. Calabretta. 1991

To determine the role of the BCR-ABL gene in the proliferation of blast cells of patients with chronic myelogenous leukemia, leukemia blast cells were exposed to synthetic 18-mer oligodeoxynucleotides complementary to two identified BCR-ABL junctions. Leukemia colony formation was suppressed, whereas granulocyte-macrophage colony formation from normal marrow progenitors was unaffected. When equal proportions of normal marrow progenitors and blast cells were mixed, exposed to the oligodeoxynucleotides, and assayed for residual colony formation, the majority of residual cells were normal. These findings demonstrate the requirement for a functional BCR-ABL gene in maintaining the leukemic phenotype and the feasibility of gene-targeted selective killing of neoplastic cells.

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Citations in the corpus

• EgoNet: identification of human disease ego-network modules (2014, background): “The ABL1 proto-oncogene encodes a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell differentiation, cell division, and so on [36].”