bcr-abl oncogene renders myeloid cell line factor independent: potential autocrine mechanism in chronic myeloid leukemia.
In chronic myeloid leukemia (CML), a chromosome translocation has fused the bcr gene to the c-abl oncogene, such that a chimeric bcr-abl polypeptide can be made. To explore the biological properties of bcr-abl and compare them with those of the Abelson virus (AMuLV) transforming gene (gag-v-abl), we have used either a synthetic bcr-v-abl gene that mimics the translocation product or, in some experiments, a bcr-c-abl cDNA. A new retroviral vector was used to introduce the genes into the factor-dependent myeloid line FDC-P1. Both bcr-abl and v-abl efficiently rendered the myeloid cells factor independent and tumorigenic. Their fully autonomous growth may be due to the myeloid growth factor interleukin-3 (IL-3) made in small amounts by the infected cells. Hence autocrine factor production may feature in CML development and Abelson virus transformation.
Hariharan
I K
IK
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.
Adams
J M
JM
Cory
S
S
D000818:Animals; D002455:Cell Division; D002460:Cell Line; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D016044:Fusion Proteins, bcr-abl; D005786:Gene Expression Regulation; D005818:Genetic Engineering; D006133:Growth Substances / Q000096:biosynthesis*; D007377:Interleukin-3 / Q000096:biosynthesis; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000473:pathology* / Q000503:physiopathology; D051379:Mice; D009363:Neoplasm Proteins / Q000502:physiology*; D009374:Neoplasms, Experimental / Q000235:genetics* / Q000473:pathology; D014162:Transfection
D006133:Growth Substances; D007377:Interleukin-3; D009363:Neoplasm Proteins; D016044:Fusion Proteins, bcr-abl