Unexpected heterogeneity of BCR-ABL fusion mRNA detected by polymerase chain reaction in Philadelphia chromosome-positive acute lymphoblastic leukemia.

Arthur L. Hooberman, John J. Carrino, D Leibowitz, J D Rowley, Michelle M. Le Beau, Z Arlin, Carol A. Westbrook

Proceedings of the National Academy of Sciences · 1989 · 66 citations · 34 references

DOIFull text

Open access

Concepts

TL;DR

The Philadelphia chromosome fuses BCR and ABL genes, generating a chimeric BCR‑ABL mRNA, and in lymphoblastic leukemias two molecular subtypes exist—one with a BCR breakpoint producing an 8.5‑kb fusion mRNA common to CML, and another without the breakpoint producing a 7.0‑kb fusion mRNA unique to ALL. The study aimed to determine the molecular subtype of the Philadelphia chromosome in 11 Ph1‑positive ALL cases, including two with prior CML, by using a sensitive PCR‑based mRNA analysis. The authors employed a sensitive PCR assay to analyze BCR‑ABL mRNA species. The PCR analysis revealed unexpected heterogeneity: one of six bcr‑rearranged and one of five bcr‑unrearranged cases lacked known fusion mRNAs, while another bcr‑rearranged case expressed both, suggesting additional fusion species may drive disease progression, yet the method’s high false‑negative rate limits its use as a sole detection tool.

Abstract

The Philadelphia (Ph1) chromosome results in a fusion of portions of the BCR gene from chromosome 22 and the ABL gene from chromosome 9, producing a chimeric BCR-ABL mRNA and protein. In lymphoblastic leukemias, there are two molecular subtypes of the Ph1 chromosome, one with a rearrangement of the breakpoint cluster region (bcr) of the BCR gene, producing the same 8.5-kilobase BCR-ABL fusion mRNA seen in chronic myelogenous leukemia (CML), and the other, without a bcr rearrangement, producing a 7.0-kilobase BCR-ABL fusion mRNA that is seen only in acute lymphoblastic leukemia (ALL). We studied the molecular subtype of the Ph1 chromosome in 11 cases of Ph1-positive ALL, including 2 with a previous diagnosis of CML, using a sensitive method to analyze the mRNA species based on the polymerase chain reaction (PCR). We observed unexpected heterogeneity in BCR-ABL mRNA in this population; in particular, 1 of 6 bcr-rearranged cases and 1 of 5 bcr-unrearranged cases contained none of the known fusion mRNA species, while 1 of the bcr-rearranged cases contained both. This latter case is particularly interesting because it suggests that the acquisition of an additional BCR-ABL fusion species may be a mechanism of disease progression. We conclude that the PCR gives additional information about the Ph1 chromosome gene products that cannot be obtained by genomic analysis, but that it cannot be used as the sole means of detection of this chromosomal abnormality in ALL because of the high incidence of false negative results.

References

34