Abstract

Romitt i et al. (1986) repor ted the cytogenetic characterization of four monocytic cell lines established f rom bone marrow samples of patients with hematopoiet ic diseases other than leukemia. The cell line that they referred to as case 2 FR. B/S was f rom a patient with cyclic neutropenia who later developed an acute myelomonocyt ic leukemia. The line was shown to have acquired an interstitial deletion of the long arm of chromosome 11 after 59 passages in vitro, and at this passage it was able to induce tumors in nude mice. The breakpoints were localized in bands 11q21 and 11@4. This region of chromosome 11 is frequently involved in structural rearrangements in cases of acute myeloid leukemia (M4-M5 types), acute lymphocytic leukemia, and B-cell diffuse lymphoma. Yunis et al. (1989) repor ted a patient with an acute myelomonocyt ic leukemia with evidence of amplification of eleven genes mapped at 11q23---~qter and discussed the gene order and the relevance of this region in hematological malignancies. Since the cell line seemed to have lost the band 11q23, we were interested in investigating the possible presence, loss, or transposition of the oncogene ets-1, mapped at band 11q23.3 (Rovigatti et al. 1986), for a possible relation to the tumorigenicity. A Southern blot analysis with an h-c-ets-l-specific probe (5.4-kb EcoR1 genomic f ragment kindly provided by Dr. D. Stehelin) showed a normal gene dosage and absence of any detectable rear rangement (Carrozza, unpublished), and so we per formed in situ hybridization with the same probe on chromosome preparat ions at the 134th passage, when the deletion was still present in all cells. The analysis of the distribution of the autoradiographic grains showed a positive signal present both on the normal and on the deleted chromosome 11 (Fig. 1 a). This result led us to reconsider the breakpoints of the deletion, and we reanalyzed the cell line at the 142nd passage with a high-resolution banding technique (Dutrillaux and Peguignot 1981). The banding pat terns revealed an interstitial deletion with loss only of the band 11q14 and breakpoints at l lq14.1 and 11q14.3 (Fig. lb ) .

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