Genes encoded within 8q24 on the amplicon of a large extrachromosomal element are selectively repressed during the terminal differentiation of HL-60 cells.

Human acute myeloblastic leukemia HL-60 cells become resistant to differentiation during long-term cultivation. After 150 passages, double minute chromosomes (dmins) found in early-passaged cells are replaced by large extrachromosomal elements (LEEs). In a DNA library derived from a purified fraction of LEEs, 12.

Functional cytoplasmic domains of the Mac-1 integrin receptor in phorbol ester-treated U937 cells.

The integrin receptor Mac-1 regulates adherence and survival of activated tissue macrophages but the underlying molecular mechanisms are poorly understood. Phorbol ester-induced macrophagic differentiation in U937 cells leads to surface expression of Mac-1 and its activation as well. We have attempted to determine essential amino acids for these activities in the cytoplasmic regions of CD11b and CD18 subunits by deletion mutagenesis.

Theoretical and experimental dissection of competitive PCR for accurate quantification of DNA.

We frequently use competitive PCR in the plateau phase in quantifying DNA species with a small number of cells. However, the basic issues of this method are poorly understood. Here, first we analyze this method theoretically under a generalized condition that competitor and target DNA products accumulate with different amplification efficiencies.

Loss of irreversibility of granulocytic differentiation induced by dimethyl sulfoxide in HL-60 sublines with a homogeneously staining region.

The human HL-60 acute leukemia cell line harbors double minutes (dmins) during early passages. During its continuous culture for a long term, a single marker chromosome with a homogeneously staining region (HSR) replaces the dmins. The both structures harbor amplified c-MYC sequences.

Evolution of large extrachromosomal elements in HL-60 cells during culture and the associated phenotype alterations.

In the HL-60 sublines that were isolated after a long-term continuous culture, abnormally stained or abnormally banded regions on chromosomes replaced extrachromosomal double minutes. The c-MYC gene is amplified in these structures. We followed the c-MYC gene loci during a consecutive passage by using FISH, and have found a large extrachromosomal element (LEE) that preexisted at the earliest passage in a very small fraction of cells.