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PubMed2002

Not so NICE for CML.

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Antineoplastic Agents↗
PubMed2003

Molecular monitoring of responses to DLI and DLI + IFN treatment of post-SCT relapses in patients with CML.

We monitored DLI treatment of 13 post-SCT relapses using quantitative competitive (QC) RT-PCR for BCR-ABL (sensitivity 10(-5)) and compared responses to DLI alone and DLI in combination with interferon-alpha (IFN). Ten relapses (one blast crisis, five cytogenetic and four molecular) were treated with DLI+IFN, three relapses (one cytogenetic, two molecular) were treated with DLI alone. Except the patient treated in blast crisis, who died, all the patients treated with DLI+IFN achieved complete molecular remission, with the median time interval of 3.9 months (range 0.25-10.5 months). None of the three patients treated with DLI alone have achieved complete molecular remission up to now, i.e. 32, 45, and 50 months after DLI. However, in all of them some decrease of BCR-ABL transcript level was detected. Although the retrospective analyses did not confirm that IFN improved the response to DLI, our results based on sensitive molecular monitoring suggest that DLI effect, at least in some patients, is supported by IFN administration.

Adolescent↗
PubMed2000

Evaluation at single cell level of residual Philadelphia negative hemopoietic stem cells in chronic phase CML patients.

In chronic myeloid leukemia, accurate determination of Ph(-) Hemopoietic stem cells (HSC) in peripheral blood (PB), bone marrow (BM) and leukapheresis products is important for the selection of patients for whom mobilization, collection, and autografting of Ph(-) HSC are envisaged. To this effect, the BCR/ABL fusion was assessed at the single cell level in 25 sets of PB and BM samples using dual-color I-FISH in immunophenotyped CD34(+) cells and RT-PCR of individual CFU-GM colonies. In 15 cases found to be 100% Ph(+), the respective BCR/ABL gene was absent in 30% of CD34(+) cells, while the respective transcripts could not be identified in 17% of CFU-GM. The mean percentage of BCR/ABL(-) CD34(+) cells and CFU-GM cells was higher (38% and 29%, respectively) in untreated patients than in treated patients (24% and 7%, respectively). In eight cases with cytogenetic response (CgR), the percentage of Ph(-) metaphases correlated with the level of BCR/ABL(-) colonies in BM and PB and with the proportion of BCR/ABL(-) CD34(+) cells in the BM. Immunophenotyping and FISH was fast, easy, always informative, and quantitative for the BCR/ABL(-) CD34(+) cells. Our results show that (a) at early diagnosis a high frequency of BCR/ABL(-) HSC circulate in the PB and that Ph(-) hematopoiesis is not completely suppressed; (b) although normal clonogenic cells decline rapidly within a few months after diagnosis, appreciable numbers of normal CD34(+) cells survive in chronic phase, especially in patients with CgR.

Antigens, CD34↗
PubMed1997

Ph-positive CML in blastic phase with monosomy 7 in a Down syndrome patient. Monitoring by interphase cytogenetics and demonstration of maternal allelic loss.

We report a case of Ph-positive chronic myelocytic leukemia in blastic phase in an 11-year-old boy with Down syndrome. Monosomy 7 was the only additional chromosomal anomaly in the blastic clone. Fluorescence in situ hybridization analysis on interphase nuclei with a centromeric probe specific to chromosome 7 proved to be efficient in disease monitoring, and showed, together with the results of chromosome analysis on metaphases, that B-lymphocytes at the origin of an EBV-established line were not part of the leukemic clone. The study of DNA polymorphisms showed that the origin of the constitutional trisomy 21 was a maternal anaphase I nondisjunction, that the chromosome 7 lost in the blastic marrow clone was the maternal one, and led us to postulate that the mother's chromosomes are prone to impairment of normal disjunction. The study of allelic losses of chromosome 7 loci proved to be a further possibility for disease monitoring.

Adult↗