| Autor: |
Amare Kadam PS; Cancer Cytogenetics Laboratory, Tata Memorial Hospital, Parel, Mumbai 400012, India. pratibha.amare@gmail.com, Raje GC, Pais AP, Banavali S |
| Jazyk: |
angličtina |
| Zdroj: |
Cancer genetics and cytogenetics [Cancer Genet Cytogenet] 2008 Apr 01; Vol. 182 (1), pp. 27-32. |
| DOI: |
10.1016/j.cancergencyto.2007.12.012 |
| Abstrakt: |
Out of 76 pediatric cases of B-cell precursor acute lymphoblastic leukemia (BCP-ALL) positive for ETV6/RUNX1 (previously TEL/AML1) resulting from t(12;21), 7 cases revealed coexistence of ETV6/RUNX1 and MLL aberrations. One case of der(21) duplication with ETV6/RUNX1 exhibited a novel MLL translocation variant t(6;11)(p21.1p23;q13q25), with translocation of 3' telomeric MLL and deletion of 5' centromeric MLL. Another case of der(21) duplication with ETV6/RUNX1 showed MLL rearrangement upon Southern blotting. The remaining five ETV6/RUNX1-positive cases had MLL allelic deletion. ETV6/RUNX1 and MLL aberration clone size in these cases was suggestive of ETV6/RUNX1 as an early primary event, originating in the embryonic or infant stage and developing into leukemia by later acquisition of MLL aberration, ETV6 loss, and ETV6/RUNX1 duplication as secondary events. To date, the prognosis has been favorable, which seems to be compatible with ETV6/RUNX1-positive ALL. We conclude that the cases with coexisting ETV6/RUNX1 and MLL aberrations probably exist as a small, hidden group of ETV6/RUNX1-positive BCP-ALL, which invites further investigation, in large series from different populations, to confirm the findings and establish the biological mechanisms and prognostic significance. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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