𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Genomic segmental duplications on the basis of the t(9;22) rearrangement in chronic myeloid leukemia

✍ Scribed by Albano, F; Anelli, L; Zagaria, A; Coccaro, N; D'Addabbo, P; Liso, V; Rocchi, M; Specchia, G

Book ID
109972263
Publisher
Nature Publishing Group
Year
2010
Tongue
English
Weight
704 KB
Volume
29
Category
Article
ISSN
0950-9232

No coin nor oath required. For personal study only.

πŸ“œ SIMILAR VOLUMES

Genomic deletions on other chromosomes i
Genomic deletions on other chromosomes involved in variant t(9;22) chronic myeloid leukemia cases
✍ Francesco Albano; Giorgina Specchia; Luisa Anelli; Antonella Zagaria; Clelia Tiz πŸ“‚ Article πŸ“… 2003 πŸ› John Wiley and Sons 🌐 English βš– 564 KB

## Abstract The Philadelphia (Ph) chromosome is the cytogenetic hallmark of chronic myeloid leukemia (CML) and is observed in more than 90% of CML cases. At diagnosis, in 5–10% of CML patients the Ph chromosome is derived from variant translocations other than the standard t(9;22). Deletions adjace

Breakpoints of variant 9;22 translocatio
Breakpoints of variant 9;22 translocations in chronic myeloid leukemia locate preferentially in the CG-richest regions of the genome
✍ Andrew M. Fisher; Paul Strike; Claire Scott; Anthony V. Moorman πŸ“‚ Article πŸ“… 2005 πŸ› John Wiley and Sons 🌐 English βš– 211 KB

## Abstract From 5% to 10% of 9;22 translocations in chronic myeloid leukemia (CML) are reported to occur in variant form, that is, with the involvement of other regions of the genome in 3‐way or more rearrangements. The literature indicates that the alternative breakpoints are not distributed rand

Heterogenic molecular basis for loss of
Heterogenic molecular basis for loss of ABL1-BCR transcription: Deletions in der(9)t(9;22) and variants of standard t(9;22) in BCR-ABL1-positive chronic myeloid leukemia
✍ Ivan F. Loncarevic; Jennifer RΓΆmer; Heike Starke; Anita Heller; Cordula Bleck; M πŸ“‚ Article πŸ“… 2002 πŸ› John Wiley and Sons 🌐 English βš– 881 KB

The objective of this study was to characterize the ABL1-BCR fusion gene in 76 BCR-ABL1-positive chronic myeloid leukemia (CML) patients regarding expression as well as genomic status, to assess the frequency of ABL1-BCR gene deletion in these patients, which has been reported to be an adverse progn