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Cloning and characterization of the T(15;17) translocation breakpoint region in acute promyelocytic leukemia

✍ Scribed by Dr. Richard S. Lemons; David Eilender; Richard A. Waldmann; Matt Rebentisch; Ann-Kristin Frej; David H. Ledbetter; Cheryl Willman; Thomas McConnell; Peter O'Connell

Publisher: John Wiley and Sons
Year: 1990
Tongue: English
Weight: 881 KB
Volume: 2
Category: Article
ISSN: 1045-2257
DOI: 10.1002/gcc.2870020202

No coin nor oath required. For personal study only.

✦ Synopsis

A reciprocal chromosomal translocation, t( I 5; I7)(q22;q I I .2-I2), is characteristic of acute promyelocytic leukemia (APL) of French-American-British (FAB) subtype M3, and is not associated with any other human malignancy. The non-random pattern of the APL translocations suggests that specific genes on chromosomes I 5 and I 7 are somehow altered or deregulated as a consequence of the rearrangement. Translocation breakpoints in APL patients provide physical landmarks that suggest an approach to isolating the APL gene+). Genetic and physical maps constructed for the APL breakpoint region on chromosome I 7 have indicated that two fully-linked DNA markers, defining loci for THRA I and D I7S80, map to opposite sides of an APL breakpoint yet reside on a common 350-kb Ci a1 fragment. Cosmid-walking experiments to clone this APL breakpoint have revealed a 38-kilobase deletion on chromosome 17. Studies in additional APL patients have shown that the breakpoint region on chromosome I 7 spans at least 80 kilobases.

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