Detection of XXXX -associated @entity50070 translocation early during chemotherapy with DNA topoisomerase II inhibitors.

@entity1 @entity5 @entity11626 @entity3052 @entity1778 @entity521 @entity50070
@entity1778 with @entity11626 gene translocations are a complication of primary @entity5 treatment with DNA topoisomerase II inhibitors. How early translocations appear during primary @entity5 treatment has not been investigated. We tracked the leukemic clone with an @entity11626 gene translocation during @entity521 therapy in a @entity1 who developed @entity3052 . The karyotype of the leukemic clone showed del(11)(q23). We used panhandle PCR-based methods to isolate the breakpoint junction involving @entity11626 and an unknown partner gene. Marrow DNA from @entity521 diagnosis and DNA and RNA from serial preleukemic marrows were examined for the translocation. The karyotypic del(11)(q23) was a cryptic t(11;17). @entity50070 , a growth arrest-specific gene at chromosome band 17p13, was the partner gene of @entity11626 . Two different @entity50070 fusion transcripts were expressed. The translocation was already detectable by 1.5 months after the start of @entity521 treatment. The translocation was not detectable in the marrow at @entity521 diagnosis or in peripheral blood lymphocyte DNAs of six normal subjects. @entity50070 is a new partner gene of @entity11626 in treatment-related @entity3052 . @entity11626 gene translocations can be present early during anticancer treatment at low cumulative doses of DNA topoisomerase II inhibitors. Although @entity11626 has many partner genes and most have not been characterized, panhandle PCR strategies afford new means for detecting @entity11626 gene translocations early during therapy when the partner gene is unknown.
