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Lineage switch in Philadelphia chromosome‐ positive acute lymphoblastic leukemia
Author(s) -
Reardon David A.,
Castle Valerie P.,
Hanson Curtis A.,
Rofh Mark S.
Publication year - 1994
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19940301)73:5<1526::aid-cncr2820730534>3.0.co;2-e
Subject(s) - philadelphia chromosome , medicine , lineage (genetic) , acute leukemia , leukemia , acute lymphocytic leukemia , abl , cancer , fusion transcript , breakpoint cluster region , cancer research , lymphoblastic leukemia , chromosomal translocation , oncology , immunology , biology , genetics , gene , receptor , tyrosine kinase
Background . An 8‐year‐old boy, initially diagnosed with Philadelphia chromosome‐positive (Ph+) acute lymphoblastic leukemia (ALL) (French‐American‐British [FABI‐Ll), relapsed with Ph+ acute myelogenous leukemia [AML) (FAB‐M2) 21 months after successful ALL treatment with standard therapy. Methods . The initial ALL presentation and subsequent AML relapse were analyzed by conventional morphologic, cytochemical, immunophenotypic, and cytogenetic studies. Results. Molecular analysis based on the polymerase chain reaction identified the presence of a bcr‐I‐abl fusion transcript at initial ALL presentation, the completion of ALL therapy, and AML relapse. Conclusions . The cytogenetic and molecular results support a common clonal origin for this process. This is case of lineage switch in a Ph+ acute leukemia. This case thus illustrates a manifestation of heterogeneous lineage differentiation among Ph+ acute leukemias. Cancer 1994; 73:1526‐32.