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Clonal B lymphocytes lack bcr rearrangement in Ph‐positive chronic myelogenous leukaemia
Author(s) -
Ferraris Anna Maria,
Canepa Letizia,
Melani Cecilia,
Miglino Maurizio,
Broccia Giorgio,
Gaetani Gian Franco
Publication year - 1989
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1989.tb00218.x
Subject(s) - biology , clone (java method) , breakpoint cluster region , bone marrow , philadelphia chromosome , myeloid , microbiology and biotechnology , lymphoblast , chronic myelogenous leukemia , gene rearrangement , chromosomal translocation , immunology , cancer research , leukemia , virology , gene , genetics , cell culture
Summary. Philadelphia (Ph) chromosome‐positive chronic myelogenous leukaemia (CML) was studied in a subject heterozygous for the X chromosome‐linked alloenzyme system of glucose‐6‐phosphate dehydrogenase (G6PD). Determination of G6PD mosaicism showed homogeneous expression in granulocytes, erythrocytes and platelets. Cytogenetic studies showed the typical Ph translocation in all metaphases from bone marrow and peripheral blood myeloid cells, bcr rearrangement was detected in bone marrow and in granulocytes. B cells were stimulated with Epstein‐Barr virus (EBV) in order to evaluate involvement of lymphocytes, EBV‐transformed lymphoblastoid cells expressed a single G6PD pheno‐type and therefore probably derived from the leukaemic stem cell. However they had a normal karyotpye and a constitutional bcr restriction pattern. Molecular analysis in this case of CML clarifies the differentiative potential of cells belonging to the leukaemic clone, by demonstrating that clonal Phnegative B cells maintain normal differentiative capacity and have a bcr gene sequence which is not rearranged.