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Detection of bcl‐2 rearrangement in HIV‐related follicular lymphoid hyperplasia
Author(s) -
Molina Thierry J.,
Devez Francis,
Bigorgne Claude,
Le Tourneau Agnès,
Joulin Virginie,
Audouin Josée,
Diebold Jacques
Publication year - 1996
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 - 10.1046/j.1365-2141.1996.d01-1837.x
Subject(s) - gene rearrangement , immunoglobulin heavy chain , breakpoint , lymph , lymphoid hyperplasia , biology , southern blot , pseudolymphoma , germinal center , b cell , lymphoma , antibody , polymerase chain reaction , lymphatic system , follicular phase , follicular hyperplasia , cancer research , pathology , microbiology and biotechnology , gene , immunology , medicine , genetics , chromosome
Rearrangement of the bcl‐2 gene at the MBR (major breakpoint region) locus with the immunoglobulin heavy‐chain joining region has been reported in a high proportion of follicular lymphomas. This rearrangement has also been reported in very few normal B cells of the blood, tonsils, follicular lymphoid hyperplasia (FLH) of the lymph nodes. HIV infection is often associated at the onset of the disease with FLH, but the presence of rearranged bcl‐2 B cells in these lymph nodes has not been described. In using a standard PCR assay with Southern blot or a semi‐nested PCR on 48 cases of FLH, we demonstrated that there were a few bcl‐2 rearranged B cells in HIV FLH, at almost the same level as that in non‐HIV‐related FLH. The usual absence of bcl‐2 rearrangement in the HIV‐associated B‐cell lymphomas suggests that the bcl‐2 oncogene in the rearranged B cells of FLH is not cooperating with other oncogenes during HIV lymphomagenesis.