Open AccessLymphoplasmacytic lymphoma associated with diffuse large B-cell lymphoma: Progression or divergent evolution?
Author(s) -
Macarena BoizaSánchez,
Rebeca Manso,
Olga Balagué,
Cristina Chamizo,
Elham Askari,
Rocío Salgado,
Carlos Blas,
Elena Aguirregoicoa-García,
Javier Menárguez,
Carlos Santonja,
Magdalena Adrados,
Miguel Ángel Limeres-González,
Miguel Á. Piris,
Socorro María RodríguezPinilla
Publication year - 2020
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0241634
Subject(s) - diffuse large b cell lymphoma , bcl6 , lymphoplasmacytic lymphoma , lymphoma , cancer research , mutation , biology , pathology , mutation testing , bone marrow , b cell , medicine , gene , waldenstrom macroglobulinemia , genetics , antibody , germinal center
Aim Lymphoplasmacytic lymphoma (LPL) is an indolent mature B-cell-neoplasm with involvement of the bone marrow. At least 90% of LPLs carry MYD88-L265P mutation and some of them (~10%) transform into diffuse large B-cell-lymphoma (DLBCL). Material and methods Over the past 15 years we have collected 7 cases where the both LPL and DLBCL were diagnosed in the same patient. Clinical records, analytical data and histopathological specimens were reviewed. FISH studies on paraffin-embedded tissue for MYC , BCL2 and BCL6 genes were performed, as well as MYD88-L265P mutation and IGH rearrangement analysis by PCR. A mutational study was done by massive next generation sequencing (NGS). Results There were 4 women and 3 men between 36–91 years of age. Diagnoses were made simultaneously in 4 patients. In two cases the LPL appeared before the DLBCL and in the remaining case the high-grade component was discovered 5 years before the LPL. In 6 cases both samples shared the MYD88-L265P mutation. IGH rearrangement analysis showed overlapping features in two of 6 cases tested. Mutational study was evaluable in three cases for both samples showing shared and divergent mutations. Conclusions These data suggest different mechanisms of DLBCL development in LPL patients.