Heterogenous mutation spectrum and deregulated cellular pathways in aberrant plasma cells underline molecular pathology of light-chain amyloidosis

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Authors

CHYRA Zuzana SEVIKOVA Tereza VOJTA Petr PUTEROVÁ Janka KUBÍNOVÁ Lucie GROWKOVÁ Kateřina FILIPOVA Jana ZATOPKOVA Martina GROSICKI Sebastian BARCHNICKA Agnieszka WIKTOR-JEDRZEJCZAK Wieslaw WASZCZUK-GAJDA Anna JUNGOVA Alexandra MIKULASOVA Aneta HAJDÚCH Marian MOKREJŠ Martin POUR Luděk ŠTORK Martin HARVANOVA Lubica MISTRIK Martin MIKALA Gabor ROBAK Pawel CZYZ Anna DEBSKI Jakub USNARSKA-ZUBKIEWICZ Lidia JURCZYSZYN Artur STEJSKAL Lukas MORGAN Gareth KRYUKOV Fedor BUDINSKÁ Eva SIMICEK Michal JELINEK Tomas HRDINKA Matous HAJEK Roman

Year of publication 2021
Type Article in Periodical
Magazine / Source haematologica
MU Faculty or unit

Faculty of Science

Citation
Web https://haematologica.org/article/view/9744
Doi http://dx.doi.org/10.3324/haematol.2019.239756
Keywords AL AMYLOIDOSIS
Description Light-chain (AL) amyloidosis (ALA) is a rare but fatal monoclonal gammopathy (MG) causing organ and tissue damage resulting from the deposition of misfolded immunoglobulin free light chains in the form of amyloid fibrils.1 In some cases, ALA coexists with multiple myeloma (MM) (ALA+MM), which is the second most common blood cancer and is caused by the proliferation of clonal plasma cells (PC).2 Due to insufficient knowledge of ALA and ALA+MM biology, therapeutic options have mirrored treatment regimens of MM, which focus on the elimination of clonal PC.3,4 We investigated the mutation and gene expression profiles in clonal aberrant PC (aPC) in order to better understand ALA and ALA+MM etiology and to clarify the molecular differences between individual MG diagnoses.

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