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@ARTICLE{Dampmann:301923,
author = {M. Dampmann and B. von Tresckow$^*$ and H. C. Reinhardt$^*$
and R. Küppers$^*$ and J. von Tresckow},
title = {{I}nsights into the pathogenesis and biology of chronic
lymphocytic leukemia through analysis of its {B}-cell
receptor.},
journal = {Leukemia and lymphoma},
volume = {nn},
issn = {1026-8022},
address = {London [u.a.]},
publisher = {Taylor $\&$ Francis Group},
reportid = {DKFZ-2025-01193},
pages = {nn},
year = {2025},
note = {epub},
abstract = {The B-cell antigen receptor (BCR) plays an essential role
in the pathogenesis of B-cell malignancies such as chronic
lymphocytic leukemia (CLL). CLL exhibits two main subtypes
based on immunoglobulin heavy chain variable (IGHV) region
mutational status: About half of the cases carry somatically
mutated immunoglobulin V genes and hence derive from
germinal center experienced memory B cells, whereas
unmutated CLL derives from (likely CD5-positive)
antigen-stimulated, but germinal center independent mature B
cells. CLL precursor cells can be found years before
diagnosis. The IGHV mutational status of CLL clones serves
as one of the strongest prognostic markers. CLL often
carries highly similar, i.e. stereotyped BCRs pointing to
recognition of a restricted set of antigens. Indeed, the
BCRs of many CLL clones are autoreactive for particular
autoantigens, including the BCR itself. Pathogenic antigens
are further drivers in CLL development. Thus, BCR-mediated
signaling and antigen recognition play a major role in CLL
pathogenesis.},
subtyp = {Review Article},
keywords = {Autoreactivity (Other) / B-cell receptor (Other) / chronic
lymphocytic leukemia (Other) / somatic hypermutation (Other)
/ stereotypy (Other)},
cin = {ED01},
ddc = {610},
cid = {I:(DE-He78)ED01-20160331},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:40493712},
doi = {10.1080/10428194.2025.2513005},
url = {https://inrepo02.dkfz.de/record/301923},
}