The nuclear factor κB or NF-κB transcription
factor family plays a key role in several cellular functions,
i.e. inflammation, apoptosis, cell survival, proliferation,
angiogenesis, and innate and acquired immunity. The constitutive
activation of NF-κB is typical of most malignancies
and plays a major role in tumorigenesis. In this review,
we describe NF-κB and its two pathways: the canonical
pathway (RelA/p50) and the non-canonical pathway (RelB/
p50 or RelB/p52). We then consider the role of the NF-κB
subunits in the development and functional activity of B
cells, T cells, macrophages and dendritic cells, which are
the targets of hematological malignancies. The relevance of
the two pathways is described in normal B and T cells and
in hematological malignancies, acute and chronic leukemias
(ALL, AML, CLL, CML), B lymphomas (DLBCLs,
Hodgkin’s lymphoma), T lymphomas (ATLL, ALCL) and
multiple myeloma. We describe the interaction of NF-κB
with the apoptotic pathways induced by TRAIL and the
transcription factor p53. Finally, we discuss therapeutic
anti-tumoral approaches as mono-therapies or combination
therapies aimed to block NF-κB activity and to induce
apoptosis (PARAs and Nutlin-3).
