@article {3487,
	title = {NF-κB pathways in hematological malignancies.},
	journal = {Cell Mol Life Sci},
	volume = {71},
	year = {2014},
	month = {2014 Jun},
	pages = {2083-102},
	abstract = {<p>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{\textquoteright}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).</p>},
	keywords = {Antineoplastic Agents, B-Lymphocytes, Carcinogenesis, Dendritic Cells, Gene Expression Regulation, Neoplastic, Hematologic Neoplasms, Humans, Imidazoles, Macrophages, NF-kappa B, Piperazines, Signal Transduction, T-Lymphocytes, TNF-Related Apoptosis-Inducing Ligand, Transcription Factor RelA, Transcription Factor RelB, Tumor Suppressor Protein p53},
	issn = {1420-9071},
	doi = {10.1007/s00018-013-1545-4},
	author = {Gasparini, Chiara and Celeghini, Claudio and Monasta, Lorenzo and Zauli, Giorgio}
}
@article {1930,
	title = {NF-κB as a target for modulating inflammatory responses.},
	journal = {Curr Pharm Des},
	volume = {18},
	year = {2012},
	month = {2012},
	pages = {5735-45},
	abstract = {<p>The inflammatory response is of major importance in host defence, but is involved in all acute and chronic diseases. Multiple inflammatory cells and molecules are involved. Among the latter, the Nuclear Factor -κB (NF-κB) has been found to be most important and present in all cell types. NF-B regulates the expression of a large number of genes involved in inflammation. NF-κB plays a key role in the orchestration of the multifaceted inflammatory response, not only in the first pro-inflammatory phase, but also later in the regulation of the resolution of inflammation, when anti-inflammatory genes are expressed and apoptosis is induced. The review describes NF-κB and its two pathways: the canonical, mediated by the p65 and p50 subunits, and the non-canonical, mediated by the subunits RelB, p52 and p50. The relevance of the kinases and interactions leading to NF-κB activation is considered in different primary cells (i.e. macrophages, dendritic cells, fibroblasts, cells from inflammatory tissues), together with the response induced and the ligand involved. Then we overview the different steps to NF-B activation that can be targeted (IKKs, IκBα or NF-κB subunits themselves) with various technologies available i.e. small molecules peptides or nucleic acids. A rationale is provided for possible targets to consider, in the light that NF-κB signaling pathways regulates both pro-inflammatory and anti-inflammatory responses. The possibility of using NF-κB targeted dendritic cells in immunotherapy is considered.</p>},
	keywords = {Acute Disease, Animals, Chronic Disease, Dendritic Cells, Gene Expression Regulation, Humans, Immunotherapy, Inflammation, NF-kappa B, Signal Transduction},
	issn = {1873-4286},
	author = {Gasparini, Chiara and Feldmann, Marc}
}
