New monoclonal antibodies against B-cell antigens: Possible new strategies for diagnosis of primary cutaneous B-cell lymphomas

Fanoni, Daniele; Tavecchio, Simona; Recalcati, Sebastiano; Balice, Ylenia; Venegoni, Luigia; Fiorani, R.; Crosti, C.; Berti, Emilio

doi:10.1016/j.imlet.2010.09.022

Cited by 98 publications

(56 citation statements)

References 6 publications

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“…FL cells are known to produce the ligand for CXCR5, CXCL13, and it is believed they express CXCR5 to respond to CXCL13 and form the architecture of lymphoid follicles [138]. Monoclonal antibodies targeting CXCR5 were found to be reactive against primary cutaneous FL but not closely related lymphomas [139] and have been shown to inhibit tumor growth in mouse models [140]. A trifunctional bispecific antibody targeting CXCR5::CD3 suppressed tumor growth and increased survival in a xenograft model of B cell lymphoma by recruiting T cells to CXCR5-expressing B cells and co-stimulating the activation of CD4+ and CD8+ T cells to lyse B cells [140].…”

Section: Follicular Lymphomamentioning

confidence: 99%

The role of G protein-coupled receptors in lymphoid malignancies

Nugent

Proia

2017

Cellular Signalling

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B cell lymphoma consists of multiple individual diseases arising throughout the lifespan of B cell development. From pro-B cells in the bone marrow, through circulating mature memory B cells, each stage of B cell development is prone to oncogenic mutation and transformation, which can lead to a corresponding lymphoma. Therapies designed against individual types of lymphoma often target features that differ between malignant cells and the corresponding normal cells from which they arise. These genetic changes between tumor and normal cells can include oncogene activation, tumor suppressor gene repression and modified cell surface receptor expression. G protein-coupled receptors (GPCRs) are an important class of cell surface receptors that represent an ideal target for lymphoma therapeutics. GPCRs bind a wide range of ligands to relay extracellular signals through G protein-mediated signaling cascades. Each lymphoma subgroup expresses a unique pattern of GPCRs and efforts are underway to fully characterize these patterns at the genetic level. Aberrations such as overexpression, deletion and mutation of GPCRs have been characterized as having causative roles in lymphoma and such studies describing GPCRs in B cell lymphomas are summarized here.

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Section: Follicular Lymphomamentioning

confidence: 99%

The role of G protein-coupled receptors in lymphoid malignancies

Nugent

Proia

2017

Cellular Signalling

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“…Extensive preclinical work has demonstrated the blockade of PD-1 enhances immune function. In contrast to CTLA-4, PD-1 is not only expressed on T cells, but also B cells ad NK cells[162, 163]. PD-1 expression is induced on T cells when they become activated[164].…”

Section: Checkpoint Blockadementioning

confidence: 99%

Mechanisms of action of therapeutic antibodies for cancer

Redman

Hill

Aldeghaither

et al. 2015

Molecular Immunology

144

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The therapeutic utility of antibodies and their derivatives is achieved by various means. The FDA has approved several targeted antibodies that disrupt signaling of various growth factor receptors for the treatment of a number of cancers. Rituximab, and other anti-CD20 monoclonal antibodies are active in B cell malignancies. As more experience has been gained with anti-CD20 monoclonal antibodies, the multifactorial nature of their anti-tumor mechanisms has emerged. Other targeted antibodies function to dampen inhibitory checkpoints. These checkpoint inhibitors have recently achieved dramatic results in several cancers, including melanoma. These and related antibodies continue to be investigated in the clinical and pre-clinical settings. Novel antibody structures that target two or more antigens have also made their way into clinical use. Tumor targeted antibodies can also be conjugated to chemo- or radiotherapeutic agents, or catalytic toxins, as a means to deliver toxic payloads to cancer cells. Here we provide a review of these mechanisms and a discussion of their relevance to current and future clinical applications.

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“…Similar to CTLA4, PD1 is highly expressed on T reg cells, where it may enhance their proliferation in the presence of a ligand [36]. PD1 is more broadly expressed than CTLA4, as it is induced on other activated non T cell subsets, including B cells and the Natural Killer (NK) cells [37,38]. Therefore, although PD1 blockade is typically viewed as enhancing the activity of effector T cells in the tumor microenvironment, it probably enhances NK cell activity and may also enhance the antibody production either indirectly or through directeffects on PD1+ B cells [39].…”

Section: Pd1 Immune Checkpointmentioning

confidence: 99%

Developing Cancer Immunotherapies by the manipulation of Immune Checkpoints

Yogesh¹

2012

iosrphr

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New monoclonal antibodies against B-cell antigens: Possible new strategies for diagnosis of primary cutaneous B-cell lymphomas

Cited by 98 publications

References 6 publications

The role of G protein-coupled receptors in lymphoid malignancies

The role of G protein-coupled receptors in lymphoid malignancies

Mechanisms of action of therapeutic antibodies for cancer

Developing Cancer Immunotherapies by the manipulation of Immune Checkpoints

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