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dc.contributor.authorOkkenhaug, Klaus
dc.contributor.authorBurger, Jan A
dc.date.accessioned2018-06-28T08:37:40Z
dc.date.available2018-06-28T08:37:40Z
dc.date.issued2016
dc.identifier.issn0070-217X
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/277592
dc.description.abstractB cells provide immunity to extracellular pathogens by secreting a diverse repertoire of antibodies with high affinity and specificity for exposed antigens. The B cell receptor (BCR) is a transmembrane antibody, which facilitates the clonal selection of B cells producing secreted antibodies of the same specificity. The diverse antibody repertoire is generated by V(D)J recombination of heavy and light chain genes, whereas affinity maturation is mediated by activation-induced cytidine deaminase (AID)-mediated mutagenesis. These processes, which are essential for the generation of adaptive humoral immunity, also render B cells susceptible to chromosomal rearrangements and point mutations that in some cases lead to cancer. In this chapter, we will review the central role of PI3K s in mediating signals from the B cell receptor that not only facilitate the development of functional B cell repertoire, but also support the growth and survival of neoplastic B cells, focusing on chronic lymphocytic leukemia (CLL) B cells. Perhaps because of the central role played by PI3K in BCR signaling, B cell leukemia and lymphomas are the first diseases for which a PI3K inhibitor has been approved for clinical use.
dc.format.mediumPrint
dc.languageeng
dc.publisherSpringer International Publishing
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectB-Lymphocytes
dc.subjectAnimals
dc.subjectHumans
dc.subjectReceptors, Antigen, B-Cell
dc.subjectSignal Transduction
dc.subjectCell Survival
dc.subjectLeukemia, Lymphocytic, Chronic, B-Cell
dc.subjectPhosphatidylinositol 3-Kinases
dc.titlePI3K Signaling in Normal B Cells and Chronic Lymphocytic Leukemia (CLL).
dc.typeArticle
prism.endingPage142
prism.publicationDate2016
prism.publicationNameCurr Top Microbiol Immunol
prism.startingPage123
prism.volume393
dc.identifier.doi10.17863/CAM.24910
rioxxterms.versionofrecord10.1007/82_2015_484
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2016-01
dc.contributor.orcidOkkenhaug, Klaus [0000-0002-9432-4051]
dc.identifier.eissn2196-9965
rioxxterms.typeJournal Article/Review
cam.issuedOnline2015-09-09
cam.orpheus.successThu Jan 30 13:00:15 GMT 2020 - The item has an open VoR version.
rioxxterms.freetoread.startdate2100-01-01


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International