Critical signal transduction pathways in CLL
Advances in Experimental Medicine and Biology, ISSN: 0065-2598, Vol: 792, Page: 215-239
2013
- 12Citations
- 31Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations12
- Citation Indexes12
- 12
- CrossRef8
- Captures31
- Readers31
- 31
Book Chapter Description
Receptor tyrosine kinases (RTKs) are cell-surface transmembrane receptors that contain regulated kinase activity within their cytoplasmic domain and play a critical role in signal transduction in both normal and malignant cells. Besides B cell receptor (BCR) signaling in chronic lymphocytic leukemia (CLL), multiple RTKs have been reported to be constitutively active in CLL B cells, resulting in enhanced survival and resistance to apoptosis of the leukemic cells induced by chemotherapeutic agents. In addition to increased plasma levels of various types of cytokines/growth factors in CLL, we and others have detected that CLL B cells spontaneously produce multiple cytokines in vitro which may constitute an autocrine loop of RTK activation on the leukemic B cells. Moreover, aberrant expression and activation of non-RTKs, for example, Src/Syk kinases, induce resistance of the leukemic B cells to therapy. Based on current available knowledge, we detailed the impact of aberrant activities of various RTKs/non-RTKs on CLL B cell survival and the potential of using these signaling components as future therapeutic targets in CLL therapy. © 2013 Springer Science+Business Media New York.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84934439133&origin=inward; http://dx.doi.org/10.1007/978-1-4614-8051-8_10; http://www.ncbi.nlm.nih.gov/pubmed/24014299; https://link.springer.com/10.1007/978-1-4614-8051-8_10; https://dx.doi.org/10.1007/978-1-4614-8051-8_10; https://link.springer.com/chapter/10.1007/978-1-4614-8051-8_10; http://link.springer.com/content/pdf/10.1007/978-1-4614-8051-8_10; https://link.springer.com/content/pdf/10.1007%2F978-1-4614-8051-8_10.pdf; http://link.springer.com/chapter/10.1007%2F978-1-4614-8051-8_10; http://link.springer.com/10.1007/978-1-4614-8051-8_10
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