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Piddock, Rachel E., Bowles, Kristian M. 
ORCID: https://orcid.org/0000-0003-1334-4526 and Rushworth, Stuart A.
(2017)
The role of PI3K isoforms in regulating bone marrow microenvironment signaling focusing on acute myeloid leukemia and multiple myeloma.
Cancers, 9 (4).
ISSN 2072-6694
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Abstract
Despite the development of novel treatments in the past 15 years, many blood cancers still remain ultimately fatal and difficult to treat, particularly acute myeloid leukaemia (AML) and multiple myeloma (MM). While significant progress has been made characterising small-scale genetic mutations and larger-scale chromosomal translocations that contribute to the development of various blood cancers, less is understood about the complex microenvironment of the bone marrow (BM), which is known to be a key player in the pathogenesis of chronic lymphocytic leukaemia (CLL), AML and MM. This niche acts as a sanctuary for the cancerous cells, protecting them from chemotherapeutics and encouraging clonal cell survival. It does this by upregulating a plethora of signalling cascades within the malignant cell, with the phosphatidylinositol-3-kinase (PI3K) pathway taking a critical role. This review will focus on how the PI3K pathway influences disease progression and the individualised role of the PI3K subunits. We will also summarise the current clinical trials for PI3K inhibitors and how these trials impact the treatment of blood cancers.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | aml,myeloma,microenvironment,pi3k,sdg 3 - good health and well-being ,/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being |
| Faculty \ School: | Faculty of Medicine and Health Sciences > Norwich Medical School |
| UEA Research Groups: | Faculty of Medicine and Health Sciences > Research Groups > Cancer Studies Faculty of Medicine and Health Sciences > Research Centres > Metabolic Health |
| Related URLs: | |
| Depositing User: | Pure Connector |
| Date Deposited: | 04 Apr 2017 05:29 |
| Last Modified: | 24 Oct 2023 00:49 |
| URI: | https://ueaeprints.uea.ac.uk/id/eprint/63160 |
| DOI: | 10.3390/cancers9040029 |
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