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XPO1.md
| ... | ... | @@ -3,11 +3,14 @@ bibliography: 'morinlab.bib' |
| 3 | 3 | csl: 'NLM.csl' |
| 4 | 4 | link-citations: true |
| 5 | 5 | nocite: | |
| 6 | - @jardinRecurrentMutationsExportin2016, @mareschalWholeExomeSequencing2016, @reddyGeneticFunctionalDrivers2017, |
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| 6 | + @jardinRecurrentMutationsExportin2016, @mareschalWholeExomeSequencing2016, @reddyGeneticFunctionalDrivers2017 |
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| 7 | 7 | --- |
| 8 | 8 | |
| 9 | 9 | [[_TOC_]] |
| 10 | 10 | |
| 11 | +## Overview |
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| 12 | + |
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| 13 | +XPO1 encodes exportin-1 (CRM1), a key nuclear export protein that regulates the cytoplasmic trafficking of many tumour suppressors and growth regulators, including TP53, RB, and FOXO family members[@balasubramanianSelectiveInhibitionNuclear2022]. In mature B-cell neoplasms, XPO1 is frequently overexpressed and recurrently mutated (most commonly E571K), particularly in primary mediastinal B-cell lymphoma, classical Hodgkin lymphoma, and subsets of DLBCL[@miloudiXPO1E571KMutationModifies2020; @camusXPO1CellHematological2017]. These alterations are thought to enhance nuclear export efficiency, functionally dampening tumour suppressor activity without requiring their genetic loss[@balasubramanianSelectiveInhibitionNuclear2022]. As a result, many B-cell lymphomas exhibit a shared dependency on XPO1-mediated nuclear export, providing a biologic rationale for XPO1 inhibition independent of mutation status. |
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| 11 | 14 | |
| 12 | 15 | ## Experimental Evidence |
| 13 | 16 |