The RUNX/CBFβ Complex in Breast Cancer: A Conundrum of Context
Dissecting and identifying the major actors and pathways in the genesis, progression and aggressive advancement of breast cancer is challenging, in part because neoplasms arising in this tissue represent distinct diseases and in part because the tumors themselves evolve. This review attempts to illu...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-02-01
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| Series: | Cells |
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| Online Access: | https://www.mdpi.com/2073-4409/12/4/641 |
| _version_ | 1797621732231610368 |
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| author | Adiba S. Khan Kirsteen J. Campbell Ewan R. Cameron Karen Blyth |
| author_facet | Adiba S. Khan Kirsteen J. Campbell Ewan R. Cameron Karen Blyth |
| author_sort | Adiba S. Khan |
| collection | DOAJ |
| description | Dissecting and identifying the major actors and pathways in the genesis, progression and aggressive advancement of breast cancer is challenging, in part because neoplasms arising in this tissue represent distinct diseases and in part because the tumors themselves evolve. This review attempts to illustrate the complexity of this mutational landscape as it pertains to the <i>RUNX</i> genes and their transcription co-factor CBFβ. Large-scale genomic studies that characterize genetic alterations across a disease subtype are a useful starting point and as such have identified recurring alterations in <i>CBFB</i> and in the <i>RUNX</i> genes (particularly <i>RUNX1</i>). Intriguingly, the functional output of these mutations is often context dependent with regards to the estrogen receptor (ER) status of the breast cancer. Therefore, such studies need to be integrated with an in-depth understanding of both the normal and corrupted function in mammary cells to begin to tease out how loss or gain of function can alter the cell phenotype and contribute to disease progression. We review how alterations to RUNX/CBFβ function contextually ascribe to breast cancer subtypes and discuss how the in vitro analyses and mouse model systems have contributed to our current understanding of these proteins in the pathogenesis of this complex set of diseases. |
| first_indexed | 2024-03-11T09:01:05Z |
| format | Article |
| id | doaj.art-971f57fb9ef542789f475e0f97c6871a |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-11T09:01:05Z |
| publishDate | 2023-02-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-971f57fb9ef542789f475e0f97c6871a2023-11-16T19:45:12ZengMDPI AGCells2073-44092023-02-0112464110.3390/cells12040641The RUNX/CBFβ Complex in Breast Cancer: A Conundrum of ContextAdiba S. Khan0Kirsteen J. Campbell1Ewan R. Cameron2Karen Blyth3Cancer Research UK Beatson Institute, Garscube Estate, Switchback Rd, Glasgow G61 1BD, UKCancer Research UK Beatson Institute, Garscube Estate, Switchback Rd, Glasgow G61 1BD, UKSchool of Biodiversity One Health & Veterinary Medicine, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G61 1QH, UKCancer Research UK Beatson Institute, Garscube Estate, Switchback Rd, Glasgow G61 1BD, UKDissecting and identifying the major actors and pathways in the genesis, progression and aggressive advancement of breast cancer is challenging, in part because neoplasms arising in this tissue represent distinct diseases and in part because the tumors themselves evolve. This review attempts to illustrate the complexity of this mutational landscape as it pertains to the <i>RUNX</i> genes and their transcription co-factor CBFβ. Large-scale genomic studies that characterize genetic alterations across a disease subtype are a useful starting point and as such have identified recurring alterations in <i>CBFB</i> and in the <i>RUNX</i> genes (particularly <i>RUNX1</i>). Intriguingly, the functional output of these mutations is often context dependent with regards to the estrogen receptor (ER) status of the breast cancer. Therefore, such studies need to be integrated with an in-depth understanding of both the normal and corrupted function in mammary cells to begin to tease out how loss or gain of function can alter the cell phenotype and contribute to disease progression. We review how alterations to RUNX/CBFβ function contextually ascribe to breast cancer subtypes and discuss how the in vitro analyses and mouse model systems have contributed to our current understanding of these proteins in the pathogenesis of this complex set of diseases.https://www.mdpi.com/2073-4409/12/4/641breast cancerRUNX1CBFβRUNX2RUNX3estrogen receptor (ER) |
| spellingShingle | Adiba S. Khan Kirsteen J. Campbell Ewan R. Cameron Karen Blyth The RUNX/CBFβ Complex in Breast Cancer: A Conundrum of Context Cells breast cancer RUNX1 CBFβ RUNX2 RUNX3 estrogen receptor (ER) |
| title | The RUNX/CBFβ Complex in Breast Cancer: A Conundrum of Context |
| title_full | The RUNX/CBFβ Complex in Breast Cancer: A Conundrum of Context |
| title_fullStr | The RUNX/CBFβ Complex in Breast Cancer: A Conundrum of Context |
| title_full_unstemmed | The RUNX/CBFβ Complex in Breast Cancer: A Conundrum of Context |
| title_short | The RUNX/CBFβ Complex in Breast Cancer: A Conundrum of Context |
| title_sort | runx cbfβ complex in breast cancer a conundrum of context |
| topic | breast cancer RUNX1 CBFβ RUNX2 RUNX3 estrogen receptor (ER) |
| url | https://www.mdpi.com/2073-4409/12/4/641 |
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