SLX1B is active during transformation and controls relapse and resistance in human cancer.
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| Natura: | Recurso digital |
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Zenodo
2025
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| _version_ | 1866902290485477376 |
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| author | Mamoor, Shahan |
| author_facet | Mamoor, Shahan |
| contents | <p>We recently discovered SLX1B induction in a Brca1-deficient setting. To gain insight into processes SLX1B participates in, we quiered a collection of whole transcriptome datasets for SLX1B activation. A dataset describing transcriptional activity in TNBC cells in vitro comparing cells with response or no response to the chemotherapeutic agent irinotecan was retrieved. In vivo, SLX1B expression distinguished partial versus complete response in patients treated with trastuzumab for HER2+ breast cancer. Genetic manipulation of a master homeobox factor also resulted in SLX1A/B perturbation. </p> <p>The data supported a hypothesis arguing that genomic instability, and changes in expression of any machinery that can generate such instability is a recurrent trigger that ultimately drives disease relapse in cancer (recurrence) and treatment failure during treatment for cancer (partial response, residual disease or complete response).</p> |
| format | Recurso digital |
| id | zenodo_https___doi_org_10_5281_zenodo_15576044 |
| institution | Zenodo |
| language | |
| publishDate | 2025 |
| publisher | Zenodo |
| record_format | zenodo |
| spellingShingle | SLX1B is active during transformation and controls relapse and resistance in human cancer. Mamoor, Shahan <p>We recently discovered SLX1B induction in a Brca1-deficient setting. To gain insight into processes SLX1B participates in, we quiered a collection of whole transcriptome datasets for SLX1B activation. A dataset describing transcriptional activity in TNBC cells in vitro comparing cells with response or no response to the chemotherapeutic agent irinotecan was retrieved. In vivo, SLX1B expression distinguished partial versus complete response in patients treated with trastuzumab for HER2+ breast cancer. Genetic manipulation of a master homeobox factor also resulted in SLX1A/B perturbation. </p> <p>The data supported a hypothesis arguing that genomic instability, and changes in expression of any machinery that can generate such instability is a recurrent trigger that ultimately drives disease relapse in cancer (recurrence) and treatment failure during treatment for cancer (partial response, residual disease or complete response).</p> |
| title | SLX1B is active during transformation and controls relapse and resistance in human cancer. |
| url | https://doi.org/10.5281/zenodo.15576044 |