Model of tumor dormancy/recurrence after short-term chemotherapy.
Although many tumors regress in response to neoadjuvant chemotherapy, residual tumor cells are detected in most cancer patients post-treatment. These residual tumor cells are thought to remain dormant for years before resuming growth, resulting in tumor recurrence. Considering that recurrent tumors...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2014-01-01
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| Series: | PLoS ONE |
| Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0098021&type=printable |
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| _version_ | 1850151140124000256 |
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| author | Shenduo Li Margaret Kennedy Sturgis Payne Kelly Kennedy Victoria L Seewaldt Salvatore V Pizzo Robin E Bachelder |
| author_facet | Shenduo Li Margaret Kennedy Sturgis Payne Kelly Kennedy Victoria L Seewaldt Salvatore V Pizzo Robin E Bachelder |
| author_sort | Shenduo Li |
| collection | DOAJ |
| description | Although many tumors regress in response to neoadjuvant chemotherapy, residual tumor cells are detected in most cancer patients post-treatment. These residual tumor cells are thought to remain dormant for years before resuming growth, resulting in tumor recurrence. Considering that recurrent tumors are most often responsible for patient mortality, there exists an urgent need to study signaling pathways that drive tumor dormancy/recurrence. We have developed an in vitro model of tumor dormancy/recurrence. Short-term exposure of tumor cells (breast or prostate) to chemotherapy at clinically relevant doses enriches for a dormant tumor cell population. Several days after removing chemotherapy, dormant tumor cells regain proliferative ability and establish colonies, resembling tumor recurrence. Tumor cells from "recurrent" colonies exhibit increased chemotherapy resistance, similar to the therapy resistance of recurrent tumors in cancer patients. Previous studies using long-term chemotherapy selection models identified acquired mutations that drive tumor resistance. In contrast, our short term chemotherapy exposure model enriches for a slow-cycling, dormant, chemo-resistant tumor cell sub-population that can resume growth after drug removal. Studying unique signaling pathways in dormant tumor cells enriched by short-term chemotherapy treatment is expected to identify novel therapeutic targets for preventing tumor recurrence. |
| format | Article |
| id | doaj-art-774729aa917646fba8b2ccbd6589284f |
| institution | OA Journals |
| issn | 1932-6203 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-774729aa917646fba8b2ccbd6589284f2025-08-20T02:26:20ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0195e9802110.1371/journal.pone.0098021Model of tumor dormancy/recurrence after short-term chemotherapy.Shenduo LiMargaret KennedySturgis PayneKelly KennedyVictoria L SeewaldtSalvatore V PizzoRobin E BachelderAlthough many tumors regress in response to neoadjuvant chemotherapy, residual tumor cells are detected in most cancer patients post-treatment. These residual tumor cells are thought to remain dormant for years before resuming growth, resulting in tumor recurrence. Considering that recurrent tumors are most often responsible for patient mortality, there exists an urgent need to study signaling pathways that drive tumor dormancy/recurrence. We have developed an in vitro model of tumor dormancy/recurrence. Short-term exposure of tumor cells (breast or prostate) to chemotherapy at clinically relevant doses enriches for a dormant tumor cell population. Several days after removing chemotherapy, dormant tumor cells regain proliferative ability and establish colonies, resembling tumor recurrence. Tumor cells from "recurrent" colonies exhibit increased chemotherapy resistance, similar to the therapy resistance of recurrent tumors in cancer patients. Previous studies using long-term chemotherapy selection models identified acquired mutations that drive tumor resistance. In contrast, our short term chemotherapy exposure model enriches for a slow-cycling, dormant, chemo-resistant tumor cell sub-population that can resume growth after drug removal. Studying unique signaling pathways in dormant tumor cells enriched by short-term chemotherapy treatment is expected to identify novel therapeutic targets for preventing tumor recurrence.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0098021&type=printable |
| spellingShingle | Shenduo Li Margaret Kennedy Sturgis Payne Kelly Kennedy Victoria L Seewaldt Salvatore V Pizzo Robin E Bachelder Model of tumor dormancy/recurrence after short-term chemotherapy. PLoS ONE |
| title | Model of tumor dormancy/recurrence after short-term chemotherapy. |
| title_full | Model of tumor dormancy/recurrence after short-term chemotherapy. |
| title_fullStr | Model of tumor dormancy/recurrence after short-term chemotherapy. |
| title_full_unstemmed | Model of tumor dormancy/recurrence after short-term chemotherapy. |
| title_short | Model of tumor dormancy/recurrence after short-term chemotherapy. |
| title_sort | model of tumor dormancy recurrence after short term chemotherapy |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0098021&type=printable |
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