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EMT, CTCs and CSCs in tumor relapse and drug-resistance
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// Abhisek Mitra 1 , Lopa Mishra 2 and Shulin Li 1 1 Department of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA 2 Department of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, TX, USA Correspondence to: Shulin Li, email: // Keywords : tumor relapse, CTCs, CSCs, EMT, clinical trials Received : February 02, 2015 Accepted : April 20, 2015 Published : May 08, 2015 Abstract Tumor relapse and metastasis are the primary causes of poor survival rates in patients with advanced cancer despite successful resection or chemotherapeutic treatment. A primary cause of relapse and metastasis is the persistence of cancer stem cells (CSCs), which are highly resistant to chemotherapy. Although highly efficacious drugs suppressing several subpopulations of CSCs in various tissue-specific cancers are available, recurrence is still common in patients. To find more suitable therapy for relapse, the mechanisms underlying metastasis and drug-resistance associated with relapse-initiating CSCs need to be identified. Recent studies in circulating tumor cells (CTCs) of some cancer patients manifest phenotypes of both CSCs and epithelial-mesenchymal transition (EMT). These patients are unresponsive to standard chemotherapies and have low progression free survival, suggesting that EMT-positive CTCs are related to co-occur with or transform into relapse-initiating CSCs. Furthermore, EMT programming in cancer cells enables in the remodeling of extracellular matrix to break the dormancy of relapse-initiating CSCs. In this review, we extensively discuss the association of the EMT program with CTCs and CSCs to characterize a subpopulation of patients prone to relapses. Identifying the mechanisms by which EMT-transformed CTCs and CSCs initiate relapse could facilitate the development of new or enhanced personalized therapeutic regimens.
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TBK1 Regulates Prostate Cancer Dormancy through mTOR Inhibition
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Metastasis Awakening: Targeting dormant cancer
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Late Recurrence of Non-Small Cell Lung Cancer More Than 5 Years After Complete Resection
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Phase II Study of Dasatinib (BMS-354825) in Patients With Metastatic Adenocarcinoma of the Pancreas
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The nutritional phenome of EMT-induced cancer stem-like cells
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Forward genetic screens in mice uncover mediators and suppressors of metastatic reactivation
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Metadata
- Authors
- Mitra, A., Mishra, L., & Li, S.
- Venue
- Oncotarget
- Publisher
- Impact Journals, LLC
- Published
- 2015-05-08
- Volume
- 6
- Issue
- 13
- Pages
- 10697-10711
- ISSN
- 1949-2553 (ISSN-L)
- OpenAlex
- W1842991947
- Cited by
- 465
- References
- 131
- FWCI
- 30.55
- Type
- journal article
- Language
- en
- Open access
- diamond
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.