The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Drug resistance and Cancer stem cells
Open accessAbstract
Therapy resistance is a major problem when treating cancer patients as cancer cells develop mechanisms that counteract the effect of therapeutic compounds, leading to fit and more aggressive clones that contribute to poor prognosis. Therapy resistance can be both intrinsic and/or acquired. These are multifactorial events, and some are related to factors including adaptations in cancer stem cells (CSCs), epithelial-mesenchymal transition (EMT), deregulation of key signaling pathways, drug efflux through ABC transporters, acquired mutations, evading apoptosis, and activation of DNA damage response among others. Among these factors, CSCs represent the major source of therapy resistance. CSCs are a subset of tumor cells that are capable of self-renewal and multilineage progenitor expansion that are known to be intrinsically resistant to anticancer treatments. Multiple clones of CSCs pre-exist, and some can adopt and expand easily to changes in the tumor microenvironment (TME) and/or in response to radio- and chemotherapy. A combination of both intrinsic and extrinsic factors contributes to CSC-mediated therapy resistance. In this review, we will focus on CSCs and therapy resistance as well as suggest strategies to eliminate CSCs and, therefore, overcome resistance.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Galluzzi, L., Vitale, I., Aaronson, S. A., Abrams, J. M., Adam, D., Agostinis, P., Alnemri, E. S., Altucci, L., Amelio, I., Andrews, D. W., et al. (2018) · Cell Death & Differentiation · doi:10.1038/s41418-017-0012-4 · Cited by 6,680
Wnt/β-catenin signaling and disease
Clevers, H., & Nusse, R. (2012) · Cell · doi:10.1016/j.cell.2012.05.012 · Cited by 5,554
Hippo pathway in organ size control, tissue homeostasis, and cancer
Yu, F.-X., Zhao, B., & Guan, K.-L. (2015) · Cell · doi:10.1016/j.cell.2015.10.044 · Cited by 2,206
Bmi-1 is required for maintenance of adult self-renewing haematopoietic stem cells.
Park, I.-K., Qian, D., Kiel, M., Becker, M. W., Pihalja, M., Weissman, I. L., Morrison, S. J., & Clarke, M. F. (2003) · Nature · doi:10.1038/nature01587 · Cited by 1,871
Vaure, C., & Liu, Y. (2014) · Frontiers in Immunology · doi:10.3389/fimmu.2014.00316 · Cited by 842
Metastatic Latency and Immune Evasion through Autocrine Inhibition of WNT
Malladi, S., Macalinao, D. G., Jin, X., He, L., Basnet, H., Zou, Y., de Stanchina, E., & Massagué, J. (2016) · Cell · doi:10.1016/j.cell.2016.02.025 · Cited by 791 · cited 1×
“Study from the Massague J laboratory demonstrated that latency competent cancer (LCC) cells show stem-cell-like characteristics and express SOX2 and SOX9 transcription factors, which are essential for their survival and resistance to therapy in host organs under immune surveillance and for metastatic outgrowth under p…”
BackgroundPollyea, D. A., Stevens, B. M., Jones, C. L., Winters, A., Pei, S., Minhajuddin, M., D’Alessandro, A., Culp-Hill, R., Riemondy, K. A., Gillen, A. E., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0233-1 · Cited by 778
The Hippo effector YAP promotes resistance to RAF- and MEK-targeted cancer therapies
Lin, L., Sabnis, A. J., Chan, E., Olivas, V., Cade, L., Pazarentzos, E., Asthana, S., Neel, D., Yan, J. J., Lu, X., et al. (2015) · Nature Genetics · doi:10.1038/ng.3218 · Cited by 551
Peiris-Pagès, M., Martinez-Outschoorn, U. E., Pestell, R. G., Sotgia, F., & Lisanti, M. P. (2016) · Breast Cancer Research · doi:10.1186/s13058-016-0712-6 · Cited by 465
An integrin β3-KRAS-RalB complex drives tumour stemness and resistance to EGFR inhibition
Seguin, L., Kato, S., Franovic, A., Camargo, M. F., Lesperance, J., Elliott, K. C., Yebra, M., Mielgo, A., Lowy, A. M., Husain, H., et al. (2014) · Nature Cell Biology · doi:10.1038/ncb2953 · Cited by 374
Cited by
Unveiling the mechanisms and challenges of cancer drug resistance
Khan, S. U., Fatima, K., Aisha, S., & Malik, F. (2024) · Cell Communication and Signaling · doi:10.1186/s12964-023-01302-1 · Cited by 417
scDrugMap: benchmarking large foundation models for drug response prediction
Wang, Q., Pan, Y., Zhou, M., Tang, Z., Wang, Y., Wang, G., & Song, Q. (2025) · Nature Communications · doi:10.1038/s41467-025-67481-2 · Cited by 12
Pan-cancer analyses suggest kindlin-associated global mechanochemical alterations
Chowdhury, D., Mistry, A., Maity, D., Bhatia, R., Priyadarshi, S., Wadan, S., Chakraborty, S., & Haldar, S. (2024) · Communications Biology · doi:10.1038/s42003-024-06044-5 · Cited by 5
Metadata
- Authors
- Li, Y., Wang, Z., Ajani, J. A., & Song, S.
- Venue
- Cell Communication and Signaling
- Published
- 2021-02-15
- Volume
- 19
- Issue
- 1
- Pages
- 19-19
- ISSN
- 1478-811X (ISSN-L)
- OpenAlex
- W3129607550
- Cited by
- 331
- References
- 12
- FWCI
- 17.20
- Type
- journal article
- Language
- en
- Open access
- gold
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.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
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.
