The DOI matches its Crossref record.
Evolving Views of Breast Cancer Stem Cells and Their Differentiation States
Abstract
Cellular heterogeneity is a prominent characteristic of breast cancers, and accumulating evidence indicates that variability in the differentiation state of tumor cells contributes to this phenomenon. Breast cancers are among the tumor types in which the existence of cancer stem cells has been widely supported, and specific markers, including CD44/CD24 and ALDH1, have been consistently used to identify such cells. Recent studies have revealed the potential for dynamic bidirectional transitions of breast cancer cells between differentiated and stem-like phenotypes. In addition, the potential importance of intermediate states along differentiation axes, including the epithelial-to-mesenchymal transition and the basal-luminal differentiation axis, has emerged. These findings provide a view of breast cancer stem cells that departs from the traditional unidirectional hierarchical model, as well as new insights into the mechanisms by which differentiation events contribute to breast cancer biology. Herein we discuss these advances.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“When DNA damage is excessive, ATM drives the activation of NF‐κB to accelerate TNF‐α production and to mediate phosphorylation of receptor‐interacting kinase 1 (RIP1).”
From p21 maintains senescent cell viability under persistent DNA damage response by restraining JNK and caspase signaling (2017) · cites this paper as Condiotti et al, 2014
In the citing paper
“RIP1 kinase promotes the JNK‐mediated induction of interleukin (IL)‐8 production and the recruitment of the FADD adapter protein to activate caspase‐8 and trigger programmed cell death (Biton & Ashkenazi, 2011; Condiotti et al, 2014).”
From p21 maintains senescent cell viability under persistent DNA damage response by restraining JNK and caspase signaling (2017) · cites this paper as Condiotti et al, 2014
Citations
Cites
Still being checked.
Cited by
Sorted by citations
Yosef, R., Pilpel, N., Papismadov, N., Gal, H., Ovadya, Y., Vadai, E., Miller, S., Porat, Z., Ben‐Dor, S., & Krizhanovsky, V. (2017) · The EMBO Journal · doi:10.15252/embj.201695553 · Cited by 293
Bliss, S. A., Paul, S., Pobiarzyn, P. W., Ayer, S., Sinha, G., Pant, S., Hilton, H., Sharma, N., Cunha, M. F., Engelberth, D. J., et al. (2018) · Scientific Reports · doi:10.1038/s41598-017-18834-5 · Cited by 25
Dou, X., Tong, P., Huang, H., Zellmer, L., He, Y., Jia, Q., Zhang, D., Peng, J., Wang, C., Xu, N., et al. (2020) · Journal of Cancer · doi:10.7150/jca.41324 · Cited by 7
Cancer stem cells in tumor pathogenesis after cryoablation
Goltsev, А., Diabina, O. A., Ostankov, M. V., Bondarovich, N. A., & Yampolskaya, E. E. (2015) · Problems of Cryobiology and Cryomedicine · doi:10.15407/cryo25.03.205 · Cited by 3
Стволовые раковые клетки в патогенезе опухолевого процесса после криодеструкции
Goltsev, А., Diabina, O. A., Ostankov, M. V., & Bondarovich, N. A. (2015)
Metadata
- Authors
- Condiotti, R., Guo, W., & Ben-Porath, I.
- Affiliations
- Hebrew University of Jerusalem (IL)
- Albert Einstein College of Medicine (US)
- ORCID
- Guo, Wenjun
- Venue
- Critical Reviews in Oncogenesis
- Publisher
- Begell House
- Published
- 2014
- Volume
- 19
- Issue
- 5
- Pages
- 337-348
- ISSN
- 0893-9675 (ISSN-L)
- OpenAlex
- W2080602366
- Cited by
- 7
- References
- 0
- Citations by year
- 2020: 1 · 2018: 1 · 2017: 3 · 2015: 2
- FWCI
- 0.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Critical Reviews™ in Oncogenesis (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Mesenchymal stem cell research
- Keywords
- breast cancer stem cells, cellular heterogeneity, CD44/CD24, ALDH1, epithelial-mesenchymal transition, tumor microenvironment
- MeSH terms
- Breast Neoplasms, Cell Differentiation, Humans, Neoplastic Stem Cells, Epithelial-Mesenchymal Transition
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