Residual breast cancers after conventional therapy display mesenchymal as well as tumor-initiating features

By Chad Creighton, Xiaoxian Li, M. Landis, J. Dixon, V. Neumeister, Ashley B Sjolund, David L. Rimm, H. Wong, Angel A. Rodriguez, Jason I. Herschkowitz and 13 more. Proceedings of the National Academy of Sciences of the United States of America, 2009

1,423 citations recorded by the source corpus.

Subfields: Cancer Research, Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/bb3c16ce871db0689c9dd1094aca146f7c5f46d7

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. R. Weinberg
2. M. Nieto
3. D. Hanahan
4. Thomas Brabletz
5. Aleix Prat
6. Jane E. Visvader
7. Lisa A. Carey
8. X. Ye

In Oncology

1. R. Weinberg
2. M. Nieto
3. Thomas Brabletz
4. D. Hanahan
5. Jing Yang
6. Simone Brabletz
7. Aleix Prat
8. X. Ye

In Pulmonary and Respiratory Medicine

1. R. Weinberg
2. Thomas Brabletz
3. M. Nieto
4. X. Ye
5. Yongheng Chen
6. S. Leonov
7. Carlos L. Arteaga
8. Huajun Zhang

Citations in the corpus

• Network-based inference of protein activity helps functionalize the genetic landscape of cancer (2016, neutral): “While gene expression data are ubiquitous in cancer research 9–12 , methods for the genome-wide assessment of protein activity are still elusive.”
• Direct Signaling Between Platelets and Cancer Cells Induces an Epithelial-Mesenchymal-Like Transition and Promotes Metastasis (2011, neutral): “, 2005) CREIGHTON_CSC (Creighton et al., 2009) VANTVEER_BREAST_CANCER_POOR_PROGNOSIS MSigDB, (van 't Veer et al.”
• Cancer stem cells: current status and evolving complexities. (2012, background): “Furthermore, the analysis of breast tissue taken from patients pre- and postendocrine therapy or chemotherapy for gene expression changes revealed that residual breast cancers may be enriched for tumor cells with CSC-like and mesenchymal characteristics (Creighton et al., 2009).”
• Stochastic state transitions give rise to phenotypic equilibrium in populations of cancer cells. (2011, positive): “Additionally, because anticancer therapies preferentially kill specific cancer cell states, treatment can result in selective changes in phenotypic proportions within tumors (Creighton et al., 2009; Gupta et al., 2009; Li et al., 2008; Woodward et al., 2007).”
• Core epithelial-to-mesenchymal transition interactome gene-expression signature is associated with claudin-low and metaplastic breast cancer subtypes (2010, background): “found that the GESderived frombreast tumor-initiating cells was also enriched in claudin-low tumors, but likewise did not serve as a useful prognostic marker for clinical progression (53).”
• Dynamic EMT: a multi‐tool for tumor progression (2021, positive): “…stress adaptation, exemplified by analysis of post-therapy specimens, e.g., in esophageal and breast cancer after chemotherapy and in CRC after radiotherapy, showing decreased E-cadherin and elevated SNAIL and Vimentin levels (Creighton et al , 2009; Kawamoto et al , 2012; Hara et al , 2014).”
• The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, background): “In fact, after therapy, residual breast tumors display both the EMT and tumor-initiating characteristics (Creighton et al. 2009).”
• Triple-negative breast cancer: disease entity or title of convenience? (2010, background): “This subgroup is also notable for expression of cell–cell junction proteins and for the possession of stem-cell signatures and EMT characteristics with upregulation of mesenchymal markers”
• Epithelial–mesenchymal transition in tumor metastasis (2016, background): “Finally, expression of EMT-TFs has been correlated negatively with pathologic response to treatment, suggesting a role in chemoresistance (Creighton et al., 2009; Farmer et al., 2009).”
• Epithelial-Mesenchymal Plasticity: A central regulator of cancer progression (2015, background): “Besides promoting systemic dissemination, the EMT program also appears to serve as a major driver of drug resistance and subsequent disease recurrence in breast cancer patients (Cheng et al., 2014; Creighton et al., 2009; Oliveras-Ferraros et al., 2012).”
• Overcoming Endocrine Resistance in Breast Cancer (2020, positive): “Residual tumors that survive endocrine therapy can be enriched with cancer cell populations exhibiting classical tumorinitiating features such as CD44+/CD24−/low cell surface markers, high aldehyde dehydrogenase activity, and enhanced mammosphere formation (Creighton et al., 2009; Rodriguez et al., ”