Core epithelial-to-mesenchymal transition interactome gene-expression signature is associated with claudin-low and metaplastic breast cancer subtypes

By J. Taube, Jason I. Herschkowitz, K. Komurov, A. Zhou, Supriya Gupta, Jing Yang, Kimberly A. Hartwell, T. Onder, Piyush B. Gupta, K. Evans and 6 more. Proceedings of the National Academy of Sciences of the United States of America, 2010

1,021 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/9ea11aea3bc266c58524b351e8b610ec00e1d21f

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In Cancer Research

1. M. Nieto
2. D. Hanahan
3. R. Weinberg
4. Aleix Prat
5. Jacques E. Dumont
6. A. Richardson
7. Charles M. Perou
8. Vincent Detours

In Molecular Biology

1. R. Weinberg
2. M. Nieto
3. Jing Yang
4. D. Hanahan
5. K. Yeung
6. Herbert Levine
7. Wenjun Guo
8. C. Scheel

In Oncology

1. R. Weinberg
2. M. Nieto
3. D. Hanahan
4. Jing Yang
5. K. Yeung
6. C. Scheel
7. Christine L. Chaffer
8. Aleix Prat

Citations in the corpus

• The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, background): “Other types of intermediate states can be observed during the early migration of cranial neural crest in Xenopus and zebrafish (Figure 2d).”
• Epithelial–mesenchymal transition in tumor metastasis (2016, background): “Certain subtypes of cancer with poor prognosis (i.e., basal-like, claudin low subtype of breast cancer) have a strong EMT signature (Liu et al., 2013; Sarri o et al., 2008; Taube et al., 2010).”
• KRAS and YAP1 converge to regulate EMT and tumor survival (2014, neutral): “This may be attributed to different baseline levels of MAPK/PI3K signaling in the two systems, or the influence of wild-type KRAS (To et al., 2013).”
• Deconstructing the molecular portraits of breast cancer (2010, background): “…a mesenchymal state in a mammary epithelial cell (also known as epithelial-to-mesenchymal transition [EMT]) is associated with the acquisition of undifferentiated mammary stem cell-like features (Taube et al., 2010; Morel et al., 2008; Gupta et al., 2009; Shipitsin et al., 2007; Mani et al., 2008).”
• Hallmarks of cancer: the next generation. (2011, positive): “…tumor types and have been shown in experimental models of carcinoma formation to be causally important for programming invasion; some have been found to elicit metastasis when ectopically overexpressed (Micalizzi et al., 2010; Taube et al., 2010; Schmalhofer et al., 2009; Yang and Weinberg, 2008).”
• Most Random Gene Expression Signatures Are Significantly Associated with Breast Cancer Outcome (2011, background): “These include signatures of stem cells [13–15], aneuploidy [16], wound healing [17,18], hypoxia [19,20], stromal component [21], epithelialmesenchymal transition [22–24]; of mutations in TP53 [25], ALK5 [26]; of loss of PTEN [27]; of perturbations of E2F1 [28], bromodomain 4 [29], mir31 targets [30]”
• Epithelial-mesenchymal transition spectrum quantification and its efficacy in deciphering survival and drug responses of cancer patients (2014, neutral): “These results corroborate the cancer-specific EMT signature scoring, which forms the basis of the generic EMT signature.”
• Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis (2015, result): “Experiments showing that SNAIL can initiate repression of E-cadherin but ZEB is required for its complete inhibition (41), and that most genes repressed during EMT are inhibited by ZEB irrespective of the EMT-inducing signal (42), are consistent with either model; both approaches argue for ZEB activ”