ErbB2, but not ErbB1, reinitiates proliferation and induces luminal repopulation in epithelial acini

By S. Muthuswamy, Dongmei Li, S. Lelièvre, Mina J. Bissell, J. Brugge. Nature Cell Biology, 2001

616 citations recorded by the source corpus.

Subfields: Immunology and Allergy, Oncology, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/a3af8c38f0b946bdcb1b40e34ebb0ae438c5beab

How researchers see this paper

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

In Immunology and Allergy

1. J. Joyce
2. Valerie M. Weaver
3. J. Brugge
4. Jayanta Debnath
5. J. Erler
6. T. Cox
7. W. C. Hines
8. Mina J. Bissell

In Oncology

1. J. Joyce
2. J. Brugge
3. J. Erler
4. T. Cox
5. Jayanta Debnath
6. A. Cano
7. G. Moreno-Bueno
8. Valerie M. Weaver

In Radiology, Nuclear Medicine and Imaging

1. J. Joyce
2. Carlos L. Arteaga
3. M. Moasser
4. Lewis C. Cantley
5. N. Iqbal
6. N. Iqbal
7. T. Yuan

Citations in the corpus

• The role of apoptosis in creating and maintaining luminal space within normal and oncogene-expressing mammary acini. (2002, methodology): “Except for this minor modification in fixation and permeablization, the immunostaining of acinar structures was carExperimental Procedures ried out as previously described (Muthuswamy et al., 2001).”
• The morphologies of breast cancer cell lines in three‐dimensional assays correlate with their profiles of gene expression (2007, background): “The two outliers in this correlation were MCF-10A and MCF-12A, both Basal B but highly un-invasive.”
• Matrix Crosslinking Forces Tumor Progression by Enhancing Integrin signaling (2009, background): “In these MECs, addition of the synthetic bivalent FKBP ligand, AP1510, drives homodimerization of ErbB2, activation of the kinase domain, and initiation of ErbB2 signaling (Muthuswamy et al., 2001).”
• Herceptin-induced inhibition of phosphatidylinositol-3 kinase and Akt Is required for antibody-mediated effects on p27, cyclin D1, and antitumor action. (2002, background): “Dysregulated signaling by this receptor network has been causally associated with early transformation of mammary epithelial cells (11, 12) as well as with enhanced breast cancer cell proliferation and shorter survival in patients with mammary carcinomas (13, 14).”
• The oncogene HER2: its signaling and transforming functions and its role in human cancer pathogenesis (2007, background): “The experimental homodimerization and activation of HER2 leads to disruption of tight junctions, loss of cell polarity and proliferative disarray in breast epithelial cell acinar structures, although the basal membrane is preserved and invasive features are not induced (Muthuswamy et al., 2001).”
• The organizing principle: microenvironmental influences in the normal and malignant breast. (2002, neutral): “6) (Muthuswamy et al., 2001).”
• Collective cell guidance by cooperative intercellular forces (2010, neutral): “We chose these cell lines because each exhibits pronounced morphological differences as well as diverse levels of transforming potential, expression of cell–cell junction proteins, and cell proliferatio”
• Why don’t we get more cancer? A proposed role of the microenvironment in restraining cancer progression (2011, background): “Studies of this type have suggested the cellular response to drugs used in the clinic is, not surprisingly, context dependen”
• Transcriptional regulation of cell polarity in EMT and cancer (2008, background): “Indeed, activation of ErbB2 was shown to disrupt apical–basal polarity of mammary epithelial cells and of epithelial acini in three-dimensional cultures (Muthuswamy et al., 2001).”
• Therapeutic targeting of the tumor microenvironment. (2005, positive): “Both organotypic 3D culture sys­ tems, as pioneered by Bissell and adopted by Brugge and oth­ ers (Muthuswamy et al., 2001; Petersen et al., 1992; Schmeichel and Bissell, 2003), and the recent development of a “humanized” mammary gland xenograft model (Kuperwasser et al., 2004), allow human…”
• Remodeling and homeostasis of the extracellular matrix: implications for fibrotic diseases and cancer (2011, positive): “…in a physiologically relevant topographical context if they are to respond in a physiologically relevant manner to signaling molecules (Weaver et al., 1996; Weaver et al., 1997; Muthuswamy et al., 2001), so that both the environmental biochemical and biomechanical cues mimic the in vivo situation.”
• Mutant p53 drives invasion by promoting integrin recycling. (2009, background): “After oncogenic stimulation such as expression of V12Ras or ErbB2 (NeuT) or coexpression of ErbB1 and TGF-b, these cells can be induced to form invasive structures (Muthuswamy et al., 2001; Seton-Rogers et al., 2004).”