Effects of PTEN Loss and Activated KRAS Overexpression on Mechanical Properties of Breast Epithelial Cells
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Title
Effects of PTEN Loss and Activated KRAS Overexpression on Mechanical Properties of Breast Epithelial Cells
Authors
Keywords
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Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 19, Issue 6, Pages 1613
Publisher
MDPI AG
Online
2018-05-31
DOI
10.3390/ijms19061613
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Note: Only part of the references are listed.- Mechanical Properties of the Cytoskeleton and Cells
- (2017) Adrian F. Pegoraro et al. Cold Spring Harbor Perspectives in Biology
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- (2017) Sandra Tavares et al. Nature Communications
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- (2016) K Bhattacharya et al. Oncogenesis
- Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging
- (2016) Linda S. Steelman et al. Aging-US
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- (2015) Kozaburo Hayashi et al. Journal of the Mechanical Behavior of Biomedical Materials
- The combinatorial activation of the PI3K and Ras/MAPK pathways is sufficient for aggressive tumor formation, while individual pathway activation supports cell persistence
- (2015) Keyata N. Thompson et al. Oncotarget
- Mechanical phenotype of cancer cells: cell softening and loss of stiffness sensing
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- Deregulation of the EGFR/PI3K/PTEN/Akt/mTORC1 pathway in breast cancer: possibilities for therapeutic intervention
- (2015) Nicole M. Davis et al. Oncotarget
- PI3K and MEK inhibitor combinations: examining the evidence in selected tumor types
- (2013) Carolyn D. Britten CANCER CHEMOTHERAPY AND PHARMACOLOGY
- Targeting the PI3K/AKT/mTOR and Raf/MEK/ERK pathways in the treatment of breast cancer
- (2013) Kamal S. Saini et al. CANCER TREATMENT REVIEWS
- The Ras-ERK pathway modulates cytoskeleton organization, cell motility and lung metastasis signature genes in MDA-MB-231 LM2
- (2013) C Choi et al. ONCOGENE
- Prognostic and Predictive Significance of MYC and KRAS Alterations in Breast Cancer from Women Treated with Neoadjuvant Chemotherapy
- (2013) Cynthia Brito Lins Pereira et al. PLoS One
- A physical sciences network characterization of non-tumorigenic and metastatic cells
- (2013) Scientific Reports
- Measuring the Mechanical Properties of Living Cells Using Atomic Force Microscopy
- (2013) Gawain Thomas et al. Jove-Journal of Visualized Experiments
- The Clinical Effect of the Dual-Targeting Strategy Involving PI3K/AKT/mTOR and RAS/MEK/ERK Pathways in Patients with Advanced Cancer
- (2012) T. Shimizu et al. CLINICAL CANCER RESEARCH
- Combined PI3K/mTOR and MEK Inhibition Provides Broad Antitumor Activity in Faithful Murine Cancer Models
- (2012) P. J. Roberts et al. CLINICAL CANCER RESEARCH
- The clonal and mutational evolution spectrum of primary triple-negative breast cancers
- (2012) Sohrab P. Shah et al. NATURE
- Comprehensive molecular portraits of human breast tumours
- (2012) Daniel C. Koboldt et al. NATURE
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- (2012) M I Vitolo et al. ONCOGENE
- Cell Stiffness Is a Biomarker of the Metastatic Potential of Ovarian Cancer Cells
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- The effect of matrix stiffness on the differentiation of mesenchymal stem cells in response to TGF-β
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- Hallmarks of Cancer: The Next Generation
- (2011) Douglas Hanahan et al. CELL
- The Ras-ERK and PI3K-mTOR pathways: cross-talk and compensation
- (2011) Michelle C. Mendoza et al. TRENDS IN BIOCHEMICAL SCIENCES
- Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer
- (2010) Alfonso Sánchez-Muñoz et al. BMC CANCER
- Effects of KRAS, BRAF, NRAS, and PIK3CA mutations on the efficacy of cetuximab plus chemotherapy in chemotherapy-refractory metastatic colorectal cancer: a retrospective consortium analysis
- (2010) Wendy De Roock et al. LANCET ONCOLOGY
- Deletion of PTEN Promotes Tumorigenic Signaling, Resistance to Anoikis, and Altered Response to Chemotherapeutic Agents in Human Mammary Epithelial Cells
- (2009) M. I. Vitolo et al. CANCER RESEARCH
- Basal Subtype and MAPK/ERK Kinase (MEK)-Phosphoinositide 3-Kinase Feedback Signaling Determine Susceptibility of Breast Cancer Cells to MEK Inhibition
- (2009) O. K. Mirzoeva et al. CANCER RESEARCH
- In vivo Antitumor Activity of MEK and Phosphatidylinositol 3-Kinase Inhibitors in Basal-Like Breast Cancer Models
- (2009) K. P. Hoeflich et al. CLINICAL CANCER RESEARCH
- PI3K pathway activation in breast cancer is associated with the basal-like phenotype and cancer-specific mortality
- (2009) Elena López-Knowles et al. INTERNATIONAL JOURNAL OF CANCER
- AFM indentation study of breast cancer cells
- (2008) Q.S. Li et al. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Deformability study of breast cancer cells using microfluidics
- (2008) H. W. Hou et al. BIOMEDICAL MICRODEVICES
- Mutations in the Phosphatidylinositol-3-Kinase Pathway Predict for Antitumor Activity of the Inhibitor PX-866 whereas Oncogenic Ras Is a Dominant Predictor for Resistance
- (2008) N. T. Ihle et al. CANCER RESEARCH
- Targeting AKT/mTOR and ERK MAPK signaling inhibits hormone-refractory prostate cancer in a preclinical mouse model
- (2008) Carolyn Waugh Kinkade et al. JOURNAL OF CLINICAL INVESTIGATION
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