Dual specificity phosphatase 4 gene expression in association with triple-negative breast cancer outcome

[1]  F. Bertucci,et al.  Personalized medicine: present and future of breast cancer management. , 2014, Critical reviews in oncology/hematology.

[2]  M. Leary,et al.  Genetic and epigenetic aspects of breast cancer progression and therapy. , 2014, Anticancer research.

[3]  S. Cagnol,et al.  Oncogenic KRAS and BRAF activation of the MEK/ERK signaling pathway promotes expression of dual-specificity phosphatase 4 (DUSP4/MKP2) resulting in nuclear ERK1/2 inhibition , 2013, Oncogene.

[4]  J. Jonkers,et al.  MEK inhibition as a strategy for targeting residual breast cancer cells with low DUSP4 expression , 2012, Breast Cancer Research.

[5]  G. Mills,et al.  Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance , 2012, Nature Medicine.

[6]  L. Harris,et al.  Evaluation of prognostic and predictive value of microtubule associated protein tau in two independent cohorts , 2011, Breast Cancer Research.

[7]  Nikolai Daraselia,et al.  Exploring molecular pathways of triple-negative breast cancer. , 2011, Genes & cancer.

[8]  X. Shu,et al.  Distinct distribution and prognostic significance of molecular subtypes of breast cancer in Chinese women: a population-based cohort study , 2011, BMC Cancer.

[9]  R. Plevin,et al.  Deletion of the Dual Specific Phosphatase-4 (DUSP-4) Gene Reveals an Essential Non-redundant Role for MAP Kinase Phosphatase-2 (MKP-2) in Proliferation and Cell Survival* , 2011, The Journal of Biological Chemistry.

[10]  M. Pegram,et al.  Triple negative breast cancer: unmet medical needs , 2011, Breast Cancer Research and Treatment.

[11]  Gen Sheng Wu,et al.  Post-translational regulation of mitogen-activated protein kinase phosphatase-2 (MKP-2) by ERK , 2010, Cell cycle.

[12]  Stefan Joos,et al.  Epigenetic downregulation of mitogen-activated protein kinase phosphatase MKP-2 relieves its growth suppressive activity in glioma cells. , 2010, Cancer research.

[13]  X. Shu,et al.  Soy food intake and breast cancer survival. , 2009, JAMA.

[14]  P. Conte,et al.  A prognostic model based on nodal status and Ki-67 predicts the risk of recurrence and death in breast cancer patients with residual disease after preoperative chemotherapy. , 2009, Annals of oncology : official journal of the European Society for Medical Oncology.

[15]  A. Nobel,et al.  Supervised risk predictor of breast cancer based on intrinsic subtypes. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[16]  Jennifer L. Osborn,et al.  Direct multiplexed measurement of gene expression with color-coded probe pairs , 2008, Nature Biotechnology.

[17]  S. Narod,et al.  Triple-Negative Breast Cancer: Clinical Features and Patterns of Recurrence , 2007, Clinical Cancer Research.

[18]  C. Mackay,et al.  Targeting dual-specificity phosphatases: manipulating MAP kinase signalling and immune responses , 2007, Nature Reviews Drug Discovery.

[19]  W. Sauerbrei,et al.  REporting recommendations for tumor MARKer prognostic studies (REMARK) , 2006, Breast Cancer Research and Treatment.

[20]  Van,et al.  A gene-expression signature as a predictor of survival in breast cancer. , 2002, The New England journal of medicine.

[21]  J. Downward.  Targeting RAS signalling pathways in cancer therapy , 2003, Nature Reviews Cancer.