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Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies.
Gen expression profiles from 21 breast cancer data sets and identified 587 TNBC cases may be useful in biomarker selection, drug discovery, and clinical trial design that will enable alignment of TNBC patients to appropriate targeted therapies.
Definition of a consensus binding site for p53
Recent experiments have suggested that p53 action may be mediated through its inter action with DNA. We have now identified 18 human genomic clones that bind to p53 in vitro. Precise mapping of the…
Refinement of Triple-Negative Breast Cancer Molecular Subtypes: Implications for Neoadjuvant Chemotherapy Selection
Pre-clinical data is provided that could inform clinical trials designed to test the hypothesis that improved outcomes can be achieved for TNBC patients, if selection and combination of existing chemotherapies is directed by knowledge of molecular TNBC subtypes.
Oncogenic forms of p53 inhibit p53-regulated gene expression.
C Cotransfection experiments showed that wild-type p53 activated the expression of genes adjacent to a p53 DNA binding site, which correlated with DNA binding in vitro and provided a basis for the selection of such mutants during tumorigenesis.
Oncoprotein MDM2 conceals the activation domain of tumour suppressor p53
- J. Oliner, J. Pietenpol, S. Thiagalingam, J. Gyuris, K. Kinzler, B. Vogelstein
- 29 April 1993
It is shown that, when expressed in Saccharomyces cerevisiae, human MDM2 inhibits human p53's ability to stimulate transcription by binding to a region that nearly coincides with the p53 acidic activation domain.
WAF1/CIP1 is induced in p53-mediated G1 arrest and apoptosis.
The results support the idea that WAF1/CIP1 is a critical downstream effector in the p53-specific pathway of growth control in mammalian cells.
A tale of two proteins: Differential roles and regulation of Smad2 and Smad3 in TGF‐β signaling
The current understanding of Smad2 and Smad3‐mediated TGF‐β signaling and their relative roles are discussed, in addition to potential mechanisms for the selective activation ofSmad2 versus Smad 3.
Differential Response to Neoadjuvant Chemotherapy Among 7 Triple-Negative Breast Cancer Molecular Subtypes
The clinical relevancy of the 7-subtype classification of triple-negative breast cancer reported by Lehmann and colleagues is confirmed, and may spur innovative personalized medicine strategies for patients with TNBC.
Molecular profiling of the residual disease of triple-negative breast cancers after neoadjuvant chemotherapy identifies actionable therapeutic targets.
UNLABELLED Neoadjuvant chemotherapy (NAC) induces a pathologic complete response (pCR) in approximately 30% of patients with triple-negative breast cancers (TNBC). In patients lacking a pCR, NAC…
Identification and use of biomarkers in treatment strategies for triple‐negative breast cancer subtypes
Common themes emerge from the proposed strategies, such as the use of biomarkers to identify tumours with genomic instability, targeting adapted molecular states resulting from tumour suppressor loss, and targeting altered metabolic pathways.