We have invested in world-class research for over two decades, resulting in several refereed publications. This page serves to highlight some of our most important and relevant publications that are in alignment with our goals.
1. Inhibition of RSK with the novel small-molecule inhibitor LJI308 overcomes chemoresistance by eliminating cancer stem cells.
Davies AH, Reipas K, Hu K, Berns R, Firmino N, Stratford AL, Dunn SE. (2015)
Blocking the RSK Pathway kills Triple Negative Breast Cancer (TNBC) cells that our resistant to chemotherapies that patients typically receive in the clinic.
2. YB-1 transforms human mammary epithelial cells through chromatin remodeling leading to the development of basal-like breast cancer.
Davies AH, Reipas KM, Pambid MR, Berns R, Stratford AL, Fotovati A, Firmino N, Astanehe A, Hu K, Maxwell C, Mills GB, Dunn SE. (2014)
The RSK Pathway activates the YB-1 protein, leading to the development of TNBC. TNBC is also called 'basal-like' breast cancer.
3. Targeting p90 ribosomal S6 kinase eliminates tumor-initiating cells by inactivating Y-box binding protein-1 in triple-negative breast cancers.
Stratford AL, Reipas K, Hu K, Fotovati A, Brough R, Frankum J, Takhar M, Watson P, Ashworth A, Lord CJ, Lasham A, Print CG, Dunn SE. (2012)
RSK was identified as the most important drug target for TNBC.
4. Targeting tumour-initiating cells to improve the cure rates for triple-negative breast cancer.
Stratford AL, Reipas K, Maxwell C, Dunn SE. (2010)
Inhibiting Tumor-initiating cells or cancer stem cells are a promising way of attacking TNBC.
5. The promise and challenges of targeting RSK for the treatment of cancer.
Stratford AL, Dunn SE. (2011)
Invited review of explaining why RSK is an excellent drug target.
6. Y-box binding protein-1 induces the expression of CD44+ and CD49f leading to enhanced self-renewal, mammosphere growth, and drug resistance.
To K, Fotovati A, Reipas KM, Law JH, Hu K, Wang J, Astanehe A, Davies AH, Lee L, Stratford AL, Raouf A, Johnson P, Berquin IM, Royer HD, Eaves CJ, Dunn SE. (2010)
The transcription factor YB-1 is activated by RSK leading to an increase in the cancer stem cells. Cancer stem cells are identified by the expression of the cell surface receptors CD44+ and CD49f.
7. The expression of activated Y-box binding protein-1 serine 102 mediates trastuzumab resistance in breast cancer cells by increasing CD44+ cells.
Dhillon J1, Astanehe A, Lee C, Fotovati A, Hu K, Dunn SE. (2010)
Activation of the YB-1 by RSK increases drug resistance. Specifically activation is the RSK/YB-1 pathway is associated with resistance to trastuzumab - also called Herceptin. Herceptin is a drug used to treat a certain type of breast cancer that possesses high levels of the Her-2 receptor.
8. Y-box binding protein-1 serine 102 is a downstream target of p90 ribosomal S6 kinase in basal-like breast cancer cells.
Stratford AL, Fry CJ, Desilets C, Davies AH, Cho YY, Li Y, Dong Z, Berquin IM, Roux PP, Dunn SE. (2008)
RSK is the major kinase responsible for activating YB-1 in Triple Negative Breast Cancer ( also called 'basal like' breast cancer).
9. Interplay between YB-1 and IL-6 promotes the metastatic phenotype in breast cancer cells
Bàrbara Castellana, Trond Aasen, Gema Moreno-Bueno, Sandra E. Dunn, Santiago Ramón y Cajal (2015)
Describes a novel signaling network in which YB-1 regulates IL-6, and vice versa, creating a positive feed-forward loop driving EMT-like metastatic features during breast cancer progression.