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Damian A. Johnson

Researcher at The Breast Cancer Research Foundation

Publications -  5
Citations -  6026

Damian A. Johnson is an academic researcher from The Breast Cancer Research Foundation. The author has contributed to research in topics: Cell migration & Breast cancer. The author has an hindex of 5, co-authored 5 publications receiving 5298 citations.

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Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy

TL;DR: BRCA1 or BRCA2 dysfunction unexpectedly and profoundly sensitizes cells to the inhibition of PARP enzymatic activity, resulting in chromosomal instability, cell cycle arrest and subsequent apoptosis, illustrating how different pathways cooperate to repair damage.
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FGFR Signaling Promotes the Growth of Triple-Negative and Basal-Like Breast Cancer Cell Lines Both In Vitro and In Vivo

TL;DR: Basal-like breast cancer cell lines, and breast cancers, express autocrine FGF2 and show sensitivity to FGFR inhibitors, identifying a potential novel therapeutic approach for these cancers.
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The collagen receptor Endo180 (CD280) Is expressed on basal-like breast tumor cells and promotes tumor growth in vivo.

TL;DR: It is shown that high levels of Endo180 are found in a subset of basal-like breast cancers and that this expression is an independent prognostic marker for shorter disease-free survival, arguing that elevated expression of this receptor in tumor cells could have important consequences in subsets of basal -like carcinomas for which there is a current lack of effective treatment.
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An In Vivo Functional Screen Identifies ST6GalNAc2 Sialyltransferase as a Breast Cancer Metastasis Suppressor

TL;DR: It is demonstrated that the prometastatic role of galectin-3 is regulated by its ability to bind to the tumor cell surface and highlighted the potential of monitoring ST6GalNAc2 expression to stratify patients with breast cancer for treatment with galectine-3 inhibitors.
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Endoglin expression in breast tumor cells suppresses invasion and metastasis and correlates with improved clinical outcome

TL;DR: It is demonstrated that endoglin is expressed in a subset of invasive breast cancers and cell lines and is subject to epigenetic silencing by gene methylation, which correlates with poor clinical outcome in a large cohort of invasive Breast Cancer patients.