The dawn of targeted therapies for triple negative breast cancer (TNBC): a snapshot of investigational drugs in phase I and II trials.

Introduction: Triple negative breast cancer (TNBC) was once thought to be an insurmountable disease marked by a lack of targeted treatments. However, we are now witnessing the dawn of targeted therapies for TNBC in which progress has stemmed from an improved understanding of the components that make TNBC unique. The identification of biomarkers, such as BRCA1/2, PIK3CA and RSK2, have advanced the field remarkably and there is considerable interest in finding novel therapeutics for TNBC that offer durable clinical benefit with fewer adverse events.

Concise review: bullseye: targeting cancer stem cells to improve the treatment of gliomas by repurposing disulfiram.

Cancer stem cells (CSCs) are thought to be at the root of cancer recurrence because they resist conventional therapies and subsequently reinitiate tumor cell growth. Thus, targeting CSCs could be the bullseye to successful cancer therapeutics in the future. Brain tumors are some of the most challenging types of cancer to treat and the median survival following the initial diagnosis is 12-18 months.

YB-1 transforms human mammary epithelial cells through chromatin remodeling leading to the development of basal-like breast cancer.

There is growing evidence that cancer-initiation could result from epigenetic changes. Y-box binding protein-1 (YB-1) is a transcription/translation factor that promotes the formation of tumors in transgenic mice; however, the underlying molecular events are not understood. To explore this in a human model system, YB-1 was expressed in mammary epithelial cells under the control of a tetracycline-inducible promoter.

Personalizing the treatment of pediatric medulloblastoma: Polo-like kinase 1 as a molecular target in high-risk children.

Medulloblastoma is the most common malignant brain tumor in children. This disease is heterogeneous and is composed of four subtypes of medulloblastoma [WNT, Sonic Hedgehog (SHH), Group 3, and Group 4]. An immediate goal is to identify novel molecular targets for the most aggressive forms of medulloblastoma.

Overcoming resistance to Sonic Hedgehog inhibition by targeting p90 ribosomal S6 kinase in pediatric medulloblastoma.

Background: Molecular subtyping has allowed for the beginning of personalized treatment in children suffering from medulloblastoma (MB). However, resistance inevitably emerges against these therapies, particularly in the Sonic Hedgehog (SHH) subtype. We found that children with SHH subtype have the worst outcome underscoring the need to identify new therapeutic targets.