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New Cancer Stem Cell Sorting Strategy to Boost Breast Cancer Research

Sorting breast cancer cells using a new reporter construct allows the interrogation of a highly pure population of cancer stem cells and may allow for the discovery of new therapeutic targets

Hedgehog and Epithelial to Mesenchymal Transition: Partners in Crime in Cancer Drug Resistance

Elevated Hedgehog signaling and EMT transcription factor expression allows cancer cells to gain tumor-initiating capabilities and chemoresistant properties

Growth Factor Double Team Promotes Breast Cancer

Researchers determine the roles of proNGF and NGF in breast cancer stem cell regulation, and uncover potentially druggable targets.

Guiding Breast Cancer Therapy through Epigenetic Analysis

DNA methylation studies in cancer stem cells may aid choice of therapy in breast cancer

Utility of Statin Use for Inflammatory Breast Cancer Treatment

A new study suggests that statin use may be justified as a radiosensitizing agent through assessments of cell line activity in vitro and information garnered from a prospective clinical trial.

Cool-1 Therapy for Glioblastoma

Alternately targeted therapy for the treatment of Glioblastoma multiforme shown to be effective in vitro.

Therapeutic Targets to Limit Glioblastoma Recurrence Uncovered

“Cellular Plasticity Confers Migratory and Invasive Advantages to a Population of Glioblastoma-Initiating Cells that Infiltrate Peritumoral Tissue”

From Stem Cells

Treatment of glioblastoma multiforme (GBM) is often problematic due to infiltration of the peritumoral (PT) parenchyma by tumour cells (Kelly et al, Martiroysan et al and Stevenson et al) leading to tumour regrowth.   Additionally, studies into GBM also support the existence of cancer stem cells (CSCs) which survive traditional treatments and initiate tumour recurrence (Eyler and Rich).   As CSCs from GBM (or Glioblastoma Initiating Cells – GICs) have been found in peritumoral regions (Glas et al), studies into the mechanisms behind the ability of GICs to migrate and infiltrate may allow the development of new therapeutic interventions.   In their current study, researchers from the laboratory of Jose L. Fernandez-Luna at the Hospital Universitario Marqués de Valdecilla and Instituto de Formación e Investigación Marques de Valdecilla (IFIMAV), Santander, Spain have shown that GICs isolated from the PT have an invasive advantage over GICs from the tumour mass (TM), and that this is governed by an upregulation in αVβ3 integrin, which promotes Rac1 activation (Dey et al) and is involved in sensing matrix rigidity during cell spreading (Jiang et al) and the downregulation of p27, which can inhibit RhoA activation (Besson et al) (Ruiz-Ontañon et al).

Vaccine against Tumour Spread?

Original article from STEM CELLS

"Preventive Cancer Stem Cell-Based Vaccination Reduces Liver Metastasis Development in a Rat Colon Carcinoma Syngeneic Model"

Cancer stem cells (CSCs) represent a minor population of self-renewing cells that fuel tumour growth and have recently been identified in solid tumors, including those in the colon (O'Brien et al, Ricci-Vitiani et al and Visvader and Lindeman). Colon carcinoma is the second most common cause of cancer-related morbidity due, in part, to the appearance of metastases in the liver in 50%–60% of patients (Steele and Ravikumar). In a recent study published in Stem Cells, researchers from the group of Valérie Pierrefite-Carle at the Université de Nice Sophia Antipolis, Nice, France, using a rat model of colon carcinoma, demonstrate that a preventive vaccination generated using a CSC lysate can protect against the development of this liver metastasis, suggesting that CSC-based vaccination could be an efficient treatment to reduce tumour relapse in colon carcinoma (Duarte and Momier et al).

 

Tumour Stem Cell Marker Identified

“Dclk1 distinguishes between tumor and normal stem cells in the intestine”

The study of tumour stem cells (TSCs) has been hindered by the lack of selective markers which can differentiate between normal stem cells (NSCs) and TSCs. In the intestine, many markers of NSCs and TSCs are shared (Delarba et al, O’Brien et al, Zhu et al and Todaro et al) and so identifying TSC-specific markers is an important challenge. In the following study, researchers from the laboratory of Tsutomu Chiba at Kyoto University Graduate School of Medicine, Japan have studied the doublecortin-like kinase 1 (Dclk1) gene, previously identified in mouse and human intestine (May et al 2008 and May et al 2009) and associated with mouse intestinal tumors and human colorectal carcinomas (May et al 2008 and Gerbe et al), and have found that Dclk1 does not mark NSCs in the intestine but instead marks TSCs, with specific ablation of Dclk1-positive TSCs leading to the regression of intestinal polyps (Nakanishi et al).

Disrupting Metabolism to Eliminate Cancer Stem Cells

"Effective Elimination of Cancer Stem Cells By a Novel Drug Combination Strategy"

Effective means to target cancer stem cells (CSCs) using pharmaceutical agents have been hindered by their seemingly intrinsic resistance to chemotherapeutic agents (Gilbert and Ross). CSCs in Glioblastoma multiforme (GBM) have been shown to be resistant to common chemotherapeutics and radiation (Kang and Kang and Beier et al), and glioblastoma cancer stem cells (GSCs) have been found to reside in hypoxic niches which further promotes drug resistance (Lei et al, Heddleston et al and Li et al). This suggests that the glycolytic pathway may be utilised in these cells to generate energy, giving researchers a potential target for chemotherapeutic intervention. Now researchers from the laboratories of Peng Huang from the State Key Laboratory of Oncology in South China, Guangdong, China and The University of Texas MD Anderson Cancer Center, Texas, USA, in a study published in Stem Cells, have found that 3-bromo-2-oxopropionate-1-propyl ester (3-BrOP), which affects key enzymes in the glycolytic pathway and reduces ATP generation (Ko et al, Geschwind et al and Xu et al), allows the efficient elimination of CD133+ GSCs when used in combination with other common chemotherapeutic agents (Yuan and Wang et al).

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