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This Week in Cancer Discovery: Jun 13, 2012


In Cancer Discovery this week, researchers in New York and California report that microRNA-23a promotes the transition of colorectal cancer from indolent to invasive disease. The team profiled somatic copy number alterations in noninvasive adenomas and invasive adenocarcinomas from mouse models and identified a recurrent amplicon on mouse chromosome 8 encoding miRNA-23a and -27a, both of which were upregulated in mouse intestinal adenocarcinomas as well as in human colorectal cancer samples and colorectal cancer cell lines. "Functionally, miR-23a promotes the migration and invasion of colorectal cancer cells and stem cells, whereas miR-27a primarily promotes proliferation," the authors write. "We computationally and experimentally validated that metastasis suppressor 1 is a direct miR-23a target and similarly validated that the ubiquitin ligase FBXW7 is a direct miR-27a target."

Also in Cancer Discovery this week, researchers in Italy report that gene signatures associated with medulloblastoma cancer stem cells can be used to predict the molecular classification of human medulloblastoma and identify novel molecular mediators involved in the disease's genesis. The team compared distinct postnatal hindbrain-derived neural stem cells from mouse brains with murine compound Ptch/p53 mutant medulloblastoma cancer stem cells and found that transcriptome analysis of both results in the identification of gene signatures reminiscent of specific human medulloblastoma molecular subclasses. "These data indicate that gene expression analysis of medulloblastoma [cancer stem cells] holds great promise not only for understanding functional differences between distinct [cancer stem cell] populations but also for identifying meaningful signatures that might stratify medulloblastoma patients beyond histopathologic staging," the authors write.

Finally in Cancer Discovery this week, researchers in the US and UK describe a novel mechanism of inducing apoptosis in cancer cells through the inhibition of the protein kinase WEE1. The team shows that WEE1 inhibition forces S-phase-arrested cells into mitosis without letting them complete DNA synthesis. This results in highly abnormal mitoses and, ultimately, mitotic exit and apoptosis. "This mechanism of cell death is shared by CHK1 inhibitors, and combined WEE1 and CHK1 inhibition forces mitotic entry from S-phase in the absence of chemotherapy," the authors write. "We show that p53/p21 inactivation combined with high expression of mitotic cyclins and EZH2 predispose to mitotic entry during S-phase with cells reliant on WEE1 to prevent premature cyclin-dependent kinase (CDK)1 activation." This suggests that WEE1 inhibition could be a targeted therapy for aggressive breast cancer, they add.

The Scan

New Study Investigates Genomics of Fanconi Anemia Repair Pathway in Cancer

A Rockefeller University team reports in Nature that FA repair deficiency leads to structural variants that can contribute to genomic instability.

Study Reveals Potential Sex-Specific Role for Noncoding RNA in Depression

A long, noncoding RNA called FEDORA appears to be a sex-specific regulator of major depressive disorder, affecting more women, researchers report in Science Advances.

New mRNA Vaccines Offer Hope for Fighting Malaria

A George Washington University-led team has developed mRNA vaccines for malaria that appear to provide protection in mice, as they report in NPJ Vaccines.

Unique Germline Variants Found Among Black Prostate Cancer Patients

Through an exome sequencing study appearing in JCO Precision Oncology, researchers have found unique pathogenic or likely pathogenic variants within a cohort of Black prostate cancer patients.