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This Week in BMC Cancer: Feb 6, 2012

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In BMC Cancer, researchers at the University of Porto in Portugal and Vanderbilt University examined the pathogenicity of somatic mitochondrial DNA mutations found in cancer. They compared the predicted pathogenicity of the mtDNA mutations to variations seen in the human populations and all possible variations. "Our results show that the somatic mtDNA mutations reported over all tumors are indistinguishable from a random selection from the set of all possible amino acid variations, and have therefore escaped the effects of purifying selection that act strongly at the population level," the researchers write.

Researchers led by Qiang Wu at Anhui Medical University in China report that miR-133 expression is lost in breast cancer cells. Further, lower expression of miR-133 was linked to lymph nodes metastasis, worse clinical stage, and shorter relapse-free survival. "Functionally, miR-133a can suppress tumor cell invasion and migration and targeted the expression of FSCN1," Wu et al. write. "Future study will verify whether detection of miR-133a expression can [serve] as a novel biomarker for breast cancer progression and patient prognosis."

Finally in BMC Cancer, Peng Hou at Jiaotong University School of Medicine in Xi'an, China, and colleagues found that PIK3CA amplification occurs in 67 percent of gastric cancer patients and that such amplification was linked with increased levels of phosphorylated Akt. In addition, PIK3CA amplification was associated with poor survival. "PIK3CA amplification was closely associated with elevated p-Akt, suggesting that this genetic alteration may be a major mechanism in activating the PI3K/Akt signaling pathway, and contribute to gastric tumorigenesis," the researchers write. "Thus, specific genotype-based targeting against the PI3K/Akt signaling pathway may be an effective therapeutic strategy for gastric cancer."

The Scan

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Nucleic Acids Research Papers on SomaMutDB, VThunter, SCovid Databases

In Nucleic Acids Research this week: database of somatic mutations in normal tissue, viral receptor-related expression signatures, and more.