New research published in the open access journal BMC Cancer sheds more light on the suspected association between olive oil-rich Mediterranean diets and reductions in breast cancer risk.

Javier Menendez from the Catalan Institute of Oncology and Antonio Segura-Carretero from the University of Granada in Spain led a team of researchers who set out to investigate which parts of olive oil were most active against cancer. Menendez said, "Our findings reveal for the first time that all the major complex phenols present in extra-virgin olive oil drastically suppress overexpression of the cancer gene HER2 in human breast cancer cells".

Extra-virgin olive oil is the oil that results from pressing olives without the use of heat or chemical treatments. It contains phytochemicals that are otherwise lost in the refining process. Menendez and colleagues separated the oil into fractions and tested these against breast cancer cells in lab experiments. All the fractions containing the major extra-virgin phytochemical polyphenols (lignans and secoiridoids) were found to effectively inhibit HER2.

Although these findings provide new insights on the mechanisms by which good quality oil, i.e. polyphenol-rich extra-virgin olive oil, might contribute to a lowering of breast cancer risk in a HER2-dependent manner, extreme caution must be applied when applying the lab results to the human situation. As the authors point out, "The active phytochemicals (i.e. lignans and secoiridoids) exhibited tumoricidal effects against cultured breast cancer cells at concentrations that are unlikely to be achieved in real life by consuming olive oil".

Nevertheless, and according to the authors, "These findings, together with the fact that that humans have safely been ingesting significant amounts of lignans and secoiridoids as long as they have been consuming olives and extra-virgin oil, strongly suggest that these polyphenols might provide an excellent and safe platform for the design of new anti breast-cancer drugs".

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The two found that the CRISPR locus can block the transfer of plasmids from one S. epidermidis strain to another or between S. epidermidis and S. aureus strains. The researchers' experiments show that the CRISPR locus limits the ability of the S. epidermidis strain to act as a plasmid recipient, essentially denying entry to the genes carrying the resistance.

They also found that "CRISPR interference," as this phenomenon is known, involves the targeting of the incoming plasmid or virus DNA directly. The CRISPR locus gives rise to RNA molecules (chemical cousins of DNA) that apparently recognize the incoming plasmid or virus DNA by the classic base pairing defined by Watson and Crick. This recognition then appears to lead to DNA destruction by unknown mechanisms.

Virtually any DNA molecule could be targeted with CRISPR interference. This blocking mechanism can, in principle, be "programmed" by incorporating into the CRISPR locus any desired A, T, G, C sequence that would match a target. It could potentially be used to fight antibiotic resistance in other pathogenic bacteria, including those that cause anthrax, tuberculosis, cholera and plague.

The programmable nature of CRISPR interference makes it analogous to RNA interference (RNAi), which has received much attention for its ability to block the functions of specific genes in human cells. Unlike RNAi, however, CRISPR interference operates naturally in bacteria.

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