Killing Cancer Cells with a Trojan Horse Strategy

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Really fascinating talk by Johns Hopkins University researcher Peter L. Pedersen, PhD. Dr. Pedersen’s lab is studyiTrojanHorseng a compound that disrupts cancer cells’ mitochondria, the energy-producing part of the cell. If cancer cells can’t produce energy – they die. But disrupting the mitochondria in cancer cells is challenging: there are two sources of energy in cancer cells – only one in healthy cells – and the trick is to target only the cancer cells, not the healthy one, said Dr. Pedersen.

Dr. Pedersen presented his lab’s findings on a compound called 3-BrPA for short, which appears to stop liver cancer cells from producing energy. 3-BrPA sneaks into a cancer cells’ mitochondria using the Trojan Horse strategy. It’s structurally similar to another compound (lactic acid) found in high amounts in cancer cells. The cancer cells mistakes 3-BrPA for lactic acid and transports it inside. There, 3-BrPA gets in the way of the two pathways in energy production.

In animal studies, Dr. Pedersen’s lab has had promising results. For example, out of 33 animals with advanced liver cancer: the tumors of the 19 animals treated with 3-BrPA all went away within 1 to 4 weeks; the tumors in the untreated animals continued to grow.

While exciting, right now this research is still only in the laboratory phase.

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    Investigating the Energy-Cancer Link

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    More news on calorie restriction, from Dr. Stephen D. Hursting, a researcher at the University of Texas at Austin. If restricting calories delays and/or prevents tumor formation – as a wide body of research shows – the question is how. And why does obesity increase the risk of cancer? (It does: If you haven’t already read about it – take a look at AICR’s new analysis on the obesity-cancer link.)

    Dr. Hursting’s lab is trying to figure out what’s going on in the link between energy intake and cancer. He talks about the animal research involving a key factor in metabolizing energy: IGF-1, which is linked to increased risk of cancer. His research has shown that calorie restriction and obesity both appear to share a common signaling pathway.

    He also spoke about some intriguing, relatively new research looking at how exercise plays a role in cancer prevention and energy. Although it looks like exercise does add to the calorie restriction effect, he said, obesity prevention by exercise is not the same as by weight. Two animals can be the same weight – one by diet and the other by exercise – yet there appear to be different signaling effects and gene expressions happening.

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      Restricting Calories: Preventing Cancer?

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      The morning research conference session starts out with the tantalizing question of how can delay aging, asked by Rafael de Cabo, PhD. Dr. Cabo, who works at NIH’s National Institute on Aging, said how in the lab, the only way that we can restrict aging so far is by calorie restriction. Caloric restriction also delays tumor formation. (In lab research, caloric restriction diets are usually extreme.)

      Caloric restriction seems counter-intuitive, he explains. You would think that lowering one’s calories – energy – would lead to fatigue and the organisms’ functions would shut down. But that is not the case; it somehow uses the energy it has in a different way.

      Somehow, Dr. Cabo said, the organism or cell has a way to sense the nutrients. Dr. Cabo presented his lab’s research on the link between a specific gene — Nrf2 – and caloric restriction. He is looking at if Nrf2 activates the effect of calorie restriction, and if so, how it works. As usual, his research is turning up more questions and is ongoing.

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