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We've previously looked at the development of cancer treatments that deliver drugs directly into cancer cells before releasing their chemotherapeutic payload to reduce the damage done to healthy cells. But a new protein "switch" approach developed by researchers at Johns Hopkins University changes the game again by instructing cancer cells to produce their own cancer medication and cause the cancer cells to self-destruct while sparing healthy tissue. The protein switch strategy would see a doctor administering a "prodrug," which is an inactive form of a cancer-fighting drug that would only be activated when it detects the presence of a cancer marker, triggering the cellular switch to turn the harmless prodrug into a potent form of chemotherapy. "The switch in effect turns the cancer cell into a factory for producing the anti-cancer drug inside the cancer cell," said Marc Ostermeier, a Johns Hopkins chemical and biomolecular engineering professor in the Whiting School of Engineering, who supervised development of the switch. "The healthy cells will also receive the prodrug and ideally it will remain in its non-toxic form. Our hope is that this strategy will kill more cancer cells while decreasing the unfortunate side effects on healthy cells." The research team made the cancer-fighting switch by fusing together two different proteins; one that detects a marker that cancer cells produce and another protein extracted from yeast that can turn an inactive prodrug into a cancer-cell killer. "When the first part of the switch detects cancer, it tells its partner to activate the chemotherapy drug, destroying the cell," Ostermeier explained. For the technique to work, the switch first needs to get inside the cancer cells. Ostermeier says this can be done in one of two ways; by delivering the switch protein itself into the cells or, alternatively, delivering the switch gene inside the cell where it serves as the blueprint from which the cell's own machinery constructs the protein switch. Once the switches are in place, the patient would receive the inactive chemotherapy drug, which would then be activated inside the cells where the switch has been flipped on. "The protein switch concept changes the game by providing a mechanism to target production of the anti-cancer drugs inside cancer cells instead of targeting delivery of the anti-cancer drug to cancer cells," Ostermeier said. Although the novel cancer-fighting strategy hasn't yet been tested on human patients, the research team has successfully tested the switches on human colon cancer and breast cancer cells in the lab. The next step is animal testing, which is expected to begin within a year. "This is a radically different tool to attack cancers," said James R. Eshleman, a professor of pathology and oncology in the Johns Hopkins School of Medicine and a co-author of the paper that appears in the Proceedings of the National Academy of Sciences, "but many experiments need to be done before we will be able to use it in patients."

 

Spanish scientists trial promising HIV vaccine

Researchers at the Spanish Superior Scientific Research Council (CSIC) have successfully completed Phase I human clinical trials of a HIV vaccine that came out with top marks after 90% of volunteers developed an immunological response against the virus. The MVA-B vaccine draws on the natural capabilities of the human immune system and "has proven to be as powerful as any other vaccine currently being studied, or even more", says Mariano Esteban, head researcher from CSIC's National Biotech Centre.

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The MVA-B vaccine first showed promising signs back in 2008 when clinical trials involving mice and macaque monkeys demonstrated a very high efficiency against Simian immunodeficiency virus (SIV). The recent human trials involved 30 healthy volunteers, where 24 were treated with MVA-B, while the other 6 were treated with a placebo, carried out over a 48 week period.
Development of MVA-B is based on the insertion of four HIV genes in a previously used vaccine (MVA) for smallpox. When injected with the vaccine, a healthy immune system can react against the MVA, whilst the HIV genes are incapable of self-replicating. This guarantees a safe clinical trial for HIV free volunteers. Furthermore by trialing the vaccine on healthy patients, the immune system can learn how to detect and combat the HIV virus components. "It is like showing a picture of the HIV so that it is able to recognize it if it sees it again in the future", says Esteban.
"Our body is full of lymphocytes, each of them programmed to fight against a different pathogen" continued Esteban. "Training is needed when it involves a pathogen, like the HIV one, which cannot be naturally defeated".

The trial demonstrated how the vaccine stimulates the production of lymphocytes B, which produces HIV attacking antibodies that block the virus from infecting healthy cells. Blood tests during the 48th week revealed that 72.7% of the treated volunteers had developed these HIV fighting antibodies. However generating a long lasting response against future attacks truly renders the vaccine effective. This is achieved when the body maintains a basic memory level of T lymphocytes, which are generated after the first attack and can circulate the body for years. The T lymphocytes are responsible for stimulating the attacked cell's immune response, which can then identify and destroy the HIV virus. Blood tests during the 48th week revealed that the 85% of the patients maintained the memory T lymphocytes immune response.
"MVA-B immune profile meets, initially, the requirements for a promising HIV vaccine," says Esteban. Although it does not remove the virus from the body, the immune response induced by the vaccine could keep the virus under control by destroying the infected cell.
According to CSIC, "if this genetic cocktail passes Phase II and Phase III future clinic trials, and makes it into production, in the future HIV could be compared to herpes virus nowadays".
Phase I clinic trials will also commence with HIV infected volunteers to test its efficiency as a therapeutic vaccine.
Source: Spanish Superior Scientific Research Council (Spanish).