Dallas (TX) - Researchers at the University of Texas Southwestern Medical Center have announced a discovery which could have a profound impact in the treatment of lung cancer, certain types of breast cancer and some other cancers. Lead researcher Xiaodong Wang, the Howard Hughes Medical Institute investigator at UofT, has developed a therapy which has been shown to cause implanted human cancer cells in mice to commit suicide.
Normal cells that become defective undergo a natural form of suicide, called cellular apoptosis. When this happens, a protein called SMAC, which is short for "second mitochondria-derived activator of apoptosis" is called into action, shown by the hand-drawn illustration on the left (by Sean Petersen, courtesy of Howard Hughes Medical Institute, colorized by TG Daily). That protein is part of every cell's internal "kill yourself" circuitry. It's normally activated only when fatal flaws are found. However, in cancer cells when that circuitry should be activated, there is a type of short-circuit which actually turns it off. This disabling allows the cancer cells to continue living even though they are not viable, should be killed, and are actually quite harmful to the body.
Wang and his researchers were able to develop a short chain molecule which mimics the SMAC protein, or mimetic. When introducing the altered protein, they discovered that in presence of some other proteins and mechanisms which are known to be part of the cell's natural "life-giving circuitry", called TNFa, the artificial SMAC molecule re-activates the internal death pathways. This tells the cancer cell to go ahead and kill itself. And all of this happens in spite of the cancer cell's natural ability to disable the real SMAC signal. The new artificial SMAC molecule steps in and seals the deal.
Studies have shown that some forms of lung cancer, breast cancer, and a few other forms of skin cancer, when mice are injected with cancer cells from a human host and cancerous tumors result, those tumors are significantly reduced in size with this treatment. In a few cases, they were completely eradicated without any other form of treatment which would affect the cancer cells. Wang and others also indicate that the harm to normal, healthy cells within the body would likely be significantly less than existing treatments, specifically those which attack the body at large, making SMAC-derived protocols very promising future treatment possibilities.
Wang said, "People have suspected for a long time that some cancer cells may somehow turn on their apoptotic pathway. And now that we know what pathway they turn on and why, we can take advantage of this phenomenon for potential cancer therapies by switching a [faulty] signal into a deadly one with SMAC mimetics."
Wang and his team recently announced this latest research. His work follows previous research in the same area as a form of brain cancer called glioblastoma was studied in 2004. His research team was able to demonstrate that SMAC could be used to kill cells in the lab. This new report indicates that the SMAC molecule works in other forms of cancer. Wang and his team are currently investigating the various cell lines to determine what it is that makes these particular types of cells susceptible to SMAC, while other cancers resist the treatment.
Normal cells that become defective undergo a natural form of suicide, called cellular apoptosis. When this happens, a protein called SMAC, which is short for "second mitochondria-derived activator of apoptosis" is called into action, shown by the hand-drawn illustration on the left (by Sean Petersen, courtesy of Howard Hughes Medical Institute, colorized by TG Daily). That protein is part of every cell's internal "kill yourself" circuitry. It's normally activated only when fatal flaws are found. However, in cancer cells when that circuitry should be activated, there is a type of short-circuit which actually turns it off. This disabling allows the cancer cells to continue living even though they are not viable, should be killed, and are actually quite harmful to the body.Wang and his researchers were able to develop a short chain molecule which mimics the SMAC protein, or mimetic. When introducing the altered protein, they discovered that in presence of some other proteins and mechanisms which are known to be part of the cell's natural "life-giving circuitry", called TNFa, the artificial SMAC molecule re-activates the internal death pathways. This tells the cancer cell to go ahead and kill itself. And all of this happens in spite of the cancer cell's natural ability to disable the real SMAC signal. The new artificial SMAC molecule steps in and seals the deal.
Studies have shown that some forms of lung cancer, breast cancer, and a few other forms of skin cancer, when mice are injected with cancer cells from a human host and cancerous tumors result, those tumors are significantly reduced in size with this treatment. In a few cases, they were completely eradicated without any other form of treatment which would affect the cancer cells. Wang and others also indicate that the harm to normal, healthy cells within the body would likely be significantly less than existing treatments, specifically those which attack the body at large, making SMAC-derived protocols very promising future treatment possibilities.
Wang said, "People have suspected for a long time that some cancer cells may somehow turn on their apoptotic pathway. And now that we know what pathway they turn on and why, we can take advantage of this phenomenon for potential cancer therapies by switching a [faulty] signal into a deadly one with SMAC mimetics."
Wang and his team recently announced this latest research. His work follows previous research in the same area as a form of brain cancer called glioblastoma was studied in 2004. His research team was able to demonstrate that SMAC could be used to kill cells in the lab. This new report indicates that the SMAC molecule works in other forms of cancer. Wang and his team are currently investigating the various cell lines to determine what it is that makes these particular types of cells susceptible to SMAC, while other cancers resist the treatment.
Shop Keywords: cancer treatment lung breast skin melanoma SMAC TNFa University of Texas Southwestern Medical Center Xiaodong Wang Howard Hughes second mitochondria derived activator of apoptosis




