Release date: 2014-11-03
The uncontrolled growth of cancer cells is due to their ability to hijack the normal growth processes and checkpoints of cells. Usually after treatment, the main cancer signaling pathway will turn off another cancer signal transduction pathway, thus opening a clever escape route for cancer cell survival. Recently, researchers at Case Western Reserve University in the United States said that the use of two drugs from the beginning can predict and block that alternate track. The results of the study were led by Professor Ruth Keri, deputy director of the Case Comprehensive Cancer Research Center and vice president of the Department of Pharmacology, and published in the recent issue of Cancer Research.
Of course, this effort is not simply doubled. Scientists must choose a specific drug that precisely counters the behavior of cancer cells. Basically, Keri and her colleagues used a drug, rapamycin, to stop the growth of cancer cells, and another drug, dasatinib, to induce cancer cells to think of their original growth. It is still going on quickly.
The scientists chose the drug rapamycin, an inhibitor of the mTOR (mammalian rapamycin target protein) protein, and dasatinib, a drug that blocks Src family kinases (SFKs). Interestingly, both drugs did not show significant clinical efficacy in breast cancer treatment when used alone. In ongoing clinical trials, combining dasatinib or rapamycin with other therapies has proven promising; however, this study demonstrates for the first time that the combination of these two drugs is in the treatment of breast cancer It may be beneficial.
How do cancer cells grow, how does rapamycin and dasatinib interrupt this process? mTOR signals that cells with cancer characteristics grow rapidly. If the mTOR signal is blocked, another protein, AKT (protein kinase B), will take over and signal the cancer to continue to grow and survive. SFKs also work with mTOR and AKT to send signals to promote tumor growth.
Researchers at Keri Labs found that dasatinib blocked the transmission of SFKs. Without the SKF signal, AKT did not receive the message that "mTOR signal has been turned off by rapamycin." Therefore, AKT does not know how to intervene and take over mTOR "send the necessary signals to continue to grow tumors."
Keri said: "We found that if you put these two drugs together, you can kill the tumor better than using one of the drugs alone. This is an important finding. Using two drugs is better than choosing only one of them. a drug."
The researchers used two different mouse models of breast cancer to demonstrate the efficacy of this combination. Magnetic resonance imaging (MRI), the same type of imaging, allows researchers to periodically observe a patient's tumor growth. When the mice eventually formed a tumor, one experimental group received dual treatment with rapamycin and dasatinib, the other experimental group was treated with rapamycin alone, and the other experimental group was treated with only dasatinib. One group was treated with placebo as a control.
In mice treated with a combination of rapamycin and dasatinib, the tumor shrinks or disappears. When receiving dual therapy, none of the mice in this experimental group experienced tumor growth. In contrast, in an experimental group that received only one drug treatment, the mice experienced sustained tumor growth. In the placebo control group, tumors grew rapidly throughout the study.
To make matters worse, in the experimental group receiving monotherapy, when the treatment was stopped, the tumors would return to their original size or even become larger within a few days. When combined drug therapy was stopped, tumor regrowth was greatly delayed by several weeks. “Double treatment can significantly delay tumor regrowth,†Keri said.
Keri and her team then hope to launch a clinical trial to determine whether this combination therapy has the same effect in mice as humans. The first step will be to assess whether humans can respond to this combination of drugs without being overwhelmed by their toxicity. For them, the mice did not show toxicity problems.
Keri said: "We hope to see the same effect in the mouse model in human trials, and ultimately, stop or significantly delay tumor growth."
Source: Biopass
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