延缓癌症发展 z-bo 2020-10-07 379

　　The latest research from the University of Nebraska-Lincoln, Weststar Institute and other institutes shows that locking the biochemical gate can slow down the speed of energy substances entering the immunosuppressive cells, and more and more tumors progress and help treat various Kind of cancer. A recent study published in the journal Nature found that elevated levels of fatty acid transporter 2 (FATP2) in cells are known to suppress immune responses and interfere with cancer treatment. After isolating tumor cells from humans and mice, the researchers also found that the amount of energy lipids that help FATP2 are produced and transported to the cells has greatly increased.

　　Generally, the results of this study indicate that FATP2 is involved in the most common malicious reorganization process of human white blood cells. As a result, these white blood cells can no longer be the first responders to fight infection. When the researchers eliminated the gene associated with FATP2, they found that certain cancers (including lymphoma, lung cancer, colon cancer, and pancreatic cancer) slowed down significantly in mice. Earlier, Concetta DiRusso in Nebraska discovered Lipofermata, a compound that inhibits FATP2. When used with drugs that interfere with cell replication, it can also help slow or inhibit tumor growth. according to

　　Research, targeting FATP2 in immunosuppressive cells can prevent lipid accumulation and slow down the progression of tumors without serious side effects.

　　"I think the special thing is that this is not for a specific cancer. This excites us." Dirusso is one of the collaborators of this research at George Holmes University. I am a professor of biochemistry. "It is very exciting to be able to target some common cells in different cancers.

　　"It cannot completely eliminate (tumors), but it has a certain inhibitory effect. Yes. Now, we are more interested in combination therapies. Because tumors are smart, they target tumors in many ways, not just one. Target. Tumors have found a way to bypass our best drugs. This is why the combination of these drugs is so powerful, and we hope it will be more effective."

　　Dmitry Gabrilovich of the Wistar Institute and his colleagues first noticed an increase in FATP2 in solid tumors a few years ago. Their observations put Gabrilovich in contact with Paul Black, a Nebraska biochemist who studies fat molecules. The basic principle of how to cross the cell membrane In the early research of black yeast, fatty acids were activated and transported into the cell, and then they were metabolized into energy or entered the cell membrane. Found an implantable gene fragment and related protein, the protein is FATP2, the director of the Biochemical Black Division Charles Bessey (Charles Bessey) said: "Control the amount of fat entering the body into the cell membrane. When you have gated When the right and start to control the gate, it will affect downstream substances. If cancer cells need to provide lipids to metastasize and cause serious diseases, it will increase protein content. Therefore, this gate plays a very important role in all these metabolic systems Role."

　　Black's previous study confirmed that FATP2 has two gene mutations. One is the main metabolic fatty acid, and the other is used to transport them across the cell membrane. This important difference is a study by the DiRusso Institute. Provide evidence: The laboratory has screened more than 100,000 anti-FATP2 compounds, which may help fight obesity and type 2 diabetes

　　The most effective drug candidate, Lipofermata, is basic. When Gabrilovich got in touch with Black, he was able to eliminate fat accumulation in tissue culture and reduce lipid absorption in rats by more than 60%, while DiRusso received a treatment Patent for drugs for metabolic disorders. Contact DiRusso immediately, and the two became Gabrilovich (Gabrilovich), who provided the biochemical views, samples and lipofermata needed for the team experiment. "Whether it is cancer biology or diabetes, or what you are pursuing in this biomedical world, you can't do it yourself. Please sit down." We sit down and do our own thing, like a small shaft, I can do it. The times have passed. Some of our early mechanical work did this, but now it is too complicated. A lot of information.

　　"I don't know the background of the problem, but the published data will make this problem very fast."