The scientist discovers the survive new mechanism of stimulative cancer cell

The scientist discovered a kind of sealed mechanism before this, one kind calls cuticular cell to grow factor accepts put oneself in another's position (EGFR) cheese ammonia acerbity kinase is not kinase to depend on what the mechanism promotes cancer cell to survive through a kind.

　　 scientist discovered a kind of sealed mechanism before this, one kind calls cuticular cell to grow factor accepts put oneself in another's position (EGFR) cheese ammonia acerbity kinase is not kinase to depend on what the mechanism promotes cancer cell to survive through a kind. The clinical trial result that this research disturbs kinase activity for latter and mere with a view to fares badly offerred a kind of explanation, hinted the possible new way that treats strategy.

　　 EGFR and cellular hyperplasia, survive and closely related excessive expression, and often can observe in the cancer of epithelial origin the activation of EGFR. Up to now, people thinks the most function of EGFR gets the adjusting control of its kinase activity, the development in the process that treats these cancer in with a view to went a few kinds to restrain the compound of this kinase activity technically. However, up to now clinical experience makes clear, the activity that mere block stops acerbity kinase of EGFR cheese ammonia cannot bring about clear clinical result on most patient body.
　
　 　 "EGFR is related the expressive level in cancerous organization and prognosis, but the reaction with therapeutics of depressor of acerbity to EGFR cheese ammonia kinase is not relevant, lai Jiji of this clew EGFR notting comply's enzymatic activity is opposite possibly also the development of cancer has contribution, "The Dr. IsaiahJ.Fidler explanation that biology of cancer of Anderson cancer center is the university says the author of this research, Dekesasi. Dr. Fidler and his colleague was designed a series of experiment, the hurried that the blame kinase of the EGFR in investigating cancer cell thereby depends on lives function.

This group of scientists discover 　 　 the mechanism that EGFR depends on through be not kinase with a kind stabilizes sodium - dextrose turns in all vehicle 1(SGLT1) , let human cancer cell maintain level of the dextrose inside enough cell thereby. Dextrose is the content end the main energy of all cells, if lack the dextrose of proper amount, the cell can call the procedure that dies from bite sex cell through starved to death oneself. Cancer cell is very active in metabolic respect, used up more dextrose than normal cell; In addition, the excessive expression of EGFR and relevant SGLT1 stability increase can let tumor cell be in live below not quite ideal to normal cell condition even.

　 　 " our result hints EGFR Lai Jiji notting comply's enzymatic activity also can maintain level of the dextrose inside basic cell, because this prevented cancer cell,the trend dies from bite sex. This kind of function of possible EGFR more the viability below the case that strengthened cancer cell to exist in the medicaments that change cure, "Dr. Mien-ChieHung puts forward one of authors of research. The kinase activity that this group of scientists offer to restrain the SGLT1 stability that gets EGFR adjusting control and EGFR at the same time may be epithelial to eradicating cancer is necessary.