Researchers keep it up developing new medication to fight cancer, and whereas some square measure so effective, others ne’er full-fill their promise.
A new study currently explains why some cancer medication might not add the method their developers suppose they are doing. But within the problem also lies the solution.
Cancer affects many individuals around the world, and in some cases, it does not respond to the forms of therapy that doctors usually prescribe.
For this reason, researchers keep it up trying to find the ever simpler medication that may stop cancer in its tracks. Sometimes, these new medical specialties live up to their developers’ expectations, whereas at alternative times they let down.
As the explore for improved metastatic tumor medication continues, a replacement study has discovered that a lot of the new medications that work usually target completely different mechanisms than those the scientists intended them for. This may additionally make a case for why several new medications fail to figure.
The finding comes from a team of scientists at the Cold Spring Harbor Laboratory in New York, who originally set out to study a different issue. Jason Sheltzer, Ph.D., and the team initially wanted to identify the genes that had links to low survival rates among people receiving cancer treatment.
But this work led them to find something they did not expect that MELK, a protein formerly linked with cancer growth, does not affect tumor progression. Because cancer tumors contain high levels of MELK, researchers had thought that cancer cells used this supermolecule to proliferate.
They thought that by stopping MELK production, this would also slow down tumor growth. However, Sheltzer and colleagues found that this was not true.
If a therapeutic target that researchers believed to control most promise didn’t add the method that scientists had expected, could this also be true of other therapeutic targets? “My intention was to researchable whether or not MELK was an aberration,” notes Sheltzer.
