Vital protein to stop tumour growth identified
Scientists
have found that researchers should not give up on the beta3-integrin
protein, which has been a major target in cancer drug design for the
last two decades.
LONDON: In what can be called a major relief for scientists working on
cancer research, a new study has reassured the potential of a protein
that can be targetted to stop tumour growth.
Scientists from the University of East Anglia in Britain have found that researchers should not give up on the beta3-integrin protein, which has been a major target in cancer drug design for the last two decades.
"These findings have re-established the expression of beta3-integrin as a valid clinical target when treating cancer. Efforts must now be re-focused to either develop new drugs to target beta3-integrin, or figure out how to more effectively use the drugs that already exist," said Stephen Robinson of the School of Biological Sciences, University of East Anglia.
The research, published in American Heart Association's journal "Circulation Research", also explained why the most advanced version of avAY3-integrin - a stem cell marker and driver of tumour cell resistance - failed clinical trials to treat aggressive forms of brain cancer.
"This research helps to explain why these very promising drugs aren't meeting with the success that was anticipated and it suggests a way forward - how to make them work better," Robinson said.
"We have shown how tumours continue to grow despite treatment which should block blood vessel recruitment. They modulate how they are recruiting their blood vessels by using a different pathway from the one that is being targeted," he said.
"Our research also shows that timing is critical when targeting the protein beta3-integrin," he added.
Scientists from the University of East Anglia in Britain have found that researchers should not give up on the beta3-integrin protein, which has been a major target in cancer drug design for the last two decades.
"These findings have re-established the expression of beta3-integrin as a valid clinical target when treating cancer. Efforts must now be re-focused to either develop new drugs to target beta3-integrin, or figure out how to more effectively use the drugs that already exist," said Stephen Robinson of the School of Biological Sciences, University of East Anglia.
The research, published in American Heart Association's journal "Circulation Research", also explained why the most advanced version of avAY3-integrin - a stem cell marker and driver of tumour cell resistance - failed clinical trials to treat aggressive forms of brain cancer.
"This research helps to explain why these very promising drugs aren't meeting with the success that was anticipated and it suggests a way forward - how to make them work better," Robinson said.
"We have shown how tumours continue to grow despite treatment which should block blood vessel recruitment. They modulate how they are recruiting their blood vessels by using a different pathway from the one that is being targeted," he said.
"Our research also shows that timing is critical when targeting the protein beta3-integrin," he added.
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