CANCER
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Bloodwise 13<br />
STRATEGIC REPORT<br />
FUELLING FASTER GROWTH<br />
Many cancer cells grow quickly, and need a<br />
rapid energy supply to fuel the production<br />
of new cells. To do this, the cancer quickly<br />
churns out energy-carrying molecules by<br />
hijacking mechanisms normally reserved for times<br />
when oxygen is low or lots of cells are urgently needed<br />
to fight infection. This has been known for a long time,<br />
but has gained renewed interest as scientists have<br />
realised that blocking it is a possible way of starving<br />
the cancer of its fuel.<br />
At University College London Dr Stephen Daw is<br />
leading the UK arm of a large international clinical<br />
trial for children, adolescents and young adults with<br />
newly diagnosed Hodgkin lymphoma. Cure for these<br />
patients often comes after gruelling treatment and<br />
at the expense of long-term health problems because<br />
of the side effects of the treatment, particularly<br />
radiotherapy. By using PET scans that detect abnormal<br />
metabolic activity in cancer cells, the trial aims to<br />
reduce the use of radiotherapy in lower risk patients<br />
who respond well to initial chemotherapy, and to<br />
reduce the intensity of radiotherapy in patients who<br />
still need it.<br />
FOOT ON THE GAS<br />
Normal cells can’t multiply without<br />
the right level of ‘go ahead’ message<br />
from growth signals within the tissue.<br />
But cancer cells don’t rely on external<br />
stimulation: they’re self-sustaining.<br />
They keep themselves alive by making growth signals<br />
themselves, by becoming super sensitive to signals<br />
around them or turning the light switch to ‘always on’.<br />
Many targeted therapies, such as imatinib, work by<br />
dampening these ‘go’ signals.<br />
Professors Conny Bonifer and Peter Cockerill have<br />
a £1.5 million programme at the University of<br />
Birmingham which is focusing on regulator proteins<br />
that have gone awry in one of the biggest blood<br />
cancer killers, acute myeloid leukaemia (AML). As a<br />
consequence the activities of hundreds of genes under<br />
their control are inappropriately altered.<br />
The team want to understand how these changes affect<br />
the growth signalling pathways in different types<br />
of AML and whether drugs can be used to target or<br />
reverse the changes.<br />
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