CANCER

Bloodwise 12
STRATEGIC REPORT
at Imperial College have developed a new drug that
blocks faulty NF-kB signals in myeloma, and a new
project seeks to test whether the same effects can be
seen in diffuse large B-cell lymphoma.
A WOUND THAT NEVER HEALS
Inflammation in tissues is how the body
responds to injury. It helps bring in the
cells needed to remove old cells and
make new ones. Just as the immune cells
gather near a site of injury to begin tissue repair,
cancers mimic these signals to surround themselves
with immune cells to promote their uncontrolled cell
growth.
A new project at Kings College in London will
investigate how corrupted non-cancerous cells in
leukaemia potentially block the action of killer
white blood cells, preventing removal of the cancer
cells. This is to develop strategies to re-educate the
corrupted surrounding cells to improve new and
existing immunotherapies.
GENETIC CHAOS
Cancer is a disease of the genes. Errors
in DNA – sometimes inherited but more
often acquired during a person’s lifetime
– disrupt the normal ‘stop / go’ switches,
leading to cells growing out of control.
As the safety switches and repair mechanisms
are bypassed, the cancer cells become a hotbed
of genetic faults – further disrupting the cellular
machinery. Different daughter cells pick up different
combinations of abnormalities, and daughter cells
with faults that best allow them to survive and grow
will dominate. They pass on the ‘cancer-promoting’
genetic abnormalities to their daughter cells and the
vicious circle continues.
Our scientists at the Institute of Cancer, led by
Professor Mel Greaves, Sutton are cataloguing the
series of genetic abnormalities acquired by cancer cells
in acute lymphoblastic leukaemia in children. This is
highlighting the key steps that need to happen for the
disease to occur, raising the possibility that we’ll be
able to develop preventative therapies.
We’ve also supported a national consortium to
decipher the DNA sequence of individual patients
with aggressive non-Hodgkin lymphomas, with the
aim to match them to particular drugs that target the
specific biological faults driving the cancer. The goal
is to design a broad genetic profiling test to identify, in
advance, the drugs patients are most likely to benefit
from, especially if they relapse.
REFUSING TO DIE
When a cell divides to make new cells,
it has to duplicate its DNA and produce
all the cellular machinery needed in the
new cells. Each cell has a series of in-built
quality control steps – if the cell has any damage, the
cell division process is stopped until the damage is
repaired. If the damage is too great to repair, the cell
gets stalled at one of the checkpoints and initiates a
tidy cell death program that leaves no trace of the cell
behind. Genetic faults in cancer cells bypass these
safety checkpoints and let it escape the cell death
program, meaning damaged cancerous cells can carry
on growing.
Drugs like imatinib have been transformational in
controlling chronic myeloid leukaemia, but they don’t
cure the disease and relapse is possible. Professor
Tessa Holyoake in Glasgow has a £1.8 million
programme which is investigating whether crippling
other molecular gatekeepers of cell growth and
division can eliminate the ‘master’ leukaemia stem
cells.
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