By GEORGE JOHNSON
PUBLISHED: 23:50 GMT, 26 August 2013 | UPDATED: 09:06 GMT, 27 August
2013
At the start it all seemed so innocent. My wife Nancy was doing sit-ups
in the gym when she noticed a lump on the inside of her right leg. It didn’t go
away, and she was diagnosed with a tumour that had started for no good reason
in her uterus and burned down into her groin. You start looking for a reason —
how can a cell minding its own business transmogrify into a monster growing
within?
As a science journalist I found something sickly fascinating about the
way a single cell can break from the pack and start multiplying, creating something alien. Nancy
had some known risk factors. She was 43 and we had no children — something we
often argued about. The less frequently a woman is pregnant, the more monthly
menstrual cycles she endures.
With each period a jolt of oestrogen causes cells in the uterus and
mammary glands in the breast to begin multiplying, duplicating their DNA,
preparing for a child that may not come.
Each menstrual cycle is an opportunity
for copying errors that might result in a rogue cell emerging. Oestrogen (along
with asbestos, benzene, gamma rays, and mustard gas) is on the list of known
human carcinogens published by the U.S. government’s National Toxicology
Program.
Women are now also exposed to more monthly doses of oestrogen because
they are beginning to menstruate much earlier, possibly increasing breast
cancer risk. At the same time, women spend less of their fertile life pregnant
or nursing. Lactation also appears to hold oestrogen in check. The result is
that a teenager today may have already experienced more menstrual cycles than
her grandmother did during her entire life. When Nancy’s cancer was discovered,
batteries of tests were needed to discover its precise nature. We didn’t know
for weeks where it started, only that it was shedding cancerous cells into her
body.
Finally, we learned she had cancer of the uterus. That can be relatively
good news if caught early. Nancy’s cancer had, however, advanced to a lymph
node in her groin, which lowers the average survival rate to about 15 per cent.
But those are just averages. Nancy’s youth gave hope for a better than normal
outcome. She was strong and could tolerate multiple rounds of sickening chemo
and burning radiation.
When the postsurgical report came back from the lab, the story became
more complicated. The cancer in her uterus was weak. How could it have spread
so quickly? The answer seemed to lie in a polyp, a centimetre in size, that had
also been cut from Nancy’s uterus. What had marched with such determination
down the ligament and into the groin was a very rare cancer called uterine
papillary serous carcinoma (UPSC) — typically a cancer of older women striking
long after menopause.
It is not believed to be tied to increased oestrogen exposure. Indeed,
‘there are no risk factors’, as two researchers bluntly put it.
Cancer can take decades to develop, so in most cases it is almost
impossible to work out what triggered a rogue cell to become cancerous. It has
been estimated that every second, four million cells in our body are dividing,
copying their DNA (their genetic blueprint). With every division there are
imperfections. Some can go catastrophically wrong.
Research has found some of the causes of cancer: smoking, environmental
pollutants and infections (for example, the human papillomavirus that can cause
cervical cancer). Naturally occurring radiation from sunlight and radon gas
also contribute. Evidence also shows
that a large percentage of cancer cases can be attributed to lifestyle. Opinion
still varies on just what is most important when it comes to food — how much
red and processed meat is bad, how many fruits and vegetables are good.
Nancy always ate her vegetables — obsessively, it sometimes seemed —
and her fibre, bringing home breakfast cereals that tasted like their cardboard
box. But there was nothing rigid about Nancy’s dietary pursuits. We both loved
steaks and hamburgers (though for penance would have fish sometimes).
But the science on food is not persuasive, giving way to suspicion that
lack of exercise and excess weight are more to blame.
Our cells are constantly exchanging chemical signals, conferring on
when to start multiplying and creating new tissue. As each cell receives this
information, it sends instructions to its nucleus for activating the
appropriate genes. A cancer cell is one that, because of some fault, has cut
itself out of this discussion. Random events — triggered by a cosmic ray, a
carcinogenic chemical, or dumb luck — must have altered the DNA inside one of
Nancy’s cells, causing it to lose touch.
These errors happen all the time. We usually don’t get cancer because
other genes react to sudden bursts of activity by reining back the rogue cell’s
growth. But another bad mutation in the cell can cause that safeguard to fail,
by blocking the body’s tumour-suppressing genes. Even if that safeguard fails,
the rogue cell can sense its own inner turmoil and will send itself suicide
signals, killing itself for the common good — a process called apoptosis. But
yet another bad mutation can undermine
this defence.
That still leaves another barrier against runaway growth. A normal cell
can divide only 50 or 60 times. The count is kept by telomeres — caps on the
ends of your chromosomes (which carry your DNA). These telomeres get shorter
each time around, and once they fall below a certain size, the cell is taken
offline.
Once again, however, there is a problem. Cells like those in the immune
system, which must divide repeatedly,
manufacture telomerase, an enzyme that keeps replacing the caps on the
chromosomes’ ends. A cancer cell will learn this trick, acquiring through the
trial and error of mutation the information needed to produce its own
telomerase.
It can then replicate indefinitely, producing a mass of mutant
offspring — a tumour. That is still not enough to give you cancer. It takes
more mutations for the cell to learn how to invade surrounding tissues, to
become malignant. And, even then, the tumour can only grow to the size of a
ballpoint pen’s tip before it risks starving for lack of food or drowning in
its own waste.
To continue expanding, it must somehow reach into the circulatory
system and suck it like a vampire. With these nutrients, the cells multiply
even more aggressively, increasing the probability of more mutations. The cancer spins out one
cell variation after another — hopeful monsters trying to gain an upper hand.
Some cells might learn to consume energy more efficiently, others to suppress
the immune system. Others still will learn to send signals that con healthy
cells into growing new blood vessels that feed the tumour and new tissues that
help to build it.
Finally, the fittest cancer cells will set sail into the bloodstream
and explore new ground. Their chances of
survival are low. Most perish immediately in the river of blood — smashed
against a vessel wall, pinched to death in an impassable strait or destroyed by
the body’s immune cells.
So many dangers — which make it all the more extraordinary that some
beat the odds.
Some research suggests that the swimming cancer cells can surround
themselves with platelets (blood-clotting cells) for protection. Or if they get
stuck inside a tiny capillary, some may be able to jettison enough of their own
bodies to slim down and squeeze through. However they survive the journey, they
still must find a berth downstream. Here, again, most will perish. After 24
hours only 0.1 per cent are alive, and less than 0.01 per cent go on to form
tumours. The odds seem almost comforting, but of all the seeds a tumour can
shed, it takes only one to start another
cancer. Once the cancer cells arrive at a promising location, a new cascade of
events begins. They exchange signals with the natives — the cells of the tissue they are set to
invade — recruiting their help in coming ashore.
If co-operation is not forthcoming, a cancer cell might lie dormant in
its new home, hiding for years until
reawakened by some new random event. When the cancer cells have finally
established their first colony, some will move on to other sites. They may even
return to the mother tumour to rejoin the battle at home. This self-seeding
might help explain the recurrence of
cancers that surgeons are confident they
had completely removed.
Besides the blood, there is another course the seeds can follow from
the tumour — through the lymphatic vessels. The lymph system is a primitive
sewer, sluggishly draining clear, watery waste from cracks between cells. Along
the way it is filtered by the lymph nodes. Tumours can learn to create
connections to the lymphatic system. They may even send signals to a nearby
lymph node, instructing it to sprout more blood vessels to accommodate the
forthcoming invasion.
The lymphatic system — this key component of the body’s defences
designed to filter out infectious organisms, produce white blood cells and
generate antibodies — is turned into a tumour’s ally.
The first sign is a lump growing inside a lymph node, the barrier whose
purpose is to stop such attacks. That apparently is what happened with Nancy.
Inside my body, meanwhile, ten trillion cells are battling the same
inevitable slump towards failure — and the possibility of cancer. It is eerie
to think that inside each one, invisible to the eye, so much is happening. The
cell doesn’t know it has DNA or telomeres. There are no labels, no genetic
alphabet written anywhere, no instructions.
Somehow it all just works. And when it doesn’t, we rage against the
machine.
George Johnson is an award-winning science journalist who has written
for the New York Times and National Geographic; he is the author of nine other
books.
Source: http://www.dailymail.co.uk/health/article-2402396/Monster-inside-body-How-does-single-rogue-cell-turn-deadly-cancer.html#ixzz2dFqcNsLc
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