R
Roger
Guest
At least according to the article below. Seems to
completely change the approach to dealing with cancer since
the cancer stem cells don't have a life cycle like
cancerous non-stem cells.
Roger
------
http://virtualtrials.com/news3.cfm?item=2410
March 11, 2004
Stem Cells in Tumors May Help Explain Some Cancer Mysteries
If anyone still has doubts that the 1950s are a bygone era,
consider some experiments scientists conducted then without
raising eyebrows (let alone lawsuits).
To probe the basics of cancer, a team of scientists injected
cells from patients' colon, lung, ovarian and other tumors
into the patients' own thighs. After trying this with
varying numbers of cells, the scientists found that the
transplants regenerated a tumor in the thigh (or in a mouse)
only if at least one million cells were injected.
If the bioethics of the 1950s fell short of today's, the
science was a harbinger of an upheaval now shaking cancer
biology. After going nowhere for decades, those old results
have finally led to a revolutionary insight.
"Within a tumor mass, there is only a small population of
cells that can spawn more tumor; other cells in the tumor
can't," says cancer biologist Robert Weinberg of the
Whitehead Institute, Cambridge, Mass., who discovered the
first human oncogene.
The existence of these "tumor stem cells" promises to
explain one of the more perplexing, and tragic, mysteries of
cancer treatment. Biologists have made great strides in
identifying molecular pathways by which cancer cells grow
and spread. But although Iressa shrinks non-small-cell lung
cancers, Erbitux shrinks advanced colorectal cancers and the
just-approved Avastin shrinks metastatic colorectal cancer
-- in each case, in only some patients -- the drugs prolong
survival by mere months or not at all.
The reason, says Dr. Weinberg, may be that "killing off the
majority of cells in a tumor will still leave it with the
ability to regenerate another tumor, from these stem cells."
Eradicating the non-stem cells in a tumor "may result in a
remission" and even the appearance of being cancer-free,
explains molecular biologist John **** of the University of
Toronto, but "the disease will relapse if the tumor-
initiating cells are not eliminated."
Discovering that only some cancer cells are able to generate
more tumor has been a struggle, as the lag between those
1950s experiments and today shows.
"The idea of cancer stem cells has been around for a long
time," says biologist Irving Weissman of Stanford
University. But no stem cell (normal or cancerous) had been
isolated until he and his colleagues identified blood-
forming stem cells in mice in 1987, and in humans in 1992.
Seizing on this method for differentiating stem cells from
others, Dr. **** and his team discovered in 1994 that, in
leukemia, only some cells have the ability to spawn more
tumor. The Toronto team dubbed them "leukemic stem cells."
It was an uphill struggle to figure out whether blood
cancers are unique, or whether solid tumors have cancer stem
cells, too. But after begging the university for a crucial
$500,000 machine, biologists led by Michael Clarke and
Muhammad Al-Hajj of the University of Michigan, Ann Arbor,
found last year that breast cancer consists of a few cancer-
initiating cells that can make more breast-cancer cells,
seemingly forever, surrounded by an ocean of noncancer-
initiating cells.
Although the two kinds of cells looked identical, on closer
inspection there were several "markers" -- think of them as
microscopic flags poking up from the cell's surface -- that
distinguish a breast-cancer stem cell from the cells in a
breast tumor that can't generate more tumor. When the
Michigan team injected as few as 100 cells of the former
into mice, breast tumors grew every time. Not even tens of
thousands of noncancer stem cells produced a tumor. Since
the Michigan discovery, researchers in Japan and Canada have
found brain-cancer stem cells; stem cells likely exist in
other solid tumors, too.
Dr. Clarke estimates that breast cancer stem cells make up
as little as 3% to 5% of some tumors. That's the good
news. Those are the only cells you have to kill to cure
cancer, because non-stem cells eventually die off on
their own. Even when non-stem cells spread, they don't
pose much danger because they die after dividing a few
times. The goal of current chemotherapy, to kill as many
cells as possible, can probably be dialed back.
The bad news is that standard chemo hits tumor cells at a
vulnerable point in their life cycle, but cancer stem cells
don't seem to cycle this way. "I think the reason cancer
therapy does not cure all cancers has to do with the unique
properties" of the cancer stem cell, says Dr. ****.
Ever more sobering, the molecular pathways that scientists
have recently identified, with much fanfare, as allowing
cancer cells to grow may not be critical after all. If such
a pathway promotes growth in the zillions of cells that are
not cancer stem cells, it may be inconsequential. The only
pathways that matter are those that keep the miscreants
alive and thriving. Or as Dr. Weinberg told me, "tumor stem
cells may explain why you can have tumor shrinkage but not
life extension. If current chemotherapies don't target tumor
stem cells, the cells keep making more tumor."
On the bright side, knowing which cells they have to kill
gives scientists a better shot at finding therapies that
do that. "I'm optimistic we can figure this out," says
Dr. Clarke.
completely change the approach to dealing with cancer since
the cancer stem cells don't have a life cycle like
cancerous non-stem cells.
Roger
------
http://virtualtrials.com/news3.cfm?item=2410
March 11, 2004
Stem Cells in Tumors May Help Explain Some Cancer Mysteries
If anyone still has doubts that the 1950s are a bygone era,
consider some experiments scientists conducted then without
raising eyebrows (let alone lawsuits).
To probe the basics of cancer, a team of scientists injected
cells from patients' colon, lung, ovarian and other tumors
into the patients' own thighs. After trying this with
varying numbers of cells, the scientists found that the
transplants regenerated a tumor in the thigh (or in a mouse)
only if at least one million cells were injected.
If the bioethics of the 1950s fell short of today's, the
science was a harbinger of an upheaval now shaking cancer
biology. After going nowhere for decades, those old results
have finally led to a revolutionary insight.
"Within a tumor mass, there is only a small population of
cells that can spawn more tumor; other cells in the tumor
can't," says cancer biologist Robert Weinberg of the
Whitehead Institute, Cambridge, Mass., who discovered the
first human oncogene.
The existence of these "tumor stem cells" promises to
explain one of the more perplexing, and tragic, mysteries of
cancer treatment. Biologists have made great strides in
identifying molecular pathways by which cancer cells grow
and spread. But although Iressa shrinks non-small-cell lung
cancers, Erbitux shrinks advanced colorectal cancers and the
just-approved Avastin shrinks metastatic colorectal cancer
-- in each case, in only some patients -- the drugs prolong
survival by mere months or not at all.
The reason, says Dr. Weinberg, may be that "killing off the
majority of cells in a tumor will still leave it with the
ability to regenerate another tumor, from these stem cells."
Eradicating the non-stem cells in a tumor "may result in a
remission" and even the appearance of being cancer-free,
explains molecular biologist John **** of the University of
Toronto, but "the disease will relapse if the tumor-
initiating cells are not eliminated."
Discovering that only some cancer cells are able to generate
more tumor has been a struggle, as the lag between those
1950s experiments and today shows.
"The idea of cancer stem cells has been around for a long
time," says biologist Irving Weissman of Stanford
University. But no stem cell (normal or cancerous) had been
isolated until he and his colleagues identified blood-
forming stem cells in mice in 1987, and in humans in 1992.
Seizing on this method for differentiating stem cells from
others, Dr. **** and his team discovered in 1994 that, in
leukemia, only some cells have the ability to spawn more
tumor. The Toronto team dubbed them "leukemic stem cells."
It was an uphill struggle to figure out whether blood
cancers are unique, or whether solid tumors have cancer stem
cells, too. But after begging the university for a crucial
$500,000 machine, biologists led by Michael Clarke and
Muhammad Al-Hajj of the University of Michigan, Ann Arbor,
found last year that breast cancer consists of a few cancer-
initiating cells that can make more breast-cancer cells,
seemingly forever, surrounded by an ocean of noncancer-
initiating cells.
Although the two kinds of cells looked identical, on closer
inspection there were several "markers" -- think of them as
microscopic flags poking up from the cell's surface -- that
distinguish a breast-cancer stem cell from the cells in a
breast tumor that can't generate more tumor. When the
Michigan team injected as few as 100 cells of the former
into mice, breast tumors grew every time. Not even tens of
thousands of noncancer stem cells produced a tumor. Since
the Michigan discovery, researchers in Japan and Canada have
found brain-cancer stem cells; stem cells likely exist in
other solid tumors, too.
Dr. Clarke estimates that breast cancer stem cells make up
as little as 3% to 5% of some tumors. That's the good
news. Those are the only cells you have to kill to cure
cancer, because non-stem cells eventually die off on
their own. Even when non-stem cells spread, they don't
pose much danger because they die after dividing a few
times. The goal of current chemotherapy, to kill as many
cells as possible, can probably be dialed back.
The bad news is that standard chemo hits tumor cells at a
vulnerable point in their life cycle, but cancer stem cells
don't seem to cycle this way. "I think the reason cancer
therapy does not cure all cancers has to do with the unique
properties" of the cancer stem cell, says Dr. ****.
Ever more sobering, the molecular pathways that scientists
have recently identified, with much fanfare, as allowing
cancer cells to grow may not be critical after all. If such
a pathway promotes growth in the zillions of cells that are
not cancer stem cells, it may be inconsequential. The only
pathways that matter are those that keep the miscreants
alive and thriving. Or as Dr. Weinberg told me, "tumor stem
cells may explain why you can have tumor shrinkage but not
life extension. If current chemotherapies don't target tumor
stem cells, the cells keep making more tumor."
On the bright side, knowing which cells they have to kill
gives scientists a better shot at finding therapies that
do that. "I'm optimistic we can figure this out," says
Dr. Clarke.
