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Senior Health & Medicine
Cancers Cured in Mice by Blood Cell Transfers from
Immune Mouse
 Also
offered protection for the lifespan of the recipient mouse
May 9, 2006 - White blood cells from a strain of
cancer-resistant mice cured advanced cancers in ordinary laboratory mice
and appears to have made them immune from new cancers, researchers at
Wake Forest University School of Medicine reported yesterday.
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“Even highly aggressive forms of malignancy with
extremely large tumors were eradicated,” Zheng Cui, M.D., Ph.D., and
colleagues reported in this week’s on-line edition of Proceedings of the
National Academy of Sciences.
The transplanted white blood cells not only killed
existing cancers, but also protected normal mice from what should have
been lethal doses of highly aggressive new cancers.
“This is the very first time that this
exceptionally aggressive type of cancer was treated successfully,” said
Cui. “Never before has this been done with any other therapy.”
The original studies on the cancer-resistant mice –
reported in 2003 – showed that such resistance could be inherited, which
had implications for inheritance of resistance in humans, said Mark C.
Willingham, M.D., a pathologist and co-investigator. “This study shows
that you can use this resistant-cell therapy in mice and that the
therapy works. The next step is to understand the exact way in which it
works, and perhaps eventually design such a therapy for humans.”
The cancer-resistant mice all stem from a single
mouse discovered in 1999. “The cancer resistance trait so far has been
passed to more than 2,000 descendants in 14 generations,” said Cui,
associate professor of pathology. It also has been bred into three
additional mouse strains. About 40 percent of each generation inherits
the protection from cancer.
The original group of cancer-resistant mice, also
described in Proceedings of the National Academy of Sciences,
successfully fought off a range of virulent transplanted cancers.
“Now we know that we can take white blood cells
from this strange mouse and put them into a normal mouse and these cells
will still kill cancers,” said Willingham, professor of pathology and
head of the Section on Tumor Biology. “This is therapy in a mouse that
does not have this magical genetic inheritance.”
The transplanted white blood cells included natural
killer cells, and other white blood cells called neutrophils and
macrophages that are part of the body’s “innate immune system.” This
system forms a first line of host defense against pathogens, such as
bacteria.
“Their activation requires no prior exposure, but
rather depends on a pre-determined mechanism to recognize specific
patterns on the cancer cell surface,” the researchers said.
Moreover, preliminary studies show that the white
blood cells also kill “endogenous” cancers – cancers that spring up
naturally in the body’s own cells.
Cui and Willingham said the research produced many
other surprises. For one thing, if a virulent tumor was planted in a
normal mouse’s back, and the transplanted white blood cells were
injected into the mouse’s abdomen, the cells still found the cancer
without harming normal cells. The kind of cancer didn’t seem to matter.
A single injection of cancer-resistant macrophages
offered long-term protection for the entire lifespan of the recipient
mouse, something very unexpected, they said.
“The potency and selectivity for cancer cells are so high that, if we
learned the mechanism, it would give us hope that this would work in
humans,” said Cui. “This would suggest that cancer cells send out a
signal, but normal white blood cells can’t find them.”
Cui said the findings “suggest a cancer-host
relationship that may point in a new therapeutic direction in which
adverse side effects of treatment are minimal.”
The next steps include understanding the molecular
mechanism. “The real key is finding the mutation, which is an ongoing
investigation in collaboration with several other laboratories,” said
Willingham.
Cui, Willingham and their colleagues also showed
that highly purified natural killer cells, macrophages and neutrophils
taken from the cancer-resistant mice killed many different types of
cancer cells in laboratory studies in test tubes.
Besides Cui and Willingham, the team includes Amy
M. Hicks, Ph.D., Anne M. Sanders, B.S., Holly M. Weir, M.S., Wei Du,
M.D., and Joseph Kim, B.A., from pathology, Greg Riedlinger, B.S., from
cancer biology, Martha A. Alexander-Miller, Ph.D., from microbiology and
immunology, Mark J. Pettenati, Ph.D., and C. Von Kap-Herr, M. Sc., from
medical genetics, and Andrew J.G. Simpson, Ph.D., and Lloyd J. Old,
M.D., of the Ludwig Institute for Cancer Research in New York.
The primary support for the research came from the
Cancer Research Institute, a New York based group founded to foster the
science of cancer immunology, on the premise that the body's immune
system can be mobilized against cancer. The research also had support
from the National Cancer Institute and the Charlotte Geyer Foundation.
What Do These Results Mean For Human Cancer Therapy?
By the study authors
First, we should point out that in this mouse
system the donor and recipient mice were both in the same in-bred
laboratory strains of mice. Thus, except for the SR/CR mutation, they
are genetically identical. Our transfer of immune cells between these
mice is basically a transplantation experiment between identical twins.
If we tried this therapy in human patients, the transferred immune cells
would probably not survive, since the donor and recipient would be very
different genetically.
However, these results show that the concept would
work under the right circumstances. For example, if we identified the
gene, it might be possible to take immune cells from a patient and
insert that mutant gene into those cells in the test tube, then give
these cells back to the same patient; this would then perhaps allow the
mutant immune mechanism to work to reject tumor cells without the loss
of the immune cells due to transplant rejection. However, this is a
complex strategy that can have many potential problems.
A more important message from this work is that
such a mechanism is actually possible in intact animals, and that a
thorough understanding of the underlying molecular events could
potentially lead to a new strategy for more specific cancer therapy.
There is second important message from this work.
The fact that the cancer-resistant immune cells can specifically sort
out cancer cells for rapid destruction suggests a fundamental difference
between cancer cells and normal cells.
We can say with confidence that the killing of
cancers by the SR/CR immune cells is remarkably tumor-specific without
causing significant harm to normal tissues in an otherwise normal
mouse. For some reason, the immune cells from these special mice are
capable of detecting these differences.
An important question is: “What are the common
properties of different cancer cells that allow them to be distinguished
by these special immune cells?” While it is possible that cancer cells
express something that activates these SR/CR white blood cells, it is
also possible that these cancer cells may fail to inhibit these SR/CR
white blood cells. That is, the success of cancer growth may be through
the ability of cancer cells to inhibit controls that normally limit the
growth and spread of cells.
The SR/CR immune cells may ignore this common
inhibitory function released by cancer cells, and treat them like any
other out-of-control tissue. We hope that by understanding this
interaction between cells we can uncover clues to these underlying
molecular mechanisms.
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