Treatments: Should Cancer Stem-Cells BeTheFocus?

(IMO stem cells are what Beard describes as the germ cells
in trophoblast thesis of cancer) There was a recent article
on stem cells and Beard's thesis in New Scientist - you
might want to try chasing it up. www.newscientist.com Basic
theory is that cancer is a placenta (The theory still stands
up to scrutiny today - this doesn't mean it is right!). In
pregnancy at (56 days *I think*?) the babies pancreas
becomes active and it starts pumping out proteolytic enzymes
trypsin/chymotrypsin. These enzymes kill the invasive cells
of the placenta and stop it from growing/invading the
mother. Anth

<[email hidden]> wrote in message news:12914-40990CD5-119@storefull-
3195.bay.webtv.net...

Quoted message said:

google.comsearchOpen ↗

From what I just read, the currect cancer treatments might
be the wrong approach, because they don't target cancer
stem-cells.

I was reading about cDNA, gene-chips, & cancer.

Susan, Su_Texas my opinions

U-M scientists find "stem cells" in human breast cancer =A0
Discovery could explain current treatment failures, and lead
to more effective therapies for many cancers: added 02/24/03

ANN ARBOR, Mich. - Of all the neoplastic cells in human
breast cancers, only a small minority - perhaps as few as
one in 100 - appear to be capable of forming new malignant
tumors, according to just-published research by scientists
in the University of Michigan Comprehensive Cancer Center.

The discovery could help researchers zero in on the most
dangerous cancer cells, to develop new more-effective
treatments.

"These tumor-inducing cells have many of the properties of
stem cells," says Michael Clarke, M.D., a U-M professor of
internal medicine, who directed the study. "They make copies
of themselves - a process called self-renewal - and produce
all the other kinds of cells in the original tumor."

Although similar cells have been identified in human
leukemia, these are the first to be found in solid tumors,
Clarke adds.

The cells were isolated from primary or metastatic breast
cancers, removed from nine women treated for cancer at the
U-M's Cancer Center.

The discovery - reported this week in the online early
edition of the Proceedings of the National Academy of
Sciences - also may explain why current treatments for
metastatic breast cancer often fail, says Max S. Wicha,
M.D., an oncologist and director of the U-M Comprehensive
Cancer Center.

"The goal of all our existing therapies has been to kill as
many cells within the tumor as possible," Wicha says. "This
study suggests that the current model may not be getting us
anywhere, because we have been targeting the wrong cells
with the wrong treatments. Instead, we need to develop drugs
targeted at the tumor's stem cells. If we are to have any
real cures in advanced breast cancer, it will be absolutely
necessary to eliminate these cells.

"What this means for women with cancer is that, for the
first time, we can define what we believe are the important
cells - the cells which determine whether the cancer will
come back or be cured," Wicha adds. "Before this, we didn't
even know there were such cells."

All cancer cells have a unique pattern of proteins, similar
to a fingerprint, on their surface membranes, explains
Muhammad Al-Hajj, Ph.D., a U-M post-doctoral fellow and
first author of the PNAS paper. " We used specific
antibodies and flow cytometry technology, to segregate the
phenotypically heterogenous cancer cells within a tumor,
into isolated populations based on their surface protein
markers," Al-Hajj says.

These isolated cell populations were then individually
injected into immune-deficient mice, and the mice were
examined for tumor growth every week for up to six months.

Al-Hajj found [that] a small group of cells, with a
phenotype common to all but one of the human tumors in the
study, could form new cancers in
mice. These cells all expressed a protein marker called
CD44, in addition to having either very low levels or
no levels of a marker called CD24.

"As few as 100 to 200 of these tumor-inducing cells,
isolated from eight of nine tumors in the study, easily
formed tumors in mice, while tens of thousands of the other
cancer cells from the original tumor failed to do so,"
Clarke says.

The fact that tumor-inducing stem cells from eight of nine
women, showed a common surface marker pattern is
significant, Wicha explains. "Even though it's only nine
patients, it shows that the markers identifying these stem
cells, were expressed in the majority of breast cancer
patients in the study. This may not be the only expression
pattern on every patient's stem cells, but it demonstrates
the validity of the cancer stem cell model."

To test the stem cell's ability to regenerate the
original tumor, U-M scientists repeated the experiment up
to four times.

First, 200 cells with the unique two-marker surface pattern,
were isolated from the original human tumor. When these
cells produced a breast tumor in a mouse, Al-Hajj removed
the mouse tumor, and used flow cytometry to isolate 200 stem
cells from it. These cells were then injected into another
mouse to produce another tumor. Once again, the tumor was
harvested, stem cells were separated, and injected into
another mouse. Each procedure is called a passage.

"Tumor cells with this particular surface marker pattern,
produced a new tumor in the next generation of mouse every
time," Clarke explains. "When we examined the tumors after
each passage, we found their cell diversity to be the same
as the original tumor."

Given that tumor-inducing cells now have been identified in
breast and blood cancers, Wicha and Clarke believe it is
likely that similar cells drive the development of other
types of cancer, as well.

The U-M Comprehensive Cancer Center is establishing a new
research program, to identify stem cells in other cancers
and develop new therapies to destroy them.

"What we are working on now, is finding out what makes these
tumor stem cells different from the other cells in a tumor,"
Wicha says. "Now that we can actually identify them, we can
start developing treatments to specifically target and
hopefully eliminate them."

"This is not a cure for cancer," Clarke emphasizes. "But it
is a very promising lead, which will focus our efforts to
try to find a cure for cancer."

In addition to Al-Hajj, Wicha and Clarke, Sean J. Morrison,
Ph.D., a Howard Hughes Medical Institute assistant
investigator and U-M assistant professor of internal
medicine, is a collaborator in the research study. The U-M
study was funded by the National Cancer Institute.

The U-M has applied for a patent on the identity and
function of tumor stem cells.

Special notes on this release:

Though promising, this research is still in the animal
testing stage.

Additional research will be needed, before this research
progresses to the point, where it could benefit breast
cancer patients.

["]http://www.cancer.med.umich.edu/news/stemcell.htm]

----------------

Susan, Su_Texas my opinions

["]http://www.genomenewsnetwork.org/articles/03_03/stem_c.shtml]

The Real Problem in Breast Tumors: Cancer Stem Cells=A0=A0By
Nancy Touchette, March 7, 2003

The quest for a cancer cure seems like the ending to a Kafka
novel: so close, yet so far away. Decades of research and
billions of dollars in funding have revealed much about the
molecular events that lead to cancer. But overall, today's
cancer cure rates are not much better than they were 30
years ago.

Part of the problem, a new study suggests, is that current
cancer therapies may be targeting the wrong cells. The real
issue may be a small population of cells in tumors that
resemble adult stem cells (the self-replicating cells that
give rise to specialized cells in tissues).

Michael F. Clarke and Max S. Wicha, and their colleagues at
the University of Michigan in Ann Arbor, have identified a
small population of cells in breast tumors, that can seed
the growth of new cancers. These cancer-causing cells, which
make up a tiny fraction of cells within tumors, have
properties similar to those of stem cells.

"This study creates a whole new conceptual paradigm, of how
tumors form," says Robert A. Weinberg of the Whitehead
Institute for Biomedical Research, an early pioneer in the
study of cancer-causing genes. "It changes our thinking."

Researchers have traditionally thought of cancer, as a
collection of cells all growing exponentially. "This paper
demonstrates convincingly, that the model is wrong," says
Weinberg. "Only a few cells are endowed with the ability to
replicate. It has profound implications, for how we think
tumors evolve and how we treat tumors."

Conventional cancer therapies do an effective job killing
the majority of cells within the tumor, but they may miss
cancer stem cells, according to the new research published
in Proceedings of the National Academy of Sciences. As a
result, cancers often recur.

This is the first time that cells with stem-cell-like
properties, have been found in solid tumors. However,
researchers had previously found similar cells in leukemia.

"This is a landmark study," says Irving L. Weissman of
Stanford University in California, who discovered
leukemia stem cells. "It is significant because all of
the useful cancer drugs that we have, are those that
shrink the main body of the tumor. This study reveals
that this may not be enough."

Both non-tumorigenic and tumorigenic cells exist within
breast tumors.

"Shrinking the tumor is fine, but if it doesn't get rid of
the cancer stem cells, the cancer will grow back," according
to Weissman.

Stem cells are immature cells that can replicate or renew
themselves, and are able to differentiate or mature into all
the cells, that an organism or particular organ system need.

Three years ago, Weissman discovered that mutations and
rearrangements of the genomes of stem cells, that give rise
to all the cells of the blood, can lead to some forms of
leukemia. Weissman proposed that these changes could
underlie the development of cancers in many tissues.

"Ideas are cheap," says Weinberg. "Without evidence, we
could only treat Weissman's idea as speculation. Now it
seems that he was right on the mark."

In the present study, the Michigan researchers examined
cells from nine human breast tumors and tumor metastases.
They looked for "markers"=97proteins attached to the outside
of only some cells=97to distinguish cells.

Using three different markers, the researchers grouped the
tumor cells into two different classes.

The difference between the two cell types became evident,
when they transplanted them into mice. When as few as 200 of
one cell type were injected into mice, tumors developed. But
when they implanted as many as 10,000 cells of the second
type, no tumors developed.

"This is the classic definition of a stem cell," says
Weissman. "Take a small subset of cells and put it in the
organism, and see if it regenerates the original tissue.
This is just what happens when they implant the tumor stem
cells. All the cells of the original tumor are generated."

The key to developing new cancer therapies, may be to focus
on these cancer stem cells. But this is likely to be
difficult.

"Stem cells are more difficult to kill," says Wicha.
"Because they are so important throughout a person's
lifetime, they have developed mechanisms that protect
themselves."

For example, tumor stem cells are able to resist toxic
substances, such as cancer drugs. More mature cells are
easier to kill than stem cells, because these mechanisms are
not always active.

Normal Stem Cells vs. Cancer Stem Cells

The stem cells in tumors discovered by researchers at the
University of Michigan, are not the same type of stem cells
being explored as potential therapies, to treat degenerative
diseases. Both normal embryonic and adult stem cells are
being actively studied for their ability, to proliferate and
replace damaged cells in diseases such as diabetes,
Parkinson's disease, and heart disease.

But stem cells in tumors develop, because of mutations that
accumulate over years and often decades. The mutations are
thought to promote the tumor stem cells' ability to
proliferate, eventually leading to cancer.

The next step is to figure out what makes the cancer stem
cells different from the other cells in the tumor. The
researchers are currently using DNA microarrays (or "gene
chips"😉 to identify genes that are active in the cancer-
causing cells, compared to benign tumor cells.

Some of these genes might control the cell's ability to
replicate and metastasize. Identifying these genes may
suggest new drug targets, that could selectively kill the
cancer cells.

"The only cells within an organism, that live long enough
to accumulate the mutations that lead to cancer, are the
stem cells," says Wicha. "When the cancer cell
differentiates, it produces other cells that have lost the
ability to self-renew."

If the researchers can find normal adult breast stem cells,
they may understand how breast cancers develop. "A key
question is what is the difference between a normal stem
cell and a tumor stem cell," says Wicha. "A normal breast
stem cell can make copies of itself, but then shuts itself
off. Cancer stem cells make too many copies of themselves."

Wicha thinks that a primary event in cancer development,
occurs when the normal stem cell loses the ability to
regulate its own growth. But many other mutations must
occur, to turn a normal stem cell into cancer stem cell.

Weissman suspects that most cancers develop from mutations
in the genomes of stem cells, in various tissues
throughout the body.

"I suspect that a lot of researchers studying different
types of cancers, are going to be looking for stem cells in
their tumors now," says Weissman.

----------------------

Susan, Su_Texas my opinions

Starts to sound like parasites, doesn't it?

"Anth" <[email hidden]> wrote in message news:ocydnZkLJucu5ATdRVn-
[email hidden]...

Quoted message said:

(IMO stem cells are what Beard describes as the germ cells
in trophoblast thesis of cancer) There was a recent
article on stem cells and Beard's thesis in New Scientist
- you might want to try chasing it up.
www.newscientist.com Basic theory is that cancer is a
placenta (The theory still stands up to scrutiny today -
this doesn't mean it is right!). In pregnancy at (56 days
*I think*?) the babies pancreas becomes active

and

Quoted message said:

it starts pumping out proteolytic enzymes
trypsin/chymotrypsin. These enzymes kill the invasive
cells of the placenta and stop it from growing/invading
the mother. Anth

<[email hidden]> wrote in message news:12914-40990CD5-119@storefull-
3195.bay.webtv.net...

Quoted message said:

google.comsearchOpen ↗

From what I just read, the currect cancer treatments
might be the wrong approach, because they don't target
cancer stem-cells.

I was reading about cDNA, gene-chips, & cancer.

Susan, Su_Texas my opinions

<[email hidden]> wrote in message news:29591-40995066-493@storefull-
3197.bay.webtv.net... U-M scientists find "stem cells" in
human breast cancer

Quoted message said:

Discovery could explain current treatment failures, and
lead to more effective therapies for many cancers:
added 02/24/03

Let's wait and see. Despite the usual journalistic hype, and
researchers making their findings sound as significant as
possible, I am not sure that this research is telling us
anything that we didn't already know, or could predict.

The cells in any cancer, unlike normal tissue cells, tend to
vary dramatically from each other, in size and shape and
even to having different numbers of chromosomes and numbers
of cell nuclei. So even morphologically (on microscopic
appearances) it is clear that there are many different
populations of cell in a cancer. It is inevitable that such
differences will extend to different cell behaviours, such
as rate of cell division and ability to produce tumours if
injected into test animals.

Also one of the authors quoted by su_texas claims that
mature cells are easier to kill than rapidly multpiplying
cells, which is just not true. Many forms of chemotherapy
can only kill cells when they are dividing, and the side
effects on bone marrow and gut (diarrhoea etc) occur
purely and simply because the cells there are rapidly
dividing. Radiotherapy is also more effective on rapidly
dividing cells.

So it is not clear how most of the cells in a cancer being
derived from a single rapidly dividing source would explain
the limitations of chemotherapy or radiotherapy. It is more
likely that there are many different cell lines sustaining
the growth of cancer and that the *slower* dividing ones
will be the ones resistant to treatment and cause cancer
recurrence if it occurs..

What do you think, Orac?

Peter Moran

Parasites not sure- could you explain? Anth

"Gymmy Bob" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

Starts to sound like parasites, doesn't it?

"Anth" <[email hidden]> wrote in message news:ocydnZkLJucu5ATdRVn-
[email hidden]...

Quoted message said:

(IMO stem cells are what Beard describes as the germ
cells in

trophoblast

Quoted message said:

Quoted message said:

thesis of cancer) There was a recent article on stem
cells and Beard's thesis in New Scientist - you might
want to try chasing it up. www.newscientist.com Basic
theory is that cancer is a placenta (The theory still
stands up to scrutiny today - this doesn't mean it is
right!). In pregnancy at (56 days *I think*?) the babies
pancreas becomes active

and

Quoted message said:

it starts pumping out proteolytic enzymes
trypsin/chymotrypsin. These enzymes kill the invasive
cells of the placenta and stop it from growing/invading
the mother. Anth

<[email hidden]> wrote in message news:12914-40990CD5-119@storefull-
3195.bay.webtv.net...

Quoted message said:

google.comsearchOpen ↗

From what I just read, the currect cancer treatments
might be the

wrong

Quoted message said:

Quoted message said:

Quoted message said:

approach, because they don't target cancer stem-cells.

I was reading about cDNA, gene-chips, & cancer.

Susan, Su_Texas my opinions

(This is what I think) Basically what you have here is
'progressive refinement.' You have a large population that
has the potential to mutate and also have offspring. When
you give the cancers chemo you kill the weakest ones and the
cells left over (the stronger ones) can rebuild the
population, thus the population is now stronger than before,
and the process repeats.

There's a considerable amount of damage to the DNA (because
of the acidic environment) so you have a lot of mutation,
the cells that fail to survive (because the DNA is messed up
sufficiently) destruct, but the ones with the necessary
mutations to survive, grow on to rebuild the next
population. So what you have is a growing resistance to the
agent used to kill them, and also growing resistance to the
persons immune system. Do you think that the DNA damage
could selectively switch on elements that make the cancer
cells invasive, grow their own blood supplies ? Anth

"Peter Moran" <[email hidden]> wrote in message news:40999184$0$10291$61c65585@uq-127creek-reader-
01.brisbane.pipenetworks.com.au...

Quoted message said:

<[email hidden]> wrote in message news:29591-40995066-493@storefull-
3197.bay.webtv.net... U-M scientists find "stem cells" in
human breast cancer

Quoted message said:

Discovery could explain current treatment failures, and
lead to more effective therapies for many cancers: added
02/24/03

Let's wait and see. Despite the usual journalistic hype,
and researchers making their findings sound as significant
as possible, I am not sure

that

Quoted message said:

this research is telling us anything that we didn't
already know, or could predict.

The cells in any cancer, unlike normal tissue cells, tend
to vary dramatically from each other, in size and shape
and even to having

different

Quoted message said:

numbers of chromosomes and numbers of cell nuclei. So
even morphologically (on microscopic appearances) it is
clear that there are many different populations of cell
in a cancer. It is inevitable that such differences will
extend to different cell behaviours, such as rate of
cell division and ability to produce tumours if injected
into test

animals.

Quoted message said:

Also one of the authors quoted by su_texas claims that
mature cells are easier to kill than rapidly multpiplying
cells, which is just not true. Many forms of chemotherapy
can only kill cells when they are dividing, and the side
effects on bone marrow and gut (diarrhoea etc) occur
purely and simply because the cells there are rapidly
dividing. Radiotherapy is

also

Quoted message said:

more effective on rapidly dividing cells.

So it is not clear how most of the cells in a cancer being
derived from a single rapidly dividing source would
explain the limitations of

chemotherapy

Quoted message said:

or radiotherapy. It is more likely that there are many
different cell lines sustaining the growth of cancer and
that the *slower* dividing ones will be the ones resistant
to treatment and cause cancer recurrence if it occurs..

What do you think, Orac?

Peter Moran

It would be interesting to see how the DNA mutations vary
across the tumour? Maybe Orac has some info on this? Anth

"Anth" <[email hidden]> wrote in message
"]news:[email hidden]... [snip]

One word. "Hulda"

"Anth" <[email hidden]> wrote in message news:OfKdnUvWeoTCCATdRVn-
[email hidden]...

Quoted message said:

Parasites not sure- could you explain? Anth

"Gymmy Bob" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

Starts to sound like parasites, doesn't it?

"Anth" <[email hidden]> wrote in message news:ocydnZkLJucu5ATdRVn-
[email hidden]...

Quoted message said:

(IMO stem cells are what Beard describes as the germ
cells in

trophoblast

Quoted message said:

Quoted message said:

thesis of cancer) There was a recent article on stem
cells and Beard's thesis in New Scientist - you might
want to try chasing it up. www.newscientist.com Basic
theory is that cancer is a placenta (The theory still
stands up

to

Quoted message said:

Quoted message said:

Quoted message said:

scrutiny today - this doesn't mean it is right!). In
pregnancy at (56 days *I think*?) the babies pancreas
becomes

active

Quoted message said:

Quoted message said:

and

Quoted message said:

it starts pumping out proteolytic enzymes
trypsin/chymotrypsin. These enzymes kill the invasive
cells of the placenta and stop it from
growing/invading the mother. Anth

<[email hidden]> wrote in message news:12914-40990CD5-119@storefull-
3195.bay.webtv.net...
> google.comsearchOpen ↗
>
> From what I just read, the currect cancer treatments
> might be the

wrong

Quoted message said:

Quoted message said:

> approach, because they don't target cancer stem-
> cells.
>
> I was reading about cDNA, gene-chips, & cancer.
>
> Susan, Su_Texas my opinions

"Anth" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

(This is what I think) Basically what you have here is
'progressive refinement.' You have a large population that
has the potential to mutate and also have offspring. When
you give the cancers chemo you kill the weakest ones and
the cells

left

Quoted message said:

over (the stronger ones) can rebuild the population, thus
the population is now stronger than

before,

Quoted message said:

and the process repeats.

There's a considerable amount of damage to the DNA
(because of the acidic environment) so you have a lot of
mutation, the cells that fail to survive (because the DNA
is messed up sufficiently) destruct, but the ones with

the

Quoted message said:

necessary mutations to survive, grow on to rebuild the
next population. So what you have is a growing resistance
to the agent used to kill them,

and

Quoted message said:

also growing resistance to the persons immune system. Do
you think that the DNA damage could selectively switch on
elements that make the cancer cells invasive, grow their
own blood supplies ? Anth

I don't think chemotherapy makes a cancer more cancerous,
but resistance to chemotherapy must depend on some cancer
cells being less susceptible to immune attack. The same
must apply when immunotherapy produces a remission, but
then fails.

Peter Moran

Quoted message said:

"Peter Moran" <[email hidden]> wrote in message

news:40999184$0$10291$61c65585@uq-127creek-reader-
01.brisbane.pipenetworks.com.au...

Quoted message said:

Quoted message said:

<[email hidden]> wrote in message news:29591-40995066-493@storefull-
3197.bay.webtv.net... U-M scientists find "stem cells"
in human breast cancer

Quoted message said:

Discovery could explain current treatment failures, and
lead to more effective therapies for many cancers:
added 02/24/03

Let's wait and see. Despite the usual journalistic
hype, and

researchers

Quoted message said:

Quoted message said:

making their findings sound as significant as possible,
I am not sure

that

Quoted message said:

this research is telling us anything that we didn't
already know, or

could

Quoted message said:

Quoted message said:

predict.

The cells in any cancer, unlike normal tissue cells,
tend to vary dramatically from each other, in size and
shape and even to having

different

Quoted message said:

numbers of chromosomes and numbers of cell nuclei. So
even morphologically (on microscopic appearances) it is
clear that there are many different populations of cell
in a cancer. It is inevitable that such differences will
extend to different cell behaviours, such as rate

of

Quoted message said:

Quoted message said:

cell division and ability to produce tumours if injected
into test

animals.

Quoted message said:

Also one of the authors quoted by su_texas claims that
mature cells are easier to kill than rapidly
multpiplying cells, which is just not true. Many forms
of chemotherapy can only kill cells when they are
dividing,

and

Quoted message said:

Quoted message said:

the side effects on bone marrow and gut (diarrhoea etc)
occur purely and simply because the cells there are
rapidly dividing. Radiotherapy is

also

Quoted message said:

more effective on rapidly dividing cells.

So it is not clear how most of the cells in a cancer
being derived from

a

Quoted message said:

Quoted message said:

single rapidly dividing source would explain the
limitations of

chemotherapy

Quoted message said:

or radiotherapy. It is more likely that there are many
different cell lines sustaining the growth of cancer and
that the *slower* dividing

ones

Quoted message said:

Quoted message said:

will be the ones resistant to treatment and cause cancer
recurrence if

it

Quoted message said:

Quoted message said:

occurs..

What do you think, Orac?

Peter Moran

Oh right Hulda - I very much doubt it? I've not touched
Hulda much mainly because her protocols have not been tested
properly. Anth

"Gymmy Bob" <[email hidden]> wrote in message news:qf-dnTHeVslQCATdRVn-
[email hidden]...

Quoted message said:

One word. "Hulda"

"Anth" <[email hidden]> wrote in message news:OfKdnUvWeoTCCATdRVn-
[email hidden]...

Quoted message said:

Parasites not sure- could you explain? Anth

[snips]

You take a tumour from a 'immune weaked mouse' and place it
into a 'non immune weaked mouse' it will not grow, because
the immune system attacks it and destroys it. It is said
that cancer cells have a thick fibrin coat to prevent the
immune system from attacking it? Then why when you
transplant the tumour into a non immune weaked mouse does
the tmuour get attacked, surely if the antigens are hidden
under a fibrin coat then the immune system won't be able to
recognise it as foreign? Anth .

"Anth" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

You take a tumour from a 'immune weaked mouse' and place
it into a 'non immune weaked mouse' it will not grow,
because the immune system attacks

it

Quoted message said:

and destroys it. It is said that cancer cells have a thick
fibrin coat to prevent the

immune

Quoted message said:

system from attacking it?

That's not true, but there are blocking antibodies coating
cancer cells that protect them from immune attack. The
immunology of cancer is extremely complex. A speaker I heard
recently said that there are at least a dozen mechanisms by
which cancers evade immune attack

When you think about it, the wonder is that some cancers are
susceptible to immune attack at all, since they are
essentially our own cells, and it is just that sometimes the
gene defects lead them to produce unusual proteins.

Peter Moran

Ongoing Treatment?

IF cancer stem-cells are the problem, & they can't easily be
killed off, then you'd probably need an ongoing treatment
designed to kill off the cancer cells as they develop, ...
that is, after you've finished all that's currently offered
to the general public, in traditional cancer care.

???

Are there ongoing treatments like that, in regular or
alternative-medicine?

Susan, Su_Texas my opinions

From: [email hidden] (Anth)

(IMO stem cells are what Beard describes as the germ cells
in trophoblast thesis of cancer) There was a recent article
on stem cells and Beard's thesis in New Scientist - you
might want to try chasing it up. www.newscientist.com Basic
theory is that cancer is a placenta (The theory still
stands up to scrutiny today - this doesn't mean it is
right!). In pregnancy at (56 days *I think*?) the babies
pancreas becomes active and it starts pumping out
proteolytic enzymes trypsin/chymotrypsin. These enzymes
kill the invasive cells of the placenta and stop it from
growing/invading the mother.

Anth

=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D

So far, can't find Beard, but did find this:

5T4 & Cancer Vaccine

["]http://www.newscientist.com/news/news.jsp?id=3Dns99994309]

Stem cell mobility linked to cancer's spread,
10:23=A024=A0October=A003=A0NewScientist.com news service=A0

A molecule present in many spreading cancers, has been
identified as key to helping stem cells to become mobile,
reveal UK scientists.

A cancer vaccine based on the molecule, has already been
successfully trialled in humans, and a "magic bullet"
treatment is also in development.

As cancers grow, cells often move out of the original tumour
and spread around the body using the blood or lymphatic
system, a process called metastasis. These widespread
cancers are especially difficult to treat.

Now scientists have discovered, that a surface molecule
called 5T4 (which is present in many different types of
tumour), is also produced by embryonic stem cells (ESCs) as
the embryo grows and develops.

Peter Stern and colleagues, at Cancer Research UK's Paterson
Institute in Manchester, found the 5T4 produced by mouse
ESCs, made the cells spread across culture plates. "We think
we've found a common factor in the movement of embryonic
cells during development, and of cancer cells during the
spread of disease," he says.

Robert Souhami, director of clinical research at Cancer
Research UK, says: "By studying fundamental developmental
biology, the new study has highlighted a potentially
exciting strategy to prevent cancer from spreading - one of
the great challenges faced by scientists."

Avoid rejection

The researchers originally came across 5T4, when they
compared the surface molecules of special ESCs called
trophoblasts, with those found on cancer cells in humans.

Trophoblasts form the interface between the placenta and a
fetus. The team focused on them, because this special layer
has to avoid rejection by the mother's immune system -
cancer cells also manage to evade the body's immune system.

They found 5T4 was common to both. The molecule was
overexpressed in cancer cells, whereas non-cancerous adult
cells did not express the molecule at all.

The new study of mouse ESCs demonstrated, that 5T4 is the
key to making developing stem cells mobile. In normal
development, 5T4 is involved in helping cells move around in
a regulated way, Stern explains. "In cancer it's not
regulated - it's out of control."

Immune response

The team has already harnessed 5T4 in human clinical trials.
Because it is expressed in the embryo only, 5T4 should be
treated as a foreign invader by the adult body.

The team, in collaboration with Oxford BioMedica, has
developed a therapeutic vaccine, based on eliciting an
immune response against cancer cells expressing 5T4. =A0=A0
=A0"The cancer vaccine has been shown to be immunogenic and
safe," Stern told New Scientist.

The team is also collaborating with Active Biotech, to
develop a "magic bullet" based on 5T4. They are using an
antibody that latches on to the molecule, to seek out
tumours and deliver a drug to kill them.

The discovery of 5T4 could even give practical help to
scientists trying to isolate pure, unspecialised ESCs,
Stern adds.

Stem cells differentiate easily, and 5T4 could be used as a
marker to weed out cells, which have started to develop from
their primitive state.

Journal reference: Journal of Cell Science (vol 116, p 4533)
=A0
----------------

Susan, Su_Texas my opinions=A0

Galectin-3, & the Modified Protein Treatment (Non-
Stick Approach)

["]http://www.newscientist.com/news/news.jsp?id=3D99993801]

Deadly spread of cancer halted,
12:21=A005=A0June=A003=A0NewScientist.com news service=A0

The spread of cancers through the body could be halted, by
targeting a protein that helps cells latch on to each other,
reveals a new study.

The spreading of cancer from an initial tumour to other
parts of the body - called metastasis - frequently means
there is little hope a person can be saved. But scientists
have now modified a naturally occurring human protein to
disrupt this deadly process, in mouse models of human
breast cancer.

"We were able to significantly reduce the spread of the
disease and decrease tumour growth, without any evidence of
toxicity," says Gary Jarvis, a microbiologist at the
University of California in San Francisco. "If we can stop
metastasis in humans, we will have gone a long way towards
successfully treating cancer."

"It's when tumours spread to essential organs, such as
the liver or lung, that they become fatal," says
colleague Constance John, a research chemist. "There is
nothing to date that has been approved by the Food and
Drug Administration, for treatment of cancer that works
on that process."

Stick together

The team modified a protein, that seems play an important
role in helping cells stick to each other. This ability aids
metastasis, by allowing cancerous cells that enter the
bloodstream, to lodge themselves in other parts of the body.

The team, lead by Jarvis in the US and Hakon Leffler at
the University of Lund in Sweden, singled out a human
protein named galectin-3. This is from a family of
proteins called lectins, that bind to sugar molecules on
the surfaces of cells.

Galectin-3 is known to play a role in cancer formation,
particularly in promoting cell-to-cell adhesion. "The idea
was to break that contact and inhibit secondary cancer
formation," says Jarvis. So the team removed the key part of
galectin-3 that normally allows cells to stick to each
other. The modified protein also occupies the site on a
cell's surface, blocking normal galectin-3 from binding.
This stops cells from adhering to each other.

The modified protein more than halved the number of mice,
that developed metastatic tumours. Cancer implanted into the
mice spread to the lymph nodes or other organs, in 11 of the
20 control mice given sham injections, but only four of the
20 mice given the truncated protein.

Slow growth

The growth of the implanted tumours was also significantly
less, in mice treated with the modified protein, compared to
the control mice.

"It's not only affecting metastasis," Leffler told New
Scientist. "It's reducing the primary tumour a lot."
Importantly, he adds, the novel treatment did not cause any
adverse reactions.

A drug therapy targeting galectin-3, might one day be
effectively used in combination with currently available
cancer medications like chemotherapy and radiation, say the
researchers. Although, the results are "optimistic", Leffler
cautions that "an animal model is not human".

"We're not trying to develop a cure for cancer," says John.
"What we're trying to do is make cancer a disease that one
can live with."

Journal reference: Clinical Cancer Research (June issue) =A0
----------------------

Susan, Su_Texas my opinions=A0

Quoted message said:

Subject: Re: Treatments: Should Cancer Stem-Cells BeTheFocus?
From: [email hidden]
Date: 5/5/04 11:15 PM Eastern Daylight Time
Message-id: <[email hidden]>

Quoted message said:

The spread of cancers through the body could be halted, by
targeting a protein that helps cells latch on to each
other, reveals a new study.

Myth. A theory in search of some data to support it.>

Quoted message said:

The spreading of cancer from an initial tumour to other
parts of the body - called metastasis

Never can happen in the real world.

Quoted message said:

Cancer implanted into the mice spread to the lymph nodes

Now that is possible.

It is not possible for the implanted cells nor the natural
cells of the tissues to enter the blood stream any more
than it is possible for the blood cells to migrate into
the tissues.

The lymphatic system is a first line of defense against
disease, including cancer. The cells of the lymphatic system
line up like the cells on a fish skin. They can open up and
allow in objects as large as other cells that need to be be
removed from the body. It is this capacity of the lymph
system which would have allowed the cells to "migrate". That
is, migrate to a node where it would be trapped and
destroyed by lysosomes.

Damn. Why is it that these jerks cannot understand the
obvious truths that they are studying?

DrC PhD

<[email hidden]> wrote in message
"]news:[email hidden]...

[snip]

===================

So far, can't find Beard, but did find this:

navi.netunitari1.htmOpen ↗ This is what the
Gonzalez/Dr Kelley therapy is based on. (High doses of
digestive proteolytic enzymes.)

5T4 & Cancer Vaccine

["]http://www.newscientist.com/news/news.jsp?id=ns99994309]

Stem cell mobility linked to cancer's spread,
10:23 24 October 03 NewScientist.com news service

A molecule present in many spreading cancers, has been
identified as key to helping stem cells to become mobile,
reveal UK scientists.

A cancer vaccine based on the molecule, has already been
successfully trialled in humans, and a "magic bullet"
treatment is also in development.

As cancers grow, cells often move out of the original tumour
and spread around the body using the blood or lymphatic
system, a process called metastasis. These widespread
cancers are especially difficult to treat.

Now scientists have discovered, that a surface molecule
called 5T4 (which is present in many different types of
tumour), is also produced by embryonic stem cells (ESCs) as
the embryo grows and develops.

Peter Stern and colleagues, at Cancer Research UK's Paterson
Institute in Manchester, found the 5T4 produced by mouse
ESCs, made the cells spread across culture plates. "We think
we've found a common factor in the movement of embryonic
cells during development, and of cancer cells during the
spread of disease," he says.

Robert Souhami, director of clinical research at Cancer
Research UK, says: "By studying fundamental developmental
biology, the new study has highlighted a potentially
exciting strategy to prevent cancer from spreading - one of
the great challenges faced by scientists."

Avoid rejection

The researchers originally came across 5T4, when they
compared the surface molecules of special ESCs called
trophoblasts, with those found on cancer cells in humans.

Trophoblasts form the interface between the placenta and a
fetus. The team focused on them, because this special layer
has to avoid rejection by the mother's immune system -
cancer cells also manage to evade the body's immune system.

They found 5T4 was common to both. The molecule was
overexpressed in cancer cells, whereas non-cancerous adult
cells did not express the molecule at all.

The new study of mouse ESCs demonstrated, that 5T4 is the
key to making developing stem cells mobile. In normal
development, 5T4 is involved in helping cells move around in
a regulated way, Stern explains. "In cancer it's not
regulated - it's out of control."

Immune response

The team has already harnessed 5T4 in human clinical trials.
Because it is expressed in the embryo only, 5T4 should be
treated as a foreign invader by the adult body.

The team, in collaboration with Oxford BioMedica, has
developed a therapeutic vaccine, based on eliciting an
immune response against cancer cells expressing 5T4.

"The cancer vaccine has been shown to be immunogenic and
safe," Stern told New Scientist.

The team is also collaborating with Active Biotech, to
develop a "magic bullet" based on 5T4. They are using an
antibody that latches on to the molecule, to seek out
tumours and deliver a drug to kill them.

The discovery of 5T4 could even give practical help to
scientists trying to isolate pure, unspecialised ESCs,
Stern adds.

Stem cells differentiate easily, and 5T4 could be used as a
marker to weed out cells, which have started to develop from
their primitive state.

Journal reference: Journal of Cell Science (vol 116, p 4533)

----------------

Susan, Su_Texas my opinions

Thanks for the info Anth