[Congressional Record Volume 153, Number 186 (Thursday, December 6, 2007)]
[Senate]
[Pages S14821-S14824]
From the Congressional Record Online through the Government Publishing Office [www.gpo.gov]
STEM CELL RESEARCH
Mr. BROWNBACK. Mr. President, I rise to discuss a recent enormous
scientific breakthrough on a topic that has engaged this body for much
of the past 8 years. I think this is a day that many of us--I think
perhaps all of us--have hoped would take place. I ask unanimous consent
to include in the Record at the end of my remarks an article that broke
lose right around Thanksgiving.
The PRESIDING OFFICER. Without objection, it is so ordered.
(See exhibit 1.)
Mr. BROWNBACK. Mr. President, this article is by Dr. James Thomson,
University of Wisconsin. Some may recognize that name. His name has
been used on this floor many times during the past 8 years on the issue
of embryonic stem cell research. He is the man who discovered human
embryonic stem cells about 10 years ago and described them as being
what is called pluripotent, which means that an embryonic stem cell
could form any other type of cell tissue in the body, whether it is for
the eye, brain, bone, or skin. Any type of cell tissue could regenerate
on a fast basis, and it was thought that these sorts of pluripotent
embryonic stem cells were going to solve a number of our human health
problems. Many of my colleagues on both sides of the aisle embraced the
news and said this is a fabulous thing and we are going to be able to
now cure a number of people from diseases who have had great problems
and difficulties, and we want cures for them.
There was an ethical glitch with it in that it took the destruction
of a human embryo to get these human embryonic stem cells, and therein
ensued a fight that engaged the country and engaged the world about the
tension between cures and an ethical recognition of human life and the
sacredness of human life. It has been a long debate. I am hopeful that
the article I submitted into the Record is the bookend on the other end
of this debate that was started by Professor Thomson and that, in many
respects, I hope is ended by Professor Thompson and his colleagues.
In this article they describe a new type of pluripotent stem cell
that is manipulated by man. They call it an induced pluripotent stem
cell. This is an elegant and simple process where they take a skin cell
from an individual and they reprogram it to be able to act like an
embryonic stem cell, or what they call an induced pluripotent stem
cell. They then are able to get it to generate more embryonic-like stem
cells that are pluripotent and which then can be used to treat diseases
or to study diseases, thus removing the need to develop and have a
human embryo destroyed, or the origination of the embryonic stem cells,
thus removing the problem of not being able to get a genetic match so
that we have to go to a cloned embryonic stem cell, or a cloned human
to create an embryonic stem cell that matches genetically. You don't
have to do that. Get a person's skin cells, reprogram them, back in,
pluripotent, to form any type of cell--elegant, simple.
There are still many barriers to go on embryonic-like stem cells
anyway because they have had a problem with tumor formation. But on the
ethical issue, I am hopeful we are on the other bookend, and it is now
over; that we don't need to destroy young human life for cures; that we
don't need to destroy them for pluripotent cells; that we can do it
much simpler and ethically and that good ethics is good science.
I put a description up here of what Dr. Thomson said on this subject.
There was a University of Tokyo professor who came out with an article
the same day, using a slightly different or modified technique, to be
able to do this in humans. The University of Tokyo professor had done
this earlier in mice and now has perfected it in human cells. He came
out saying the same thing:
These induced pluripotent cells described here meet the
defining criteria we originally proposed for human ES cells,
with the significant exception that the induced pluripotent
cells are not derived from embryos.
That was Dr. James Thomson.
I want to speak about this to my colleagues because we have had so
many debates on the Senate floor about this topic. I hope my colleagues
will research this. A number of people in the scientific field are
saying: Great, but let's not stop embryonic stem cell work and
destroying embryos for research purposes. Or let's not stop human
cloning because it appears now that the only reason to clone a human
would be to bring a human to live birth at this point in time, which
still has everybody in this body opposed to that type of human cloning.
It is noteworthy that the ``father'' of Dolly the sheep has said he
has given up on human cloning to go to this type of technique rather
than human cloning to provide these sorts of cures and research.
Mr. President, I also ask unanimous consent to be printed in the
Record at the end of my comments a Telegraph article from the United
Kingdom in which Ian Wilmut announced he is shunning human cloning.
The PRESIDING OFFICER. Without objection, it is so ordered.
(See exhibit 2.)
Mr. BROWNBACK. Mr. President, it is my hope that we can move together
in finding cures and developing research that cures humans that is
ethical and sound and doesn't destroy young human life.
We have been able to do quite a bit of this already. We recently
found there was scientific work done by a Northwestern University
professor in developing cures and treatments for type I diabetes using
stem cells. Again, this is adult stem cells, which is ethical and
moral, no problem with it. The only problem I found with it is that the
Northwestern professor was having to do this in Brazil rather than in
the United States to get support and funding. He is saying this:
Though too early to call it a cure, the procedure has
enabled the young people, who have type I diabetes, to live
insulin-free so
[[Page S14822]]
far, some as long as 3 years. The treatment involves stem
cell transplants from the patient's own blood.
For parents who are dealing with juvenile diabetes and those
difficulties, this is fabulous news in humans. We need more of it, and
we need it to take place in the United States and not Brazil. Nothing
against Brazil. I am glad for it to take place there, but I want it
here for our children. We now have--as I have said previously on the
floor--73 different human applications for adult stem cells. We have
not been able to come up with any in the embryonic field yet. I think a
bigger number--and we will verify this for my colleagues, as it is not
verified yet--is somewhere north of 400,000 people who are now being
treated with adult or cord blood stem cells in the United States and
different places around the world, the majority being U.S. citizens. Of
course, we don't have any in the embryonic field because it continues
to struggle with tumor formation as an issue. These are wonderful
numbers of treatments that we are getting in different human maladies
and, hopefully, we can verify that number of 400,000 people being
treated with stem cells, getting heart tissue and spinal cord tissue to
regenerate, and Parkinson's treatment is coming forward. This is a
beautiful set of treatments--all ethical.
I want to look at the budgetary numbers briefly to remind my
colleagues where we have invested taxpayer funding in this field. It is
my hope that as we look at the numbers--we have an ethical issue on
human embryonic stem cell research, and I believe we have crossed over
the line. I hope we can continue to look at our funding issues, where
we are putting a lot of money, and have put a lot of money, into
embryonic stem cell research. We are looking at $140 million in fiscal
year 2006 and over half a billion since 2002 in embryonic stem cell
research of both human and nonhuman types. We have not cured a single
patient yet with that money.
May I submit to my colleagues that with over half a billion dollars,
we could be treating and developing these cures in the United States
and not in Brazil.
In trying to set aside all of the sharp edges that have now been
associated with this debate, and focusing just on patients and treating
people, I hope we will say we are all in this for cures, for treating
people. So if I could take portions of these funds and put it into
treating people and getting more people treated for Parkinson's,
congestive heart failure, or diabetes--all the things that we are
actually doing in humans today but that need more research in funding--
that we would say: OK, you are right. We don't have to go the embryonic
stem cell route now. Let's go to where people are getting treated and
treat people.
This is about curing people. That is what we have debated and talked
about for some period of time, curing people. We have one that is
working and one that doesn't. Yet we have invested pretty heavily in
this.
I ask my colleagues if there is some way that we could put the swords
down and talk about this rationally, stop the fighting and say how do
we treat people. I believe that is our objective.
With that, I thank my colleagues for their indulgence in this debate.
It will continue to come up. The next issue will be human animal
crosses. I advise my colleagues on this, you will see people pushing to
cross genetic materials from animals into humans. They are going to say
it is going to cure a lot of people. I think it is an enormous ethical
boundary that we should not cross at this point in time, with our
understanding of life and what it is to be human. I hope before we go
that route, we will all get together and say we are going to pause for
a while on this one. This is too big for all of us, and we want to
think about this for a while--left, right, middle. We have a ways to go
to get some cures. We are getting them. We don't need to cross over to
that. We can think about that.
I yield the floor.
Exhibit 1
Induced Pluripotent Stem Cell Lines Derived from Human Somatic Cells
Somatic cell nuclear transfer allows trans-acting factors
present in the mammalian oocyte to reprogram somatic cell
nuclei to an undifferentiated state. Here we show that four
factors (OCT4, SOX2, NANOG, and LIN28) are sufficient to
reprogram human somatic cells to pluripotent stem cells that
exhibit the essential characteristics of embryonic stem
cells. These human induced pluripotent stem cells have normal
karyotypes, express telomerase activity, express cell surface
markers and genes that characterize human ES cells, and
maintain the developmental potential to differentiate into
advanced derivatives of all three primary germ layers. Such
human induced pluripotent cell lines should be useful in the
production of new disease models and in drug development as
well as application in transplantation medicine once
technical limitations (for example, mutation through viral
integration) are eliminated.
Mammalian embryogenesis elaborates distinct developmental
stages in a strict temporal order. Nonetheless, because
development is dictated by epigenetic rather than genetic
events, differentiation is, in principle, reversible. The
cloning of Dolly demonstrated that nuclei from mammalian
differentiated cells can be reprogrammed to an
undifferentiated state by trans-acting factors present in the
oocyte (1), and this discovery led to a search for factors
that could mediate similar reprogramming without somatic cell
nuclear transfer. Recently. four transcription factors (Oct4,
Sox2, c-myc, and Klf4) were shown to be sufficient to
reprogram mouse fibroblasts to undifferentiated, pluripotent
stem cells (termed induced pluripotent stem (iPS) cells) (2-
5). Reprogramming human cells by defined factors would allow
the generation of patient-specific pluripotent cell lines
without somatic cell nuclear transfer, but the observation
that the expression of c-Myc causes death and differentiation
of human ES cells suggests that combinations of factors
lacking this gene are required to reprogram human cells (6).
Here we demonstrate that OCT4, S0X2, NANOG, and LIN28 are
sufficient to reprogram human somatic cells.
Human ES cells can reprogram myeloid precursors through
cell fusion (7). To identify candidate reprogramming factors,
we compiled a list of genes with enriched expression in human
ES cells relative to myeloid precursors, and prioritized the
list based on known involvement in the establishment or
maintenance of pluripotency (table S1). We then cloned these
genes into a lentiviral vector (fig. S1) to screen for
combinations of genes that could reprogram the differentiated
derivatives of an OCT4 knock-in human ES cell line generated
through homologous recombination (8). In this cell line, the
expression of neomycin phosphotransferase, which make cells
resistant to geneticin, is driven by an endogenous OCT4
promoter, a gene that is highly expressed in pluripotent
cells but not in differentiated cells. Thus reprogramming
events reactivating the OCT4 promoter can be recovered by
geneticin selection. The first combination of 14 genes we
selected (table S2) directed reprogramming of adherent cells
derived from human ES cell-derived CD45+ hematopoietic cells
(7, 9), to geneticin-resistant (OCT4 positive) colonies with
an ES cell-morphology (fig. S2A) (10). These geneticin-
resistant colonies expressed typical human ES cell-specific
cell surface markers (fig. S2B) and formed teratomas when
injected into immunocompromised SCID-beige mice (fig. S2C).
By testing subsets of the 14 initial genes. we identified a
core set of 4 genes, OCT4, SOX2, NANOG, and LIN28, that were
capable of reprogramming human ES cell-derived somatic cells
with a mesenchymal phenotype (Fig. 1A and fig. S3). Removal
of either OCT4 or SOX2 from the reprogramming mixture
eliminated the appearance of geneticin resistant (OCT4
positive) reprogrammed mesenchymal clones (Fig. 1A). NANOG
showed a beneficial effect in clone recovery from human ES
cell-derived mesenchymal cells but was not required for the
initial appearance of such clones (Fig. 1A). These results
are consistent with cell fusion-mediated reprogramming
experiments, where overexpression of Nanog in mouse ES
cells resulted in over a 200-fold increase in
reprogramming efficiency (11). The expression of NANOG
also improves the cloning efficiency of human ES cells
(12). and thus could increase the survival rate of early
reprogrammed cells. LIN28 had a consistent but more modest
effect on reprogrammed mesenchymal cell clone recovery
(Fig. 1A).
We next tested whether OCT4, SOX2, NANOG, and LIN28 are
sufficient to reprogram primary, genetically unmodified,
diploid human fibroblasts. We initially chose IMR90 fetal
fibroblasts because these diploid human cells are being
extensively characterized by the ENCODE Consortium (13), are
readily available through the American Type Culture
Collection (ATCC, Catalog No. CCL-186) and have published DNA
fingerprints that allow confirmation of the origin of
reprogrammed clones. IMR90 cells also proliferate robustly
for more than 20 passages before undergoing senescence but
grow slowly in human ES cell culture conditions, a difference
that provides a proliferative advantage to reprogrammed
clones and aids in their selection by morphological criteria
(compact colonies, high nucleus to cytoplasm ratios, and
prominent nucleoli) alone (14, 15). IMR90 cells were
transduced with a combination of OCT4, SOX2, NANOG, and
LIN28. Colonies with a human ES cell morphology (iPS
colonies) first became visible after 12 days
posttransduction. On day 20, a total of 198 iPS colonies were
visible from 0.9 million starting IMR90 cells whereas no iPS
colonies were observed in non-
[[Page S14823]]
transduced controls. Forty-one iPS colonies were picked, 35
of which were successfully expanded for an additional three
weeks. Four clones (iPS(IMR90)1-4) with minimal
differentiation were selected for continued expansion and
detailed analysis.
Each of the four iPS(IMR90) clones had a typical human ES
cell morphology (Fig. 1B) and a normal karyotype at both 6
and 17 weeks of culture (Fig. 2A). Each iPS(IMR90) clone
expressed telomerase activity (Fig. 2B) and the human ES
cell-specific cell surface antigens SSEA-3, SSEA-4, Tra-1-60
and Tra-1-81 (Fig. 2C) whereas the parental IMR90 cells did
not. Microarray analyses of gene expression of the four
iPS(IMR90) clones confirmed a similarity to five human ES
cell lines (H1, H7, H9, H13 and H14) and a dissimilarity to
IMR90 cells (Fig. 3, table S3, and fig. S4). Although there
was some variation in gene expression between different
iPS(IMR90) clones (fig. S5), the variation was actually less
than that between different human ES cell lines (Fig. 3A and
table S3). For each of the iPS(IMR90) clones, the expression
of the endogenous OCT4 and NANOG was at levels similar to
that of human ES cells, but the exogenous expression of these
genes varied between clones and between genes (Fig. 3B). For
OCT4, some expression from the transgene was detectable in
all of the clones, but for NANOG, most of the clones
demonstrated minimal exogenous expression, suggesting
silencing of the transgene during reprogramming. Analyses
of the methylation status of the OCT4 promoter showed
differential methylation between human ES cells and IMR90
cells (fig. S6). All four iPS(IMR90) clones exhibited a
demethylation pattern similar to that of human ES cells
and distinct from the parental IMR90 cells. Both embryoid
body (fig. S7) and teratoma formation (Fig. 4)
demonstrated that all four of the reprogrammed iPS(IMR90)
clones had the developmental potential to give rise to
differentiated derivatives of all three primary germ
layers. DNA fingerprinting analyses (short tandem repeat-
STR) confirmed that these iPS clones were derived from
IMR90 cells and confirmed that they were not from the
human ES cell lines we have in the laboratory (table S4).
The STR analysis published on the ATCC website for IMR90
cells employed the same primer sets and confirms the
identity of the IMR90 cells used for these experiments.
The iPS(IMR90) clones were passaged at the same ratio
(1:6) and frequency (every 5 days) as human ES cells, had
doubling times similar to that of the human H1 ES cell
line assessed under the same conditions (table S5), and as
of this writing, have been in continuous culture for 22
weeks with no observed period of replicative crisis.
Starting with an initial 4 wells of a 6-well plate of iPS
cells (one clone/well, approximately 1 million cells),
after 4 weeks of additional culture, 40 total 10-cm dishes
(representing approximately 350 million cells) of the 4
iPS(IMR90) clones were cryopreserved and confirmed to have
normal karyotypes.
Since IMR90 cells are of fetal origin, we next examined
reprogramming of postnatal fibroblasts. Human newborn
foreskin fibroblasts (ATCC, Catalog No. CRL-2097) were
transduced with OCT4, SOX2, NANOG, and LIN28. From 0.6
million foreskin fibroblasts, we obtained 57 iPS colonies. No
iPS colonies were observed in non-transduced controls.
Twenty-seven out of 29 picked colonies were successfully
expanded for three passages, four of which (iPS(foreskin)-l
to 4) were selected for continued expansion and analyses. DNA
fingerprinting of the iPS(foreskin) clones matched the
fingerprints for the parental fibroblast cell line published
on the ATCC website (table S4).
Each of the four iPS(foreskin) clones had a human ES cell
morphology (fig. S8A), had a normal karyotype (fig. S8B), and
expressed telomerase, cell surface markers, and genes
characteristic of human ES cells (Figs. 2 and 3 and fig. S5).
Each of the four iPS(foreskin) clones proliferated robustly,
and as of this writing, have been in continuous culture for
14 weeks. Each clone demonstrated multilineage
differentiation both in embryoid bodies and teratomas (figs.
S9 and S10); however, unlike the iPS(IMR90) clones, there was
variation between the clones in the lineages apparent in
teratomas examined at 5 weeks. In particular, neural
differentiation was common in teratomas from iPS(foreskin)
clones 1 and 2 (fig. S9A), but was largely absent in
teratomas from iPS(foreskin) clones 3 and 4. Instead,
there were multiple foci of columnar epithelial cells
reminiscent of primitive ectoderm (fig. S9D). This is
consistent with the embryoid body data (fig. Sl0), where
the increase in PAX6 (a neural marker) in iPS(foreskin)
clones 3 and 4 was minimal compared to the other clones, a
difference that correlated with a failure to downregulate
NANOG and OCT4. A possible explanation for these
differences is that specific integration sites in these
clones allowed continued high expression of the lentiviral
transgenes, partially blocking differentiation.
PCR for the four transgenes revealed that OCT4, SOX2, and
NANOG were integrated into all four of the iPS(IMR90) clones
and all four of the iPS(foreskin) clones, but that LIN28 was
absent from one iPS(IMR90) clone (#4) and from one
iPS(foreskin) clone (#1) (Fig. 2D). Thus, although LIN28 can
influence the frequency of reprogramming (Fig. 1A), these
results confirm that it is not absolutely required for the
initial reprogramming, nor is it subsequently required for
the stable expansion of reprogrammed cells.
The human iPS cells described here meet the defining
criteria we originally proposed for human ES cells (14), with
the significant exception that the iPS cells are not derived
from embryos. Similar to human ES cells, human iPS cells
should prove useful for studying the development and function
of human tissues, for discovering and testing new drugs, and
for transplantation medicine. For transplantation therapies
based on these cells, with the exception of autoimmune
diseases, patient-specific iPS cell lines should largely
eliminate the concern of immune rejection. It is important to
understand, however, that before the cells can be used in the
clinic, additional work is required to avoid vectors that
integrate into the genome, potentially introducing mutations
at the insertion site. For drug development, human iPS cells
should make it easier to generate panels of cell lines that
more closely reflect the genetic diversity of a population,
and should make it possible to generate cell lines from
individuals predisposed to specific diseases. Human ES cells
remain controversial because their derivation involves the
destruction of human preimplantation embryos and iPS cells
remove this concern. However, further work is needed to
determine if human iPS cells differ in clinically significant
ways from ES cells.
____
Exhibit 2
Dolly Creator Prof Ian Wilmut Shuns Cloning
(By Roger Highfield)
The scientist who created Dolly the sheep, a breakthrough
that provoked headlines around the world a decade ago, is to
abandon the cloning technique he pioneered to create her.
Prof Ian Wilmut's decision to turn his back on
``therapeutic cloning'', just days after US researchers
announced a breakthrough in the cloning of primates, will
send shockwaves through the scientific establishment.
He and his team made headlines around the world in 1997
when they unveiled Dolly, born July of the year before.
But now he has decided not to pursue a licence to clone
human embryos, which he was awarded just two years ago, as
part of a drive to find new treatments for the devastating
degenerative condition, Motor Neuron disease.
Prof Wilmut, who works at Edinburgh University, believes a
rival method pioneered in Japan has better potential for
making human embryonic cells which can be used to grow a
patient's own cells and tissues for a vast range of
treatments, from treating strokes to heart attacks and
Parkinson's, and will be less controversial than the Dolly
method, known as ``nuclear transfer.''
His announcement could mark the beginning of the end for
therapeutic cloning, on which tens of millions of pounds have
been spent worldwide over the past decade. ``I decided a few
weeks ago not to pursue nuclear transfer,'' Prof Wilmut said.
Most of his motivation is practical but he admits the
Japanese approach is also ``easier to accept socially.''
His inspiration comes from the research by Prof Shinya
Yamanaka at Kyoto University, which suggests a way to create
human embryo stem cells without the need for human eggs,
which are in extremely short supply, and without the need to
create and destroy human cloned embryos, which is bitterly
opposed by the pro life movement.
Prof Yamanaka has shown in mice how to turn skin cells into
what look like versatile stem cells potentially capable of
overcoming the effects of disease.
This pioneering work to revert adult cells to an embryonic
state has been reproduced by a team in America and Prof
Yamanaka is, according to one British stem cell scientist,
thought to have achieved the same feat in human cells.
This work has profound significance because it suggests
that after a heart attack, for example, skin cells from a
patient might one day be manipulated by adding a cocktail of
small molecules to form muscle cells to repair damage to the
heart, or brain cells to repair the effects of Parkinson's.
Because they are the patient's own cells, they would not be
rejected.
In theory, these reprogrammed cells could be converted into
any of the 200 other type in the body, even the collections
of different cell types that make up tissues and, in the very
long term, organs too. Prof Wilmut said it was ``extremely
exciting and astonishing'' and that he now plans to do
research in this area.
This approach, he says, represents, the future for stem
cell research, rather than the nuclear transfer method that
his large team used more than a decade ago at the Roslin
Institute, near Edinburgh, to create Dolly.
In this method, the DNA contents of an adult cell are put
into an emptied egg and stimulated with a shock of
electricity to develop into a cloned embryo, which must be
then dismantled to yield the flexible stem cells.
More than a decade ago, biologists though the mechanisms
that picked the relevant DNA code that made a cell adopt the
identity of skin, rather than muscle, brain or whatever, were
so complex and so rigidly fixed that it would not be possible
to undo them.
They were amazed when this deeply-held conviction was
overturned by Dolly, the first mammal to be cloned from an
adult cell, a feat with numerous practical applications, most
remarkably in stem cell science.
But although ``therapeutic cloning'' offers a way to get a
patient's own embryonic stem cells to generate unlimited
supplies of cells
[[Page S14824]]
and tissue there is an intense search for alternatives
because of pressure from the pro-life lobby, the opposition
of President George W Bush and ever present concerns about
cloning babies.
Prof Wilmut's decision signals the lack of progress in
extending his team's pioneering work on Dolly to humans.
The hurdles seem to have been overcome a few years ago by a
team led by Prof Hwang Woo-Suk in South Korea, with whom he
set up a collaboration.
Then it was discovered Prof Hwang's work was fraudulent.
``We spent a long time talking to him before discovering it
was all a fraud,'' he said. ``I never really got started
again after that.''
And Prof Wilmut believes there is still a long way to go
for therapeutic cloning to work, despite the headlines
greeting this week's announcement in Nature by Dr Shoukhrat
Mitalipov and colleagues at Oregon Health & Science
University, Beaverton, that they cloned primate embryos.
In all Dr Mitalipov used 304 eggs from 14 rhesus monkeys to
make two lines of embryonic stem cells, one of which was
chromosomally abnormal. Dr Mitalipov himself admits the
efficiency is low and, though his work is a ``proof of
principle'' and the efficiency of his methods has improved,
he admits it is not yet a cost effective medical option.
Cloning is still too wasteful of precious human eggs, which
are in great demand for fertility treatments, to consider for
creating embryonic stem cells. ``It is a nice success but a
bit limited,'' commented Prof Wilmut. ``Given the low
efficiency, you wonder just how long nuclear transfer will
have a useful life.''
Nor is it clear, he said, why the Oregon team was
successful, which will hamper attempts to improve their
methods. Instead, Prof Wilmut is backing direct reprogramming
or ``de-differentiation'', the embryo free route pursued by
Prof Yamanaka, which he finds ``100 times more interesting.''
``The odds are that by the time we make nuclear transfer
work in humans, direct reprogramming will work too.
I am anticipating that before too long we will be able to
use the Yamanaka approach to achieve the same, without making
human embryos. I have no doubt that in the long term, direct
reprogramming will be more productive, though we can't be
sure exactly when, next year or five years into the future.''
Prof Yamanaka's work suggests the dream of converting adult
cells into those that can grow into many different types can
be realised remarkably easily.
When his team used a virus to add four genes (called Oct4,
Sox2, c-Myc and KIf4) into adult mouse fibroblast cells they
found they could find resulting embryo-like cells by sifting
the result for the one in 10,000 cells that make proteins
Nanog or Oct4, both typical markers of embryonic cells.
When they studied how genes are used in these reprogrammed
cells, ``called induced pluripotent stem (iPS) cells'', they
were typical of the activity seen in an embryo. In the test
tube, the new cells look and grow like embryonic stem cells.
And they were also able to generate viable chimaeras from
the cells, where the embryo cells created by the new method
could be mixed with those of a mouse embryo to grow into a
viable adult which could pass on the DNA of the reprogrammed
cells to the next generation.
Nonetheless, there will have to be much work to establish
that they behave like embryo cells, let alone see if they are
safe enough to use in the body. Even so, in the short term
they will offer an invaluable way to create lines of cells
from people with serious diseases, such as motor neuron
disease, to shed light on the mechanisms.
Given the history of fraud in this field, the Oregon
research was reproduced by Dr David Cram and colleagues at
Monash University, Melbourne. ``At this stage, nuclear
transfer to create pluripotent stem cell lines remains an
inefficient process,'' said Dr Cram.
Mr. BROWNBACK. Mr. President, I suggest the absence of a quorum.
The PRESIDING OFFICER. The clerk will call the roll.
The legislative clerk proceeded to call the roll.
Mr. CRAIG. Mr. President, I ask unanimous consent that the order for
the quorum call be rescinded.
The PRESIDING OFFICER (Mr. Salazar). Without objection, it is so
ordered.
Mr. CRAIG. Mr. President, let me inquire, we are in morning business?
The PRESIDING OFFICER. The Senator is correct.
____________________