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Permalink 09:31:17 pm, by Tom, 1420 words, 3292 views   English (UK)
Categories: Information

Pompe disease – a starring role for animal research

The new Harrison Ford film, Extraordinary Measures, hitting UK cinemas from 26 February, is a fictionalised account of the development of a treatment for Pompe disease, a rare genetic disorder. Pompe disease (glycogen storage disease type 2, acid maltase deficiency) is an enzyme deficiency with devastating effects – progressive muscle weakness and, in the severe infantile form, gross enlargement of the heart. Until fairly recently, the infantile form of the disease was invariably fatal within the first year of life. Now, however an effective treatment is in place.

While the increased awareness that the film’s fictional account brings is very welcome, the real story of how that treatment came about is a fascinating one (1) and laboratory animals play a starring role. The long road to a treatment started in 1932 with the first observation of the disease by Dr JC Pompe, after whom it is named. Pompe described accumulation of glycogen in muscle tissue, which was a puzzle, as the enzymes involved in the usual metabolism of glucose and glycogen were all present and correct. The solution to this puzzle had to wait until Christian de Duve’s 1974 Nobel Prize-winning discovery of lysosomes in 1955. These cellular compartments or organelles are the ‘recycling units’ of animal cells. They have an acid environment and their own specific set of enzymes for breaking down cellular components.

De Duve was carrying out ‘blue skies’ research, with no thought of direct medical application. However, as so often in research, a breakthrough in our basic understanding of biology led to medical applications. In this case, de Duve’s colleague Henri Hers realised that the deficiency of a lysosomal enzyme (alpha glucosidase) for the breakdown of glycogen would explain the symptoms of Pompe disease. This proved to be the case, and Hers established the principle of lysosomal storage diseases, of which around 40 have now been described, in 1965. Before moving on, let us note the role of laboratory animals in this breakthrough. I wrote to Professor de Duve and asked what part the use of animals had played in his work and he replied that “We would not have been able to make the discoveries we made without an extensive use of laboratory animals.”(2) - a statement confirmed by his Nobel Prize lecture.

Having discovered the basis of Pompe disease, the next milestone was to develop a treatment. This proved to be very difficult, largely due to the lack of animal models. A recurring refrain from the animal rights lobby is that if the humane use of animals in medical research was banned, scientists would soon find other ways to ensure medical progress. That comforting belief is belied by the series of attempts, some of them pretty desperate, to treat terminally ill children over the next 25 years. None of them worked.

The next great leap forward came from The Netherlands in 1990 and relied on the use of laboratory mice. Enzyme replacement therapy (ERT) had long been suggested as a potential treatment for lysosomal storage diseases but had never succeeded. In the case of Pompe disease, where large amounts of enzyme were needed in the muscle, introduced enzyme was simply soaked up by the liver. Two Dutch scientists, Arnold Reuser and Ans van der Ploeg, had the idea that phosphorylated enzyme would be taken via by the mannose-6-phosphate receptors in lysosomes, allowing the enzyme to be targeted.

However the supply of phosphorylated enzyme was small – nowhere near enough to treat a sick child. How could efficacy be demonstrated, in the absence of an animal model? In an ingenious experiment (3), they used specific monoclonal antibodies to demonstrate that when bovine phosphorylated alpha glucosidase was introduced to mice, it was taken up by heart and skeletal muscle lysosomes and caused a significant increase in enzyme activity – a 43% increase in skeletal muscle and 70% in the heart. An increase that, if repeated in humans, would result in the level of enzyme found in the healthy population. With characteristic understatement, van der Ploeg et al concluded "...we think that the original idea of enzyme replacement therapy for treatment of lysosomal storage diseases deserves new attention." At last, thanks to this ground-breaking work, a treatment for Pompe disease was a real possibility.

Now that there had been ‘proof of principle’ all that was needed was for a pharmaceutical company to spend millions of dollars in developing a treatment. Understandably perhaps, given the rarity of the disease and the inability to demonstrate actual efficacy, there was no immediate rush. Fortunately, at this point two animal models became available that allowed scientists to demonstrate that not only did the phosphorylated alpha glucosidase make its way to the lysosomes, it also had a beneficial effect.

From 1998 onwards, transgenic mice with Pompe disease, developed in Rotterdam and elsewhere, were used to demonstrated the efficacy of alpha-glucosidase enzyme. At the same time the potential of ERT was also illustrated, more dramatically perhaps, by YT Chen at Duke University, using quail. The quail had the same enzyme deficiency as found in humans, resulting in muscle weakness. After injection with the enzyme, they recovered to the extent of one subject actually flying around the lab (4). The evidence was therefore now pretty convincing – it was time for human trials.

The big problem was in producing enough enzyme for humans, even for babies. This required substantial industry investment. Two rival approaches were tried. A Dutch company, Pharming, produced the enzyme in the milk of transgenic animals for use in a trial led by Ans van der Ploeg, whose PhD research had led to the original breakthrough. The transgenic animal used was the rabbit, on the grounds that a human alpha-glucosidase-producing line could be established quite quickly. This work was used in a successful clinical trial, the results of which were published in The Lancet in July 2000 (5).

Another trail was carried out by YT Chen, using enzyme produced via Chinese Hamster Ovary (CHO) cell culture, by Synpac, a Taiwan-based company. This trial was also successful.

What follows next is a slightly convoluted story. The short version is that a third company, Genzyme, with an existing enzyme replacement therapy for Gaucher disease, bought out both Pharming and Synpac. In the end, they didn’t use either of the enzymes produced by these companies but developed their own, in-house CHO product, now marketed as Myozyme. This was a difficult decision – how could they decide which of the competing products should be invested in to produce a commercial treatment? The answer was what Genzyme called “The mother of all experiments” which compared the different products in transgenic Pompe mice. The result led to the availability of the treatment we have today.

However, the eventual production system is a technicality that need not concern today’s patients. Their concern is that an untreatable, terminal illness is now treatable. If you go and see Extraordinary Measures do bear in mind the starring role that doesn’t appear in the cast list – that of the mice and quail that made this treatment possible.

Kevin O’Donnell


1. http://pompestory.blogspot.com
2. Letter from Christian de Duve to Kevin O’Donnell, 4 March 1997
3. Intravenous Administration of Phosphorylated Acid Alpha-Glucosidase Leads to Uptake of Enzyme in Heart and Skeletal Muscle of Mice http://www.jci.org/articles/view/115025
4. Clinical and metabolic correction of pompe disease by enzyme therapy in acid maltase-deficient quail http://www.jci.org/articles/view/1722/pdf
5. Recombinant human alpha-glucosidase from rabbit milk in Pompe patients http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(00)02533-2/fulltext#article_upsell (free registration required)

Biographical note.

I should declare an interest. I am a professional scientist, however my involvement with Pompe disease dates from the diagnosis of our first child, Calum, with infantile Pompe disease in 1993. At that time the disease was still untreatable and Calum died at 8 months of age. Following that I had the great privilege of participating in an international community of patients and scientists that championed the development of a treatment for Pompe disease. They don’t appear in the cast list of the film either, or the book on which it is based The Cure by Geeta Anand. This prompted me to write the real story down – I think it’s a better story than either rthe book or the film though not, sadly, as well written. Your comments welcome at http://pompestory.blogspot.com You can find out more about Pompe disease from the following sites:

International Pompe Association www.worldpompe.org
Acid Maltase Deficiency Association www.amda-pompe.org
UK Pompe Group www.pompe.org.uk
Genzyme www.pompe.com


Permalink 03:23:39 pm, by Tom, 767 words, 2263 views   English (UK)
Categories: Information

Gene therapy on the brain

Hot on the heels of last weeks report of the successful use of gene therapy to treat the eye disease Leber’s congenital amaurosis comes a report that scientists lead by Nathalie Cartier and Patrick Aubourg of the French National Institute for Health and Medical Research have combined gene therapy and stem cell medicine to successfully treat two boys with the disease cerebral X-linked adrenoleukodystrophy (X-ALD).

X-ALD is caused by mutations in the ABCD1 gene that plays a key role in the transport of fatty acids within cells, and lack of ABCD1 causes long-chain fatty acids to build up within cells known as microglia and oligodendrocytes in the brain. Affected microglial cells and oligodendrocytes eventually cease to maintain the insulating myelin sheath that is required for effective transmission of electrical impolses along nerve cells, leading to brain damage and ultimately death at an early age. The disease was made famous by the film "Lorenzo's oil" which describes a dietary supplement that may delay the progression of the disease, though the only treatment that is currently considered truly effective is allogeneic hematopoietic cell transplantation where healthy bome marrow stem cells from a donor are transplanted into the X-ALD patient. Allogeneic hematopoietic cell transplantation works because the microglial gells and oligodendrocytes develop from cells that migrate to the brain from the bone marrow, so that healthy cells from the donor eventually replace some of the patient's ABCD1 deficient cells and help maintain the myeline sheath. Unfortunately it is often difficult to identify a suitable donor, and even if one is found the procedure is risky due to problems such as graft-versus-host disease where immune cells in the donated bone marrow mount an immune response against the patient's tissues.

Gene Therapy

Dr. Cartier and colleagues examined the possibility of using gene therapy to modify the patient's own hematopoietic stem cells so that they express a functioning ABCD1 gene and then injecting these cells into the patient to replace their faulty bone marrow hematopoietic cells, thereby avoiding the problem of donor and host incompatability. Rather than attempt to genetically modify and transplant all types of human bone marrow stem cells they concentrated on a subset of cells called the CD34+ cells that give rise to many cells of the immune system. These have the great advantage that they can be isolated from the blood, avoiding the need for surgery to harvest bone marrow. To assess whether genetically modified CD34+ cells could develop into cells of the immune system when injected into the bone marrow they selected the NOD/SCID mouse that lacks a functioning immune system and is often used to assess human stem cell transplantation techniques and to study aspects of the human immune system. Initial results with retroviral vectors were disappointing but using the NOD/SCID mouse model they developed a lentiviral vector based on HIV-1 that enables the functioning ABCD1 gene to safely incorporate into the genome of a significant proportion of the cells and drive ABCD1 expression in immune system cells derived from them (1). What is more they found that as well as the expected range of immune cells the genetically modified CD34+ cells migrated to the brain and differentiated into microglial cells (2). Of course if the therapy is to prevent disease progression the vector needs not only to drive expression of ABCD1 but to do so reliably for many years,. To assess whether the lentiviral vector could do this they transplanted Sca-1+ cells, the mouse equivalent of human CD34+ cells, containing the ABCD1 expressing lentiviral vector into mice that lacked a functional ABCD1 gene, and found that even 12 months after transplantation almost a quarter of microglial cells in the mouse brain expressed ABCD1 (3).

These promising results in mice were enough to persuade Dr. Cartier and her colleagues that this therapy should proceed to a pilot study in human patients who are in the early stages of this desease. While it will take several years of observation and clinical trails involving larger numbers of patients before we can be sure that this therapy is a success, this exciting news is yet another sign that gene therapy is finally coming of age.


Paul Browne

1) Benhamida S. et al "Transduced CD34+ cells from adrenoleukodystrophy patients with HIV-derived vector mediate long-term engraftment of NOD/SCID mice." Mol Ther. Volume 7(3), pages 317-324 (2003) PubMed: 12668127

2) Asheuer M. et al. "Human CD34+ cells differentiate into microglia and express recombinant therapeutic protein" Proc Natl Acad Sci U S A. Volume 101(10), pages 3557–3562 (2004) PubMed Central: PMC373501

3) Cartier N. et al. "Hematopoietic Stem Cell Gene Therapy with a Lentiviral Vector in X-Linked Adrenoleukodystrophy" Science Volume 326(5954), pages 818 - 823 DOI: 10.1126/science.1171242


Permalink 10:05:57 pm, by Tom, 537 words, 2039 views   English (UK)
Categories: Information

Mending a Broken Heart

An interesting item in the news today about research on repairing the damage to the heart caused by a heart attack. The report in PNAS can be read by those with a subscription at:

While there have been several attempts to bioengineer cardiac tissue for transplant in vitro using starting from cells seeded onto a scaffold, so far these efforts have been hampered by difficulties in getting the capillaries necessary to supply blood to enable the muscles in the tissue patch to grow properly. Due to these difficulties engrafted heart patches have until now had limited benefits on heart function in animal models of heart attack, and consequently this approach has not yet been assessed in human clinical trials.

A cross-section of the new tissue with functional blood vessels (the hollow ovals) containing red blood cells[/caption]

In this project the scientists at Ben-Gurion University started with a similar approach to that used previously by other scientists. They grew the patch of tissue from neonatal rat heart cells which were seeded in scaffolds designed to allow cardiac cell organization and blood vessel penetration after transplantation, and supplemented them with a mixture of growth factors that encourage cell survival and blood vessel growth. After the cells had been cultured in vitro for 24 hours to allow initial organization of the cells within the scaffold they introduced a new step, implanting the patch into the rat omentum, an abdominal tissue that is particularly rich in blood vessels, in the hope that the interaction with the blood vessels of the omentum would encourage the development of mature blood vessels in the heart patch.

They observed that the blood vessels of the omentum connected with those developing in the heart patch, encouraging blood vessel development and growth of cardiac muscle. The real test came when they compared the ability of omentum-grown heart patches to repair tissue damage in rats which had undergone experimentally incuced heart attacks 7 days earlier, with that of heart patches that had been grown in vitro. The result was clear, the omentum-grown heart patches had better blood vessel and muscle quality than the in-vitro grown patches and integrated more strongly into the heart. When they examined several parameters of heart function they found that the hearts of those rats which had received omentum-grown patches worked better than those of control rats and those which had received in-vitro grown patches.

So what does this mean for the treatment of heart attacks? The authors point out this is a relatively straightforward procedure that could be assessed in human trials, but also caution that the extra surgery required to grow the heart patch on the omentum would be to risky for many elderly or ill patients so it is a procedure suitable for only a minority of heart attack patients. What the authors suggest is the development of in vitro bioengineering techniques that mimic the influence of the omentum on the growth of blood vessels and muscle within the heart patch, and with this study they have begun to determine what the requirements of such in vitro systems are.

Needless to say as such in vitro techniques for stimulating heart tissue growth are developed they will need to be assessed in animal models of heart injury before they can enter clinical trials in human patients.


Dr. Paul Browne


Permalink 10:48:01 pm, by Tom, 1087 words, 3178 views   English (UK)
Categories: Information

From Mouse to Monkey to Humans: The Story of Rituximab

Modern advances in science have meant that our models of diseases have vastly improved. Be that in a dish in the laboratory, a computer simulation or through using a transgenic mouse, there have been developments across the biomedical field that have given us a greater understanding of diseases and how our bodies work.

This increase in knowledge has meant that we are finding may drugs already on the market can treat a variety of diseases – those involving the same pathway or cell type. This is precisely what happened this month with a drug called Rituximab.

Rituximab was licensed in 1997 for use in the treatment of Non-Hodgkin’s lymphoma (NHL) - a cancer where cells of the immune system called B-cells mutate and divide abnormally. The cancer then spreads around the body when the B-cells clone themselves in replication.

Since it’s initial approval for use in NHL, rituximab has been used to successfully treat advanced rheumatoid arthritis and has also been part of anti-rejection treatments for kidney transplants (both involve B cells. Then news came last week that it could even slow the progression of rheumatoid arthritis (RA) in the early stages of the disease.

Rheumatoid Arthritis

Rituximab is an interesting drug, as it is a chimeric antibody. This means that it contains portions of both human and mouse antibodies mixed together. The first papers reporting on rituximab were published in 1994. The first looked at its creation, and the second reported on the phase I clinical trials of the drug.

The human immune system works by using antibodies as their ‘messengers’. The antibodies contain multiple regions that allow them to work effectively. One part of the molecule binds with the foreign molecule; the other part then recruits the immune cells to destroy the molecule and eliminate it from the body.

The B-cells mutated in NHL and involved in RA are part of the human immune system and are responsible for making antibodies against ‘foreign invaders’. Mature forms of B-cells have a protein called CD20 on their surface.

The protein CD20 was the target for a team in San Diego (1) in 1994. Because NHL and RA are characterised by excessive levels of, or mutated B-cells, they looked at ways to reduce their numbers. The researchers determined that CD20 was the perfect target on the human B-cells as it was located on the surface of the cell and it didn’t mutate, move inside the cell or fall off in the life cycle of the B-cell. The team then produced an antibody that would attack CD20 itself, so it would bind to the outside of B-cells, flagging them to the immune system to be eliminated. They identified a mouse antibody that had high anti-CD20 activity.

They then constructed a “chimeric” antibody containing the variable domain of the mouse antibody, the portion that specifically binds CD20, along with the constant domain of human antibody, the portion that recruits other components of the immune system to the target.

The construction of a chimeric antibody (later named rituximab) was crucial, as the mouse antibody was unsuitable for direct use in humans. While the mouse antibody was able to bind to human CD20, it would not be able to then recruit the human complement system and immune cells that are needed destroy the “targeted” B cells. It would also quickly be recognised as foreign in the human body, and destroyed by the immune system, therefore by using a chimeric antibody with enough human characteristics, the antibody would not only recognise the human CD20 and target the immune system to it but would remain in the body long enough to destroy the B cells.

To test whether rituximab would work as hoped, they performed studies in cynomolgus monkeys. They choose this species because the constant domains of their antibodies are very similar to those in humans, unlike those of the mouse, allowing the chimeric antibody to function as it would in humans. Following administration of rituximab the number of B cells in the monkey’s bloodstream fell dramatically. The numbers were also reduced in the bone marrow (where B cells are produced) and the lymph nodes (where they are activated to target foreign molecules). Rituximab administration was non-toxic and in the weeks after treatment finished the number of B-cells slowly recovered. This is important as it demonstrates that the treatment didn’t harm the monkey’s bone marrow stem cells, an important consideration since these cells are required for a healthy immune system.

Rituximab was an ideal candidate to treat NHL and the promising results in monkeys prompted the scientists to conduct phase I clinical trials inhuman patients which confirmed that rituximab was safe and indicated that it could shrink tumours.

Evaluation of the effectiveness of rituximab involved many studies of patients with Non-Hodgkin’s lymphoma. While the initial clinical trial results varied, likely due to the differing sizes of tumours between the patients, they showed it was effective at reducing B-cell numbers and tumour size. Since it’s approval numerous clinical trials have confirmed that rituximab is an effective treatment for Non-Hodgkin’s lymphoma (3).

This month’s exciting study by Professor Paul-Peter Tak from the University of Amsterdam showed that rituximab in combination with the drug methotrexate could slow the progression of early stage rheumatoid arthritis (RA).

The study involved 755 patients diagnosed with RA within the last year. Methotrexate is already considered to be the best treatment for these patients and 12.5% of the patients taking only methotrexate in this study experienced significant reduction of their symptoms. However, compare this to the 30.5% of patients taking a combination of methotrexate and rituximab, and it is clear that rituximab is effective. Issues of cost have been raised in relation to rituximab, but if it turns out to be as effective in treating early RA as this study suggests, then it may ultimately save the health services and insurance companies money as slowing or stopping the progression of the disease will result in fewer patients needing the more expensive treatment and care required in advanced RA.

Emma Stokes

1) Reff M.E. et al. “Depletion of B cells in vivo by a chimeric mouse human monoclonal antibody to CD20.” Blood Volume 83(2), Pages 435-445 (1994) PubMed: 7506951

2) Maloney D.G. et al. “Phase I clinical trial using escalating single-dose infusion of chimeric anti-CD20 monoclonal antibody (IDEC-C2B8) in patients with recurrent B-cell lymphoma.” Blood Volume 84(8), Pages 2457-2466 (1994) Pubmed: 7522629

3) Schultz H. et al. “Chemotherapy plus Rituximab versus chemotherapy alone for B-cell non-Hodgkin's lymphoma.” Cochrane Database of Systematic Reviews 2007, Issue 4. Art. No.: CD003805. DOI:10.1002/14651858.CD003805.pub2.


Permalink 06:15:34 pm, by Tom, 699 words, 4204 views   English (UK)
Categories: Information

Some good news from Europe

As many of you will no doubt be aware the EU is in the process of updating Directive 86/609, the directive that covers the "laws, regulations and administrative provisions of the Member States regarding the protection of animals used for experimental and other scientific purposes". The proposals for the revision of Directive 86/609 that were adopted by the EU commission in November last year contained many welcome improvements on the previous rules, and would bring the regulation of animal research in the rest of the EU up to the high standards that we are used to in the UK.

However a few of the proposed changes led to widespread fears among European scientists that huge additional bureaucratic burdens would be placed on those undertaking animal research, often with little or no animal welfare gains. Scientists were also concerned that the proposal to limit research on monkeys and other non-human primates to projects that focus on the “avoidance, prevention, diagnosis or treatment of life-threatening or debilitating clinical conditions in human beings”, a restriction that would stop EU scientists from undertaking research on the basic function of the nervous system, even though such research greatly improves our understanding of the biology of many terrible diseases. In the UK a coalition of nine scientific organizations that together represent the overwhelming majority of medical researchers published a Declaration of concern to highlight the particular items that they felt should be changed or removed. The nine organizations included charities that fund vital research into diseases such as muscular dystrophy and Alzheimer's disease.

Fortunately on Tuesday the EU parliament's Agriculture committee, which was tasked with producing a report on proposed revisions and suggesting ammendments, listened to scientific community (including several Pro-Test members who submitted evidence and talked with MEPs) and addressed most of their concerns in its report. While they supported higher standards for animal welfare and the need for animal studies to undergo compulsory ethical assessment, they rejected some of the revisions proposed by the EU commission that would have pointlessly increased the bureaucracy associated with animal research and in particular rejected "...the idea that tests using non-human primates should be restricted to "life-threatening or debilitating" conditions, as this would seriously hinder research into some forms of cancer, multiple sclerosis and Alzheimer's disease".

As it happens science writer Ed Yong has just reposted a 2007 post on his "Not exactly rocket science" blog that illustrated just how useful research that does not address "life-threatening or debilitating" conditionsis to neuroscience. In a study published in Nature Tianming Yang and Michael Shadlen from the University of Washington measured the activity of individual nerves in Rhesus macaque monkeys in order to determine how the pattern of nerve cell activity in an area of the brain known as the lateral intraparietal area (LIP) changed as the monkeys learned to base their decisions about which of two targets to choose for a reward on the combined probabilities indicated by four shapes, each associated to a varying degree with one target or the other. The ability to calculate probablity is strongly associated with decision making and unltimately reasoning this study which gave a new insight into how nerve cells in the brain's control centres, such as the LIP, extract probabilistic information from a set of symbols and to combine this information over time in order to help later decision making. Their results also provided the first solid experimental evidence to support role of the log likelihood ratio, a statistical test for making a decision between two hypotheses, as the common currency with which the brain constructs an informed guess between two options, an important discovery that will aid future research into how we make decisions.

While the report published by the agriculture committee represents an important victory for science the future of animal research in the EU is the by no means assured, and scientists and supporters of medical research must continue to argue their case and lobby their MEPs as the revisions to Directive 86/609 go before the full EU parliament. We will soon suggest ways in which you can help us in this effort, so keep an eye on Pro-Test news and be ready to stand up for science!


Paul Browne

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