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FB 65

31/5/2018

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FB 65. I have a bit of an eye problem at the moment so this report should be brief. A minor but almost amusing news flash is that my wife (also a geneticist) and I recently volunteered to join the committee of a breed club. We were accepted and then immediately nominated as delegates to Breed Council. Attending the recent Council meeting I had expected all sorts of fireworks on JKD but instead met a very different scene. Our club proposition that Breed Council encourage member clubs to hold open meetings on the disease so that everyone at last could hear all about it was passed unanimously, on minor amendment, mostly because of persuasion by a delegate from another club. The amendment was that my club hold the first meeting, and funding to aid this was included. This seemed to be a complete turn-around from actions in past meetings, but one disappointment in this for me was that I was left in the dark as to what the past hostility had been about. I can only say that if any delegate, club or individual wants to ask me anything about my actions, or those of boxerjkd, please just contact me by email (brucecatt8@gmail.com) and I will endeavour to explain everything and anything. 
However, setting this aside, the important news is that an open meeting is being planned, amidst the difficulties of finding a free date and venue can be found in this summer season of wall-to-wall shows. The speakers will be Professor Syme of the RVC who will explain the difficulties of the disease and its diagnosis. I will summarise the genetic findings from the boxerjkd efforts which will include the evidence on the inheritance and what tools we can use to help with Boxer breeding until the responsible gene is found. And then Professor Amos will tell us how far his research to find the gene has progressed. And from what I can learn, everything is going extremely well.
Additional news of interest is presented in a Purina publication (https://www.proplan.com/media/5954/boxerupdate_spr2018.pdf). It describes a new project on kidney disease specifically in American Boxers. I think we already know the answers to many of the questions they want to address but the more information the better. Many American cases have already contributed to Professor Amos’ search to find the gene.
I finish on the sad note of new JKD cases. The worst concerns a puppy only 4 months old and seriously ill. The big question has been whether at this young age she should be put on a renal diet? I have checked with our specialist and it seems one has to choose the least of two evils, and a renal or even a senior diet is recommended. Other new cases have rattled the concept that JKD is rare; we have recently had a UK litter with at least three affected puppies, with a fourth possible, and a Polish litter appears to have broken the record with five cases in one litter. How awful for all concerned. Here I recall I have to mention another disturbing issue. I have just learned that a boxerjkd diagnosis has been questioned and this has been used to diminish the evidence on JKD. On checking back on the records I found an ndisputable veterinary diagnosis from two independent vets, including ultrasound assessment of the kidneys. They were described as abnormal (with much detail) and it seems that the owner had simply misunderstood what was described and thought that ‘kidney abnormalities’ meant ‘ kidney tumours’ and told the stud dog owner this. And the word spread. Why are people content to believe word of mouth rather than seek the truth? I endeavour to find the correct answers to all questions.
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FB 64 Update from Professor Bill Amos

9/5/2018

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FB 64. I have a piece of exciting update from Professor Amos on his research. It reads as follows: “Many of you will have seen posts asking for samples from dogs affected with JKD. I am the geneticist to whom the samples are sent and I thought you might like an update on progress. I will try to write this in non-technical language but do feel free to ask me questions if you want more detail or require something explaining further.
First, I just want to say a massive thank you to all those who have sent me samples. I now have samples from 1,100 dogs of which about 100 have JKD and the rest are used as healthy controls for comparison. The first part of my study was completed in 2017 using a relatively crude analysis applied to about 600 samples. I was pleased to find a strong indication that the faulty gene lies in one particular region on one on the dog’s 38 chromosomes. I am 90% certain this is a robust result. I don’t say 100% because there remains some room for doubt. Having said this, Bruce told me about one top dog who he was sure was homozygous (carried two copies of the faulty gene). I have samples from 13 of his offspring and they all carry a trait that is much commoner in diseased compared with control dogs. Such a pattern would be highly unlikely unless Bruce was right and if the region was not involved with the disease.
With a good ‘hit’ I now want to find the gene. With so many new samples coming in over the last 4 months I am in a good position. My next experiment is to look much more closely at the candidate chromosome region by DNA sequencing (I will read the genetic code). As a trial run to make sure the method works, I will study about 500 dogs. Sequencing will take about 5 weeks and I will post the samples off on Monday 7th May. Fingers crossed! If this works well, I will analyse the full sample set. However, even with just the first half I should be able to say with confidence that the gene does (or does not) lie in this region, and may well be able to say what the gene is. I should also be able to start developing a simple genetic test to tell whether a dog is a carrier or not.
I should end on a slight cautionary note. While the disease clearly has a genetic basis and runs in families, it is not completely simple. You may already have asked yourself how a top dog can carry two copies of the faulty gene yet still be healthy. There are several possible answers: the disease could be very variable such that some puppies die before they are born while others live well into adulthood; it could be that there is a second gene involved that actually protects against the effects of the disease gene. The truth is that we do not yet know why. Thus, while I am confident that I am well on my way to tracking down the main player, this will not be the end of the story. In future I want to understand the disease fully. In this light, more samples will always be welcome! “
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FB 63

3/3/2018

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FB 63 Looking back on previous JKD updates, it seems I always start by saying that much time has passed since my last report but that much has been happening. I can say this mega fold this time too. I have not written since before Christmas but much has been stirring, although with several hold ups. It has been a bit bumpy.
But first a word on Dr Hamilton’s bio-marker for ARVC: 
- The bio-marker system for detecting developing ARVC before disease signs or Holter indications has now been patented, 
- An upgraded manuscript on the subject has been submitted to a foremost major medical journal, and is in the process of review, 
- Funding has been raised to allow further assessment of the screen both in humans and our dogs, but more funds will be needed to show its full potential for detecting cardiomyopathy carriers in our Boxer populations. 
- American veterinary cardiologists are becoming involved and these include our own (UK) hyper-enthusiastic Simon Swift who is now working in Florida. 
- It might seem that the ABC, or ABCCF, is also now interested in the bio-marker screen.
With JKD, there has been even more of a bumpy ride of late:
- Prof Amos has been ill, twice and the search for the gene location has therefore been badly delayed, although I gather all is underway again now. 
- American JKD cases have been increasingly reported and they have been contributing substantially to the Amos DNA work 
- Lynn Kincla’s publication of new pedigrees on the Boxerjkd website has unfortunately been delayed, partly by her house move but also because of difficulties getting veterinary and other details. Most are however now publishable and will be put up on the site very shortly. They involve British and other European dogs. 
- One UK litter has come to particular attention because it contained three affected cases and the possibility of a fourth; and the litter which comprised only seven pups is only 9 months old. Fortunately, all people involved, owners of the sire, dam, and all puppies have been uniquely cooperative, and swabs for DNA from the whole litter are being supplied. And all the pups will continue to be closely monitored. 
At breeder level in the UK, it appears that views on JKD have become increasingly confused. In contrast to clear actions in past times on progressive neuropathy (PA), sub-aortic stenosis (SAS), and cardiomyopathy (ARVC) in which breeding guidelines were set up and SUCCESSFULLY applied within a few months, we are now in our 8th year with JKD without any resolution in sight. Nobody knows what to believe and what to do. Despite my facebook efforts to keep people abreast of developments, and all the information and advice from Boxerjkd, there is still a lack of understanding. Not everyone uses facebook of course, but options for providing information are increasing limited these days. Instead, information seems to be almost totally reliant on diverse and generally flawed personal opinion and ringside gossip. 
So, why is it different from former times? A major factor, I’m sure, is that with each of the earlier diseases, clubs held open meetings around the whole country at which I and specialists in each field of veterinary medicine explained the nature of the diseases and their genetics, and breeding guidelines were offered. The latter were clearly accepted by breeders as indicated by a show of hands at the end of each talk and the concepts were supported and ultimately endorsed by Breed Council. But in the 8 years since JKD recognition not a single meeting of this type has been organised. However, things may be breaking. In the last few days I have been officially asked to speak on JKD at the next (April) meeting of Breed Council and I believe that two clubs are requesting Breed Council to encourage all clubs to have open meetings on the disease such as we had for the earlier diseases. At such meetings JKD and its complications could be described, the basis for the genetic conclusions on the inheritance explained, advice given on what can be done, and equally importantly, what should NOT be done, and with further suggestions offered to help resolution of this well-established and difficult inherited problem in our breed.
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FB 62

16/11/2017

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FB 62. It has always perplexed me that scientific discoveries so often come out in twos, from different labs. I suppose people are asking the same questions based on what is known at the time, and therefore are liable to come up with the same ideas and results. And so it would seem with our Boxer stuff. Professor Amos says he has the identified the chromosome on which the JKD gene lies, and almost immediately the Swedish/American labs say the same thing. Could this be true and have they each have found the same chromosome? Either way, it seems some collaboration may result. And then no sooner do we have Dr Hamilton talking about his bio-marker for ARVC when I hear that a British cardiologist, David Connolly, who I also know from former times, is asking for ARVC cases and controls to test out something a bit similar. And just like the JKD groups, these two ARVC groups may join forces. They might even use the same dogs/blood samples. It’s all progress I suppose, but Boxers' problems are getting their share of attention. Wouldn’t you agree?
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FB 61

15/11/2017

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FB 61. Life has its ups and downs. The latest ‘down’ for me was having to put to sleep my nearly 10 year old girl and favourite, my last show bobtail, Sunny or Steynmere Sunshine Girl. Maybe by having taken up violent tug-of-war games with her much bigger brother she had damaged a disc in her neck or maybe it was a cancer symptoms but she started going through periods of agony in her neck region. There only one thing to do at her age. So she now rests among the apple tress in the garden with so many other Steynmere Boxers. I only showed her as a puppy as I was so wrapped up with cardiomyopathy that I never got her and her brother socialised normally and she did not like the show ring. Nevertheless she qualified for the Pup of the Year competition easily as a baby despite being the youngest. This is the end of an era with a vengeance.
But there have been ‘ups’, with both the ARVC and JKD research. A few days ago I visited paediatric cardiologist Robert Hamilton from Canada who was attending a cardiology conference in Wales and got an update on his bio-marker for ARVC. In a remarkable piece of outside-the-box thinking he had come up with an idea for detecting the presence of the disease before it was overtly recognisable. He had tested it out on number of his ARVC patients and all showed positive. Then he turned to Boxers affected with this same heart disease. All affected Boxers (American) also showed positive while a sample of UK Boxers, deduced by pedigree to be free of the gene responsible, proved negative. More intriguingly, but in a separate study, several dogs from a further UK sample, including some that were seemingly totally normal, although at risk by pedigree of carrying the gene, showed weakly positive suggesting they carried the gene and the test was offering an early diagnosis.
Finding this bio-marker represents a stunning discovery and it has since been probed and checked. The human work, supplemented by the main Boxer result, have been submitted for publication in a top American medical journal. I believe I have got it right when I say that only 40% of papers submitted to this journal get through the first editorial stage and go out to formal review. Dr Hamilton’s paper cleared this first hurdle immediately and I have great expectations for full reviewer acceptance as I think this a major milestone in human, and also Boxer cardiomyopathy research. For both species it opens up the possibility for a pre-clinical test which will serve virtually as a gene test for the disease. Much work still needs to be done to ascertain how early in life, and how effectively it picks up dogs which carry the gene but are apparently normal still needs to be ascertained; further investigation is needed. 
For this further Boxer work, a first requirement is funding, and application has already been made to the AKC (about $50,000 is needed) and, given its importance for American breeders, I would hope that the ABC will step in to help. The second very obvious requirement is full breeder support without which nothing can be done. Here about 50 new affected cases will be needed plus a like number of clear-by-pedigree controls, plus as many close family relatives as possible, all with pedigrees (in total confidence). Breeders interested in helping would best contact me (brucecatt8@gmail.com) in the first place. But no work or even sample collection will start until after the needed funding is obtained. In conclusion, the opportunity to get a sound working test for ARVC is now possible, but it is entirely up to Boxer breeders to help with the needed investigations. I do hope there will be major breeder support as an ARVC test is desperately needed in NA and, I’m afraid also in the UK.
Developments with JKD research are equally exciting. I wrote earlier about Professor Amos’ new findings, and progress continues He is quite confident that he has found the chromosome on which the gene for JKD lies, this indicated by an association between the disease and two of his micro-satellite markers on the chromosome. Moreover they mark the site to a small region in the chromosome where a number of genes lie, mutations in which could be responsible for the disease. He is now working through each of these genes, sequencing them for mutations. One gene has been eliminated and results on a second should be available by the end of November, and so it will continue until the gene with the causal mutation is found. If a mutation cannot be found then it all gets difficult; the mutation may lie in an inter-genic or regulatory region, which would make it very hard to find, but let’s hope for something simple.
Interestingly, we hear that the Swedish and Norwegian work has now also found what they believe is the location of the gene, and discussions on the possibility of all researchers working together henceforth are now in progress. However, although the Scandinavian interests are currently focussed on the diagnostic aspects of the work, any future collaboration will depend on agreement by everyone on the candidate region. Nobody is offering this information yet, and there are also practical problems to be resolved such as the partial duplication of material caused by the AHT contribution of swabs from UK dogs with the blood samples I sent to Norway earlier. With or without any collaboration this could bias the Scandinavian GWAS results. But it is all very exciting and illustrates the commitment of all researchers and their confidence that JKD has a basically simple inheritance. Professor Amos is still eagerly accepting swabs from affected normal dogs, and may be contacted directly for swab kits (wa100@hermes.cam.ac.uk).
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FB 60

5/9/2017

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​FB 60. It may seem that nothing is happening with JKD at the moment. As always this is far from the truth. In part this has been due to my change in email address which caused a number of reports on new cases temporarily to go astray. My first news , therefore, is that this has been rectified and all the new pedigrees are now up on the boxerjkd.com website, with few more yet to come in. They include JKD cases from countries other than the UK and the whole makes informative reading. The same pattern of inheritance is becoming evident everywhere.
Disappointingly, critical personal comments on the boxerjkd group written by Tim Hutchings have appeared in the British canine newspaper, Our Dogs. The seriousness of the JKD situation is also dismissed. Responding to this has taken up some time but the whole story to date can be viewed in the boxerjkd.com blog. It all makes for sad reading.
It seems that much of the problem is due a lack of understanding of the genetics of the disease and full appreciation of the pedigree evidence. Therefore boxerjkd.com is now trying to alleviate this by annotating the pedigrees to provide more key information; this is based on the published evidence. However, as not all pedigrees have been reported to us, notably those held by the Breed Council health committee, the annotations are incomplete. The annotated pedigrees can now be viewed on the boxerjkd website. 
It should also be noted that the Norway list is incomplete. The Norwegian Boxer Club has decided that it wants to publish its own pedigrees, although with our annotation system. This may be appropriate and would save us much work. We are therefore closing our Norway list and replacing it with a link to the Norwegian one. Little difference will be noted in practice.
Of far greater importance however are the new research findings also reported in the boxerjkd blog. These comprise the incredible news from Professor Amos that he is confident that he has identified the chromosome on which the gene for JKD lies. Finding the chromosomal location of the gene is a major milestone in identifying the gene itself. More detail is given in the blog.
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FB 58

24/6/2017

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FB 58. There must be few people in Boxers who have not heard of the inherited juvenile kidney disease (JKD) that has risen to the fore in recent years. I have tried to keep everyone aware of the situation and as a professional geneticist and former Boxer breeder I have done my best, along with others (www.boxerjkd.com) to help breeders deal with the problem. Critical to this has been the publication of pedigrees of affected dogs on the boxerjkd website. Together with appropriate breeding guidelines, this is the only available option for breeders, and will continue to be, until the gene responsible is found. But clearly not everyone agrees with this, preferring instead to keep all available information hidden and leaving breeders with only ringside gossip to help them avoid walking into the disease. Typically my efforts have involved describing other people’s experiences which is not pleasant, but when JKD comes close to me, as it now has, the tragedy of it all becomes so much more poignant. So this message gives an account of a personal experience with JKD, but the situation is relevant for all.
Last year, as things appeared to be quietening down a bit with JKD, I had the wild thought of venturing back into the show ring after a Boxer cardiomyopathy- and JKD-forced long absence. The idea was triggered by an impressive photo of a young bobtail puppy. I enquired about her to learn of a further attraction; she was the granddaughter of a champion dog of mine I collected semen from in the 1970s. Expressing an interest I was offered her on condition I would show and have a litter from her. However, to be fair, she was not as good as her photograph, but a deal is a deal and I did my best on showing, not realising the difficulties of her exuberant wild temperament and my loss of fitness after 10 and more years sitting in front of a computer dealing with Boxer health problems. In the meantime the breeder had some very bad luck and decided to give up Boxers, which I really hoped would mean I would not have to breed her. She did have obvious JKD risks in her pedigree but fairly far back as is the case for so many Boxers these days. 
But the next thing that happened was that I was contacted by an owner of a young bitch that had died of JKD earlier this year and who, on replacing the youngster with a pup from a known person in the breed, learned about my battles with JKD. But she also thought that I might have the sister. It turned out that I did. It was my young bitch. So, she could now be deduced not only to being at high risk of being a carrier, but also at risk of developing the disease herself at some point. This obviously put paid to any ideas on breeding from her, for which I was actually quite thankful, but of course left me with concerns for her future health. However what really had me fuming was that although the owner of the affected sister had reported the case to the health committee, the situation had not been reported to me. Had my interest in showing and maybe breeding not eased off I could have gone ahead in ignorance of the risks, and bred this high risk bitch, so to propagate the disease gene.
This is hardly a novel situation. Let me be clear. This note is not about me or my dog; it is about the whole breed situation. The central point is that the Breed Council health committee, supported by Council itself has a policy of NOT publishing information that could help everyone avoid JKD. How many other people, and dogs, must unknowingly be in this position? It is preposterous. I have been dismayed about this for a long time, but as it could have dragged me into the mess, I become totally disgusted. I find it quite criminal and have felt so strongly about the health committee avoiding basic action to limit propagation of the disease that I have written explaining the situation to the Kennel Club. What they can do, I don’t know, but I can say that I got a reply within the hour and am sure enquiries will be made. As it is I feel that my efforts and those of boxerjkd to help breeders avoid JKD are in effect just a waste of time. We have been handicapped by the health committee throughout, but the current withholding of pedigree information is far more serious. It should be up to breeders to decide what to do.
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FB 55

21/3/2017

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FB 55. We have a result for the prospective new ARVC test. It looks to be working. The new group of American dogs affected by ARVC all gave a positive response to the test as also did one British case that I was fortunate enough to find. More importantly for me personally was the uniformly negative response from the UK group deduced by pedigree to be free of the gene. So all in all we have a clear indication that the test serves to detect the disease. But the hope and expectation was that it would serve as a pre-clinical test. In other words would it pick up evidence of the disease before clinical signs appear and hopefully even before Holter can detect increased numbers of VPCs in runs etc to signify developing ARVC? I had included several dogs in the above study that could be deduced by pedigree to be at risk of having the gene. In other words, they had known transmitting dogs quite close up in their pedigrees and therefore might actually carry the gene although outwardly perfectly normal and free of the disease. What did they show? Amazingly, two of them gave what one might call ambiguous results. They showed positive, but only in a weak way. The simplest explanation is that we have the answer we really seek. The test is picking up normal dogs with hidden low expressing ARVC which is exactly what we hoped the test would do. It would look to be more sensitive than Holter.
It has to be proven that this is the correct interpretation but here I am on home territory as I know exactly what to do to establish the genetic facts. However, I don’t think I could convince owners and breeders to pay for more blood tests and no doubt also for Holter information. So looking forward, what can be done? And with ARVC all but extinct in the UK, what can UK breeders offer other than controls. 
I conclude that any further investigations really will have to be done in NA. But, even though the Canadian researchers seem to expect me to resolve the genetic issues, I am unhappy about intruding into other country’s affairs and it is quite probable that NA breeders would not want me interfering in their business either. Would they indeed help me by reporting cases and the breeding. Would owners of related dogs submit with them for analyses? And then there is still the funding issue.
So here we are. I believe we have an incredibly valuable test within reach, one that is probably more sensitive than Holter and almost as good as a gene test, but we need the critical supporting evidence to establish this, and it will need the cooperation of numbers of NA breeders who would be willing to submit their show dogs for study. Will any step forward to help the verification of the test? Let me know (bcattanach@steynmere.freeserve.co.uk). Pedigrees and full identification of dogs would be essential, but of course everything would be in the strictest confidence with no identities ever being disclosed. And then on top of this, there is the funding issue. Here we have a hold up, although funding is being applied for. Does anyone have any ideas? Otherwise we are pretty well stuck for the moment. So near and yet so far.
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Following FB 54

9/2/2017

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Following FB 54, I am happy to announce that despite a blip, the blood samples for the ARVC trial arrived safely and in apparently good shape in Toronto. The blip was missing a transport connection in Canada which delayed their arrival by a day. It is just as well we used a large box with 30 Kg of dry ice. Work starts on them almost immediately, and I’ll report the results if they arrive before I go on holiday next week. One trouble for me is that I don’t know what to expect; I don’t know whether the bio-marker marks the start of ARVC or only a secondary but early consequence of the disease. The test did not work perfectly in humans, but the dog disease and controls are much more clearly defined, so I have wild hopes for a 100% distinction between the two groups, although I am absolutely sure nobody else has such expectations. We’ll see.
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FB 54

6/2/2017

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FB 54. As I said in my last note, collecting blood samples for the ARVC trial has not been easy but, finally, samples from some 25 dogs were submitted to me for shipment to Canada. But what a palaver! This time the research group wanted me to take every possible precaution for safe transport. The list included creating a partial vacuum in every tube using a syringe and needle, sealing with parafilm and then wrapping each tube in its own plastic bag so that any leakages could be rescued. This morning with all finally achieved, the 60 plus tubes were loaded into a very large polystyrene traveling box filled with dry ice at -80 degrees centigrade and delivered to my old lab for collection by Fedex. What a relief to be rid of them, but now I wait in trepidation for the results. Will the test work and, more importantly for me, will my selection of dogs be correct? But I think this is the last time for me. I have had enough and it seems pretty clear that UK breeders have had enough too, as maybe also their vets. Regarding the latter, most have been very good and have collected the blood without charge. True, some have charged a standard surgery fee, but I have heard that one vet that wanted £100 for collecting from a single dog; and this exercise is for research, not for the owner. I was irate enough about this to write to the Chairman of the Veterinary Ethics committee. It is not right that owners have to pay to help research and, to be fair, neither is it right that vets should sacrifice time with their paying patients to facilitate this work. Something more formal needs to be organised. However, maybe on behalf of the various research groups involved I could thank all the breeders, owners and vets around the world who have done all that they can to help this and the other ARVC and JKD projects. Now let’s hope that the researchers can succeed in their quests for finding the Boxer ARVC and JKD genes and get this pre-clinical test for the ARVC successfully trialed.
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