Veterinary cancer care is one of the fastest growing areas of veterinary medicine in the UK. In a mirror of human medicine our patients are living longer and numerically we are seeing an ever increasing number of oncology cases.

Statistically of 10 year old dogs and 12 year old cats approximately 45% of individuals will have some form of neoplastic disease developing. This may not be clinically significant and it may only ever be known about at necropsy.

The treatment of cancer is very specialised and requires a different outlook and approach from virtually any other aspect of veterinary medicine. The principal aim of veterinary care of the cancer patient must be the quality of life for the patient and the veterinary oncologist must never lose site of this fact.
About The Cancer Treatment Unit
One of the features of these developments has been the creation of units in many countries which are dedicated to the treatment of cancer in pets.
The Cancer Treatment Unit is a small unit in Whitstable, Kent, England dedicated to the development of cancer care in the companion animal and is patient based. We are not primarily a research unit and do not forget that the patient comes first. The maintenance of a good quality of life for our patients is CTU prime aim.

The Cancer Treatment Unit(CTU) offer advisory services to veterinary surgeons throughout the world by preparing Case Assessment Reports. We provide direct referral services for the treatment of the cancer patient. In particular we are developing techniques of brachytherapy for the treatment of some forms of cancer in companion animals.


What is pet cancer?
In very general terms every kilogram of pet animal is composed of about 200,000,000,000 cells and it is more remarkable that normality prevails rather than abnormality. In healthy tissues the rate and frequency of cell division is carefully regulated both within each cell and by the interrelationship between cells. There are substantial safeguards built into the system to ensure that every cell division continues faultlessly. Only when these safeguards fail to work does a cancer start. The genetic material is held in the DNA structures of each cell.

The genes effectively produce a range of proteins into the cell which regulate how that cell works. There is a complicated system by which individual genes are turned on and off so that there is a regulation of the cell metabolism. This whole complicated system can be likened to a factory with each department producing, or not producing, components for the final product, for example, a car. When everything works properly the end product is perfect, if some of the departments produce too much or too little the car might have seven wheels and no seats or two boots but no engine! The safeguards built into cell function try to ensure that each product of the cell is in the correct proportion and that when the cell divides the two daughter cells are similarly perfect.
One of the most remarkable safeguards is an inbuilt system which is controlled by the genes in the cells which limits the number of times that a particular cell line can divide. When a cell divides the chromosomes which are made of the genetic material also divide and each time a small section at their ends fails to replicate. Therefore as the cell line continues to divide the chromosomes get shorter. The end parts of the chromosomes are called the telomeres and it is these which become progressively shorter each time the cell divides. After a predestined number of cell divisions the telomeres are shortened sufficiently to cause the cells to stop any further dividing. This is known as the cells becoming senescent. Cells in senescence will eventually die but a few of the millions of cells concerned will not be caught by this safeguard system and will continue further division. After a few more decisions the telomeres are even further shortened and there is a stop to the cycling of even the remaining cells. This second "last resort" stop is called crisis. Again the cells will stop dividing and will die out.

A few of these cells will even evade crisis and escape this second safety net. Such cells will continue to divide indefinitely and will thus become so-called immortal cells. In some cancer cells an enzyme is produced that rebuilds the telomeres of the chromosomes as they become shortened thus enabling the cells to evade these two safety nets and becoming immortal cells. The enzyme is produced by genes in the DNA of affected cancer cells. This is one mechanism whereby the genetic error in a cell can lead to cancer. In normally dividing cells the change to the cell division part of the life cycle as opposed to the resting phase is regulated by genes know as proto-oncogenes which stimulate cell division and tumour suppressor genes which inhibit cell division. The balance between these two types of genes leads to an orderly regulation of cell division.

During cell division there will be a small percentage of cases where the division is faulty and the genetic material (genes) become damaged. If this occurs to proto-oncogenes they can be transformed into oncogenes which become increasingly overactive and thus there is an unregulated increase in cell division, and these cells will all contain the genetic error. There are some special genes in each cell of which the gene P53 is probably the best known, that trigger self destruction of the cell if the DNA becomes damaged. This self destruction is known as apoptosis. This mechanism is extremely important to the clinician since both radiotherapy and some chemotherapeutic drugs work by damaging the DNA structure and relying upon apoptosis to complete the destruction of the cancer cells. Another error can occur when there is a faulty division which can stop the tumour suppressor genes working. This again results in an uncontrolled division of cells with damaged DNA.

It seems likely that although a cancer can actually start in a single cell, there must be multiple faults in the DNA cell if it is not to be caught by one of the safety mechanisms. A cell that has become cancerous enters a phase of rapid, uncontrolled reproduction which is essentially caused by the genes within that cell producing an imbalance in the proteins needed to regulate the cell life cycle. There is the internal cell production of stimulatory proteins. Some of these can leave such a damaged cell and can affect receptor sites on adjacent cells. Once this happens there is a pathway for the genetic error to be passed from one cell to another.

:How does cancer spread???

Sevice for pet

The Cancer Treatment Unit for companion animals ( CTU) was opened by the Lord Mayor of Canterbury in August 1992 as a small unit attached to a primary care veterinary practice. The aim of the CTU is stated as being that of "relieving suffering and improving care for the cancer patient."

1. Case Assessment Reports
The compilation of Case Assessment reports for primary care practices. Essentially veterinary practices send the CTU the case notes on a particular patient together with laboratory reports and we assemble a report - usually within 48 hours - giving a description of the work completed, a summary of how we see the disease process and where appropriate treatment options and if possible some idea of the prognosis. These reports are designed to be read by the client and the presenting veterinary surgeon and are aimed at being a discussion document for the management of the case. In the first 9 years we have completed nearly 1500 case assessment reports for veterinary practices. Each report is looked at individually and usually takes between 1 and 2 hours to assemble. Clearly much of the information is retrieved from data bases but each is tailored for the particular patient in question.

2. Referral Consultations
We are frequently asked by primary care practices once we have completed a Case Assessment Report, to see the patient and to discuss the case with the client. There are often questions that clients want to ask and the experience that we have in dealing with the cancer patient is helpful. We always work with the presenting veterinary practice and try to involve the client and the presenting veterinary surgeon in the management of the case by keeping both informed at all times. Clients frequently find it easier talking to a veterinary oncologist rather than their own primary care veterinary surgeon and there are times when the presenting veterinary surgeon finds the involvement of a colleague can take some of the pressure off a particular case. He/she can be confident of the support that we always give to the presenting veterinary surgeon as well as the client.

3. Referral surgery, cryosurgery and chemotherapy
Many patients are sent to us for surgery, cryosurgery or chemotherapy. We are very careful to maintain our aims of putting the life quality as our main objective for the patient. There are times when this is in conflict with advancing veterinary techniques but our priority is the patients' welfare. Where we feel there is a conflict we leave others to push forward the frontiers whilst we attend to the patients of today. Most veterinary practices are proficient in handling some of the cytotoxic drugs used routinely in veterinary medicine but there are some drugs that are probably best administered by those with experience in the field. Therefore we routinely see patients for the administration of chemotherapy. This is usually done on an out-patient basis with the patient being referred back to the presenting veterinary surgeon for the rest of the treatment.

4. Brachytherapy
The CTU has been at the forefront of developing brachytherapy for use in veterinary oncology. Brachytherapy is the use of radioactive sources such as Iridium-192 for the local treatment of neoplastic disease. We recognise that we are years (and millions of pounds!) behind the treatment of humans with comparable conditions and we are pleased to see that in some other countries forms of brachytherapy akin to human treatment is becoming available. However we are developing the use of thermolabile moulds and intracavity devices for the treatment of many types of tumour. We have developed a technique for delivering a calculated dose of radiation to intranasal tumours. The great benefit of brachytherapy in these cases is that we are treating from the inside out rather than vice versa. We would now argue that for intranasal tumours which have not traversed the medial nasal septum and which are rostrally located, brachytherapy following a unilateral rhinotomy is the treatment of choice. This is also the case for a number of skin and superficial tumours where brachytherapy is the pre-operative or post-operative treatment of choice for destroying the locally invading cancer cells. Often brachytherapy is part of a combination of treatments involving surgery, radiotherapy and sometimes chemotherapy as well. The great advantage of brachytherapy over external beam radiotherapy is that the delivery system give the potential of delivering a higher dose to a very specifically localised area. This makes the technique most suitable for those tumours which have a high invasive but low metastatic potential and which are located in the skin. There are other tumours which are much more suitably treated with external beam radiotherapy and the two systems are seldom in conflict for treatment of choice as they both have individual merits for differing situations.

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