Surgery may be difficult due to the location of these tumors. Surgery alone often leads to recurrence. Chemotherapy is very effective for TVTs. The prognosis for complete remission with chemotherapy is excellent. The most common chemotherapy agents used are vincristine, vinblastine, and doxorubicin. Radiotherapy may be required if chemotherapy does not work.

In 2010, EBC-46, a drug which cures facial tumours in dogs, cats, and horses, was proposd as a cure for DFTD.

Vaccination with irradiated cancer cells has not proven successful.

A primary research report in 2011 has suggested that picking a genetically diverse breeding stock, defined by the genome sequence, may help with for conservation efforts.

As of 2011, there was ongoing support for a research team of David Phalen and colleagues to investigate chemotherapeutic agents against DFTD.

In 2013, a study using mice as a model for Tasmanian devils suggested that a DFTD vaccine or treatment could be beneficial. In 2015, a study which mixed dead DFTD cells with an inflammatory substance stimulated an immune response in five out of six devils injected with the mixture, engendering for a vaccine against DFTD. Field testing of the potential vaccine is being undertaken as a collaborative project between the Menzies Institute for Medical Research and the Save the Tasmanian Devil Program under the Wild Devil Recovery program, and aims to test the immunisation protocol as a tool in ensuring the devil's long term survival in the wild.

In March 2017, scientists at the University of Tasmania presented an apparent first report of having successfully treated Tasmanian devils suffering from the disease, by injecting live cancer cells into the infected devils to stimulate their immune system to recognise the disease and fight it off.

Canine transmissible venereal tumors (CTVTs), also called transmissible venereal tumors (TVTs), canine transmissible venereal sarcoma (CTVS), sticker tumors and infectious sarcoma is a histiocytic tumor of the external genitalia of the dog and other canines, and is transmitted from animal to animal during mating. It is one of only three known transmissible cancers in mammals; other are devil facial tumor disease, a cancer which occurs in Tasmanian devils, and contagious reticulum cell sarcoma of the Syrian hamster.

The tumor cells are themselves the infectious agents, and the tumors that form are not genetically related to the host dog. Although the genome of a CTVT is derived from a canid (probably a dog, wolf or coyote), it is now essentially living as a unicellular, asexually reproducing (but sexually transmitted) pathogen. Sequence analysis of the genome suggests it diverged from canids over 6,000 years ago; possibly much earlier. The most recent estimates of its time of origin place date it to about 11,000 years ago. However, the most recent common ancestor of "extant" tumors is more recent: it probably originated 200 to 2,500 years ago.

Canine TVTs were initially described by Russian veterinarian M.A. Novinsky (1841–1914) in 1876, when he demonstrated that the tumor could be transplanted from one dog to another by infecting them with tumor cells.

A transmissible cancer is a cancer cell or cluster of cancer cells that can be transferred between individuals without the involvement of an infectious agent, such as an oncovirus. Transmission of cancer between humans is rare.

Contagious cancers occur in dogs, Tasmanian devils, Syrian hamsters, and some marine bivalves including soft-shell clams. These cancers have a relatively stable genome as they are transmitted.

In humans, a significant fraction of Kaposi's sarcoma occurring after transplantation may be due to tumorous outgrowth of donor cells. Although Kaposi's sarcoma is caused by a virus (Kaposi's sarcoma-associated herpesvirus), in these cases, it appears likely that transmission of virus-infected tumor cells—rather than the free virus—caused tumors in the transplant recipients.

Some studies have shown that thyroglobulin (Tg) testing combined with neck ultrasound is more productive in finding disease recurrence than full- or whole-body scans (WBS) using radioactive iodine. However, current protocol (in the USA) suggests a small number of clean annual WBS are required before relying on Tg testing plus neck ultrasound. When needed, whole body scans consist of withdrawal from thyroxine medication and/or injection of recombinant human Thyroid stimulating hormone (TSH). In both cases, a low iodine diet regimen must also be followed to optimize the takeup of the radioactive iodine dose. Low dose radioiodine of a few millicuries is administered. Full body nuclear medicine scan follows using a gamma camera. Scan doses of radioactive iodine may be I or I.

Recombinant human TSH, commercial name Thyrogen, is produced in cell culture from genetically engineered hamster cells.

Animals that have undergone population bottlenecks may be at greater risks of contracting transmissible cancers. Because of their transmission, it was initially thought that these diseases were caused by the transfer of oncoviruses, in the manner of cervical cancer caused by HPV.

- Canine transmissible venereal tumor (CTVT) is sexually transmitted cancer in dogs. It was experimentally transplanted between dogs in 1876 by M. A. Novinsky (1841–1914). A single malignant clone of CTVT cells has colonized dogs worldwide, representing the oldest known malignant cell line in continuous propagation.

- Contagious reticulum cell sarcoma of the Syrian hamster can be transmitted from one Syrian hamster to another by means of the bite of the mosquito "Aedes aegypti".

- Devil facial tumour disease (DFTD) is a transmissible parasitic cancer in the Tasmanian devil.

- Soft-shell clams, "Mya arenaria", have been found to be vulnerable to a transmissible neoplasm of the hemolymphatic system — effectively, leukemia.

- Horizontally transmitted cancers have also been discovered in three other species of marine bivalves: bay mussels ("Mytilus trossulus"), common cockles ("Cerastoderma edule") and golden carpet shell clams ("Polititapes aureus"). The golden carpet shell clam cancer was found to have been transmitted from another species, the pullet carpet shell ("Venerupis corrugata").

Antineoplastic resistance, synonymous with chemotherapy resistance, is the ability of cancer cells to survive and grow despite different anti-cancer therapies, i.e. their multiple drug resistance. There are two general causes of antineoplastic therapy failure:

Inherent resistance, such as genetic characteristics, giving cancer cells their resistance from the beginning, which is rooted in the concept of cancer cell heterogeneity and acquired resistance after drug exposure.

Recovery is most likely if it is spotted within the first 24–48 hours, and you should seek veterinary advice—a vet may choose to give the animal drugs.

The sick animal should be kept in a cage by itself so that others do not catch the disease—wet tail can be very contagious so sanitize all objects the animal has come in contact with (wheel, food dish, huts, etc.).

If the animal doesn't want to eat, then dry, unflavored oats can be hand fed, which can also help with the diarrhea. The animal should only be fed dry foods, any foods with a high water content should be avoided.

If the animal has an unclean or matted rear-end, this should not be remedied using a bath in water—instead a q-tip (cotton bud) or cotton ball can be used to very gently clean the animal's rear end to avoid discomfort or rashes.

If the animal is not drinking, hydration can be aided by scruffing (i.e. very gently holding the rodent by the extra skin on the back of the neck) the animal so that they open their mouth; then in small, short intervals, water can be provided with a 1 ml syringe. It is very important that this is done slowly, to avoid getting water down the animal's wind pipe. Unflavored pedialyte can be purchased from a grocery store and can be very helpful with wet tail. If feeding is also an issue, a suggested aide is to feed extremely small amounts of no garlic, no onion, no added sugar mashed baby food, and administered using the same scruffing method, and again at a very slow pace.

DFTD tumours are "large, solid, soft tissue masses usually with flattened, centrally ulcerated, and surfaces", which are "typically multicentric, appearing first in the oral, face, or neck regions", and are " to nodular aggregates of round to spindle-shaped cells, often within a pseudocapsule and divided into lobules by delicate fibrous septae". The disease is described as being aggressive, locally. Tumours can cover the eyes.

As Iain O'Neill notes, it also presents a "high rate of regional lymph node involvement and systemic metastasis"; of the avenues by which the cancer can spread systemically, metastasis to the lungs, spleen, and heart are observed, as is secondary "intracranial involvement". O'Neill also notes that "organ involvement and superimposed infection may... contribute to mortality." Moreover, growth of large tumours impedes feeding, and starvation is another cause of death in affected devils.

Follicular thyroid cancer or follicular thyroid carcinoma accounts for 15% of thyroid cancer and occurs more commonly in women over 50 years of age. Thyroglobulin (Tg) can be used as a tumor marker for well-differentiated follicular thyroid cancer. Follicular cells are the thyroid cells responsible for the production and secretion of thyroid hormones.

Antineoplastic resistance, often used interchangeably with chemotherapy resistance, is the multiple drug resistance of neoplastic (cancerous) cells, or the ability of cancer cells to survive and grow despite anti-cancer therapies.

There are two general causes of antineoplastic therapy failure: Inherent genetic characteristics, giving cancer cells their resistance, which is rooted in the concept of cancer cell heterogeneity and acquired resistance after drug exposure. Altered membrane transport, enhanced DNA repair, apoptotic pathway defects, alteration of target molecules, protein and pathway mechanisms, such as enzymatic deactivation.

Since cancer is a genetic disease, two genomic events underlie acquired drug resistance: Genome alterations (e.g. gene amplification and deletion) and epigenetic modifications.

Cancer cells are constantly using a variety of tools, involving genes, proteins and altered pathways, to ensure their survival against antineoplastic drugs.

While there is no cure for haemophilia, treatment improves outcomes.

Desmopressin (DDAVP) may be used in those with mild haemophilia A. Tranexamic acid or epsilon aminocaproic acid may be given along with clotting factors to prevent breakdown of clots.

Pain medicines, steroids, and physical therapy may be used to reduce pain and swelling in an affected joint.

Treatment is symptomatic and supportive. Children with hydrocephalus often need a ventriculoperitoneal shunt. Nucleoside analog ribavirin is used in some cases due to the inhibitory effect the agent has "in vitro" on arenaviruses. However, there is not sufficient evidence for efficacy in humans to support routine use. The only survivor of a transplant-associated LCMV infection was treated with ribavirin and simultaneous tapering of the immunosuppressive medications. Early and intravenous ribavirin treatment is required for maximal efficacy, and it can produce considerable side effects. Ribavirin has not been evaluated yet in controlled clinical trials.

Use of ribavirin during pregnancy is generally not recommended, as some studies indicate the possibility of teratogenic effects. If aseptic meningitis, encephalitis, or meningoencephalitis develops in consequence to LCMV, hospitalization and supportive treatment may be required. In some circumstances, anti-inflammatory drugs may also be considered. In general, mortality is less than one percent.

Treatment is directed towards (1) correcting hypotension, hypovolemia, electrolyte imbalances, and metabolic acidosis; (2) improving vascular integrity, and (3) providing an immediate source of glucocorticoids. Rapid correction of hypovolemia is the first priority.

Most patients show dramatic improvement within 24 to 48 hours of appropriate fluid and glucocorticoid therapy. Over the ensuing 2 to 4 days, a gradual transition from IV fluids to oral water and food is undertaken, and maintenance mineralocorticoid and glucocorticoid therapy is initiated. Failure to make this transition smoothly should raise suspicion of insufficient glucocorticoid supplementation, concurrent endocrinopathy (e.g. hypothyroidism), or cocurrent illness (especially renal damage).

Aggressiveness of therapy depends on the clinical status of the patient and the nature of the insufficiency (glucocorticoid, mineralocorticoid, or both). Many dogs and cats with primary adrenal insufficiency are presented in Addisonian crisis and require immediate, aggressive therapy. In contrast, secondary insufficiency often has a chronic course.

Hypoadrenocorticism is treated with fludrocortisone (trade name Florinef) or a monthly injection of Percorten-V (desoxycorticosterone pivalate, DOCP) and prednisolone or Zycortal. Routine blood work is necessary in the initial stages until a maintenance dose is established. Most of the medications used in the therapy of hypoadrenocorticism cause excessive thirst and urination. It is absolutely vital to provide fresh drinking water for a canine suffering from this disorder.

If the owner knows about an upcoming stressful situation (shows, traveling etc.), the animals generally need an increased dose of prednisone to help deal with the added stress. Avoidance of stress is important for dogs with hypoadrenocorticism. Physical illness also stresses the body and may mean that the medication(s) need to be adjusted during this time. Most dogs with hypoadrenocorticism have an excellent prognosis after proper stabilization and treatment.

Lymphoma/lymphosarcoma is the most common malignancy in ferrets. Ferret lymphosarcoma occurs in two forms -- "juvenile lymphosarcoma", a fast-growing type that affects ferrets younger than two years, and "adult lymphosarcoma", a slower-growing form that affects ferrets four to seven years old.

In juvenile ferret lymphosarcoma, large, immature lymphocytes (lymphoblasts) rapidly invade the thymus or the organs of the abdominal cavity, particularly the liver and spleen. In adult ferret lymphosarcoma, the lymph nodes in the limbs and abdominal cavity become swollen early on due to invasion by small, mature lymphocytes. Invasion of organs, such as the liver, kidney, lungs, and spleen, occurs later on, and the disease may be far advanced before symptoms are noticeable.

As in humans, ferret lymphosarcoma can be treated surgically, with radiation therapy, chemotherapy or a combination thereof. The long-term prognosis is rarely bright, however, and this treatment is intended to improve quality of life with the disease.

Cardiac and respiratory complications are treated symptomatically. Physical and occupational therapy may be beneficial for some patients. Alterations in diet may provide temporary improvement but will not alter the course of the disease. Genetic counseling can provide families with information regarding risk in future pregnancies.

On April 28, 2006 the US Food and Drug Administration approved a Biologic License Application (BLA) for Myozyme (alglucosidase alfa, rhGAA), the first treatment for patients with Pompe disease, developed by a team of Duke University researchers. This was based on enzyme replacement therapy using biologically active recombinant human alglucosidase alfa produced in Chinese Hamster Ovary cells. Myozyme falls under the FDA Orphan Drug designation and was approved under a priority review.

The FDA has approved Myozyme for administration by intravenous infusion of the solution. The safety and efficacy of Myozyme were assessed in two separate clinical trials in 39 infantile-onset patients with Pompe disease ranging in age from 1 month to 3.5 years at the time of the first infusion. Myozyme treatment clearly prolongs ventilator-free survival and overall survival. Early diagnosis and early treatment leads to much better outcomes. The treatment is not without side effects which include fever, flushing, skin rash, increased heart rate and even shock; these conditions, however, are usually manageable.

Myozyme costs an average of US$300,000 a year and must be taken for the patients' entire life, so some American insurers have refused to pay for it. On August 14, 2006, Health Canada approved Myozyme for the treatment of Pompe disease. On June 14, 2007 the Canadian Common Drug Review issued their recommendations regarding public funding for Myozyme therapy. Their recommendation was to provide funding to treat a very small subset of Pompe patients (Infants less one year of age with cardiomyopathy). Genzyme received broad approval in the European Union. On May 26, 2010 FDA approved Lumizyme, a similar version of Myozyme, for the treament of late-onset Pompe disease.

A new treatment option for this disease is called Lumizyme. Lumizyme and Myozyme have the same generic ingredient (Alglucosidase Alfa) and manufacturer (Genzyme Corporation). The difference between these two products is in the manufacturing process. Today, the Myozyme is made using a 160-L bioreactor, while the Lumizyme uses a 4000-L bioreactor. Because of the difference in the manufacturing process, the FDA claims that the two products are biologically different. Moreover, Lumizyme is FDA approved as replacement therapy for late-onset (noninfantile) Pompe disease without evidence of cardiac hypertrophy in patients 8 years and older. Myozyme is FDA approved for replacement therapy for infantile-onset Pompe disease.

Recent studies on chaperone molecules to be used with myozyme are starting to show promising results on animal models.

Immunosuppressive therapy has been effective in halting the disease for laboratory animals.

The coronavirus which causes ECE has a counterpart strain that has more systemic effects with a higher mortality rate. This systemic syndrome has been compared to Feline infectious peritonitis in cats.

Initial therapy:

- hydration, increasing salt intake, and forced diuresis.

- hydration is needed because many patients are dehydrated due to vomiting or kidney defects in concentrating urine.

- increased salt intake also can increase body fluid volume as well as increasing urine sodium excretion, which further increases urinary potassium excretion.

- after rehydration, a loop diuretic such as furosemide can be given to permit continued large volume intravenous salt and water replacement while minimizing the risk of blood volume overload and pulmonary oedema. In addition, loop diuretics tend to depress calcium reabsorption by the kidney thereby helping to lower blood calcium levels

- can usually decrease serum calcium by 1–3 mg/dL within 24 hours

- caution must be taken to prevent potassium or magnesium depletion

The goal of therapy is to treat the hypercalcaemia first and subsequently effort is directed to treat the underlying cause.

Drug therapy can slow down progression and in some cases even improve the heart condition. Standard therapy may include salt restriction, ACE inhibitors, diuretics, and beta blockers. Anticoagulants may also be used for antithrombotic therapy. There is some evidence for the benefits of coenzyme Q10 in treating heart failure.

As for other flavivirus infections, no cure is known for yellow fever. Hospitalization is advisable and intensive care may be necessary because of rapid deterioration in some cases. Different methods for acute treatment of the disease have been shown not to be very successful; passive immunisation after emergence of symptoms is probably without effect. Ribavirin and other antiviral drugs, as well as treatment with interferons, do not have a positive effect in patients.

A symptomatic treatment includes rehydration and pain relief with drugs such as paracetamol (acetaminophen in the United States). Acetylsalicylic acid (aspirin) should not be given because of its anticoagulant effect, which can be devastating in the case of internal bleeding that can occur with yellow fever.

Artificial pacemakers may be used in patients with intraventricular conduction delay, and implantable cardioverter-defibrillators in those at risk of arrhythmia. These forms of treatment have been shown to prevent sudden cardiac death, improve symptoms, and reduce hospitalization in patients with systolic heart failure.