My husband and I just subscribed last evening but have been visiting your website to learn about possible causes, medications, and effects that have been referenced in regards to our 10-year old Sheltie spayed female. In July 2000, she suddenly was stricken by something that caused her to have facial spasms, frequent shudders and weakness in her hind quarters where she fell to the floor on her side, straight down on all 4s or just her hind quarters. At first, the episodes came every 30 minutes and lasted very briefly but continued day and night and she paced for 24-hours. Then, they progress to every 15 seconds. Her only rest lasted no more than 90 minutes.
She's been to Auburn University Veterinary School where her neurologist took an MRI, CSF, CBC and tests for infectious diseases to find the root cause. All results came back normal. She was placed on phenobarbital, prednisone, doxycycline, trimethoprim-sulfa, sucralfate for seizure control (she had one full seizure the morning of her MRI), possible Rocky Mt. Spotted Fever and inflammation of her brain. She completed the doxycycline and trimethoprim but remained on phenobarbital (30 mg twice daily), prednisone (10 mg twice daily for 8 days then down to 10 mg once daily for 1 week then down to 10 mg once every other day), 1 g sucralfate 3 times daily. The neurologist offered 2 possible causes: distemper or stroke. Stroke was the less likely possibility since the onset of her problems progressively worsened over 2 weeks from mid-July to late-July. She's been current on all her innoculations since she was born in 1990 and only once missed her distemper vaccination in 1995. But we understand that batches of vaccines can sometimes be contaminated or be ineffective.
Although she wasn't her usual perky self, she was better without the spasms and shudders. She slept briefly in 2-3 hour stretches at night. Two weeks later, when she went in for her phenobarbital levels check, they were
minimally within range. Then, she started to lose her toenails, her toe pads had open sores, a tiny spot appeared on each of her eyes (corneal), she became slightly anemic and her tongue turned black for a day and again for 5 days. Her prednisone was at 10 mg every other day, so she was adjusted back to 10 mg once daily. Her regular vet suggested changing her from phenobarbital to KBr, which I was glad to do with its fewer side-effects. I covered her feet with socks to prevent her chewing them, gave her baby aspirin for her tongue and started her on KBr for the next 5 weeks (where we are today).
Then we tried to reduce her prednisone again on September 09, 2000 to 10 mg once every other day. She became too weak to stand for more than 2 minutes. She was like this for 5 days and her gums became very pale. Of
course, she was too weak to do anything but sleep...ironically, her first time for a full night's sleep. Since she was due for her KBr levels measurements in a few days, anyway, I called her regular vet to have her blood tests done and for her to be seen for the latest problems. Her KBr levels were barely within range and she was very anemic with an enlarged abdomen. An abdominal ultrasound was done showing an enlarged liver and spleen. The liver situation from her phenobarbital. The spleen was more of a concern (her 1997 radiographs indicated an enlarged spleen then). She also had a urinary tract infection with traces of blood in her urine. She was given epogen injection for her anemia and amoxi 250 mg for her infection. Her regular vet recommended we return to Auburn.
This week our dog was admitted back to Auburn where she remains. She's being examined and watched by Internal Medicine. Tests of her blood showed low counts of mature white blood cells and low count of red blood cells. There's a proliferation of immature white blood cells. She was running a fever, too. Her liver, spleen and bone marrow were aspirated. She underwent another ultrasound on her abdomen. Her spleen was free of tumors
although there are nodules. Her lungs looked clear. Her heart sounds fine. The aspirations of her liver and bone marrow showed presence of the immature white blood cells. The bone marrow showed too many of them that crowded out mature white and red blood cells. Her spleen aspiration looked fine. She was given a growth factor for her bone marrow and her red blood cell count very minimally increased. The internal medicine doctor believes she has acute leukemia. The only other possibility would be a viral attack on her bone marrow. He's taking a biopsy of her liver today to confirm the presence of immature white blood cells.
Our dog's case is puzzling Auburn. The neurology, oncology, pathology and internal medicine departments are all involved in her case this week. She's receiving growth factor daily, now, to boost her mature white blood cells. Her red blood cells remains low at 20%, but the internal medicine doctor hopes that will improve as the mature white blood cells start to increase and she's able to fight off infections on her own. Along with her prednisone (5 mg twice daily), phenobarbital, KBr, sucralfate, and amoxicycline, she's getting another antibiotic and growth factor.
Lupus has been ruled out. I've asked for a babesiosis test to be done and test results won't return from Louisiana University until next week about the same time pathology results on her liver biopsy will return.
It seems that leukemia is rare in dogs. We find no mention of it on your website. A couple of other veterinary websites we've visited discuss leukemia. However, since your explanations are more in plain English, could you explain the condition to us, please? We know that there are 2 types: acute and chronic. Chronic has better prognosis due to its slower onset and progression. Could there be any relationship between her early neurological symptoms and to her present anemic symptoms?
N. & S.
Answer: N & S -
I think that leukemias are pretty uncommon and that it is probably also likely that they do not get diagnosed as often as they occur, since the clinical signs associated with leukemias can be very variable and are easy to confuse with other disorders.
There are several kinds of white blood cells that make up the immune system. The most common one is the neutrophil, followed by lymphocytes, eosinophils, monocytes, basophils and some variants of these cells. Each of these is produced by a group of precursor cells in the bone marrow that are referred to as stem cells. The stem cells differentiate and produce the different types of white blood cells but they arise from the same basic cell line, so there are often mixed types of leukemias.
Leukemia is the presence of cancer cells in the bone marrow itself. This is different from lymphoma, the other common white blood cell cancer, because lymphoma arises from tissues outside the bone marrow, such as lymph nodes or the spleen. There are two forms of leukemia, acute and chronic. The acute form usually has poorly differentiated stem cells, produces anemia, drops in white blood cell count and a lot of secondary problems associated with anemia and a severely deficient immune system. When bone marrow is examined, acute leukemia usually causes the bone marrow to have a large number of cancer cells, making up at least 30% of the bone marrow cells. The chronic form of leukemia is different in that it is usually possible to identify the type of cell that is proliferating, such as granulocytic (neutrophil) leukemia, lymphobastic leukemia, eosinophilic leukemia or lymphoid leukemia. White blood cell counts are usually elevated and sometimes are extraordinarily high, such as 100,000 to 300,000 wbcs/ul. Clinical signs tend to be non-specific for this disorder, too but enlarged lymph nodes and spleen, weakness, lethargy, lameness, fevers, increased drinking and urinating, bleeding disorders, liver enlargement and pale gums have been reported to occur.
The prognoses for acute lymphoblastic leukemia and for acute nonlymphoid leukemia are both very grave, with most affected pets living only a short time after it is possible to make a diagnosis of these conditions, even with treatment. There is no consistently successful treatment plan that I know of but l-asparaginase (Elspar Rx) was supposed to be helpful in some cases. This medication is not currently available, as far as I know, though.
Chronic lymphocytic leukemia and chronic nonlymphoid leukemias have a better prognosis, although there isn't sure treatment for them, either. Some dogs are reported to live for months, to years, with these conditions. I think that the majority of patients probably do well for the shorter time period, though.
It is good that your sheltie is at one of the veterinary schools because there are resources there for confirming the diagnosis and for obtaining the most current therapeutic information.
I do not know how frequently neurologic signs, such as seizures, are associated with leukemias, but it they are listed as one possible symptom in Ettinger and Feldman's "Textbook of Veterinary Internal Medicine". At the present time, I do not think that initiating factors for leukemia have been identified in dogs, so there may easily be a link between the neurologic symptoms and the leukemia, if it is present, but it would be hard to be sure.
I wish that I could help with this situation but you are doing the right things and have the help of people far more expert than I am in this kind of care.
Mike Richards, DVM
Last edited 03/21/02
Original Doc: Leukemia In Dogs.doc
Hospital Prevalence Of Cancer In The Scottish Terrier
Environmental Epidemiology Branch
National Cancer institute, Bethesda, Maryland
Source: Scottish Terrier Club of America Handbook, 1986. Pages158-167.
Canis familiaris, the domestic dog, is thought to be the oldest of domesticated animal species (1). Skeletal remains have been found in association with humans dating back 12,000 years (2). Through selective breeding, man over the centuries altered the basic dog into individual types that better served his purpose. In doing this, numerous different breeds were created, each possessing a different spectrum of specific traits (e.g., shape, size, coat color, temperament, intelligence). Some breeds also developed susceptibilities for specific congenital or developmental defects and/or for neoplasia (an excessive uncontrolled new growth of cells).
If no inherent predisposition existed, one would expect only a small fraction of any breed's population to be born with or develop an anatomical abnormality or neoplasia. If such occurred, the event would be considered to be one of random chance, excluding outside influences. Numerous veterinary studies have, however, reported specific problems in certain dog breeds that were diagnosed more often than could be expected by random chance. This is true for the Scottish terrier.
The data which the subsequent information is based came from the Veterinary Medical Data Program (VMDP). For many years (1964-1977) the National Cancer Institute (NCI) sponsored the VMDP - a data collection registry composed of computerized abstracts of medical records representing each hospital visit for any reason to a participating veterinary university teaching facility in the United States and Canada. Today the program continues under the auspices of the Association of VMDP Par-ticipants, Inc., and encompasses 18 universities (3). This is the largest repository of available veterinary clinical data in the world.
Over two million hospital episodes about dogs have been reported, spanning an average of 11.7 clinic years of data per university (as of July 1983). Approximately 11,000 hospital visits were about Scotties; these represent the medical history of 3,480 uniquely identifiable patients.
It should be remembered that veterinary universities see referral patients, often for a developmental defect or neoplasm. Although no evidence has been presented showing that one breed is more likely to be referred for specialty care than another, one must be cautious with this possible uncontrollable bias when analyzing and interpreting retrospective studies of hospital data. The hazards from this are greatest when the study population comes from one treatment facility (4).
METHODS AND RESULTS
The first general analysis of neoplasia data from the VMDP, based on data provided by 12 university facilities, was published in 1971 (5). It reported that the Scottie had a 2 fold excess compared to all dogs combined for the diagnosis of any neoplasm (P < 0.001) and a 2.2 fold excess (P < 0.00 1) for malignant neoplasms. While these risk values were not the highest calculated (Boxers showed twice the risk of Scotties), they were substantial.
From the current VMDP data on file at NCI (1964-1983), 486 Scotties (14% of the total population seen) were identified with one or more microscopically confirmed neoplasms (Table 1). Seventy percent were reported as malignant, with about 26 percent of these involving the hematopoietic (blood-cell forming) and lymphatic systems.
The scope of cancer diagnosed in the Scottie is presented in Table 2. From it, we note the most frequent cancer was lymphosarcoma, followed by bladder and other transitional cell carcinomas of the lower urinary tract (renal pelvis, ureter, and urethra), and malignant melanoma. The prevalence rate of cancer cases by age and sex is presented in Figure 1. Males show a higher rate than females at each age interval from 2 to 3 years of age through 14 years of age, which most likely can be attributed to the excess risk for lymphosarcoma in males.
To access the independent effect of sex and better appreciate the number of Scotties with these cancers versus cancers expected in any purebred dog, further analysis using the relative risk (RR) methodology (6) was applied to the eight most frequently occurring malignancies. Relative risk is the ratio of the rate of disease among a test group (e.g., Scotties) to that rate in the comparison group (e.g., all purebred dogs combined). If the rate of cancer X in the Scottie was 34 cases per 3,400 patient years (hospital population denominator based on counting each patient once for each year it is brought to the treatment facility for any reason) and the overall rate in purebred dogs was 257 cases per 386,000 patient years, Scotties would have a relative risk of 15 (.01/.000666) for cancer X or, said another way, they had 15 times as much cancer X as purebred dogs in general.
Sex risk values are presented in Table 3. In each of these analyses males were used as the standard comparison group (RR= 1), and each computation was adjusted for variations in age. Females were at significant excess risk only for bladder and other lower urinary tract cancer. Females were significantly spared from lymphosarcoma and malignant melanoma, or, said another way, males had the significant percentage of these diseases.
Table 4 shows that six of eight malignancies tested were diagnosed more frequently in the Scottie than expected, with a high degree of statistical confidence. Two in particular, carcinomas of the bladder and lower urinary tract and gastric carcinoma, were quite high. Another was malignant melanoma. The inevitable question is why?
The epidemiologic features for canine tumors at many organ sites show marked similarity to those in humans, including risk by age and sex (7). Much of cancer seen in man is attributed to exposures to environmental carcinogenic factors (e.g., solar radiation, X-radiation, radioactive elements, inorganic substances, chemicals), and presumably this would hold true also for the dog. This certainly applies to bladder carcinogens; the dog was the first laboratory model in which the same urothelial response to urine-borne carcinogens as seen in man was demonstrated (8).
Tobacco usage and occupational chemical exposures are known risk factors for human bladder cancer (9). There is strong evidence that sufficient levels of some of these occupational chemical carcinogens have escaped into the general environment to place nearby inhabitants at increased risk (10). Following this lead, an investigation of VMDP dogs in geographical areas with greater industrial activity showed an increased diagnostic frequency of bladder cancer compared with other cancers. This association with industrial activity was also seen in rates for bladder cancer in both men and women living in the same geographical areas as the VMDP dogs (11). Thus, it is suggested that the pet dog is a sentinel model for this type of environmentally related cancer.
That the Scottie has the highest risk for bladder cancer of any purebred dog (12) may indicate that they are especially sensitive to environmental bladder carcinogens. Female Scotties have twice as much bladder cancer as do males (P<0.02), a situation that exists in other dogs (12). This phenomenon is thought to be related to the greater frequency of micturition of male dogs because of "scent marking" their territory. Thus, the bladder epithelium of male dogs has less time exposure to urine-borne carcinogens than that of female dogs (12).
Gastric carcinoma in man is quite common, although it is declining in incidence in the United States. This cancer shows marked geographic variations by country; occurs more often in blacks than in whites and in men than in women; presents in familial aggregations; and is linked to diet, tobacco usage, and possibly carcinogenic chemicals in air pollution (13). It is rare in the dog, but it appears to be increasingly diagnosed and has emerged as a problem in the Scottie. Canine gastric carcinoma presents a similar histologic pattern to that seen in man (14). There is no detectable sex risk known at this time in dogs. Too few cases are available to assess whether geographic variations exist. One might assume diet is a likely factor in the canine disease, but this is speculation. Obviously, further research is necessary to determine why this canine cancer occurs, which would lead to a better understanding of the Scottie's problem.
Both the incidence and mortality in man from malignant melanoma have been rising rapidly in all countries in which the disease has been studied. The prognosis is improving, probably largely because people are seeking treatment at an earlier stage of their disease, but the increase in disease is resulting in higher mortality (15). Ultraviolet radiation is decidedly an etiologic factor. Black-skinned people rarely have melanomas, whereas they are common in red-haired and blond people. Familial aggregations account for about 6% of the human cases. Familial precursor lesions have been identified with distinct clinical and histological features (16).
Malignant melanoma has been recognized for decades as a problem in the dog, and Scotties have long been known as a breed bearing a familial risk (17). Many of these lesions originate in the mouth (half in the VMDP series) and on the digits, as they do in other dogs.
Many aspects of this disease are similar in dog and man. In both, the cancer typically develops in midlife and older, similar histologic lesions are seen, and metastatic disease occurs via blood and lymph channels. There are also differences, and many questions still are unanswered (18). Why are oral malignant melanomas common in the dog and not in man? Why are nearly all oral melanomas in dogs malignant, while cutaneous and ocular ones are more often benign? Why are malignant melanomas more common among heavily pigmented dogs (e.g., Scotties), while in man, fair-skinned people have the greater susceptibility? It seems that research on this disease in the Scottie is long overdue.
It has been assumed that the inherited component of neoplasia is susceptibility to the disease. Yet the converse also seems reasonable; that a resistance or sparing to certain tumors may also be inherited (19). To this end, we know that the Scottie has not been detected with an excessive risk for tumors of the testis (20), ovary (21), perianal gland (22), mammary gland (23), kidney (24), nervous system (25), or thyroid (26), because few cases have been diagnosed relative to those in other dog breeds. As a matter of fact, the sparing from mammary cancer probably is the major reason why female Scotties do not show a greater prevalence of cancer, surpassing the male, as is seen in dogs in general (5).
As Scottie owners, we must be ever vigil to their medical abnormalities. Early detecting has proven most beneficial in treating human cancer; the same applies to dog, particularly for lymphosarcoma and mast cell sarcoma (27). Being aware of those cancers of greater risk, is the first step in this process.
The author wishes to thank Dr. Dorothy D. Greenhouse of the Scottish Terrier Club of Greater Washington, D.C., for the idea and encouragement to conduct this study.
Data from the following colleges of veterinary medicine were used in this project: Auburn, Colorado State, Cornell, Iowa State, Kansas State, Louisana State, Michigan State, The Ohio State, Purdue, and Texas A&M Universities and the Universities of California, Georgia, Guelph, Illinois, Minnesota, Missouri, Saskatchewan, and Tennessee.
(1) Shaler, N.S. DomesticatedAnimals. Charles Scribner & Sons, New York, 1895.
(2) Asdell, S.A. Dog Breeding. Reproduction and Genetics. Little, Brown and Co., Boston, p. 14,1966.
(3) Hayes, H.M., Jr., Wilson, G.P. and Moraff, H. The veterinary medical data program (VMDP): past, present, and future. In: Proceedings of the International Symposium on Animal Health and Disease Data Banks, December 4-6, 1978, Washington, D.C., USDA, APHIS, Misc. Pub. #1381, pp. 127-132,1979.
(4) Mantel, N. and Haenszel, W. Statistical aspects of the analysis of data from retrospective studies of disease. J. Nati. Cancer Inst. 22:719-748, 1959.
(5) Priester, W.A. and Mantel, N. Occurrence of tumors in domestic animals. Data from 12 United States and Canadian colleges of veterinary medicine. J. Natl. Cancer Inst. 47:1333-1344, 1971.
(6) Gart, J.J. Point and interval estimation of the common odds ratio in the combination of 2X2 tables with fixed marginals. Biometrika 57:471-475, 1970.
(7) Hayes, H.M., Jr. The comparative epidemiology of selected neoplasms between dogs, cats and humans. A review. Eur. J. Cancer 14:1299-1308, 1978.
(8) Hueper, W.C., Wiley, F.H. and Wolfe, H.D. Experimental production of bladder tumors in dogs by administration of beta-naphthylamine. J. Ind. Hyg. Toxicol. 20:46-84,1938.
(9) Cole, P. Lower urinary tract. In: Cancer Epidemiology and Prevention, D. Schot-tenfeld, ed. Charles C. Thomas, Springfield, pp. 233-262, 1975.
(10) Hoover, R. and Fraumeni, J.F., Jr. Cancer mortality in U.S. counties with chemical industries. Environ. Res. 9:196-207, 1975.
(11) Hayes, H.M., Jr., Hoover, R. and Tarone, R.E. Bladder cancer in pet dogs: a sentinel for environmental cancer? Am. J. Epidemiol. 114:229-233, 1981.
(12) Hayes, H.M., Jr. Canine bladder cancer: epidemiologic features. Am. J. Epidcmiul. 104:673-677, 1976.
(13) Fraumeni, J.F., Jr. (ed.) Persons at High Risk of Cancer. Academic Press, New York, 1975.
(19) Marnden, D.G. The nature of inherited susceptibility to cancer. Carcinogenesis 5:1535-1537,1984.
(20) Hayes, H.M., Jr. and Pendergrass, T.W. Canine testicular tumors: epidemiologic features of 4 1 0 dogs. Int. J. Cancer 18:482-487, 1976.
(21) Hayes, H.M., Jr. and Young, J.L., Jr. Epidemiologic features of canine ovarian neoplasms. Gynecol. Oncol. 6:348-353, 1978.
(22) Hayes, H.M., Jr. and Wilson, G.P. Hormone-dependent neoplasms of the canine perianal gland. Cancer Res. 37:2068-2071, 1977.
(23) Priester, W.A. Occurrence of mammary neoplasms in bitches in relation to breed, age, tumour type, and geographic region from which reported. J. small Anim. Pract. 20:1-11,1978.
(24) Hayes, H.M., Jr. and Fraumeni, J.F., Jr. Epidemiologic features of canine renal neoplasms. Cancer Res. 37:2253-2256, 1977.
(25) Hayes, H. M., Jr., Priester, W.A. and Pendergrass, T. W. Occurrence of nervous tissue tumors in cattle, horses, cats and dogs. Int. J. Cancer 15:39-47, 1975.
(26) Hayes, H.M., Jr. and Fraumeni, J.F., Jr. Canine thyroid neoplasms: epidemiologic features. J. Natl. Cancer Inst. 55:931-934, 1975.
(27) Norris, A. and Withrow, S.J. Review of cancer chemotherapy for pet animals. Can. Vet. J. 25:153-157, 1984.
Table 1. Distribution of 553 confirmed primary neoplasms diagnosed in 486 Scottish terriers brought to 18 North American university veterinary medical teaching hospitals that participate in the Veterinary Medical Data Program.
Table 2. Distribution of the more frequently confirmed primary malignant tumors diagnosed in 361 Scottish terriers brought to 18 North American university veterinary medical teaching hospitals (VMTH).
No. of VMTHs Reporting This cancer
No. of cases*
% of cancer patients
Transitional cell carcinoma
of the lower urinary tract
Mast cell sarcoma
Squamous cell carcinoma of the skin
Basal cell carcinoma
Perianal gland carcinoma
*Patients with two or more primary malignancies were counted in each category.
Table 3. Estimated relative risk (RR) for female Scotties for primary cancer versus that in male Scotties (RR = 1) seen at 18 North American university veterinary medical teaching hospitals (VMTH) using the statistical methodology of Gart (6).
Transitional cell carcinoma of the lower urinary tract
Mast cell sarcoma
Squamous cell carcinoma of the skin
*Patients with two or more primary malignancies were counted in each category.
+RR adjusted for variations in age.
**Significant at P<0.05 using 95% confidence intervals.
nsNot statistically significant, P>0.05.
Table 4. Estimated relative risk (RR) of the 8 most frequent malignant tumors diagnosed in 361 Scottish terriers brought to 18 North American university veterinary medical teaching hospitals (VMTH) compared with that diagnosed in all purebred dogs using the statistical methology of Gart (6).
*Patients with two or more primary malignancies were counted in each category.
RR adjusted for age and sex for lymphosarcoma, transitional cell carcinoma, and malignant melanoma; adjusted for age only for other cancers.
**Significant at P<0.001 using 99.9% confidence intervals.
***Significant at P 0.01 using 99% confidence intervals.
nsNot statistically significant, P>0.01.
300+ X (10-14 yrs)
| 0 ( 17.5yrs)
250+ 0 ( 10-14 yrs)
| X (7-9 yrs)
150+ 0 (7-9 yrs)
| X X ( 4-6, 7-9yrs
50+ 0 ( 7-9 yrs)
| 0X 0 ( 2-3, 4-6 yrs)
0 5 10 15 20
AGE IN YEARS
Figure 1. Hospital prevalence per 1,000 patient years at-risk for primary cancers diagnosed in Scottish terriers seen at 18 North American university veterinary medical teaching hospital by sex and age. The rates for the age intervals 2-3, 4-6, 7-9, and 10-14 years were plotted at the midpoint of each interval; 15 years was plotted at 17.5 years.
Original Doc: cancer03.doc
Hormonal Control of Canine Tumors
A summary of the veterinary field's current knowledge
of hormonal manipulation in cancer care.
by Dennis W. Macy, D. V. M., M. S.
Source: From September 1985 AKC Gazette
It is estimated that 30% of the tumors in dogs arise from parent tissue, which normally grow in response to hormones. That is, the normal parent tissues grow in the presence of hormones and cease growing when hormones are absent. When abnormal tissues (or tumors) develop, they may retain their responsiveness to hormones and thus may be controlled through hormonal manipulation. The relationship between a tissue and a hormone is very specific. A tissue will only respond to a hormone if it possesses a specific receptor for that particular hormone. Tissue without specific receptors will not be affected by a given hormone. This phenomenon is very important in that hormonal therapy is very specific and generally much less toxic than traditional anticancer therapy that tend to be less discriminatory in their cell killing.
Therapy for hormone sensitive tumors includes removing glands that secrete hormones which stimulate the tumors to grow, or by administering blocking hormones which bind to tumor receptors but do not stimulate the tissue to grow. Most of these compounds are steroid derivatives, although some newer compounds are synthetic hormoneÄlike compounds, and a few are antagonistic and have antihormone activity. More widespread use of hormonal manipulation in dogs for the control of cancer has been limited by our knowledge of which tumors have hormone receptors and to which hormones. With the development of new laboratory receptor technology, our knowledge in this area is rapidly expanding. The following discussion represents a summary of current knowledge of hormonal manipulation in the dog as it relates to cancer management.
Manipulation of sex hormones in the management of tumors is probably the most widely practiced form of hormonal manipulation in small animal clinical medicine. The most common site for cancer in the bitch is the mammary gland. In the 1960s, definitive evidence that early spaying decreased the incidence of mammary tumors in the bitch was demonstrated. Spaying bitches before their first estrous cycle eliminates the risk of development of mammary cancer almost entirely. Spaying after one estrus increased the risk factor to 8% of the nonspayed bitch's incidence rate. Any protection against mammary tumor development is lost if bitches are spayed after 2.5 years of age.
Although the advantage of hormonal manipulation is clear in the prevention of mammary tumors, the use of hormonal manipulation in the treatment of mammary tumors is still controversial. Estrogen and progesterone receptors have recently been found by a number of investigators on approximately 50% of malignant mammary tumors in the dog. Those dogs with estrogen and/or progesterone receptor positive tumors have been shown to have a better survival rate than those dogs with mammary tumors without estrogen or progesterone receptors. This observation is similar to what is observed in women with mammary tumors. Women with mammary tumors that are positive for estrogen or progesterone receptors routinely are subjected to hormonal manipulation.
The advantage of removing the estrogen and progesterone source (spaying) in bitches that have mammary tumors that are positive for estrogen and progesterone receptors, has not been established. A study that was done prior to the identification of the estrogen and progesterone receptors in canine mammary tumors failed to show an advantage of spaying in decreasing further risk of developing mammary tumors, but the study did indicate that the spaying may delay the spread of tumors to such areas as the lungs. Studies need to be carried out to determine if spaying may be an affective adjunctive means of treatment to surgical removal of bitches with estrogen or progesterone receptor positive mammary tumors.
The recent discovery of estrogen receptors in canine mammary tumors also opens the opportunity to study antiestrogen drugs like tamoxifen in the treatment of estrogen positive mammary tumors in the dog. In humans, tamoxifen acts by competitive inhibition of estrogen receptors, and is frequently used in the treatment of estrogen receptor positive mammary tumor patients. There are many species differences, and the ability of this drug to do the same thing in the dog must be established and tested before routine use can be recommended. The presence of progesterone receptors on canine mammary tumors adds additional understanding of the increased incidence of mammary tumors in dogs given various progesterone type drugs. Cat mammary tumors are low in estrogen receptors and high in progesterone receptors. A close association between the administration of progestational compounds and a condition called mammary fibroadenomatosis has been well established for this species. Knowledge then, of tissue hormone receptors may indicate the potential hazard of inducing tumor with various types of hormone for other disease conditions.
Perianal tumors and prostatic tumors in the male dog may be helped by castration or by the administration of estrogen compounds. The perianal tumors are common cancers of older male dogs and are very rare in females. Perianal gland tumors rank third in frequency of all canine tumors behind mammary and mast cell tumors. Because of the very low incidence of the tumor in females, it has been long believed that perianal tumors were dependent on male sex hormone for development and growth. Recently scientific evidence to support this belief has been reported by the discovery of sex hormone receptors in cells of perianal tumors. Surgical removal of the source of testosterone (castration) is usually followed by rapid decreases in tumor size. Similarly, castrated dogs seldom develop perianal tumors and recurrence of perianal tumors in dogs castrated as part of the therapy is very low. Castration and local surgical excision is the most frequently practical management regimen for perianal tumors.
The administration of estrogen compounds also is effective in controlling perianal tumors. One way estrogen compounds work is by blocking testosterone production by shutting off the supply of a pituitary hormone, called LH, that normally stimulates testosterone production in the testicles. Estrogen therapy however must be given frequently and can be associated with sometimes fatal bone marrow toxicities. Estrogen receptors recently have been found arising from tumors not normally associated with hormonal control like canine mast cell tumors. The role, if any, of antiestrogen or estrogen compounds in the treatment of this common malignant skin tumor is unknown at this time.
Adrenocortical steroids are used in the treatment of a number of cancers in the dog. Specific antitumor effects have been observed in two common tumors in the dog (lymphomas and mast cell tumors). The use of adrenocorticosteroids in the treatment of other tumors is primarily due to its antiinflammatory properties that tend to reduce swelling, pain, and increase appetite. Lymphomas and leukemias may respond dramatically to adrenocorticosteroids, and complete remissions are frequently observed within days from the start of therapy. Corticosteroids are frequently combined with other anticancer drugs in the treatment of lymphomas to increase remission times. In humans, the responsiveness of lymphomas to steroid therapy correlates roughly with the number of corticosteroid receptor sites present on the tumor. Unlike the relationship between testosterone receptors and perianal tumors, corticosteroids tend to kill or inhibit growth of lymphocytes that make up the tumor. Studies are ongoing in our laboratory to look for receptor sites of various types in canine lymphomas.
The antitumor effects of adrenocorticosteroids against mast cell tumors of the dog were first discovered in the 1950s and corticosteroids remain the primary treatment for this tumor today. Although this tumor is very common in the dog, it is extremely rare in humans and has not been well studied. Ironically, mast cell tumors have never been evaluated for corticosteroid receptors, however estrogen receptors have been found recently on two canine mast cell tumors by a German scientist. The role and potential use of the estrogen receptors in the management of this very common neoplasm awaits further verification and controlled studies.
Routine use of hormonal manipulation for the control of cancer in dogs is in its infancy. The three most common canine tumors (mammary, mast cell, perianal) have already been shown responsive to hormonal manipulation. A fuller understanding of the potential use of this specific relatively nontoxic form of therapy will rely on our discovery of hormone receptors in tumor tissues, and our ability to correlate these findings with responses to specific hormonal manipulation.
Original Doc: tumors03.doc
New Chemotherapy Treatment Mode
By Unknown Author
Journal of the AVMA, January 15, 1994.
A new method of chemotherapy promises hope for dogs with oral malignant melanoma. Cisplatin, a type of chemotherapy, was administered directly into the tumor instead of being injected into the bloodstream as a systemic treatment. The goal of this intralesional treatment was to control the tumor locally.
Patients whose tumors responded to treatment survived an average of 54 weeks, compared to an average of about 10 weeks for dogs without local tumor control. Dogs not responding to intralesional cisplatin did not survive any longer than dogs receiving conventional treatment, such as any combination of surgery, radiation and hyperthermia.
The authors of the study concluded that intralesional cisplatin achieves local tumor control while minimizing the systemic effects of chemotherapy, increasing tolerance to treatment.
Oral tumors are the fourth most common malignant tumor in dogs. Tumor recurrence is common after conventional treatment. Metastasis is also common, because of the aggressive nature of the tumors.
Many dogs with oral malignant melanoma ultimately die from metastases, but many are euthanized because quality of life deteriorates as the tumor grows. Intralesional cisplatin improves quality of life by decreasing tumor size for a longer period.
Early diagnosis is imperative for a cure. Examine your dog's mouth regularly for sores, bumps, lumps or anything unusual. Look at the gums, under the tongue, inside the lips, around the teeth. Be suspicious, especially if you haven't noticed something before.
Don't wait and see. Have it biopsied. The sooner the diagnosis is made, the sooner the treatment can begin. And the smaller the tumor, the more effective (and less expensive) the treatment.
Original Doc: tumor02.doc
Hope for Dogs with Nasal Tumors
By K. Ann Jeglum, V.M.D.
Journal of the AVMA, Volume 200, Number 3, February 1, 1992. Important explorations.
Frequent sneezing, nasal discharge and epistaxis (bleeding from the nose) are the most common signs of nasal tumors. When a nasal tumor is suspected, skull radiographs (X-rays) and biopsies reveal the definitive diagnosis and the extent of the problem.
If the tumor is not too extensive and has not metastasized, surgery to decrease the tumor's size and radiation to slow or halt its growth can be effective. When left untreated, however, nasal tumors grow and bleed, triggering dogs to sneeze even more frequently; nasal passages may be obstructed by tumorous tissue, making breathing through the nose difficult or impossible. In addition, facial deformity caused by destruction of the skull can occur in prolonged cases.
Until recently, chemotherapy was not thought to significantly affect nasal tumors. However, Dr. Kevin Hahn at Purdue University recently published data to the contrary. Dr. Hahn administered cisplatin to dogs with tumors so advanced that surgery and radiation were not recommended. He observed that cisplatin did slow or halt growth of nasal tumors. Perhaps of equal or greater importance, Dr. Hahn concluded that chemotherapy significantly improved quality of life: sneezing lessened and breathing eased.
Future studies will undoubtedly include cisplatin as an adjunct to surgery and/or radiation in hopes of offering a cure to dogs with nasal cancer. But as always the best chance for a cure is early detection.
Dr. Jeglum is the staff oncologist at the University of Penn
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