Mast Cell Tumors in Dogs: Symptoms, Diagnosis and Treatment
Mast cell tumors are one of the most common cancers in dogs. They develop from particular cells of the immune system called “mast cells,” which normally treat inflammation and allergic reactions in a dog’s body.
There’s no one single cause of mast cell tumors. Fortunately, the majority of mast cell tumors are localized to one spot. However, rarely they will spread to lymph nodes, the blood, the spleen, the liver, the lungs, the bone marrow, or other skin locations. If the tumor spreads, or metastasizes, to other areas of the body, multi-modality therapy will be required.
Symptoms vary depending on what organ is affected. For most dogs, mast cell tumors are not a painful cancer. In fact, mast cell tumors are typically diagnosed after a pet owner takes their dog to the veterinarian because they’ve felt a lump in or under the skin.
If other organs are also affected, you may see these signs:
Mast cells have inflammatory mediators that can cause shock-like signs:
If cells are disturbed and mediators leak out, stomach ulcers might occur. Look for:
Scientists in England have gathered definitive evidence that a kind of cancer in dogs is contagious – a peculiar exception to the age-old medical wisdom that you cant “catch” cancer. …
“I rather thought we might disprove this, but it came out the other way around,” said Professor Robin Weiss [UCL Infection & Immunity], who led the study appearing in todays issue of the journal Cell. “It is clearly a dog tumor cell behaving absolutely like a parasite.” Weiss called the tumor transmission trick “a curiosity of nature.” …
But the dog cancer, known as Stickers sarcoma, is spread by tumor cells getting passed from dog to dog through sex or from animals biting or licking each other. …
Weiss and his colleagues did genetic studies on the tumor cells from 40 dogs with Stickers sarcoma, collected from five continents. The researchers showed that the cells are not genetically related to the dogs they are in – proof that they did not arise from the dogs own cells.
Todays worldwide distribution of Stickers tumors represents a single colony of cancer cells, the new research concludes. …
In stark contrast to the fatal DFTD, another contagious cancer, canine transmissible venereal tumor (CTVT), is normally not lethal to its dog hosts. Also known as Stickers sarcoma, CTVT was initially described in 1876 and may have originated in a wolf as long as 2,500 years ago. It has been passed along among canines ever since, making it the oldest recognized malignant cell line [16, 17]. There is solid evidence that this tumor is passed on as an allograft, including the fact that CTVT cells have a strikingly different karyotype from the hosts cells, yet are similar to each other even when the hosts are from different continents. The cancer is typically transmitted during mating when the malignant tumor cells from one dog are directly transferred to another dog via coitus, licking, biting, and sniffing tumor-affected areas (the genitals, nose, or mouth). Although capable of metastasizing, CTVT often does not require treatment, as spontaneous regression is the general rule.
As for the Tasmanian devils, researchers thought they might have found an individual named Cedric who possessed immunity to DFTD and could be a savior for the dwindling population. After initially inoculating Cedric and his half-brother Clinky with irradiated tumor cells, followed by injections with live tumor cells, Clinky rapidly succumbed to the cancer. However, Cedric produced antibodies and developed no tumors, prompting speculation about the existence of resistant animals. Unfortunately, in a follow-up study, Cedric was injected with a slightly different strain of DFTD and wound up developing tumors—dashing hopes of finding a resistant population. This was naturally demoralizing news for conservationists but confirmed that there are different strains of the tumor and it may be possible for an animal to be immune to one strain but not others.
Direct transmissions of cancers are not entirely restricted to animals. There are approximately 3,500 women per year in the United States who develop a malignancy during pregnancy, and in rare cases, mother-to-fetus transmission of melanoma, lymphoma, leukemias, and carcinomas have been reported as well as fetus-to-fetus transmission in twins. Although exceedingly rare, 0.04% of organ transplant recipients contract cancer from the donor organ (mostly melanomas) and hematologic malignancies have been observed in about 0.06% of hematopoietic stem cell transplants. Penn  observed that about one third of recipients of organs from donors with some form of cancer at the time of donation eventually developed the same malignancy as in the donor. Curiously, the remaining two thirds did not show evidence of a transmitted cancer. Naturally, this could be due to an absence of neoplastic cells in the donated organ but alternatively it could be due to the hosts rejection of foreign malignant clones. The latter concept is bolstered by the fact that in cases in which cancer does develop following transplantation of an organ from a donor with cancer, the malignant process may regress after the graft has been removed and immunosuppression discontinued [19–22]. Another report described a situation in which a kidney and liver were transplanted from a donor who was found to harbor pancreatic adenocarcinoma. The liver recipient was re-transplanted shortly after the discovery of the donors cancer whereas the kidney recipient opted not to undergo removal of the transplanted organ; the kidney recipient died with metastatic pancreatic adenocarcinoma 15 months after transplantation . A slight variation of this scenario might be presented by the fact that solid organ transplantation carries a 1 out of 200 risk of Kaposi sarcoma in the United States [24, 25]. In principle the disease could originate directly from donated neoplastic cells or as a result of reactivation of the Kaposi sarcoma–associated herpesvirus (KSHV) carried along in the transplanted cells or as a result of immunosuppression that allows KSHV to induce a de novo malignancy. Barrozi et al.  showed that the KSHV-infected neoplastic cells from transplant recipients with Kaposi sarcoma in 5 of 8 renal transplant patients harbored genetic or antigenic markers of their matched donors, suggesting that they were transplanted malignancies rather than KSHV-caused Kaposi sarcomas that might have arisen due to immunosuppression. The authors even suggested the use of donor-derived KSHV-specific T cells for the control of post-transplant Kaposi sarcoma.
These infectious causes of cancer are well studied and investigations of virally caused cancers in animals have contributed immensely to the understanding about the molecular biology of cancer. However, a very different and less well-studied form of “contagious cancer” is currently wreaking havoc in the natural world—and one wonders whether a deeper understanding of these transmissible cancers might similarly prove fruitful in furthering the understanding of cancer biology and treatment.
Bacterial infections such as CagA-positive strains of Helicobacter pylori are associated with gastric carcinomas and MALT lymphomas. Chlamydia psittaci, the cause of psittacosis, has been linked to ocular adnexal lymphomas . Borellia burgdorferi, the cause of Lyme disease, has also been linked to primary cutaneous B-cell lymphomas  and Campylobacter jejuni appears associated with immunoproliferative disease of the small intestine . As far as parasites go, practically all medical students are aware of the link between squamous cell carcinoma of the bladder and Schistosoma hematobium. Opisthorchis viverrini is classified by the International Agency for Research on Cancer as a Group I Carcinogen for cholangiocarcinoma, whereas Clonorchis sinensis was categorized as a probable cause (Group 2A) .
Can cancer spread from dog to human?
Can a dog get cancer from licking other dog’s tumor?
Do dogs lick mast cell tumors?
What is the life expectancy of a dog with a mast cell tumor?