Histopathological classification and immunohistochemical characterization of canine mammary tumours Raval S.H.5,*, Joshi D.V.5, Parmar R.S.5, Patel B.J.5, Patel J.G.5, Patel V.B.1,5, Ghodasara D.J.2,5, Chaudhary P.S.3,5, Kalaria V.A.4,5, Charavala A.H.5 5Department of Veterinary Pathology, College of Veterinary Science and Animal Husbandry, Sardarkrushinagar Dantiwada Agricultural University, Sardarkrushinagar, Gujarat, India; 1Animal Disease Investigation Office, Government of Gujarat, Vadodara, Gujrat; 2Department of Veterinary Pathology, College of Veterinary Science & A.H., AAU, Anand, Gujrat; 3Chief Veterinary Surgeon, Surat Panjara Pole Trust, Nandini Veterinary Hospital, Surat, Gujarat; 4Department of Veterinary Pathology, College of Veterinary Science & A.H., Junagadh Agricultural University, Junagadh, Gujarat, India *Corresponding author: e-mail: samirraval81@gmail.com
Abstract The present study was carried out to investigate breed wise and age wise prevalence of canine mammary tumours (CMTs) along with histopathological and immunohistochemical characterization. A total of 97 CMTs samples were collected from different parts of Gujarat, India over period of three years (April 2014-March 2017). The mean age of the dogs, involvement of breeds and mammary glands were recorded. The mean±SD age of all affected dogs was 7.5±2.8 years. Among 12 breeds affected, most cases (n=77) of CMTs were recorded in four breeds viz., Pomeranian, Mongrel, Germen Shepard and Labrador. Caudal abdominal and inguinal mammary glands were frequently showed neoplastic growth. Among histological characterization of 97 CMTs, 16(16.49%) were non neoplastic proliferative/dysplastic lesions, 11 (11.34%) were benign neoplasms and 70 (72.16%) were malignant tumours. Out of 70 malignant neoplasms, epithelial neoplasms, special type epithelial neoplasms, mesenchymal neoplasms and carcinosarcomas were 53(54.64%), 6(6.19%), 8(8.25%), and 3(3.09%), respectively. Further, mixed carcinoma, tubulopapillary carcinoma, solid carcinoma, carcinoma and malignant myoepithelioma, tubular carcinoma and ductal carcinoma were frequently noted. Immunohistochemistry was found to be a powerful tool to classify the CMTs. In the present study, smooth muscle actin (SMA) helped in diagnosing complex adenoma, complex carcinoma, malignant myoepithelioma and fibrosarcoma. In complex adenoma, complex carcinoma and malignant myoepithelioma, myoepithelial cells showed strong SMA immunoreactivity, although stromal myofibroblasts and vascular smooth muscle cells also immunostained. Top Keywords Canine mammary tumours, Histopathological classification, Immunohistochemistry. Top |
INTRODUCTION Mammary glands (MG) are distinguishing feature of mammals that provide appropriate nourishment and passive immunity to their offspring. They are epidermal appendages that possibly evolved over 300 million years ago, from ancient apocrine sweat glands1. In domestic animals, mammary gland tumours are rare except dogs and cats2. Canine mammary tumours (CMTs) are the most common neoplasm in female dogs with 0.2% prevalence3. The annual incidence rate has been estimated at 205/100,0004. Due to spontaneous occurrence, similarities and differences in their molecular pathogenesis, CMTs is considered as a spontaneous animal model of human breast cancer5. |
In 1974, the World Health Organization (WHO) published the first “International Histological Classification of Tumours of Domestic Animals” which included tumours and dysplasia of the mammary gland. Other several classifications of canine mammary tumours had been proposed in past6,5,6,7,8,9-10. Recently, Goldschmidt et al.11 proposed modifications to the WHO classification criteria to create a more morphologically diverse and detailed classification system for CMTs. In few past studies, WHO classification was used to classify CMTs in India. However, no study has been undertaken in India to classify the CMTs according to classification proposed by Goldschmidt et al.11. Therefore, the present study was carried out to investigate breed wise and age wise prevalence of CMTs along with its histopathological characterization of CMTs and grading of the canine mammary carcinomas (CMCs). |
Top MATERIALS AND METHODS Collection of CMT tissues A total 97 CMTs samples were obtained from: (1) Department of Veterinary Pathology, Ananad Agricultural University, (2) Department of Veterinary Pathology, Junagadh Agricultural University, (3) Teaching Veterinary Clinical Complex (TVCC) - SDAU, Deesa, (4) Polyclinic, Vadoadara, (5) Nandini Hospital, Surat, and (6) Polyclinic, Ahmedabad, Gujarat over period of three years (April 2014 - March 2017). All tissues were fixed in 10% neutral-buffered formalin. Tissue processing and staining Mammary gland tumour tissues were fixed in 10% neutral-buffered formalin, processed routinely and embedded in paraffin wax. The 4 to 5 microns thick sections were cut and stained with Hematoxylin and Eosin (H&E)12. Clinical observations The mean age of the dogs was calculated, and the locations of the masses with respect to the lateral (left or right) and longitudinal (thoracic, abdominal, or inguinal mammary gland) axes were recorded. Furthermore, the frequencies of mammary tumours and hyperplasia/dysplasia were analysed according to breed. Histopathological classification A total 97 CMTs were classified into hyperplasia, benign tumours, and malignant tumours according to the criteria given by Goldschmidt et at.11. Immunohistochemistry Immunohistochemical analysis was performed on formalin fixed tissue sections and details of various antibodies are listed in Table 1. Paraffin sections were taken on poly-L-lysine-coated slides, deparaffinised, and rehydrated through graded alcohol and subjected to antigen retrieval. Heat-induced epitope retrieval was performed using pressure cooker for all primary antibodies. Then, the slides were rinsed in Tris-buffered saline (TBS) pH 7.4 and endogenous peroxidase was blocked by Peroxidase Suppressor (Thermo Scientific, USA) for 30 min. After pre-treatment, the sections were incubated with primary antibody. After rinsing with TBS, tissues were incubated with EnVision rabbit/mouse reagent conjugated to peroxidase (Dako REAL− Envision− HRP; Dako, Denmark) for 30 min at room temperature (RT) and colour reaction developed with 3,3'- diaminobenzidine (DAB) chromogen. The sections were counter stained with Mayer‘s hematoxylin, dehydrated, cleared and mounted. Canine mammary tumour samples, known to express all markers, were used as positive controls. Negative controls were obtained by omitting the primary antibody. Top RESULTS Clinical observations Age and sex The age of all 97 affected dogs were known except 3 cases. The mean ± SD age of all affected dogs was 7.5 ± 2.8 years (ranging between 2 to 14 years). The mean ± SD age of dogs with ectasia/hyperplasia/dysplasia was 4.4 ± 2.06 years (ranging between 2 to 11 years). The mean ± SD age of dogs with benign tumours was 7.3 ± 1.9 years (ranging between 5 to 10 years). The mean ± SD age of dogs with malignant tumours was 8.2 ± 2.7 years (ranging between 4 to 16 years). In present study, all cases of CMTs were recorded only in females. Breeds The details regarding occurrence of mammary lesions in various breed of dogs observed in present study is given in Table 2. Among 12 breeds, most cases (n = 77; 79.38%) of CMTs were recorded in four breeds; Pomeranian (n = 22; 22.68%), Mongrel (n = 21; 21.64%), Germen Shepard (n = 19; 19.59%), and Labrador (n = 15; 15.46%). The other breeds found to be affected were Spitz (n = 6), Doberman (n = 4), Great Dane (n = 4), Dachshund (n=2), Boxer (n = 1), Golden Retriever (n = 1), Lhasa Apso (n = 1), and Saint Bernard (n = 1). In the present study, Pomeranian, Mongrel, Germen Shepard, and Labrador were more prone to have malignant neoplasms (n=54; 55.67%) than benign neoplasms (n=8; 8.25%) or hyperplastic/dysplastic lesions (n=15; 15.46%). Reproductive status and mammary gland affected The reproductive status (spayed or intact) at the time of surgery was known in 36 cases out of the 97 cases studied. All 36 bitches were not underwent ovariohysterectomy at the time of tumour surgery. In the present study, all mammary glands were affected except left carinal thoracic gland. Most cases of CMTs (n=77; 79.38%) were recorded in caudal abdominal and inguinal glands. The highest incidences of CMTs were recorded in right inguinal (n=18; 18.56%) followed by left inguinal (n=16; 16.49%), left caudal abdominal (n=14;14.43%), and right caudal abdominal (n=12; 12.37%). In 17 cases, both caudal abdominal and inguinal glands of either side were affected. The incidences of CMTs involving right caudal thoracic, right cranial abdominal, left cranial abdominal, left caudal thoracic and right cranial thoracic were 6, 6, 3, 3, and 1 respectively. In one case, three glands (caudal thoracic, cranial abdominal and caudal abdominal) of right side were affected. Classification and incidences of CMTs Table 3 summarizes histological classification of canine mammary tumours into hyperplasia/dysplasia, benign and malignant tumours. Among the classified 97 CMTs; the malignant tumours were found to be the highest at 72.16 % (n=70) followed by non-neoplastic proliferative/dysplastic lesions (n=16; 16.49 %) and benign neoplasms (n=11; 11.34%). Histopathological characterization Hyperplasia/dysplasia Ductal ectasia was characterised by mild to cystic dilation of interlobular ducts. Regular lobular hyperplasia showed marked expansion of lobules due to proliferation of acini and ducts. Lobular hyperplasia with secretory activity showed marked expansion of lobules due to proliferation of acini and ducts. Interlobular ducts and acini were dilated and contained variable amount of eosinophilic secretory material. Lobular hyperplasia with fibrosis was characterised by expansion of lobules with increased numbers of intralobular ducts/ductules and acini, with increased intra and interlobular fibrous connective tissue. In epitheliosis, multiple intra and inter lobular ducts were showed proliferation of luminal epithelial cells. Proliferated epithelial cells were arranged in solid sheet or in papillary pattern without supportive fibrovascular stroma (Fig. 1). Benign mammary neoplasms In intraductal papillary adenoma, multiple dilated ducts showed either single or multiple papillary growth supported by a fibrovascular stalk (Fig. 2). Histologically, fibroadenoma was characterized by multilobulated mass, composed of tubuloacinar structures separated by dense fibrous connective tissue. In complex adenoma (adenomyoepithelioma), both epithelial and myoepithelial cells were proliferated and supported by dense fibrovascular stroma. Neoplastic epithelial cells predominantly arranged in a tubular or tubulopapillary pattern. The spindle shaped myoepithelial cells formed loosely packed islands beneath the ductal epithelium and had distinct cell borders and a moderate amount of basophilic cytoplasm. Strong immunoreactivity with smooth muscle actin (SMA) was observed in cytoplasm of myoepithelial cells. Benign mixed tumour was composed of focal extensive area of cartilage and proliferation of epithelial and myoepithelial cells supported by variable amounts of fibrovascular stroma. Microscopically, lipoma expanded the overlying dermis and was multi-lobulated neoplasm composed of mature adipocytes. Malignant neoplasms Carcinoma-tubular pattern was characterized by moderately cellular neoplasm composed of cells, predominantly arranged in a tubular fashion and supported by fibrovascular stroma. In tubule-papillary carcinoma neoplastic cells were arranged in a tubule-papillary fashion. In cystic papillary carcinoma most of the tubules were ectatic and filled with variable amount of eosinophilic secretory material admixed with other degenerated cells. In micropapillary invasive carcinoma, neoplastic cells formed irregular small papillae and aggregation of neoplastic cells in which supporting fibrovascular network were not detected (Fig. 3). Microscopically solid carcinoma was highly cellular neoplasm composed of cells, predominantly arranged in small lobules or solid sheets that lack differentiation towards tubules and had no lumen. In comedocarcinoma, central area of necrosis was detected in solid lobules (Fig. 4). Multifocally, within the central necrotic area, acellular basophilic laminated bodies (mineralization) were evident. Anaplastic carcinoma was composed of multiple islands of neoplastic cells, separated by dense fibrovascular stroma. At periphery of the islands, most of the neoplastic cells became individualized and invading the surrounding fibrous stroma (Fig. 5). Neoplastic cells were round to polygonal, large, with moderate to abundant eosinophilic cytoplasm and distinct cell border. On IHC, individualized neoplastic epithelial cells showed strong cytoplasmic immunoreactivity with pancytokeratins (Fig. 6). In complex carcinoma, there was malignant proliferation of epithelial cells, benign proliferation of myoepithelial cells and these cells were supported by fibrovascular stroma. Strong immunoreactivity with SMA was observed in cytoplasm of myoepithelial cells. Microscopically, carcinoma and malignant myoepithelioma was composed of malignant epithelial and malignant myoepithelial cells and supported by variable amounts of fibrovascular stroma (Fig. 7, 8). Microscopically, mixed carcinoma was composed of three types of cell populations (epithelial cells, myoepithelial cells and mesenchymal component (bone and/or cartilage) supported by variable amounts of fibrous stroma. In ductal carcinoma, multiple interlobular ducts showed neoplastic proliferation of epithelial cells with fibrous thickening of duct wall. Neoplastic epithelial cells either completely or partially filled the ectatic ducts. Within the ducts, neoplastic cells are arranged in solid sheet or irregular tubules. In intraductal papillary carcinoma, dilated duct showed papillary growth pattern supported by a fibrovascular stalk. Histologically, squamous cell carcinoma was unencapsulated, neoplasm composed of large round to polygonal cells arranged in islands, cords, and trabeculae supported by fibrovascular stroma with marked infiltration of inflammatory cells. Microscopically, adenosquamous carcinoma was moderately cellular neoplasm composed of neoplastic cells, predominantly arranged in solid carcinoma or tubular carcinoma pattern and focal to multifocal areas of squamous metaplasia. Malignant myoepithelioma was highly cellular neoplasm composed of spindle-shaped cells arranged in interlacing bundles (Fig. 9). On IHC, malignant myoepithelial cells showed strong immunoreactivity with SMA. Microscopically, osteosarcoma was unencapsulated, infiltrative, densely cellular neoplasm composed of oval, round or spindle-shaped cells that often surrounded the foci of eosinophilic, amorphous, and homogeneous to fibrillar matrix (osteoid) which was variably mineralized (Fig. 10). Microscopically, fibrosarcoma was unencapsulated highly cellular neoplasm infiltrating and effacing surround structures and, composed of spindle shaped cells arranged in long interlacing streams and bundles with variable vascular stroma. In two cases, occasionally neoplastic cells formed whorls (concentric arrangement of spindle cells around blood vessels, hemangiopericytoma-like pattern) around blood vessels (Fig. 11). On IHC, neoplastic cells did not show any immunoreactivity with SMA, S-100 and glial fibrillary acidic protein. Microscopically, liposarcoma effaced and expanded the overlying dermis and unencapsulated, poorly demarcated, highly cellular, infiltrative neoplasm composed of variable vacuolated pleomorphic polygonal cells that were densely packed with minimal fine fibrovascular stroma. Among three cases of carcinosarcoma, two cases showed mixture of tubule-papillary carcinoma and osteosarcoma (Fig. 12). In all sections, osteosarcoma component was predominate and made up of bony spicules and multifocal area of cartilage. Multifocally bony spicules were lined by osteoblasts. The epithelial component had lesser proportion and composed of neoplastic epithelial tubules trapped in neoplastic bony spicules. Morphology and arrangement of neoplastic epithelial cells were similar to tubule-papillary carcinoma. In one case of carcinosarcoma, neoplasm showed mixture of tubular carcinoma and fibrosarcoma. In entire neoplastic mass, tubular carcinoma component was predominate and morphology and arrangement of neoplastic epithelial cells were similar to tubular carcinoma. Within the neoplastic tissue, there was development of fibrosarcoma. On IHC, fibrosarcoma did not show any immunoreactivity with SMA, S-100 and GFAP. Top DISCUSSION The present study was carried out to investigate breed wise and age wise prevalence of CMTs along with its histopathological characterization of CMTs and grading of the CMCs. The present study findings clearly indicate the relationship between age and type of proliferation occurs in female dogs. Non-neoplastic proliferation occurs in young age female dogs (4.4 years). As age advanced, incidences of benign (7.3 years) and malignant tumours (8.2 years) increased. In the previous studies, the highest incidences of CMTs were reported between 8 to 12 years of age13,14,15,16-17. |
In present study, all cases of CMTs were recorded only in females. Most literatures on CMTs clearly indicate that, this is a disease of females, although some reports, indicates rarely CMTs found in males. Saba et at.18 histologically confirmed CMTs in eight male dogs in there retrospective study. Bearss et at.19 histologically confirmed CMTs in 18 male dogs in there retrospective study. Some other researchers also reported CMTs in male dogs20,21-22. |
It is now well-established fact that breed differences occur in cancer development in canines, and risk for developing a particular cancer varies between the breeds. Up to 7 years of age, purebred dogs have two time more risk of malignant mammary neoplasms than mixed-breed dogs23. In present study, Pomeranian, Labrador, Germen Shepard and Mongrel were predominately affected. Pomeranian, Labrador, and Germen Shepard are quite popular breed in Gujarat and there population are high as compared to other breeds of dogs. All non-descript dogs were considered as Mongrel in present study. Due to poor dog birth control programme, population of Mongrel dogs are high. Probably, the population and popularity is responsible for high incidences of CMTs in aforesaid breeds. Two genes, BRCA1 and BRCA2, were significantly associated with CMTs24. Breed-related differences are exists in altered BRCA1 expression25. In present study, BRCA1 mutation have not been studied, but this may contribute in numbers of neoplasms differs according to breeds. |
In India, numbers of pet dogs underwent ovariohysterectomy before reaching to sexual maturity is very low. This practice predisposes bitches to mammary tumour development. Schneider et at.26 found significant correlation between spaying, number of oestrus cycle and incidence of mammary tumours. There is an approximately 0.5% of the mammary cancer risk, if bitches are spayed before first oestrus. If bitches are spayed between the first and the second oestrus, mammary cancer risk increased up to approximately 8%. Bitches spayed after second or more oestrus cycle has 26% mammary cancer risk. There is equivocal effect of spaying after fourth oestrus cycles on mammary cancer risk14,26,27-28. |
The findings of present study revealed an increasing frequency of mammary tumours from the cranial to caudal. In few past studies, most incidences of CMTs were reported in two caudal pairs (inguinal and caudal abdominal) with a decreasing incidence in the more cranial glands and frequently more than one mammary gland were affected10,16,14,29,30. The actual explanation for more involvement of caudal pairs in neoplastic process is not completely elucidated. Among possible explanation, Mulligan31 suggested that it might be associated with the greater activity in response to oestrogen in the more caudal glands. Since these are the largest glands, they may be subject to a greater range of physiologic change and thus may become more susceptible to neoplasms. |
In present investigation, about 72% cases showed malignant proliferation of mammary tissue, while remaining 28% cases showed benign proliferation of mammary tissue. The ratio of benign to malignant neoplasms considerably varies in past studies. In most CMTs studies 12–83% neoplasms were diagnosed as malignant. Reported malignant neoplasms percentage were; 1232, 3533, 47.517, 5134, 6235, 6436, 6b37,38, 7939 and 83%40. The factor that influenced ratio of benign to malignant neoplasms includes, history of ovariohysterectomy, duration of lesions, representative samples collected from entire tumour mass, and experience of pathologist. |
Among malignant neoplasms, mixed carcinoma was predominated followed by tubule-papillary carcinoma, solid carcinoma, carcinoma and malignant myoepithelioma, tubular carcinoma and ductal carcinoma. Canine mammary mixed neoplasms are most commonly reported neoplasms in female dogs while rare in human breast41. In mixed neoplasms of epithelial, myoepithelial and mesenchymal components are present in variable proportion. There is controversy exist on histogenesis of cartilage or bone in mixed mammary neoplasms. Metaplastic change of the epithelial cells, myoepithelial cells, or interstitial stromal cells may form cartilage/bone in mixed mammary carcinoma11. Past studies also reported higher incidences of mixed mammary carcinoma39,42,43-44. However carcinoma arising in a complex adenoma/mixed tumour was most frequently reported malignant tumour in study conducted by Im et at.34. |
Immunohistochemistry seems to be powerful tools to classify the CMTs. In the present study smooth muscle actin (SMA) play very important role in diagnosis of complex adenoma, complex carcinoma, malignant myoepithelioma and fibrosarcoma. In complex adenoma, complex carcinoma and malignant myoepithelioma, myoepithelial cells showed strong immunoreactive, although stromal myofibroblasts and vascular smooth muscle cells also shown immunoreactivity Calponin, p63, CD10, and basal keratins were used as substitutes of SMA in few studies19,45,46,47-48. Among p63 and SMA, p63 is not expressed in myofibroblasts and vascular smooth muscle cells, hence found more sensitive and specific myoepithelial markers47. |
In the present study, 2 fibrosarcoma cases shown characteristic concentric arrangement of spindle cells around blood vessels (hemangiopericytoma-like pattern), which had documented earlier49. On immunohistochemical staining neoplastic cells were negative for SMA, desmin, S-100 and GFAP, hence warranted diagnosis of fibrosarcoma. |
Top ACKNOWLEDGEMENTS Authors are thankful to Dr. Nikita Bhatt and Dr. Anjali Rathod for their help in collection and processing of CMT samples. Authors are thankful to the Dean and Principal, College of Veterinary Science and Animal Husbandry, Sardarkrushinagar Dantiwada Agricultural University, Sardarkrushinagar, Gujarat, India for providing the necessary facilities to carry out this work. |
Top Figures | Fig. 1.: Epitheliosis: One duct showing solid proliferation of luminal epithelial cells, while other ducts showing papillary pattern. H&E ×200
|  | |
| | Fig. 2.: Intraductal papillary adenoma: Duct showing multiple papillary growths lined by single layered cuboidal to columnar epithelium and supported by fibrovascular stroma. H&E ×100
|  | |
| | Fig. 3.: Carcinoma-micropapillary invasive: Neoplastic cells forming intraluminal irregular aggregates and small papillae that lack supporting fibrovascular stalk H&E ×200
|  | |
| | Fig. 4.: Comedocarcinoma: The centre of neoplastic tubule showing area of necrosis characterised by presence of amorphous eosinophilic granular material. H&E ×200
|  | |
| | Fig. 5.: Anaplastic carcinoma: Individualized neoplastic cells showing marked pleomorphism. H&E ×200
|  | |
| | Fig. 6.: Anaplastic carcinoma: Individualized neoplastic cells, acini and ducts epithelium showing immunoreactivity with pancytokeratins. IPO-DAB-Mayer‘s haematoxylin counterstain. x100
|  | |
| | Fig. 7.: Carcinoma and malignant myoepithelioma: Few neoplastic tubules separated by malignant myoepithelial cells embedded in abundant myxoid matrix. H&E ×100
|  | |
| | Fig. 8.: Carcinoma and malignant myoepithelioma: Malignant myoepithelial cells showing strong immunoreactivity with SMA. IPO-DAB-Mayer‘s haematoxylin counterstain. x100
|  | |
| | Fig. 9.: Malignant myoepithelioma: Neoplastic cells showing distinct cell border, moderate amount of eosinophilic cytoplasm, fusiform vesicular nuclei, and numerous mitotic figures (arrow). Note entrapped acini showing reactive changes. H&E ×200
|  | |
| | Fig. 10.: Osteosarcoma: Neoplastic cells forming foci of eosinophilic, amorphous osteoid with variable mineralization. Few osteoclasts (arrows) randomly scattered in neoplasm. H&E ×100
|  | |
| | Fig. 11.: Fibrosarcoma: Neoplastic cells forming whorls (concentric arrangement of spindle cells around blood vessels, hemangiopericytoma-like pattern) around blood vessels. H&E ×200
|  | |
| | Fig. 12.: Carcinosarcoma (tubulopapillary carcinoma + osteosarcoma): Neoplasm showing malignant proliferation of epithelial cells and mesenchymal cells (bone). H&E ×100.
|  | |
|
Tables | Table 1.: Primary antibodies and immunostaining protocols used in this study.
| | Antibody | Source | Clone/Isotype | Dilution | Antigen Retrieval | Incubation | | SMA | Thermo Scientific | 1A4/IgG2a | 1:400 | Citrate pH-6; Pressure cooker | 1 hour, RT | | Pancytokeratin | Dako, Denmark | AE1-AE3/IgG1, Kappa | 1:400 | Citrate pH-6; Pressure cooker | 1 hour, RT | | S-100 | Dako, Denmark | Polyclonal | 1:800 | Citrate pH-6; Pressure cooker | 30 minutes, RT | | GFAP | Dako, Denmark | Polyclonal | 1:500 | Proteinase K-5 minutes | 1 hour, RT |
|
| Abbreviations: SMA - Smooth muscle actin; GFAP - Glial fibrillary acidic protein; RT - room temperature | | | Table 2.: Analysis of mammary lesions in various breeds of dogs.
| | Type of dog breeds | Incidence | Type of lesions | | No. | Percent | Hyperplasia/Dysplasia | Benign neoplasm | Malignant neoplasm | | Pomeranian | 22 | 22.68 | 4 | 2 | 16 | | Mongrel | 21 | 21.65 | 5 | 1 | 15 | | German Shepherd | 19 | 19.59 | 5 | 2 | 12 | | Labrador | 15 | 15.47 | 1 | 3 | 11 | | Spitz | 6 | 6.19 | 1 | 2 | 3 | | Great Dane | 4 | 4.12 | - | - | 4 | | Doberman | 4 | 4.12 | - | - | 4 | | Dachshund | 2 | 2.06 | - | - | 2 | | Golden retriever | 1 | 1.03 | - | 1 | - | | Boxer | 1 | 1.03 | - | - | 1 | | Saint Bernard | 1 | 1.03 | - | - | 1 | | Lhasa Apso | 1 | 1.03 | - | - | 1 | | Total | 97 | 100.00 | 16 | 11 | 70 |
| | | Table 3.: Histological classification of canine mammary hyperplasia/dysplasia, benign and malignant tumours.
| | Type of Proliferation | No. | Percent | | Hyperplasia/dysplasia | | | | Duct Ectasia | 6 | 6.19 | | Lobular Hyperplasia - Regular | 1 | 1.03 | | Lobular Hyperplasia with Fibrosis | 5 | 5.15 | | Lobular Hyperplasia with Secretory Activity | 2 | 2.06 | | Epitheliosis | 2 | 2.06 | | Total (A) | 16 | 16.49 | | Benign neoplasms | | | | Intraductal Papillary Adenoma | 3 | 3.09 | | Fibroadenoma | 2 | 2.06 | | Complex Adenoma | 1 | 1.03 | | Benign Mixed Tumour | 1 | 1.03 | | Lipoma | 4 | 4.12 | | Total (B) | 11 | 11.34 | | Malignant neoplasms | | | | Carcinoma - Tubular | 5 | 5.15 | | Carcinoma - Tubulopapillary | 8 | 8.25 | | Carcinoma - Cystic Papillary | 1 | 1.03 | | Carcinoma-Micropapillary Invasive | 1 | 1.03 | | Carcinoma - Solid | 7 | 7.22 | | Comedocarcinoma | 1 | 1.03 | | Carcinoma - Anaplastic | 2 | 2.06 | | Carcinoma-complex type | 3 | 3.09 | | Carcinoma and Malignant Myoepithelioma | 7 | 7.22 | | Carcinoma - Mixed Type | 12 | 12.37 | | Ductal Carcinoma | 5 | 5.15 | | Intraductal papillary carcinoma | 1 | 1.03 | | Squamous Cell Carcinoma | 1 | 1.03 | | Adenosquamous Carcinoma | 3 | 3.09 | | Malignant Myoepithelioma | 2 | 2.06 | | Osteosarcoma | 3 | 3.09 | | Fibrosarcoma | 4 | 4.12 | | Liposarcoma | 1 | 1.03 | | Carcinosarcoma | 3 | 3.09 | | Total (C) | 70 | 72.76 | | Grand total (A+B+C) | 97 | 100.00 |
| |
|