Mammary Neoplasia Research Articles

Effect of neutering timing in relation to puberty on health in the female dog-a scoping review.

Effects of neutering on bitch health have been reported, and are suggested to relate to bitch age at the time of neutering for some diseases. However, variation between published studies in terms of study populations and methodologies makes comparison and consolidation of the evidence difficult. A scoping review was designed to systematically search the available literature to identify and chart the evidence on the effect of neutering timing in relation to puberty on five health outcomes: atopy, developmental orthopaedic disease (DOD), neoplasia, obesity and urogenital disease. A protocol was registered, and literature searches were conducted in CAB Abstracts, Medline and Web of Science. Studies were reviewed against inclusion criteria. Data on study and population characteristics and health outcomes were charted for the final included studies. A total of 1,145 publications were reviewed across all five searches; 33 were retained for inclusion and charting. Only six of the 33 studies categorised the timing of surgical neutering as prepubertal or post-pubertal; one investigating mammary neoplasia and the other five, urogenital disease, commonly urinary incontinence. No studies were identified that examined the impacts of neutering bitches before or after puberty on atopy, DOD or obesity. One study considered bitches that were pre or post-pubertal at the time of the first treatment with deslorelin acetate for oestrus suppression and 26 examined the effects on health related to age, rather than pubertal status, at neutering. This scoping review suggests that robust evidence to support veterinarians, those working with dogs and dog owners when discussing the timing of neutering relative to puberty does not yet exist. The impact of neutering before or after puberty on atopy, DOD, neoplasia, obesity and urogenital disease in female domesticated dogs remains unclear.

A REVIEW OF NEOPLASIA IN PROSIMIANS IN HUMAN CARE FROM 1995 TO 2022.

This retrospective study of neoplasia in prosimians in human care reports histologically diagnosed cases from the archives of a nondomestic species pathology service between 1995 and 2022, primarily submitted from zoological institutions. To date, the only prior retrospective study of neoplasia in prosimians, published in 2009, was conducted with cases from a single institution specializing in prosimian noninvasive research and care. In the present study, a total of 153 neoplasms from 109 individuals were identified in the pathology service archives. The most commonly affected species belonged to the Lemuridae (92/109, 84.4%), particularly ring-tailed lemurs (Lemur catta; 55/109, 50.5%), black-and-white ruffed lemurs (Varecia variegata; 19/109, 17.4%), and red ruffed lemurs (Varecia rubra; 14/109, 12.8%). The digestive (49/153, 32.0%), reproductive (35/153, 22.9%), and integumentary (30/153, 19.6%) systems were most commonly affected. Hepatocellular neoplasia was the most common neoplasm overall (35/153, 22.9%), with a large proportion of hepatocellular carcinoma (23/35, 65.7%), suggesting a possible predisposition to this tumor in prosimians. The findings support aggressive behavior of these tumors in prosimians, and a majority (13/23, 56.5%) of cases had evidence of metastasis at the time of submission. Mammary neoplasia was also common (25/153, 16.3%) and predominantly malignant (18/25, 72.0%), in contrast with previous literature, although metastasis was uncommonly reported. The most common integumentary neoplasms were papillomas (12/30, 40.0%), and one report identified squamous cell carcinoma arising directly from a squamous papilloma. Several tumor types are reported herein for the first time in prosimian species, to the authors' knowledge. A literature review identifying additional cases reported since 2009 is also reported. This study contributes a large number of prosimian neoplasia cases to the existing literature to help determine trends in zoological collections and to inform captive prosimian health management.

E-cadherin staining in the diagnosis of lobular versus ductal neoplasms of the breast: the emperor has no clothes.

Categorizing breast neoplasia as ductal or lobular is a daily exercise that relies on a combination of histologic and immunohistochemical tools. The historically robust link between loss of the E-cadherin molecule and lobular neoplasia has rendered staining for E-cadherin by immunohistochemistry a staple of this diagnostic process. Unfortunately, discordances between E-cadherin expression and histomorphology, and variations in E-cadherin staining patterns and intensities abound in clinical practice, but are often neglected in favour of a binary interpretation of the E-cadherin result. In this article, we highlight the complexities of E-cadherin expression through a review of the E-cadherin protein and its associated gene (CDH1), the mechanisms leading to aberrant/absent E-cadherin expression, and the implications of these factors on the reliability of the E-cadherin immunohistochemical stain in the classification of ductal versus lobular mammary neoplasia.

Serum Extracellular Vesicles Cargo Approach in Bitches with Mammary Tumors.

This study investigated serum extracellular vesicles (EVs) in bitches with mammary neoplasms, in order to understand their size, shape, and concentration, as well as their association with tumor malignancy. Thirty bitches were categorized into control (n = 10), mammary tumor grades I and II (GI, n = 13), and grade III (GII, n = 7). Serum was separated from blood collected during mastectomy, and EVs were isolated using size exclusion chromatography. The analysis revealed no significant differences in EV concentrations among groups, with similar concentrations for control, GI, and GII. Ninety-one proteins were identified in EV-enriched samples, with six showing varied abundance across groups. Notably, keratin 18 was highly abundant in GI, while sushi domain-containing protein, EvC ciliary subunit 2, and the joining chain of multimeric IgM and IgA were increased in GII. Additionally, protocadherin 17 and albumin were upregulated in both GI and GII. ROC curves identified potential biomarkers for differentiating tumor grades. Enrichment pathway analysis revealed AFP gene upregulation in the GI. Mass spectrometry proteomics data were deposited in Mendeley Data. The study provides valuable insights into serum EV characterization in bitches, suggesting keratin 18 and protocadherin 17 as potential biomarkers for canine mammary neoplasia, with implications for future diagnostic and therapeutic strategies.

Identification of New Chemoresistance-Associated Genes in Triple-Negative Breast Cancer by Single-Cell Transcriptomic Analysis.

Triple-negative breast cancer (TNBC) is a particularly aggressive mammary neoplasia with a high fatality rate, mainly because of the development of resistance to administered chemotherapy, the standard treatment for this disease. In this study, we employ both bulk RNA-sequencing and single-cell RNA-sequencing (scRNA-seq) to investigate the transcriptional landscape of TNBC cells cultured in two-dimensional monolayers or three-dimensional spheroids, before and after developing resistance to the chemotherapeutic agents paclitaxel and doxorubicin. Our findings reveal significant transcriptional heterogeneity within the TNBC cell populations, with the scRNA-seq identifying rare subsets of cells that express resistance-associated genes not detected by the bulk RNA-seq. Furthermore, we observe a partial shift towards a highly mesenchymal phenotype in chemoresistant cells, suggesting the epithelial-to-mesenchymal transition (EMT) as a prevalent mechanism of resistance in subgroups of these cells. These insights highlight potential therapeutic targets, such as the PDGF signaling pathway mediating EMT, which could be exploited in this setting. Our study underscores the importance of single-cell approaches in understanding tumor heterogeneity and developing more effective, personalized treatment strategies to overcome chemoresistance in TNBC.

Ozone Therapy in the Integrated Treatment of Female Dogs with Mammary Cancer: Oxidative Profile and Quality of Life.

Considering the high frequency of malignant breast tumors, there is a growing search for new therapeutic strategies that control neoplastic growth and dissemination, combined with fewer adverse reactions. Therefore, this study evaluated the effects of ozone therapy in female dogs with mammary cancer undergoing chemotherapy treatment. Twenty-five canines diagnosed with malignant mammary neoplasia were divided into two groups: one treated with carboplatin alone (n = 11) and the other with carboplatin associated with ozone therapy (n = 14). Clinical and laboratory evaluations, mastectomy, analysis of the oxidative profile based on total antioxidant capacity (TAC) and serum concentrations of malondialdehyde (MDA), survival rate, and quality of life were performed. Animals in the ozone therapy group had higher concentrations of red blood cells and platelets, significantly improving the survival rate and quality of life. Furthermore, adverse reactions were less intense and frequent in this group, which was associated with an increase in TAC and a reduction in MDA. These results indicate that the combination of carboplatin and ozone therapy represents a promising complementary treatment for female dogs with mammary cancer, as it was associated with fewer adverse reactions and a better oxidative profile.

Epigenetic activation of SOX11 is associated with recurrence and progression of ductal carcinoma in situ to invasive breast cancer.

Risk of recurrence and progression of ductal carcinoma in situ (DCIS) to invasive cancer remains uncertain, emphasizing the need for developing predictive biomarkers of aggressive DCIS. Human cell lines and mouse models of disease progression were analyzed for candidate risk predictive biomarkers identified and validated in two independent DCIS cohorts. RNA profiling of normal mammary and DCIS tissues (n = 48) revealed that elevated SOX11 expression correlates with MKI67, EZH2, and DCIS recurrence score. The 21T human cell line model of DCIS progression to invasive cancer and two mouse models developing mammary intraepithelial neoplasia confirmed the findings. AKT activation correlated with chromatin accessibility and EZH2 enrichment upregulating SOX11 expression. AKT and HER2 inhibitors decreased SOX11 expression along with diminished mammosphere formation. SOX11 was upregulated in HER2+ and basal-like subtypes (P < 0.001). Longitudinal DCIS cohort (n = 194) revealed shorter recurrence-free survival in SOX11+ than SOX11- patients (P = 0.0056 in all DCIS; P < 0.0001 in HER2+ subtype) associated with increased risk of ipsilateral breast event/IBE (HR = 1.9, 95%CI = 1.2-2.9; P = 0.003). Epigenetic activation of SOX11 drives recurrence of DCIS and progression to invasive cancer, suggesting SOX11 as a predictive biomarker of IBE.

Mammary neoplasms infemale dogs: Clinical, diagnostic and therapeutic aspects.

With the increase inthe life expectancy ofdomestic animals and their increasingly affectionate relationship with their owners, itis possible toobserve anincrease incases ofneoplasms inthese animals. Mammary neoplasia mainly affects older females who have not been castrated, due tohormonal dependence for thedevelopment ofthe tumour. The main form oftreatment issurgery. This study aims tocarry out anupdated review onmammary neoplasms infemale dogs covering the anatomy, physiology, prevalence, causes, diagnoses, treatments, prevention and prognosis, based onscientific articles byrenowned researchers.

Estrogen receptors alpha and beta expression in different canine cancer types with an emphasis on hematopoietic malignancies.

Estrogen receptors (ERs) are located in both healthy and neoplastic tissues. The type of estrogen receptor expressed varies depending on its location, tumor type, and species. Estrogen action is mediated by binding to ER and activating the transcriptional and signaling processes that result in the control of gene expression. There are two main types of estrogen receptors: ER alpha (ERα) and ER beta (ERβ). Both receptors are functionally different, they may act antagonistically and are distributed in different tissues but their structure is similar - as they are composed of 5 different domains: A/B, C, D, E, and F. The signaling pathway and hence regulation of the gene expression by ERs is a complex and multifactorial process that involves both genomic and nongenomic actions. In the human reproductive tract, both ERα and β are present, with predominant expression of ERβ, while there are no satisfactory data distinguishing the type of ERs expressed in the canine reproductive tract. In mammary gland neoplasia, a decreased or lacking ERα expression in humans is associated with a poorer prognosis. This is similar to dogs, where higher ERα expression intensity was noted in benign tumors than in carcinomas. In human hematopoietic malignancies, ERβ is a predominant receptor. Selective and non-selective ERβ agonists have an antiproliferative and pro-apoptotic effect on human lymphoma cell lines and may be effective in the therapy of ERβ positive lymphomas and leukemias. In canine lymphoma tissues, none or only marginal expression of ERs was detected over the decades. Considering available data, we conducted preliminary studies proving that, in contrast to humans, the dominant ER expressed in canine hematopoietic tumors is ERα.

Different Oncogenes and Reproductive Histories Shape the Progression of Distinct Premalignant Clones in Multistage Mouse Breast Cancer Models

A remote carcinogen exposure can predispose to breast cancer onset decades later, suggesting carcinogen-induced mutations generate long-lived premalignant clones. How subsequent events influence the progression of specific premalignant clones remains poorly understood. Here, we generated multistage mouse models of mammary carcinogenesis by combining chemical carcinogen exposure (using 7,12-dimethylbenzanthracene, DMBA) with transgenes that enable inducible expression of one of two clinically relevant mammary oncogenes: c-MYC (MYC) or PIK3CAH1047R (PIK). In prior work, DMBA exposure generated mammary clones bearing signature HrasQ61L mutations, which only progressed to mammary cancer after inducible Wnt1 oncogene expression. Here, after an identical DMBA exposure, MYC versus PIK drove cancer progression from mammary clones bearing mutations in distinct Ras family paralogs. For example, MYC drove cancer progression from either Kras- or Nras-mutant clones, whereas PIK transformed Kras-mutant clones only. These Ras mutation patterns were maintained whether oncogenic transgenes were induced within days of DMBA exposure or months later. Completing a full-term pregnancy (parity) failed to protect against either MYC- or PIK-driven tumor progression. Instead, a postpartum increase in mammary tumor predisposition was observed in the context of PIK-driven progression. However, parity decreased the overall prevalence of tumors bearing Krasmut, and the magnitude of this decrease depended on both the number and timing of pregnancies. These multistage models may be useful for elucidating biological features of premalignant mammary neoplasia.

Genistein Supplementation and Bone Health in Breast Cancer in Rats.

The aim of our study was to analyse the effect of supplementation with various forms of genistein (nano-, micro-, and macro-) on the mineral status of rat femurs in conditions of DMBA-induced mammary gland neoplasia. Thirty-two 30-day-old Sprague Dawley rats were used in the study. The rats were divided into four experimental groups: a control group (without supplementation) and groups supplemented with nanosized (92 ± 41 nm), microsized (587 ± 83 nm), and macrosized genistein. Micromorphometric and histological examination of the rat femurs were performed, as well as analysis of the weight and mineral composition (17 elements). Quadrupole ICP-MS was used for analysis of all trace elements. Supplementation with genistein (nano-, micro-, and macro-) was shown to cause changes in the mineral composition of the bones. In the rats receiving nanogenistein, disintegration of the bone tissue was observed. The femurs of these animals had higher content of calcium (by nearly 300%) and potassium (by 25%) than the other groups, while the level of magnesium was about 22% lower. In the case of microelements, there were increases in copper (by 67%), boron (48%), manganese (13%), and nickel (100%), and a 16% decrease in strontium compared to the bones of rats without genistein supplementation. Changes in micromorphometric parameters, resulting in increased bone fragility, were observed. Administration of genistein was found to have an effect on the amount of trace elements in the bone tissue of rats with breast cancer.

Inflammation Factors and Genistein Supplementation in Cancer-Preliminary Research.

The purpose of this study was to evaluate the effect of genistein in nano, micro, and macro forms on the intensity of the DMBA-induced tumor process in rats and to understand the mechanisms of this action. The effect of genistein supplementation on the content of selected eicosanoids (HETEs, HODE, and HEPE) in the serum of rats was evaluated. The levels and expression of genes encoding various pro-inflammatory cytokines (IL-1, IL-6) and MMP-9 in the blood of rats were also investigated. The biological material for the study was blood obtained from female rats of the Sprague Dawley strain (n = 32). The animals were randomly divided into four groups: animals without supplementation, and animals supplemented at a dose of 0.2 mg/kg b.w. (0.1 mg/mL) with macro, micro (587 ± 83 nm), or nano (92 ± 41 nm) genistein. To induce mammary neoplasia (adenocarcinoma), rats were given 7,12-dimethyl-1,2-benz[a]anthracene (DMBA). The content of selected eicosanoids was determined by liquid chromatography with UV detection. An immunoenzymatic method was used to determine the content of cytokines and MMP-9. The expression of the IL-6, IL-1beta, and MMP-9 genes was determined with quantitative real-time PCR (qRT-PCR) using TaqMan probes. Based on the study, it was shown that supplementation of animals with genistein in macro, micro, and nano forms increased the intensity of the tumor process in rats. It was shown that the content of 12-HEPE, HODE, and 12-HETE in the serum of genistein-supplemented rats was statistically significantly lower with respect to the content of the aforementioned markers in the serum of rats receiving only a standard diet, devoid of supplementation. It was found that animals supplemented with nano-, micro-, and macrogenistein had higher levels of metalloproteinase-9, MMP-9, compared to animals without supplementation. There was a significant increase in MMP-9 gene expression in the blood of macrogenistein-supplemented animals, relative to the other groups of rats. On the basis of the study, it was shown that supplementation of animals with nano-, micro-, and macrogenistein had an effect on the development of the tumor process. Dietary supplementation with genistein significantly decreased the level of selected eicosanoids, which may have significant impacts on cancer development and progression.

Programmed Death-Ligand (PD-L1), Epidermal Growth Factor (EGF), Relaxin, and Matrix Metalloproteinase-3 (MMP3): Potential Biomarkers of Malignancy in Canine Mammary Neoplasia.

Gene expression has been suggested as a putative tool for prognosis and diagnosis in canine mammary neoplasia (CMNs). In the present study, 58 formalin-fixed paraffin-embedded (FFPE) paraffined canine mammary neoplasias from 27 different bitches were included. Thirty-seven tumours were classified as benign, whereas thirty-one were classified as different types of canine carcinoma. In addition, mammary samples from three healthy bitches were also included. The gene expression for vascular endothelial growth factor-α (VEGFα), CD20, progesterone receptor (PGR), hyaluronidase-1 (HYAL-1), programmed death-ligand 1 (PD-L1), epidermal growth factor (EGF), relaxin (RLN2), and matrix metalloproteinase-3 (MMP3) was assessed through RT-qPCR. All the assessed genes yielded a higher expression in neoplastic mammary tissue than in healthy tissue. All the evaluated genes were overexpressed in neoplastic mammary tissue, suggesting a role in the process of tumorigenesis. Moreover, PD-L1, EGF, relaxin, and MMP3 were significantly overexpressed in malignant CMNs compared to benign CMNs, suggesting they may be useful as malignancy biomarkers.

Comparison of the Serum Protein Electrophoretic Pattern and Concentrations of Acute Phase Proteins in Bitches with and Without Mammary Gland Tumors

Abstract Alterations in the serum protein pattern may be associated with many diseases, including neoplastic processes. In veterinary medicine, these changes are poorly understood. Therefore, this study was aimed at the analysis of the distribution of blood serum protein fractions separated by agarose gel electrophoresis, and at the determination of the concentrations of main acute phase proteins in bitches with mammary gland neoplasia. The evaluation was conducted on twelve female dogs with palpable single or multiple nodules in the parenchyma of the mammary gland and on ten tumor-free clinically healthy bitches to compare the possible differences in the obtained results. Blood serum was used to perform agarose gel electrophoresis of the main blood serum protein fractions and to analyze the concentrations of total serum proteins and the following canine acute phase proteins: serum amyloid A, haptoglobin, C-reactive protein and α1-acid glycoprotein. The concentrations of total serum proteins were slightly higher in bitches with mammary gland tumors. Serum protein electrophoresis showed lower mean concentrations of albumin and α1-globulins in the affected dogs, while the concentrations of α2-and β1-globulins were significantly higher (P=0.0032 and P=0.0021, respectively) compared to dogs without mammary gland tumors. In the concentrations of acute phase proteins, significantly higher mean concentrations of C-reactive protein and haptoglobin were obtained in dogs with mammary tumors (P=0.0025 and P=0.0002, respectively). The values of α1-acid glycoprotein did not vary markedly between the bitches with and without mammary tumors. Presented data suggest that neoplastic processes in the mammary gland may also alter the electrophoretic pattern of blood serum proteins and induce changes in the production of some inflammatory proteins.

Molecular Action of Tamoxifen in the Ovaries of Rats with Mammary Neoplasia

Tamoxifen (TAM) is a drug commonly used in patients with breast cancer. The anticancer effect of TAM occurs via its ability to antagonize estrogen-dependent growth of mammary epithelial cells. Previously, we demonstrated that TAM prevented the chemotherapy-induced loss of ovarian follicular reserves in both cancer-free rats and rats with cancer. Such follicular loss is a main cause of infertility in young women treated for cancer. The current study was undertaken to discover the molecules and intracellular pathways involved in the action of TAM in the ovaries of rats with mammary tumors. To meet this goal we used transcriptomic (RNA-Seq) and proteomic (2D-DIGE/MS) approaches. TAM inhibited the expression of genes and lncRNAs involved in ovarian steroidogenesis. Moreover, TAM altered the expression of genes related to primordial follicle activation or arrest. In addition, proteomic screening indicated the importance of basic metabolic processes in the ovarian actions of TAM. Although simple extrapolation of these data to humans is not possible, the results of this study emphasize the need to explore the ability of TAM to affect ovarian function in women undergoing cancer treatment.

PROSPECTIVE POSTMORTEM ASSESSMENT OF THE INCIDENCE OF MAMMARY NEOPLASIA IN CHIMPANZEES (PAN TROGLODYTES).

When evaluating the last 25 yr of morbidity and mortality from adult chimpanzees managed within the Association of Zoo and Aquarium Chimpanzee Species Survival Plan® for North American zoos, only two female chimpanzees were diagnosed with mammary neoplasia: one incidentally antemortem and one with a terminal metastatic neoplasia. When comparing this observation of prevalence of mammary neoplasia to humans, a substantial disparity is apparent. Mammary neoplasia is the second most common cancer in adult female humans, with a lifetime risk of 1:8 in the United States. The reason for the disparity between humans and chimpanzees, as closely related species, is unknown. The true prevalence in chimpanzees may be higher than currently noted, because routine examination of mammary tissue in chimpanzees is generally less complete than for other tissues postmortem, and antemortem assessment is generally limited to mammary palpation. This study was performed on intact, bilateral mammary glands harvested at postmortem examination of adult female chimpanzees (n = 7) from six institutions. With mammography, complete histopathologic sectioning, and genetic evaluation, the risk of mammary neoplasia was evaluated more thoroughly than during a typical postmortem exam in zoo populations during 2017-2019. No chimpanzees in the study were diagnosed with mammary neoplasia. Overall, this study supports the previous impression that chimpanzees do not develop mammary neoplasia at a similar rate as humans, even when comparable diagnostic modalities for evaluation are used.

ERCC6L facilitates the onset of mammary neoplasia and promotes the high malignance of breast cancer by accelerating the cell cycle

BackgroundBreast cancer (BC) is the leading cause of morbidity and the second leading cause of death among female malignant tumors. Although available drugs have been approved for the corresponding breast cancer subtypes (ER-positive, HER2+) currently, there are still no effective targeted drugs or treatment strategies for metastatic breast cancer or triple-negative breast cancer that lack targets. Therefore, it is urgent to discover new potential targets. ERCC6L is an essential protein involved in chromosome separation during cell mitosis. However, the effect of ERCC6L on the tumorigenesis and progression of breast cancer is unclear.Methods and resultsHere, we found that ERCC6L was highly expressed in breast cancer, especially in TNBC, which was closely related to poor outcomes of patients. An ERCC6L conditional knockout mouse model was first established in this study, and the results confirmed that ERCC6L was required for the development of the mammary gland and the tumorigenesis and progression of mammary gland cancers. In in vitro cell culture, ERCC6L acted as a tumor promoter in the malignant progression of breast cancer cells. Overexpression of ERCC6L promoted cell proliferation, migration and invasion, while knockdown of ERCC6L caused the opposite results. Mechanistically, ERCC6L accelerated the cell cycle by regulating the G2/M checkpoint signalling pathway. Additionally, we demonstrated that there is an interaction between ERCC6L and KIF4A, both of which are closely related factors in mitosis and are involved in the malignant progression of breast cancer.ConclusionsWe first demonstrated that ERCC6L deficiency can significantly inhibit the occurrence and development of mammary gland tumors. ERCC6L was found to accelerate the cell cycle by regulating the p53/p21/CDK1/Cyclin B and PLK/CDC25C/CDK1/Cyclin B signalling pathways, thereby promoting the malignant progression of breast cancer cell lines. There was a direct interaction between KIF4A and ERCC6L, and both are closely associated with mitosis and contribute to growth and metastasis of breast tumor. To sum up, our results suggest that ERCC6L may be used as a promising target for the treatment of BC.

Canine Mammary Neoplasia Induces Variations in the Peripheral Blood Levels of CD20, CD45RA, and CD99.

The idea of using tumour biomarkers as diagnostic tools is progressively increasing. Of these, serum biomarkers are of particular interest, as they can provide rapid results. In the present study, serum samples from 26 bitches diagnosed with mammary tumours, plus 4 healthy bitches, were obtained. The samples were analysed using CD antibody microarrays targeting 90 CD surface markers and 56 cytokines/chemokines. A total of five CD proteins, namely CD20, CD45RA, CD53, CD59, and CD99, were selected and further analysed, utilizing immunoblotting techniques to validate the microarray results. CD45RA showed a significantly lower abundance in the serum samples from the bitches carrying mammary neoplasia in comparison to the healthy animals. Regarding CD99, the serum samples from the neoplastic bitches showed it in a significantly higher abundance than those from the healthy patients. Finally, CD20 showed a significantly higher abundance in bitches carrying a malignant mammary tumour in comparison to healthy patients, but no differential expression between malignant and benign tumours was observed. According to these results, both CD99 and CD45RA are indicators of mammary tumour presence, but without distinguishing between malignant and benign.

The prognostic significance of the activities of matrix metalloproteinases-2 and -9 in dogs for mammary gland neoplasia (pilot study)

The aim of this study was to determine the activity of matrix metalloproteinase-2 and -9 in blood and tumour tissue of female dogs with benign and malignant mammary gland neoplasias. The increased activity of matrix metalloproteinase-2 and -9 was registered in 3.8–8.9% of canines with benign neoplasias (adenoma, mixed tumour) and in 32.5–63.5% of those with malignant neoplasias (carcinoma: mixed type, ductal, tubular, tubulopapillary). Neoplastic transformation is accompanied by blood level increase of both latent and active enzyme forms. The dogs with malignant mammary gland neoplasias were diagnosed with credible increase of matrix metalloproteinases-2 activity up to 1.59–1.96 in blood plasma and up to 21.57–24.84 in tumour tissue and the increase of matrix metalloproteinases-9 activity up to 2.16–2.67 and 29.53–35.26 respectively. For benign mammary neoplasms, the proportion of dogs with enhanced expression of matrix metalloproteinase-2 was higher than the number of patients in whom an increase in the level of matrix metalloproteinase-9 or both of these enzymes was registered by 1.7 times, for dogs with malignant tumours – in blood plasma – by 1.4–1.6 times, dogs with neoplastic changed functional tissue – 1.7 and 1.9 times, respectively. Histological type and metastatic foci presence did not correlate with enzymes’ activity. The enzymes’ activity figures in benign neoplasias fluctuated within those in clinically healthy animals. A positive characteristic of determining the plasma and tissue expression level of matrix metalloproteinases in dogs with mammary tumours is the low degree of invasiveness of the method against the background of the high informativeness of the results obtained in the preoperative period. The obtained results prove the possibility of using matrix metalloproteinases-2 and -9 to predict the course and to control the treatment of mammary neoplasia.

Prevalence of affected breasts and histopathology of female dogs submitted to mastectomies in a private clinic in the city of Dourados, Mato Grosso

The increase in the life expectancy of dogs in response to the evolution of veterinary medicine regarding the prevention and treatment of diseases is remarkable. Likewise, the rise of pathologies that affect animals of advanced age is evident, such as mammary neoplasms, which affect mainly females, elderly, unspayed or noncastrated after several estrous cycles, without racial predisposition. This research aims to collect data from the analysis of clinical data and histopathological reports of female dogs treated in Dourados, Mato Grosso (Brazil) with mammary tumors. In this survey, it was observed that of 15 female dogs with mammary neoplasia, 87% had malignant neoplasia while 13% had benign neoplasia. The caudal abdominal breasts (M4) were the most affected. Tumor sizes varied between one and five centimeters in diameter, with tumors measuring up to three centimeters being the most recurrent, and the only two benign tumors measuring 1.5 cm. Thus, it is concluded that the caudal abdominal breasts (M4) were the most affected with breast neoplasms, malignant neoformations are the most common and neoplasms with benign conformations have smaller sizes.