scholarly journals Immune Cells and Immunoglobulin Expression in the Mammary Gland Tumors of Dog

Animals ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 1189
Author(s):  
Alessandra Sfacteria ◽  
Ettore Napoli ◽  
Claudia Rifici ◽  
Daria Commisso ◽  
Giada Giambrone ◽  
...  

Inflammatory cells have a role in tumor progression and have prognostic and therapeutic potential. The immunohistochemical expression for Mast Cell Tryptase, Macrophage Marker, CD79a, IgA, IgM and IgG on 43 cases of canine mammary gland lesions was analyzed. In hyperplasia, a few B cells (BCs) and Tumor-Associated Macrophages (TAMs) were observed, while the number of Tumor-Associated Mast Cells (TAMCs) was the highest. In the peritumoral stroma of malignant lesions, low number of TAMCs and a high number of TAMAs and BCs were present. Immune cells of each type were always lower in the intratumoral than peritumoral stroma. Positivity to CD79a was also detected in the epithelial cells of simple and micropapillay carcinomas. Immunoglobulin reactivity was mainly located in the epithelial cells where an intense positivity to IgA and IgG and a weak positivity for IgM were detectable. On the basis of our preliminary results and literature data, we suggest that such cells and molecules could be directly involved in the biology of canine mammary gland tumors. In breast cancer, stromal inflammatory cells and cancer derived immunoglobulins have been correlated with the progression, malignancy and poor prognosis of the tumor. The results herein reported show that the dog’s mammary gland epithelium also expresses immunoglobulins, and they mostly show a direct relationship with the infiltration of macrophages. In addition, this study shows that the infiltration of mast cells, B-cells and macrophages varies depending on the degree of malignancy of neoplasia.

2015 ◽  
Vol 77 (11) ◽  
pp. 1465-1471
Author(s):  
Huanan WANG ◽  
Xu YANG ◽  
Yipeng JIN ◽  
Shimin PEI ◽  
Di ZHANG ◽  
...  

2018 ◽  
Vol 55 (4) ◽  
pp. 597-597
Author(s):  
Sara Belluco

The article “CD204-Expressing Tumor-Associated Macrophages Are Associated With Malignant, High-Grade, and Hormone Receptor–Negative Canine Mammary Gland Tumors” does not provide evidence that CD204 is a marker for M2 macrophages.


2019 ◽  
Vol 6 (1) ◽  
Author(s):  
Ka-Kyung Kim ◽  
Byung-Joon Seung ◽  
Dohyun Kim ◽  
Hee-Myung Park ◽  
Sejoon Lee ◽  
...  

2012 ◽  
Vol 74 (2) ◽  
pp. 227-230 ◽  
Author(s):  
Kohei SAEKI ◽  
Yoshifumi ENDO ◽  
Kazuyuki UCHIDA ◽  
Ryohei NISHIMURA ◽  
Nobuo SASAKI ◽  
...  

Diagnostics ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 104 ◽  
Author(s):  
Faiz Muhammad Khand ◽  
Da-Wei Yao ◽  
Pan Hao ◽  
Xin-Qi Wu ◽  
Asghar Ali Kamboh ◽  
...  

Early diagnosis of mammary gland tumors is a challenging task in animals, especially in unspayed dogs. Hence, this study investigated the role of microsatellite instability (MSI), MMR gene mRNA transcript levels and SNPs of MMR genes in canine mammary gland tumors (CMT). A total of 77 microsatellite (MS) markers in 23 primary CMT were selected from four breeds of dogs. The results revealed that 11 out of 77 MS markers were unstable and showed MSI in all the tumors (at least at one locus), while the other markers were stable. Compared to the other markers, the ABC9TETRA, MEPIA, 9A5, SCNA11 and FJL25 markers showed higher frequencies of instability. All CMT demonstrated MSI, with eight tumors presenting MSI-H. The RT-qPCR results revealed significant upregulation of the mRNA levels of cMSH3, cMLH1, and cPMSI, but downregulation of cMSH2 compared to the levels in the control group. Moreover, single nucleotide polymorphisms (SNPs) were observed in the cMSH2 gene in four exons, i.e., 2, 6, 15, and 16. In conclusion, MSI, overexpression of MMR genes and SNPs in the MMR gene are associated with CMT and could be served as diagnostic biomarkers for CMT in the future.


Endocrinology ◽  
2016 ◽  
Vol 157 (7) ◽  
pp. 2750-2758 ◽  
Author(s):  
Duangjai Rieanrakwong ◽  
Titaree Laoharatchatathanin ◽  
Ryota Terashima ◽  
Tomohiro Yonezawa ◽  
Shiro Kurusu ◽  
...  

It has been demonstrated that mammary gland involution after lactation is initiated by accumulation of milk in alveoli after weaning. Here, we report that involution is also dependent on mammary GnRH expression that is suppressed by PRL during lactation. Reduction of plasma prolactin (PRL) by the withdrawal of suckling stimuli increased GnRH and annexin A5 (ANXA5) expression in the mammary tissues after lactation with augmentation of epithelial apoptosis. Intramammary injection of a GnRH antagonist suppressed ANXA5 expression and apoptosis of epithelial cells after forcible weaning at midlactation, whereas local administration of GnRH agonist (GnRHa) caused apoptosis of epithelial cells with ANXA5 augmentation in lactating rats. The latter treatment also decreased mammary weight, milk production, and casein accumulation. Mammary mast cells were strongly immunopositive for GnRH and the number increased in the mammary tissues after weaning. GnRHa was shown to be a chemoattractant for mast cells by mammary local administration of GnRHa and Boyden chamber assay. PRL suppressed the mammary expression of both ANXA5 and GnRH mRNA. It also decreased mast cell numbers in the gland after lactation. These results are the first to demonstrate that GnRH, synthesized locally in the mammary tissues, is required for mammary involution after lactation. GnRH is also suggested to introduce mast cells into the regressing mammary gland and would be in favor of tissue remodeling. The suppression of these processes by PRL is a novel physiological function of PRL.


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