Mast cells and eosinophilic leukocytes in the formation of mammary gland tumors in female rats irradiated with ? rays at the age of 4 weeks

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

Animals ◽

10.3390/ani11051189 ◽

2021 ◽

Vol 11 (5) ◽

pp. 1189

Author(s):

Alessandra Sfacteria ◽

Ettore Napoli ◽

Claudia Rifici ◽

Daria Commisso ◽

Giada Giambrone ◽

...

Keyword(s):

Mammary Gland ◽

B Cells ◽

Mast Cells ◽

Epithelial Cells ◽

Immune Cells ◽

Therapeutic Potential ◽

Inflammatory Cells ◽

Mammary Gland Tumors ◽

Peritumoral Stroma ◽

Canine Mammary Gland

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.

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The effect of bromocriptine on mammary-gland ultrastructure of hyperprolactinemic rats

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100111136 ◽

1984 ◽

Vol 42 ◽

pp. 204-205

Author(s):

I.C. Murray

Keyword(s):

Mammary Gland ◽

Dopamine Agonist ◽

Alveolar Epithelium ◽

Mammary Glands ◽

Female Rats ◽

Control Group ◽

Cell Hyperplasia ◽

Once Daily ◽

Long Evans

In women, hyperprolactinemia is often due to a prolactin (PRL)-secreting adenoma or PRL cell hyperplasia. RRL excess stimulates the mammary glands and causes proliferation of the alveolar epithelium. Bromocriptine, a dopamine agonist, inhibits PRL secretion and is given to women to treat nonpuerperal galactorrhea. Old female rats have been reported to have PRL cell hyperplasia or adenoma leading to PRL hypersecretion and breast stimulation. Herein, we describe the effect of bromocriptine and consequently the reduction in serum PRL levels on the ultrastructure of rat mammary glands.Female Long-Evans rats, 23 months of age, were divided into control and bromocriptine-treated groups. The control animals were injected subcutaneously once daily with a 10% ethanol vehicle and were later divided into a normoprolactinemic control group with serum PRL levels under 30 ng/ml and a hyperprolactinemic control group with serum PRL levels above 30 ng/ml.

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Ultrastructural Changes in the Mammary Epithelial Cell Population During Neoplastic Development Induced by A Chemical Carcinogen.

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100091238 ◽

1976 ◽

Vol 34 ◽

pp. 250-251 ◽

Cited By ~ 2

Author(s):

J. Russo ◽

W. Isenberg ◽

M. Ireland ◽

I.H. Russo

Keyword(s):

Mammary Gland ◽

Cell Population ◽

Virgin Female ◽

Histological Change ◽

Mammary Epithelial ◽

Female Rats ◽

Ultrastructural Changes ◽

Post Inoculation ◽

Chemical Carcinogen ◽

Sprague Dawley

The induction of rat mammary carcinoma by the chemical carcinogen DMBA is used as a model for the study of the human disease (1). We previously described the histochemical changes that occur in the mammary gland of DMBA treated animals before the earliest manifested histological change, the intraductal proliferation (IDP), was observed (2). In the present work, we demonstrate that a change in the stable cell population found in the resting mammary gland occurs after carcinogen administration.Fifty-five day old Sprague-Dawley virgin female rats were inoculated intragastrically with 20mg of 7,12-dimethylbenz(a)anthracene (DMBA) in 1ml sesame oil. Non-inoculated, age-matched females were used as controls. Mammary glands from control and inoculated rats were removed weekly from the time of inoculation until 60 days post-inoculation. For electron microscopy, the glands were immersed in Karnovsky's fixative, post-fixed in 1% OsO4, dehydrated, and embedded in an Epon-Araldite mixture. Thick (lμ) sections were stained with 1% toluidine blue and were used for selecting areas for ultrastructural study.

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US EPA's regulatory pesticide evaluations need clearer guidelines for considering mammary gland tumors and other mammary gland effects

Molecular and Cellular Endocrinology ◽

10.1016/j.mce.2020.110927 ◽

2020 ◽

Vol 518 ◽

pp. 110927 ◽

Cited By ~ 2

Author(s):

Bethsaida Cardona ◽

Ruthann A. Rudel

Keyword(s):

Mammary Gland ◽

Mammary Gland Tumors

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Systemic Polyomavirus Genome Increase and Dissemination of Capsid-Defective Genomes in Mammary Gland Tumor-Bearing Mice

Journal of Virology ◽

10.1128/jvi.74.15.6975-6983.2000 ◽

2000 ◽

Vol 74 (15) ◽

pp. 6975-6983 ◽

Cited By ~ 4

Author(s):

Julie J. Wirth ◽

Li Chen ◽

Michele M. Fluck

Keyword(s):

Mammary Gland ◽

Viral Genome ◽

Wild Type Strain ◽

Neonatal Infection ◽

Wild Type ◽

Coding Region ◽

Live Virus ◽

Viral Genomes ◽

Mammary Gland Tumors ◽

Low Levels

ABSTRACT BALB/c mice that developed tumors 7 to 8 months following neonatal infection by polyomavirus (PYV) wild-type strain A2 were characterized with respect to the abundance and integrity of the viral genome in the tumors and in 12 nontumorous organs. These patterns were compared to those found in tumor-free mice infected in parallel. Six mice were analyzed in detail including four sibling females with mammary gland tumors. In four of five mammary gland tumors, the viral genome had undergone a unique deletion and/or rearrangement. Three tumor-resident genomes with an apparently intact large T coding region were present in abundant levels in an unintegrated state. Two of these had undergone deletions and rearrangements involving the capsid genes and therefore lacked the capacity to produce live virus. In the comparative organ survey, the tumors harboring replication-competent genomes contained by far the highest levels of genomes of any tissue. However, the levels of PYV genomes in other organs were elevated by up to 1 to 2 orders of magnitude compared to those detected in the same organs of tumor-free mice. The genomes found in the nontumorous organs had the same rearrangements as the genomes residing in the tumors. The original wild-type genome was detected at low levels in a few organs, particularly in the kidneys. The data indicate that a systemic increase in the level of viral genomes occurred in conjunction with the induction of tumors by PYV. The results suggest two novel hypotheses: (i) that genomes may spread from the tumors to the usual PYV target tissues and (ii) that this dissemination may take place in the absence of capsids, providing an important path for a virus to escape from the immune response. This situation may offer a useful model for the spread of HPV accompanying HPV-induced oncogenesis.

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