Mammary Tumors in Mice Following Transplantation of Mammary Tissue

1946 ◽  
Keyword(s):  
Mammary Tumors ◽  
Mammary Tissue

scholarly journals FAMILIAL MAMMARY TUMORS IN THE RABBIT

1939 ◽  
Vol 70 (2) ◽  
pp. 167-184 ◽  
Author(s):  
Harry S. N. Greene
Keyword(s):  
Mammary Tumors ◽  
Mammary Tissue ◽  
Tumor Type ◽  
Natural Classification ◽  
Tumor Bearing ◽  
Clinically Normal ◽  
Experimental Induction ◽  
Papillary Structure ◽  
Natural Counterpart

The clinical and pathological course of 25 mammary tumors in rabbits has been described. The antecedent breast history and morphology of the growths allowed a natural classification into two distinct types, one of which was distinguished by a preexisting cystic mastitis and a papillary structure, while the other originated in clinically normal mammary tissue and was characterized by an adenomatous structure. The two types of neoplasia occurred almost exclusively in two family groups and heredity played a fundamental rôle both in the occurrence of the tumors and in the determination of tumor type. Endocrine changes, comparable with those found in animals after long continued administration of estrogenic substances, occurred in tumor-bearing rabbits and it was inferred that the spontaneous growths represented a natural counterpart of the experimental induction of neoplasia with estrone.

scholarly journals Localization of alpha-casein gene transcription in sections of epoxy resin-embedded mouse mammary tissues by in situ hybridization.

1988 ◽  
Vol 36 (12) ◽  
pp. 1503-1510 ◽  
Author(s):  
D S Liscia ◽  
P J Doherty ◽  
G H Smith
Keyword(s):  
In Situ Hybridization ◽  
Epoxy Resin ◽  
Specific Activity ◽  
Mammary Tumors ◽  
Image Resolution ◽  
Hybridization Signal ◽  
Mammary Tissue ◽  
Positive Hybridization ◽  
Mammary Tissues

The objective of our study was to evaluate the suitability of aldehyde-fixed, epoxy resin-embedded tissue for efficient and reproducible detection of casein mRNA in mouse mammary tissue by in situ hybridization. We used mouse alpha-casein-specific, 35S-labeled riboprobes generated from a Gemini-3 vector. Both complementary (anti-sense) and homologous (sense) RNA probes were utilized in our study (specific activity ranged from 5-7 x 10(8) cpm/micrograms). We tested the stability of newly synthesized [3H]-uridine-labeled RNA in tissue sections subjected to epoxy plastic solvents and found that no detectable loss of label occurred during preparation of semi-thin (1-2 micron) plastic sections for situ hybridization. In addition, it was possible to detect alpha-casein mRNA in deplasticized sections of mammary gland tissue taken from normal, pregnant, or lactating mice, pre-neoplastic mammary alveolar hyperplasias, explant cultures, and mammary tumors. A positive hybridization signal was consistently obtained in sections of mammary tissues where the estimated average copy number for total casein mRNA was greater than or equal to 250/cell. In mammary tumors, where the estimated casein mRNA content was much lower (less than 5/cell), our positive hybridization signal occurred in regions of the tumor that, in consecutive sections, stained positive for casein by immunoperoxidase. After formaldehyde-glutaraldehyde fixation, loss of hybridizable RNA from epoxy-embedded tissues and sections appears to be minimal. Image resolution was greatly enhanced over frozen or paraffin sections of mammary tissue. Non-specific binding of the radioactive probes was very low. Protease treatment of the sections was not necessary for detection of hybridizable signal.

scholarly journals THE RELATION OF COAT COLOR TO THE SPONTANEOUS INCIDENCE OF MAMMARY TUMORS IN MICE

1934 ◽  
Vol 59 (2) ◽  
pp. 229-250 ◽  
Author(s):  
C. C. Little
Keyword(s):  
Lower Incidence ◽  
Mammary Cancer ◽  
Coat Color ◽  
Virgin Female ◽  
Mammary Tumors ◽  
Color Difference ◽  
Tumor Formation ◽  
Mammary Tissue ◽  
Biological Phenomenon ◽  
Pass Through

1. The material included in this paper consists of F1 and F2 virgin female mice derived from a cross between a strain high in mammary cancer incidence (dilute brown) and one relatively low in incidence of mammary cancer but relatively high in the incidence of various internal tumors (yellow). 2. In the F1 and F2 hybrid generations the yellow animals have a significantly lower incidence of mammary tumors than do the non-yellows. This is the first clear case of a difference in the incidence of spontaneous tumors in mice associated with a color difference. 3. Mammary tumors occur, however, significantly earlier in the yellow mice and are just as malignant as those appearing in the non-yellows. 4. The incidence of tumors other than mammary is not significantly different in the yellow and non-yellow hybrids. Such tumors, however, occur distinctly later in life than do the mammary tumors. This provides additional evidence that, in mice, mammary tumors cannot be considered to be the same biological phenomenon as are other types of tumor. 5. A study of the physiology of reproduction of yellow and non-yellow mice within the yellow stock suggests that the yellows pass through their reproductive cycle earlier than do the non-yellows. The duration of the cycle in the two forms is essentially equal. This fact would satisfactorily explain the earlier incidence of mammary tumors in yellow mice. 6. The lower incidence of mammary tumors in yellows as compared with non-yellows may be at least in part due to the same phenomenon. This would follow because the opportunity for mammary tissue in yellow mice of cancer age to be continuously affected by ovarian secretion would be less than in non-yellows. This would result in a higher percentage of yellows reaching an age at which stimuli from the ovary ceased before the mammary tissue had reached an age at which tumor formation is most frequent. 7. There is some evidence that, in this cross, dilute (dbdb) mice are less apt to form mammary tumors than are intensely pigmented animals. This point, however, needs further investigation before it can be considered to be established. 8. The facts recorded in this paper demonstrate that not all forms of tumor or all colors of mice can be lumped together in studying either the physiology or genetics of spontaneous tumor incidence.

scholarly journals Immunohistochemical Analysis of Na+/K+-ATPase and Bone Morphogenetic Protein-2 Expressions in Both Parenchymal and Stromal Cells from Benign and Malignant Canine Mammary Tumors

2021 ◽  
Author(s):  
ozlem ozmen
Keyword(s):  
Stromal Cells ◽  
Malignant Tumors ◽  
Breast Tumors ◽  
Mammary Tumors ◽  
Bone Morphogenetic Protein 2 ◽  
Mammary Tissue ◽  
Benign Tumors ◽  
Ion Pump ◽  
Human Breast ◽  
Canine Mammary Tumors

Abstract Canine mammary tumors are the most common type of dog tumor, and they are similar to human breast tumors. Na+/K+-ATPase is a common plasma membrane ion pump with important physiological and pathophysiological functions. In mammary tumors, the tumor microenvironment was composed of a heterogeneous population of tumor cells and nearby endogenous stromal cells. Bone morphogenetic proteins (BMPs) regulate fetal development, tissue homeostasis and differentiation, and a variety of cellular functions. The purpose of this study is to examine the immunohistochemical expression of Na+/K+-ATPase and BMP-2 in tumoral and stromal cells from benign and malignant canine mammary tumors. In this study, ten benign and ten malignant mammary tumors from the archives of the Department of Pathology were used, with five normal breast tissues serving as controls. The results of the revealed that tumors had higher levels of Na+/K+-ATPase and BMP-2 expressions than normal mammary tissue. While both markers were expressed negatively or mildly in benign tumors, they increased significantly in malignant tumors. Both Na+/K+-ATPase and BMP-2 are expressed by tumoral and stromal cells in canine mammary tumors. When compared to compared to BMP-2, Na+/K+-ATPase expression was found to be more severe. This study found that Na+/K+-ATPase and BMP-2 can be used as markers of malignancy in canine mammary tumors and that stromal cells also play an important role in tumor progression. These findings also indicated that Na+/K+-ATPase and BMP-2 may be used for early diagnosis or as a potential target for treatment of canine and human breast tumors in the future.

scholarly journals Detection of mutations within exons 4 to 8 of the p53 tumor suppressor gene in canine mammary glands

2012 ◽  
Vol 64 (2) ◽  
pp. 341-348 ◽  
Author(s):  
D.M.B. Souza ◽  
M.G.O. Barros ◽  
J.S.C. Silva ◽  
M.B. Silva ◽  
Z.F. Coleto ◽  
...  
Keyword(s):  
Cell Nucleus ◽  
Mammary Tumor ◽  
P53 Gene ◽  
Mammary Tumors ◽  
Mammary Glands ◽  
Suppressor Gene ◽  
Mammary Tissue ◽  
Missense Mutations ◽  
P53 Tumor Suppressor Gene ◽  
Detection Of Mutations

Fifteen female canines with mammary tumors and 6 normal females were used to study mutations in exons 4 to 8 of the p53 gene. DNA samples from the tumors, respective adjacent normal mammary tissue and mammary glands from healthy animals were sequenced and analyzed for the presence of mutations. Mutations were found in 71.8% of the samples and the most frequent were missense mutations. The most attacked exons in the mammary tumor were 5, 7 and 8, with 23.4, 31.6 and 23.4% mutations, respectively. Canine mammary tumors are related to mutations in gene p53 and mutations mostly occur in the region of the protein that is linked to the DNA in the cell nucleus, which can change the functionality of the cell and propitiate tumor growth. Despite being macroscopically normal, the mammary tissue adjacent to the tumors has mutations that can lead to recurrence if not removed together with the tumor.

scholarly journals Development of mammary cancer in γ-irradiated F1 hybrids of susceptible Sprague-Dawley and resistant Copenhagen rats, with copy-number losses that pinpoint potential tumor suppressors

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0255968
Author(s):  
Mayumi Nishimura ◽  
Kazuhiro Daino ◽  
Maki Fukuda ◽  
Ikuya Tanaka ◽  
Hitomi Moriyama ◽  
...  
Keyword(s):  
Copy Number ◽  
Mammary Cancer ◽  
Mammary Carcinogenesis ◽  
Mammary Tumors ◽  
Copy Number Variations ◽  
F1 Hybrids ◽  
Mammary Tissue ◽  
Pcr Analysis ◽  
Sprague Dawley ◽  
Genetic Trait

Copenhagen rats are highly resistant to mammary carcinogenesis, even after treatment with chemical carcinogens and hormones; most studies indicate that this is a dominant genetic trait. To test whether this trait is also dominant after radiation exposure, we characterized the susceptibility of irradiated Copenhagen rats to mammary carcinogenesis, as well as its inheritance, and identified tumor-suppressor genes that, when inactivated or mutated, may contribute to carcinogenesis. To this end, mammary cancer–susceptible Sprague-Dawley rats, resistant Copenhagen rats, and their F1 hybrids were irradiated with 4 Gy of γ-rays, and tumor development was monitored. Copy-number variations and allelic imbalances of genomic DNA were studied using microarrays and PCR analysis of polymorphic markers. Gene expression was assessed by quantitative PCR in normal tissues and induced mammary cancers of F1 rats. Irradiated Copenhagen rats exhibited a very low incidence of mammary cancer. Unexpectedly, this resistance trait did not show dominant inheritance in F1 rats; rather, they exhibited intermediate susceptibility levels (i.e., between those of their parent strains). The susceptibility of irradiated F1 rats to the development of benign mammary tumors (i.e., fibroadenoma and adenoma) was also intermediate. Copy-number losses were frequently observed in chromosome regions 1q52–54 (24%), 2q12–15 (33%), and 3q31–42 (24%), as were focal (38%) and whole (29%) losses of chromosome 5. Some of these chromosomal regions exhibited allelic imbalances. Many cancer-related genes within these regions were downregulated in mammary tumors as compared with normal mammary tissue. Some of the chromosomal losses identified have not been reported previously in chemically induced models, implying a novel mechanism inherent to the irradiated model. Based on these findings, Sprague-Dawley × Copenhagen F1 rats offer a useful model for exploring genes responsible for radiation-induced mammary cancer, which apparently are mainly located in specific regions of chromosomes 1, 2, 3 and 5.

Antineoplastic effect of iodine and iodide in dimethylbenz[a]anthracene-induced mammary tumors: association between lactoperoxidase and estrogen-adduct production

2011 ◽  
Vol 18 (4) ◽  
pp. 529-539 ◽  
Author(s):  
Ofelia Soriano ◽  
Guadalupe Delgado ◽  
Brenda Anguiano ◽  
Pavel Petrosyan ◽  
Edith D Molina-Servín ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Dna Adducts ◽  
Mammary Cancer ◽  
Mammary Tumors ◽  
Molecular Iodine ◽  
Mammary Tissue ◽  
Normal Mammary Gland ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Antineoplastic Effect

Several groups, including ours, have reported that iodine exhibited antiproliferative and apoptotic effects in various cancer cells only if this element is supplemented as molecular iodine, or as iodide, to cells that are able to oxidize it with the enzyme thyroperoxidase. In this study, we analyzed the effect of various concentrations of iodine and/or iodide in the dimethylbenz[a]anthracene (DMBA) mammary cancer model in rats. The results show that 0.1% iodine or iodide increases the expression of peroxisome proliferator-activated receptor type γ (PPARγ), triggering caspase-mediated apoptosis pathways in damaged mammary tissue (DMBA-treated mammary gland) as well as in frank mammary tumors, but not in normal mammary gland. DMBA treatment induces the expression of lactoperoxidase, which participates in the antineoplastic effect of iodide and could be involved in the pro-neoplastic effect of estrogens, increasing the formation of DNA adducts. In conclusion, our results show that a supplement of 0.1% molecular iodine/potassium iodide (0.05/0.05%) exert antineoplastic effects, preventing estrogen-induced DNA adducts and inducing apoptosis through PPARγ/caspases in pre-cancer and cancerous cells. Since this iodine concentration does not modify the cytology (histology, apoptosis rate) or physiology (triiodothyronine and thyrotropin) of the thyroid gland, we propose that it be considered as an adjuvant treatment for premenopausal mammary cancer.

scholarly journals In Vivo Dielectric Properties of Healthy and Benign Rat Mammary Tissues from 500 MHz to 18 GHz

Sensors ◽  
2020 ◽  
Vol 20 (8) ◽  
pp. 2214 ◽  
Author(s):  
Tuba Yilmaz ◽  
Fatma Ates Alkan
Keyword(s):  
Dielectric Properties ◽  
Animal Models ◽  
Ex Vivo ◽  
Mammary Tumors ◽  
Mammary Tissue ◽  
Low Grade ◽  
Healthy Human ◽  
Tissue Alteration ◽  
Mammary Tissues

This work investigates the in vivo dielectric properties of healthy and benign rat mammary tissues in an attempt to expand the dielectric property knowledge of animal models. The outcomes of this study can enable testing of microwave medical technologies on animal models and interpretation of tissue alteration-dependent in vivo dielectric properties of mammary tissues. Towards this end, in vivo dielectric properties of healthy rat mammary tissues and chemically induced benign rat mammary tumors including low-grade adenosis, sclerosing adenosis, and adenosis were collected with open-ended coaxial probes from 500 MHz to 18 GHz. The in vivo measurements revealed that the dielectric properties of benign rat mammary tumors are higher than the healthy rat mammary tissues by 9.3% to 35.5% and 19.6% to 48.7% for relative permittivity and conductivity, respectively. Furthermore, to our surprise, we found that the grade of the benign tissue affects the dielectric properties for this study. Finally, a comparison with ex vivo healthy human mammary tissue dielectric properties revealed that the healthy rat mammary tissues best replicate the dielectric properties of healthy medium density human samples.

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