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 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.

Kolaviron Ameliorates 7, 12-Dimethylbenzanthracene - Induced Mammary Damage in Female Wistar Rats

2021 ◽  
Vol 21 ◽  
Author(s):  
Rabiatu B. Suleiman ◽  
Aliyu Muhammad ◽  
Ismaila A. Umara ◽  
Mohammed A. Ibrahima ◽  
Ochuko L. Erukainure ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Sialic Acid ◽  
Wistar Rats ◽  
Mrna Level ◽  
Estrogen Receptor Α ◽  
Tumor Formation ◽  
Mammary Tissue ◽  
Standard Drug ◽  
Female Wistar Rats ◽  
Α Level

Background: Kolaviron (KV) is a flavonoid rich portion obtained from Garcinia kola seeds with a number of reported pharmacological effects. However, its ameliorative effects on 7,12-Dimethylbenzanthracene (DMBA)-induced mammary damage has not been fully investigated, despite the reported use of the seeds in the treatment of inflammatory related disorders. Objective: To evaluate the ameliorative effects of KV on DMBA-induced mammary damage in female Wistar rats. Methods: Forty-nine (49) female Wistar rats were randomly assigned into seven groups of seven rats each. DMBA was administered orally to rats in five of the groups as a single dose of 80 mg/kg body wt while the remaining two groups received the vehicle. The rats were palpated weekly for 3 months to monitor tumor formation. After 3 months of DMBA administration, 1 ml of blood was collected to assay for estrogen receptor- α (ER-α) level. Thereafter, the vehicle (dimethyl sulfoxide) was daily administered to the negative control and positive control groups for the 14 days duration of the experiment while three groups were each given a daily oral dose of 50, 100 and 200 mg/kg body wt of KV for the duration of the experiment. The last DMBA-induced group received 10 mg/kg body wt of the standard drug tamoxifen twice in a week and the remaining DMBA-free group received 200 mg/kg body wt KV. Subsequently, the animals were humanly sacrificed and ER-α, sialic acids, sialidase, sialyltransferase levels were assay for in blood and mammary tissues followed by histopathological examinations. Results: Significantly higher levels of estrogen receptor-α (ER-α), formation of lobular neoplastic cells, epithelial hyperplasia, lymphocyte infiltration and increased sialylation were detected in DMBA-induced rats. Treatment with KV at 50, 100 and 200 mg/kg body weight resulted in a significant (p<0.05) decrease in ER-α level, significantly (p<0.05) lower free serum sialic acid (21.1%), total sialic acid level of the mammary tissue (21.57%), sialyltransferase activity (30.83%) as well as mRNA level of the sialyltransferase gene (ST3Gal1) were observed after KV interventions. Conclusion: The findings suggest that KV could be further explored in targeting DMBA-induced mammary damage implicated in mammary carcinogenesis.

Estrogen Decreases Chemokine Levels in Murine Mammary Tissue: Implications for the Regulatory Role of MIP-1 Alpha and MCP-1/JE in Mammary Tumor Formation

Endocrine ◽  
2003 ◽  
Vol 22 (2) ◽  
pp. 161-168 ◽  
Author(s):  
Peter Fanti ◽  
Michael Nazareth ◽  
Robert Bucelli ◽  
Michael Mineo ◽  
Kathleen Gibbs ◽  
...  
Keyword(s):  
Mammary Tumor ◽  
Tumor Formation ◽  
Regulatory Role ◽  
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 Canine mammary cancer

2020 ◽  
Vol 51 (4) ◽  
pp. 425-439
Author(s):  
Alejandro Clavijo-Maldonado ◽  
Enio Ferreira ◽  
Carlos Vargas-Hernández ◽  
Fredy A. Rivera-Páez
Keyword(s):  
Mammary Cancer ◽  
Cellular Proliferation ◽  
Mammary Tissue ◽  
Clinical Approach ◽  
Comparative Oncology ◽  
Clinical Prognosis ◽  
Canine Mammary Cancer ◽  
Clinical Relationship ◽  
Her 2 ◽  
Poor Clinical Prognosis

Canine mammary cancer (CMC) is one of the most common neoplasms in intact females in comparison to other species. Several risk factors have been identified, including breed, genetic predisposition, age, reproductive history, hormonal influence, diet, and body condition, in addition to previous lesions to the mammary gland, such as mammary atypical hyperplasia. An understanding of the genetic markers for the disease and a clinical approach are important for establishing a specific therapy that can allow adequate patient survivorship. Overexpression of the HER-2 gene in canines and humans is associated with a poor clinical prognosis, mainly short survivorship, although the clinical relationship is not clear. The incidence of HER-2 in female dogs can range from 29.7% to 38%. However, overexpression of HER-2 is not necessarily associated with malignancy processes of the mammary tissue, although it participates in cellular proliferation. Finally, canines remain one of the most important models for comparative oncology with humans due to the great similarity in the spontaneous presentation and development of cancer, and in the high homology in the amino acid sequence.

scholarly journals INFLUENCE OF MATERNAL PHENOTYPE ON METABOLIC DIFFERENTIATION OF AGOUTI LOCUS MUTANTS IN THE MOUSE

Genetics ◽  
1978 ◽  
Vol 88 (3) ◽  
pp. 529-539
Author(s):  
George L Wolff
Keyword(s):  
Reciprocal Cross ◽  
Coat Color ◽  
Inbred Strains ◽  
Tumor Formation ◽  
Phenotypic Differentiation ◽  
Metabolic Characteristics ◽  
Agouti Locus ◽  
Uterine Environment ◽  
Strain Genome ◽  
Extensive Breeding

ABSTRACT The results of extensive breeding experiments indicate that the phenotypic differentiation of embryos carrying the viable yellow, Avy, or mottled, am, mutations is influenced to a major extent by the agouti locus genotype and the strain genome of the dam. The Avy/a and am/a genotypes are each expressed in a spectrum of coat color phenotypes. These can be grouped into two classes, mottled and pseudoagouti.—In a reciprocal cross of C57BL/6JNIcrWf and AM/Wf-am/am mice, 29.5% of the offspring of C57BL/6 dams were of the pseudoagouti phenotype, whereas no pseudoagouti offspring were produced by AM strain dams.—Mottled yellow Avy/a mice become obese and tumor formation is enhanced in these mice in comparison with the lean pseudoagouti Avy/a siblings.—In two different reciprocal crosses using four different inbred strains, the proportion of pseudoagouti Avy/a offspring differed according to the strain of the dam. Regardless of strain, mottled yellow Avy/a dams produced significantly fewer pseudoagouti Avy/a offspring than did black a/a dams.—The data suggest that metabolic differentiation of Avy/a zygotes into phenotypic classes with different susceptibilities to obesity and tumor formation is influenced to a considerable degree by the metabolic characteristics of the oviductal and uterine environment of the dam.

scholarly journals Immunohistochemical and molecular expression of laminin-332 gamma-2 chain in canine mammary tumors

2011 ◽  
Vol 63 (1) ◽  
pp. 28-35
Author(s):  
D.A.P.C Zuccari ◽  
R Castro ◽  
B.V Jardim ◽  
U.M Mancini ◽  
G.M Polachini
Keyword(s):  
Western Blot ◽  
Mammary Cancer ◽  
Malignant Tumors ◽  
Mammary Tumors ◽  
Malignant Potential ◽  
Rt Pcr ◽  
Canine Mammary Tumors ◽  
Weak Expression ◽  
Molecular Expression ◽  
Laminin 332

Forty-eight cases of canine mammary cancer were investigated to evaluate the immunohistochemical distribution of the γ2 chain of laminin-332. Tumor cells were compared to a pool of normal mammary tissues using quantitative RT-PCR. The western blot was performed in eight tumor samples as complementary test to evaluate protein integrity. Immunohistochemistry experiments showed negative, focal, and weak expression of laminin-332 γ2 in tumors with the worst prognosis. Quantitative PCR revealed downregulation of the gene in 27 (56.2%) of the animals. Out of the 16 dogs with γ2 chain overexpression, seven were still alive. The western blot results showed bands generation of 36, 50, and 98kDa, suggesting degradation of laminin-332 γ2 in malignant tumors. The results suggest that, in the future, low expression and/or degradation of laminin-332 γ2 chain in canine mammary tumors may be used as an indicator of malignant potential. However, further studies are necessary to corroborate these results

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