Disease relevance of Mammary Neoplasms, Animal

• High-affinity saturatable estrogen binding by breast cancer cytosols distinguishes endocrine-responsive mammary neoplasms from autonomous breast cancers [1].
• The authors recently demonstrated the basal and hypoxia-stimulated expression of Epo and EpoR in human breast carcinoma cell lines and in breast carcinomas, suggesting a role for autocrine Epo signaling in the hypoxic adaptations of mammary neoplasms [2].

High impact information on Mammary Neoplasms, Animal

• Since no interactions were found for the usual measure of carcinogenesis, namely, incidence of rats with 1 or more neoplasms, the overall conclusion is that DMBA, PCZ, and x-ray act additively in the induction of mammary neoplasms in the female Sprague-Dawley rat [3].
• Induction of mammary neoplasms in the ACI rat by 430-keV neutrons, X-rays, and diethylstilbestrol [4].
• Nearly all bitransgenic males develop mammary neoplasms within 8 months of birth, whereas only 15% of Wnt-1 transgenic males and none of the int-2 transgenic males have tumors [5].
• However, a comparison of the immunotitration and immunodiffusion experiments indicated that the mammary-gland acetyl-CoA carboxylase might differ from the enzyme present in mammary neoplasms [6].
• Here we show that a non-steroidal aromatase inhibitor, which competitively inhibits the conversion of androstenedione to oestrone, prevents the development of both benign and malignant spontaneous mammary neoplasms in female Sprague-Dawley ats [7].

Chemical compound and disease context of Mammary Neoplasms, Animal

• Binding of fluorescein isothiocyanate conjugated lectins to MXT mouse mammary neoplasm and their relation to steroid receptor status [8].
• 312C8-1 and 13H5 antibodies are specific for canine mammary basal and luminal epithelium, respectively, and by employing these antibodies, the origin and differentiation of canine mammary neoplasms can be determined more accurately than on the basis of hematoxylin and eosin-stained tissue alone [9].
• The aim of the study was to evaluate the possible changes in the alpha 5 beta 1 integrin receptor and its ligand fibronectin in relation to the metastatic capacity of canine mammary neoplasms [10].

Biological context of Mammary Neoplasms, Animal

• As previous studies have suggested a hormone dependence of binding sites for peanut agglutinin in mammary neoplasm, this feature has been thought to be correlated to steroid receptor status [8].
• In conclusion, the expression and distribution of connexins and E-cadherin are inversely correlated to cell proliferation in malignant mammary neoplasms of dogs and may well be related to their more aggressive histologic type and biologic behavior [11].

Anatomical context of Mammary Neoplasms, Animal

• Removal of an endogenous EGF stimulus by surgical ablation of the submaxillary glands, the major EGF-producing organ in mice, produced significantly slower growth of rodent mammary neoplasms, decreased success rate of transplantation, and an increase in the latent period before growth occurred [12].

Gene context of Mammary Neoplasms, Animal

• As revealed in this study, the exclusive overexpression of SFRP2 in canine MGTs suggests that SFRP2 is a potential candidate gene for further investigation of mammary tumorigenesis and complex etiology of the canine model of mammary neoplasms [13].
• BACKGROUND: The p53 gene mutations have been associated with the development of human breast and canine mammary neoplasms; breast carcinoma patients with alterations of p53 gene are considered to have a poor prognosis [14].
• Angiogenesis was evaluated by immunohistochemistry for platelet endothelial cell adhesion molecule (CD31) in a series of benign and malignant canine mammary neoplasms [15].
• Interleukin-2 alterations in the immune status of patients with mammary neoplasm [16].

References