Mammary tumors were promoted in male rats of the Wistar WAG strain by continuous and simultaneous administration of 17 beta-estradiol and progesterone. Tumor induction and growth were dependent on estradiol and on progesterone. Their histological features were comparable with those of human breast cancers. Hormone receptors were present in tumor cells. Estradiol receptor was found in 95% of them, at a higher level in nuclei than in cytosol. Progesterone receptor was present in 75% of tumors. In all cases, the level of androgen receptor was low.

Download full-text PDF

Source
http://dx.doi.org/10.1016/0022-4731(82)90635-5DOI Listing

Publication Analysis

Top Keywords

mammary tumors
8
simultaneous administration
8
administration beta-estradiol
8
beta-estradiol progesterone
8
estrogen progesterone
4
progesterone receptors
4
receptors mammary
4
tumors induced
4
induced rats
4
rats simultaneous
4

Similar Publications

β-Glucuronidase-Responsive Albumin-Binding Prodrug of Colchicine-Site Binders for Selective cancer Therapy.

ChemMedChem

January 2025

UMR-CNRS 7285, Institut de Chimie des Milieux et des Matériaux de Poitiers, groupe « Systèmes Moléculaires Programmés », Faculté des Sciences Fondamentales et Appliquées, 4 rue Michel Brunet, TSA 51106, 86073, Poitiers, FRANCE.

The development of novel therapeutic strategies enabling the selective destruction of tumors while sparing healthy tissues is of great interest to improve the efficacy of cancer chemotherapy. In this context, we designed a β-glucuronidase-responsive albumin-binding prodrug programmed to release a potent Isocombretastatin A-4 analog within the tumor microenvironment. When injected at a non-toxic dose in mice bearing orthotopic triple-negative mammary tumors, this prodrug produced a significant anticancer activity, therefore offering a valuable alternative to the systemic administration of the parent drug.

View Article and Find Full Text PDF

Uncommon metastatic journey: unusual breast metastases of medullary thyroid carcinoma: a case report.

BMC Womens Health

January 2025

Department of Surgical Oncology, Salah Azaiez Institute, Faculty of Medicine of Tunis, University of Tunis El Manar, Boulevad 9 Avril Bab Saadoun 1006, Tunis, Tunisia.

Medullary thyroid carcinoma is a neuroendocrine tumor derived from thyroid C-cells. It is a rare aggressive tumor, known to metastasize to lymph nodes, liver, bones, and lungs. We report a case of a young patient with a family history of breast cancer, who developed breast metastases six months post-treatment for medullary thyroid carcinoma.

View Article and Find Full Text PDF

RANK pathway has attracted increasing interest as a promising target in breast cancer, given the availability of denosumab, an anti-RANKL drug. RANK signaling mediates progesterone-driven regulation of mammary gland development and favors breast cancer initiation by controlling mammary cell proliferation and stem cell fate. RANK activation promotes luminal mammary epithelial cell senescence, acting as an initial barrier to tumorigenesis but ultimately facilitating tumor progression and metastasis.

View Article and Find Full Text PDF

Rat Models of Breast Cancer.

Adv Exp Med Biol

January 2025

Lester & Sue Smith Breast Center, Baylor College of Medicine, Houston, TX, USA.

As the first mammal to be domesticated for research purposes, rats served as the primary animal model for various branches of biomedical research, including breast cancer studies, up until the late 1990s and early 2000s. During this time, genetic engineering of mice, but not rats, became routine, and mice gradually supplanted rats as the preferred rodent model. But recent advances in creating genetically engineered rat models, especially with the assistance of CRISPR/Cas9 technology, have rekindled the significance of rats as a critical model in exploring various facets of breast cancer research.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!