4.4 Article

C(3)1-TAg in C57BL/6 J background as a model to study mammary tumor development

Journal

HISTOCHEMISTRY AND CELL BIOLOGY
Volume 156, Issue 2, Pages 165-182

Publisher

SPRINGER
DOI: 10.1007/s00418-021-01995-w

Keywords

Mammary gland; Genetically engineered mouse model; Breast cancer; Tumor development

Funding

  1. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq-PQ2)
  2. Instituto Serrapilheira [Serra-1708-15285]
  3. Pro-reitoria de Pesquisa/Universidade Federal de Minas Gerais (PRPq/UFMG) [05/2016]
  4. Fundacao de Amparo a Pesquisa do Estado de Minas Gerais-FAPEMIG [Rede Mineira de Engenharia de Tecidos e Terapia Celular (REMETTEC)] [RED-00570-16]
  5. FAPEMIG [Rede De Pesquisa Em Doencas Infecciosas Humanas E Animais Do Estado De Minas Gerais] [RED-00313-16]
  6. MCTIC/CNPq [28/2018]
  7. National Institute of Health [1R01CA179072-01A1]
  8. American Cancer Society Mentored Research Scholar grant [124443-MRSG-13-121-01-CDD]
  9. FAPEMIG (BDCTI -I) [27915-FAPEMIG/ICB]
  10. CAPES
  11. postdoctoral fellowship (PNPD) from CAPES
  12. CNPq

Ask authors/readers for more resources

The study utilized a C3(1)-TAg mouse model to investigate breast cancer in the C57BL/6 J background, finding the development of solid-basaloid adenoid cystic carcinoma with increased fibrosis and decreased adipocytes, which are triple-negative tumors. Additionally, tumor development was observed to be slower in the C57BL/6 J background compared to the FVB strain, suggesting it serves as a better model for studying different stages in breast cancer progression.
Diagnosis and prognosis of breast cancer is based on disease staging identified through histopathological and molecular biology techniques. Animal models are used to gain mechanistic insights into the development of breast cancer. C(3)1-TAg is a genetically engineered mouse model that develops mammary cancer. However, carcinogenesis caused by this transgene was characterized in the Friend Virus B (FVB) background. As most genetic studies are done in mice with C57BL/6 J background, we aimed to define the histological alterations in C3(1)-TAg C57BL/6 J animals. Our results showed that C3(1)-TAg animals with C57BL/6 J background develop solid-basaloid adenoid cystic carcinomas with increased fibrosis, decreased area of adipocytes, and a high proliferative index, which are triple-negative for progesterone, estrogen, and human epidermal growth factor receptor 2 (HER2) receptors. Our results also revealed that tumor development is slower in the C57BL/6 J background when compared with the FVB strain, providing a better model to study the different stages in breast cancer progression.

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