Abstract 3601: Dietary phosphatidylcholine depletion reduces tumor development independent of autotaxin inhibition in hyperlipidemic mouse models of breast cancer

2019 ◽  
Author(s):  
Fredrick O. Onono ◽  
Ebubechi Adindu ◽  
Baoxiang Yan ◽  
Sony Soman ◽  
Courtney Hammill ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mouse Models ◽  
Tumor Development

Preclinical testing using tumors from genetically engineered mouse mammary models

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 10067-10067
Author(s):  
L. Varticovski ◽  
M. G. Hollingshead ◽  
M. R. Anver ◽  
A. I. Robles ◽  
J. E. Green ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Clinical Trials ◽  
Mouse Models ◽  
Metastatic Disease ◽  
Tumor Development ◽  
Genetically Engineered ◽  
Cell Suspensions ◽  
Preclinical Testing ◽  
Primary Tumors ◽  
Tumor Bearing

10067 Background: Mouse models have been used extensively in preclinical testing of anticancer drugs. However, few of these models reflect the progression of human disease, and even fewer predict the performance of these drugs in clinical trials. Testing anticancer therapies in genetically engineered mouse (GEM) holds the promise of improving preclinical models and guiding the design of clinical trials. Unfortunately, the use of tumor-bearing GEM is hampered by the difficulty in simultaneously obtaining sufficient numbers of animals with the same stage of tumor development. The additional complexity in testing breast cancer therapies in the mouse is that all 10 mammary glands can develop tumors, frequently at different times. Methods: To circumvent the variable tumor latency and lack of synchrony in GEM, we transplanted tumor fragments or cell suspensions from multiple mammary tumor-bearing GEM into the mammary fat pad or subcutaneously into naïve syngeneic, immunodeficient athymic nude, or scid mice. Results: Tumors transplanted as fragments or cell suspensions derived from anterior mammary gland grew faster than the posterior tumors for serial passages without any significant morphologic differences. Cell suspensions using fresh or frozen cells were equally effective in generating tumors, and increasing the numbers of transplanted cells resulted in faster tumor growth. The transplantation strategy was reproducible in multiple breast cancer mouse models, including MMTV-PyMT, -Her2/neu, -wnt1/p53, BRCA1/p53, and others. Metastatic disease in the lungs was evident after removing the primary tumors at different rates for each mouse model. The transplanted primary tumors and the tumors arising in the original GEM had similar morphologic appearance and sensitivity to several chemotherapeutic and novel molecular targeted agents. Conclusions: We have established transplantable synchronous mammary tumors from GEM which also develop metastatic disease. These valuable mouse models are suitable for studying tumor-host interactions, tumor progression, and preclinical testing in a well-characterized molecular and genetic background. Testing these GEM tumors for conventional and novel molecular targeted therapies will be discussed. No significant financial relationships to disclose.

scholarly journals Validation of transgenic models of breast cancer: ductal carcinoma in situ (DCIS) and Brca1-mutation-related breast cancer

2005 ◽  
Vol 8 (8) ◽  
Author(s):  
M. S. Frech ◽  
L. P. Jones ◽  
P. A. Furth
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Mouse Model ◽  
Mouse Models ◽  
Ductal Carcinoma ◽  
Brca1 Mutation ◽  
Tumor Development ◽  
Estrogen Receptor Α ◽  
Mammary Tissue

Available mouse models of ductal carcinomain situ(DCIS) and BRCA1-mutation-related breast cancer are reviewed. The best validated mouse models of human DCIS are the conditional estrogen receptor α in mammary tissue (CERM) model initiated by deregulated estrogen receptor α and the serial explant mouse model initiated by p53 deficiency. At present the most useful and best validated mouse model of BRCA1-mutation-related breast cancer uses the cre-lox system to make a conditional Brca1 deletion targeted to mammary epithelial cells. The major shortcoming of the non-conditional Brca1 models is the high incidence of non-mammary tumor development. The use of mammary gland transplants or explants from these mice into nude hosts is one approach that could be used to circumvent this deficiency. Development and validation of a Brca1-mutation-related mouse model of basal cell breast cancer is an important next step.

CASC15：A tumor-associated long non-coding RNA

2020 ◽  
Vol 26 ◽  
Author(s):  
Bei Wang ◽  
Wen Xu ◽  
Yuxuan Cai ◽  
Chong Guo ◽  
Gang Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Therapeutic Target ◽  
Cancer Colorectal ◽  
Tumor Development ◽  
Pathophysiological Mechanism ◽  
Biological Processes ◽  
Non Coding Rna ◽  
Cancer Côlon ◽  
The Relationship ◽  
Long Non Coding Rna

Background: CASC15, one of long non-coding RNA, is involved in the regulation of many tumor biological processes, and is expected to become a new biological therapeutic target. This paper aims to elucidate the pathophysiological function of CASC15 in various tumors. Methods: The relationship between CASC15 and tumors was analyzed by searching references, and summarizes the specific pathophysiological mechanism of CASC15. Results: LncRNA CASC15 is closely related to tumor development, and has been shown to be abnormally high expressed in all kinds of tumors, including breast cancer, cervical cancer, lung cancer, hepatocellular carcinoma, gastric cancer, bladder cancer, colon cancer, colorectal cancer, cardiac hypertrophy, intrahepatic cholangiocarcinoma, leukemia, melanoma, tongue squamous cell carcinoma, nasopharyngeal carcinoma. However, CASC15 has been found to be downexpressed abnormally in ovarian cancer, glioma and neuroblastoma. Besides, it is identified that CASC15 can affect the proliferation, invasion and apoptosis of tumors. Conclusion: LncRNA CASC15 has the potential to become a new therapeutic target or marker for a variety of tumors.

scholarly journals Studying the role of RANKL in breast cancer and bone metastasis mouse models

Bone Reports ◽  
2021 ◽  
Vol 14 ◽  
pp. 100900
Author(s):  
Evi Gkikopoulou ◽  
Anthi Kolokotroni ◽  
Vagelis Rinotas ◽  
Melina Dragolia ◽  
Vasileios Ntafis ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Bone Metastasis ◽  
Mouse Models
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