Behavior of Human Breast Tumor Cells in Vivo on Chorioallantoic Membrane. A Preliminary Report

1982 ◽  
Vol 68 (1) ◽  
pp. 53-56
Author(s):  
Suneeti S. Sawant ◽  
Soumendra Nath Ghosh ◽  
Prabhaker N. Shah

The invasive properties of 2 types of breast cancers were tested on an « in vivo » model system in which 9-day-old chorioallantoic membrane (CAM) of chick embryo was used. Similar to HeLa and ALL cells, the breast « negative » cells invaded the blood vessels of the host, whereas the breast « positive » cells were seen in the mesoderm away from blood vessels of the host. This finding probably explains the intrinsic aggressive property of breast « negative » cells.

Wound Healing ◽  
2003 ◽  
pp. 161-178
Author(s):  
Peter J. Polverini ◽  
Jacques E. Nör ◽  
Martin C. Peters ◽  
David J. Mooney

Nanoscale ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 4258-4266 ◽  
Author(s):  
Jie Tang ◽  
Christopher B. Howard ◽  
Stephen M. Mahler ◽  
Kristofer J. Thurecht ◽  
Leaf Huang ◽  
...  

An optimized dual-target lipid-coated calcium phosphate-based nanoplatform efficiently delivers the drug/gene to triple-negative human breast tumor cells in vitro and in vivo.


Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 942
Author(s):  
Mei Qi Kwa ◽  
Rafael Brandao ◽  
Trong H. Phung ◽  
Jianfeng Ge ◽  
Giuseppe Scieri ◽  
...  

MRCKα is a ubiquitously expressed serine/threonine kinase involved in cell contraction and F-actin turnover, which is highly amplified in human breast cancer and part of a gene expression signature for bad prognosis. Nothing is known about the in vivo function of MRCKα. To explore MRCKα function in development and in breast cancer, we generated mice lacking a functional MRCKα gene. Mice were born close to the Mendelian ratio and showed no obvious phenotype including a normal mammary gland formation. Assessing breast cancer development using the transgenic MMTV-PyMT mouse model, loss of MRCKα did not affect tumor onset, tumor growth and metastasis formation. Deleting MRCKα and its related family member MRCKβ in two triple-negative breast cancer cell lines resulted in reduced invasion of MDA-MB-231 cells, but did not affect migration of 4T1 cells. Further genomic analysis of human breast cancers revealed that MRCKα is frequently co-amplified with the oncogenes ARID4B and AKT3 which might contribute to the prognostic value of MRCKα expression. Collectively, these data suggest that MRCKα might be a prognostic marker for breast cancer, but probably of limited functional importance.


1997 ◽  
Vol 6 (6) ◽  
pp. 353-360 ◽  
Author(s):  
Majella S. de Lange ◽  
Bert Top ◽  
Caro Lambrechts ◽  
Riks A. Maas ◽  
Hans L. Peterse ◽  
...  

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi217-vi217
Author(s):  
Joseph Lagas ◽  
Lihua Yang ◽  
Oren Becher ◽  
Joshua Rubin

Abstract Diffuse Intrinsic Pontine Glioma (DIPG) is a devastating pediatric high-grade glioma that occurs in the brainstem with a median survival of less than 1 year. A greater understanding of the early tumorigenic events is essential for the development of effective therapeutics. DIPG is characterized by founder mutations in histone H3, either H3.1K27M or H3.3K27M. These mutations cause global hypomethylation, resulting in aberrant gene expression. It is unknown how this mechanism contributes to tumorigenesis. Interestingly, H3.1K27M DIPG show an increased incidence in females, whereas H3.3K27M DIPG shows no sex difference. This illustrates that the tumorigenic potential of H3.1K27M may be different between the sexes. Few models of DIPG incorporate the study of H3.1K27M despite the fact that it represents a unique opportunity to obtain valuable information on the tumorigenesis of DIPG through the study of the sex difference. Thus, we have created an in vitro and in vivo model system for H3.1K27M DIPG utilizing the RCAS mouse model system. This system utilizes RCAS vectors and a RCAS-ntva transgenic mouse line to deliver specific mutations to nestin expressing cells in the brainstem, including oligodendrocyte progenitor cells (OPCs), the predicted cell of origin. Delivering H3.1K27M, ACVR1 R206H, and PDGFaa at postnatal day 7 produces DIPG-like tumors in vivo, confirmed by H and E staining, between 60 – 110 days post injection. Additionally, confirmed through immunofluorescence staining, we can isolate a pure population of OPCs via immunopanning and infect them with RCAS vectors in vitro to produce stable expression of H3.1K27M. Introduction of H3.1K27M alone into male and female OPC cultures provides an opportunity to compare the early tumorigenic effects of H3.1K27M between the sexes in vitro. These results demonstrate that we have created an in vitro and in vivo H3.1K27M DIPG model system for the study of sex differences and tumorigenesis in DIPG.


2003 ◽  
Vol 36 (9) ◽  
pp. 1127-1129 ◽  
Author(s):  
Hideaki Nagami ◽  
Keiichi Yamamoto ◽  
Hideaki Ichihara ◽  
Yoko Matsumoto ◽  
Ryuichi Ueoka

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