To investigate, Joan Massagué and his colleagues at the Memorial Sloan - Kettering Cancer Center in New York city injected
human breast cancer cells into the arteries of mice.
The study, published in the Journal of the National Cancer Institute (JNCI), identified four genes that are linked to tamoxifen resistance and poor prognosis of breast cancer, by comparing results obtained in a new animal model, in
human breast cancer cells grown in culture, and in publically available datasets collected from thousands of estrogen receptor positive breast cancer patients treated with tamoxifen.
To more directly assess the role of GSTO1 and RYR1 in the breast tumor response to chemotherapy, the researchers
injected human breast cancer cells into the mammary gland of mice and then treated the mice with carboplatin after tumors had formed.
Soll's team, in a paper published in PLOS One in March 2015, previously showed that
human breast cancer cells form tumors by extending cables — bridges of sorts — between small aggregates of cancer cells.
Mass spectrometry ‐ based cellular thermal shift assay (MS ‐ CeTSA) analysis of CDK4 / 6 inhibitor palbociclib targets in
MCF7 human breast cancer cells identifies protein complexes including the 20S proteasome.
So it came as a shock when researchers at the University of Minnesota published a study showing that doses of morphine similar to those used to ease pain actually spurred the growth of
human breast cancer cells grafted into mice.
The researchers observed the effect of the synthetically produced molecule, JK - 31, on the growth and proliferation of a
model human breast cancer cell line and found that it effectively blocked the protein cyclin - dependent kinase 1 (CDK1), which plays a key part in the process of the division of cancer cells, and therefore inhibited the proliferation of the cells.
In this new study, described Feb. 21 in Cell Reports, Semenza and his colleagues conducted gene expression analysis of
multiple human breast cancer cell lines grown in the laboratory after exposure to chemotherapy drugs, like carboplatin, which stops tumor growth by damaging cancer cell DNA.
Now, University of Pennsylvania researchers have revealed how a reduction in mitochondrial DNA content
leads human breast cancer cells to take on aggressive, metastatic properties.
Using an optimized hypoxia and reoxygenation regimen, we identified a novel cycling hypoxia - selected subpopulation
from human breast cancer cell lines and demonstrated that a stem - like breast cancer cell subpopulation could be expanded through repetitive hypoxia / reoxygenation cycles without genetic manipulation.
When the Cornell team
cultured human breast cancer cells on matrix deposited by fat - derived cells from obese mice, the cancer cells grew faster than they did on the matrix of cells from slimmer mice.
To determine whether the NSC - secreted anti-HER2 antibody binds specifically to the HER2 receptor, HB1.F3 - H2IgG cells were co-cultured overnight with either
MCF7 human breast cancer cells that express low levels of HER2, or MCF7 / HER2 cells, an MCF7 line stably transfected to overexpress HER2 [16].
To study the effect of hypoxia / reoxygenation cycles on breast cancer, we exposed two
metastatic human breast cancer cell lines (MDA - MB 231 and BCM2) to cycles of chronic hypoxia and nutrient deprivation.
Working
with human breast cancer cells and mouse models of breast cancer, scientists identified a new protein that plays a key role in reprogramming cancer cells to migrate and invade other organs.
In tests
on human breast cancer cells and in special immunodeficient mice with tissue grafts, the scientists found that both agents interfered with genes involved with breast cancer cell growth, resulting in more cancer cells.
In tumors formed
by human breast cancer cells, DNA damage (brown staining) is increased by simultaneous Olaparib treatment and PGAM1 suppression (right) when compared to either Olaparib treatment (left) or PGAM1 suppression (center) alone.
Bloch's colleagues at the National Institute of Environmental Health Sciences tested the oils in gene expression studies on lab - grown
human breast cancer cells and found that they could mimic estrogens, the primary female sex hormones, and inhibit androgens, the primary male sex hormones.
Lab testing showed that the plant - made virus particles, which naturally bind to receptors on cancer cells, were taken in by
human breast cancer cells.
To see whether cancer stem cell renewal involves a chain of events similar to that used by embryonic stem cells, and whether the process was affected by oxygen levels, Semenza and graduate student Chuanzhao Zhang focused their studies on two
human breast cancer cell lines that responded to low oxygen by ramping up production of the protein ALKBH5, which removes methyl groups from mRNAs.
Working with
human breast cancer cells and mice, scientists at The Johns Hopkins University say new experiments explain how certain cancer stem cells thrive in low oxygen conditions.
Working with
human breast cancer cells and mice, researchers at Johns Hopkins say they have identified a biochemical pathway that triggers the regrowth of breast cancer stem cells after chemotherapy.