The research team confirmed those results by testing the four compounds at a low dose in mice injected
with ovarian cancer cells.
Although this research was conducted
on ovarian cancer cells, the ground - breaking results are applicable to a wider range of cancers.
The scientists found that, at certain concentrations, one of the compounds of the series selectively killed human
ovarian cancer cells without harming healthy cells.
The researchers exposed patient - derived
epithelial ovarian cancer cells growing in their laboratory to a specific NSAID, indomethacin, and confirmed the DrugPredict finding.
«We found that targeting only glutaminase will miss the less
aggressive ovarian cancer cells because they are at a metabolic stage where they are not yet glutamine - dependent.»
The scientists then analyzed 25
different ovarian cancer cell lines in the laboratory and discovered that the higher the amount of active SYK in the cell lines, the more resistant those cells were to paclitaxel treatment.
In order to find out how and why
ovarian cancer cells grow and take on such lethal characteristics, Dr. Shepherd and his team grow the cancer cells in 3D structures, called «spheroids» — the same way the cancer cells grow in patients.
Ovarian cancer cells use autophagy all of the time, but also lose several copies of autophagy genes resulting in a compromised capacity.
To test this idea, they experimentally reduced the expression of the DNM30S lncRNA, which resulted in reduced
ovarian cancer cell migration and invasion.
A Rice University - led analysis of the metabolic profiles of hundreds of ovarian tumors has revealed a new test to determine
whether ovarian cancer cells have the potential to metastasize, or spread to other parts of the body.
«We think that by isolating the CA125 - negative tumor cells we have uncovered this reservoir of carboplatin - resistant high - grade
serous ovarian cancer cells.»
Combined expression of KLK4, KLK5, KLK6, and KLK7
by ovarian cancer cells leads to decreased adhesion and paclitaxel - induced chemoresistance.
The researchers then used a combination of existing United States Food and Drug Administration - approved drugs to target autophagy and
found ovarian cancer cells to be highly sensitive to these drugs in several different mouse cancer models — even among cells resistant to standard chemotherapy.
In a previous study, Shih, Wang and their colleagues found that paclitaxel resistance may occur because of higher levels of an enzyme found in
ovarian cancer cells called spleen tyrosine kinase, or SYK.
Working in cell cultures and mice, researchers at Johns Hopkins have found that an experimental drug called fostamatinib combined with the chemotherapy drug paclitaxel may
overcome ovarian cancer cells» resistance to paclitaxel.
«Previous studies stated that LKB1 was a tumour suppressor in ovarian cancer, meaning that tumour cells need to get rid of LKB1 to cause cancer,» says Dr. Shepherd «but our work is in direct conflict with these studies, because we definitively show that
ovarian cancer cells still have LKB1 and that this molecule allows ovarian cancer spheroids to change their metabolism, promote tumour cell survival and make them more resistant to chemotherapy.»
«We showed FER was essential
for ovarian cancer cell motility and invasiveness, both in vitro and in vivo,» Tonks says.
Researchers at Women & Infants Hospital of Rhode Island have developed a biologic drug that would prevent the production of a protein known to
allow ovarian cancer cells to grow aggressively while being resistant to chemotherapy.
When the researchers tested the circuit in vitro, they found that it was able to
detect ovarian cancer cells from amongst other noncancerous ovarian cells and other cell types.
First, we produced PARP1 -
KO ovarian cancer cell lines using CRISPR / Cas9 gene editing to test the loss of PARP - 1 as a resistance mechanism to all clinically used PARP inhibitors.
Growth inhibition induced by antiprogestins RU - 38486, ORG - 31710, and CDB - 2914 in
ovarian cancer cells involves inhibition of cyclin dependent kinase 2.
The particles were designed to release doxorubicin when exposed to ultraviolet light — here,
ovarian cancer cells turn red as the doxorubicin is released over time (Photo: Erik Dreaden and Kevin Shopsowitz)
The authors administered NK cells via intraperitoneal injection into a xenograft mouse model established using
bioluminescent ovarian cancer cell lines which allow for tumor monitoring via bioluminescent imaging (BLI).
Once ovarian cancer cells reach the omentum, they quickly develop the tools to devour the sustenance provided by this fatty tissue, reprogramming their metabolism to thrive on lipids acquired from fat cells.
Four compounds significantly inhibited
key ovarian cancer cell functions in the early steps of metastasis at low doses.
Their theory was first confirmed
with ovarian cancer cell lines and then the Peter / Lengyel team tested HGMA2 protein levels in tumor samples from 100 patients with ovarian cancer.
«For example, we found that highly
aggressive ovarian cancer cells are glutamine - dependent, and in our laboratory studies, we showed that depriving such cells of external sources of glutamine — as some experimental drugs do — was an effective way to kill late - stage cells.
Researchers at Rice University's Laboratory for Systems Biology of Human Diseases analyzed the metabolic profiles of hundreds of ovarian tumors and discovered a new test to determine
whether ovarian cancer cells have the potential to metastasize.
«This study provides evidence that CA125 - negative high - grade
serous ovarian cancer cells have stem properties and are inherently platinum resistant.
In the case of one particular ITC in cruciferous vegetables (sulphoraphane), a cell cycle (the G1 cell cycle) normally participated in
by ovarian cancer cells has been shown to be disrupted in the presence of this ITC.