«Unstable chromosomes have been associated with
cancer cell resistance to a number of drugs,» says Rebecca Burrell of Cancer Research UK's London Research Institute.
Tissue engineering provides a more practical means for researchers to study cell behavior, such as
cancer cell resistance to therapy, and test new drugs or combinations of drugs to treat many diseases.
Not exact matches
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.
As a result, P - gp causes
resistance of the diseased
cells to a majority of drugs currently available for the treatment of
cancer, as well as drugs used for treatment of infectious diseases like HIV / AIDS.
But Whitehead Institute researchers have found a mechanism underlying this
resistance — a mechanism that naturally occurs in many diverse
cancer types and that may expose vulnerabilities to drugs that spur the natural
cell - death process.
Now a University of Colorado
Cancer Center study published online ahead of print in the journal Oncogene offers compelling evidence explaining this failure and offering a possible strategy for the use of retinoic acid or other retinoids against some breast cancers: Because early clinical trials are often offered to patients who have already tried other more established therapies, breast cancer cells may have been pushed past an important tipping point that offers retinoic acid resis
Cancer Center study published online ahead of print in the journal Oncogene offers compelling evidence explaining this failure and offering a possible strategy for the use of retinoic acid or other retinoids against some breast
cancers: Because early clinical trials are often offered to patients who have already tried other more established therapies, breast
cancer cells may have been pushed past an important tipping point that offers retinoic acid resis
cancer cells may have been pushed past an important tipping point that offers retinoic acid
resistance.
The ability for
cancer cells to develop
resistance to chemotherapy drugs — known as multi-drug
resistance — remains a leading cause for tumor recurrence and
cancer metastasis, but recent findings offer hope that oncologists could one day direct
cancer cells to «turn off» their
resistance capabilities.
The use of proteasome inhibitors to treat
cancer has been greatly limited by the ability of
cancer cells to develop
resistance to these drugs.
«For years, researchers have focused on delivering more chemotherapy drugs into
cancer cells using nanoparticles, without targeting the root of drug
resistance,» He said.
Women with high levels of FGF1 were less likely to respond to platinum - based drugs, but blocking the gene makes their
cells lose their
resistance (British Journal of
Cancer, DOI: 10.1038 / bjc.2012.410).
While researchers have long worked with nanoparticles for drug delivery, the findings put forth by He and his team represent a crucial breakthrough in addressing multidrug
resistance in
cancer cells.
A new study by researchers at The Ohio State University Comprehensive
Cancer Center — Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC — James) has identified a mechanism by which cancer cells develop resistance to a class of drugs called fibroblast growth factor receptor (FGFR) inhib
Cancer Center — Arthur G. James
Cancer Hospital and Richard J. Solove Research Institute (OSUCCC — James) has identified a mechanism by which cancer cells develop resistance to a class of drugs called fibroblast growth factor receptor (FGFR) inhib
Cancer Hospital and Richard J. Solove Research Institute (OSUCCC — James) has identified a mechanism by which
cancer cells develop resistance to a class of drugs called fibroblast growth factor receptor (FGFR) inhib
cancer cells develop
resistance to a class of drugs called fibroblast growth factor receptor (FGFR) inhibitors.
Researchers at Roswell Park
Cancer Institute (RPCI) have identified a mechanism of breast cancer cells that leads to chemotherapy resistance in inflammatory breast c
Cancer Institute (RPCI) have identified a mechanism of breast
cancer cells that leads to chemotherapy resistance in inflammatory breast c
cancer cells that leads to chemotherapy
resistance in inflammatory breast
cancercancer.
«Breakthrough technique combats
cancer drug
resistance: Researchers «turn off» multi-drug
resistance capabilities in
cancer cells.»
Although proteasome inhibitors are very efficient in selective killing of
cancer tumor
cells grown in a dish (in - vitro), their success in the clinic has largely been undermined by the development of
resistance — mechanisms of which are poorly understood.
Cancer stem - like
cells are thought to be the root cause of chemotherapy
resistance, leading to treatment failure in patients with advanced disease and the triggers of tumour recurrence and metastasis (regrowth).
Analyzing data from thousands of
cancer lines and tumors, the researchers found that those demonstrating
resistance to proteasome inhibitor drugs were marked by suppressed expression of one or more of the
cells» proteasome cap subunits (which are a subsets of the larger proteasome).
Designing molecules that selectively target thiols produced by
cancer cells that cause drug
resistance is the focus of many years» work by Dimmock, Das and their collaborators.
Das explained that since the compounds they've developed make
cancer cells more sensitive to attack, they also remove
resistance to standard chemotherapy drugs — a serious problem in current therapies.
«Study identifies how
cancer cells may develop
resistance to FGFR inhibitors.»
Adult drug resistant
cancer cells may contribute to this problem, and the authors discuss these and other
cancer drug
resistance mechanisms in their recent publication in the September issue of the journal
Cancers.
He and his group had been looking for evidence that normal
cells in the
cancer's environment contribute to chemotherapy
resistance.
The team found that if they raised glutathione levels in
cancer cells in the lab, they reversed
resistance to the drug erlotinib, and the treatment was once again able to kill
cancer cells.
Although alternative drugs are available once erlotinib stops working, these are much more expensive — and they can also stop working due to
cancer cells developing
resistance.
«Recent studies suggest that epigenetic modifications may contribute to the development of
cancer progenitor
cells that can induce drug
resistance and the relapse of different types of
cancer,» said Sibaji Sarkar, PhD, instructor of medicine at BUSM.
Such a lag time, says Hahn, could allow
cancer cells to develop
resistance to a drug by finding some other way to maintain their telomeres.
The drug that they have developed appears to target
cancer stem
cell activity, which suggests it will prevent metastatic recurrence and be useful in combatting drug
resistance.»
Unfortunately, the drug usually stops working within a few months, due to
cancer cells developing
resistance to the treatment.
«We've also started exchanging ideas and information with scientists facing related challenges, such as
resistance to herbicides in weeds and
resistance to drugs in
cancer cells,» Tabashnik said.
My
cancer systems biology team at the University of California, Merced, is tackling diagnosis and treatment of therapy - resistant
cancers by elucidating the network of changes within
cells as a way to identify new drug targets and circumvent
cancer resistance.
While the combination of targeted therapies improves patient outcomes, any remaining
cancer cells can lead to drug
resistance.
«Further research into the detailed mechanisms underlying ASIS in naked mole - rats may shed new light on
cancer resistance in the mole - rats and contribute to the generation of non-tumorigenic human - iPSCs, enabling safer
cell - based therapeutics,» said Kyoko Miura, an assistant professor at Hokkaido University.
Researchers targeting colorectal
cancer stem
cells — the root cause of disease,
resistance to treatment and relapse — have discovered a mechanism to mimic a virus and potentially trigger an immune response to fight the
cancer like an infection.
«Immune
cells help reverse chemotherapy
resistance in ovarian
cancer.»
Tests with kidney
cancer and two human uterine sarcoma
cell lines, one with multidrug
resistance, showed that 10 of these new compounds were impressively potent against all three
cell lines, the researchers reported.
Semenza says previous studies have shown that
resistance to chemotherapy arises from the hardy nature of
cancer stem
cells, which are often found in the centers of tumors, where oxygen levels are quite low.
The regrowth of
cancer stem
cells is responsible for the drug
resistance that develops in many breast tumors and the reason that for many patients, the benefits of chemo are short - lived.
Interferon - inducible protein 6 - 16 (IFI 6 - 16), a protein not previously known to be associated with other misfolding diseases but that was uniquely found misfolded in the urine of women with preeclampsia, is known to help prevent
cell death and, in breast
cancer cells, is responsible for
resistance to treatment.
In animal and
cell culture studies, the drug inhibited growth both in estrogen - dependent breast
cancer cells and in
cells that had developed
resistance to the anti-estrogen tamoxifen and / or to the aromatase inhibitors, two of the most widely used types of drugs to prevent and treat estrogen - dependent breast
cancer.
This analysis, done on separate samples from the same patient, revealed that many of the affected genes confer advantages to
cancer cells by, for example, enhancing
cell migration or
resistance to chemotherapy.
Many investigators had assumed that once breast
cancer cells developed
resistance to tamoxifen, they would be resistant to all drugs that target the estrogen receptor, McDonnell explained.
Cancer stem
cells are strongly associated with the growth and recurrence of all
cancers and are especially difficult to eradicate with normal treatment, which also leads to tumours developing
resistance to other types of therapy.
The new study shows that a «constitutively active» signaling circuit can trigger
cells to grow into tumors and drive therapy
resistance in advanced prostate
cancer.
A new study led by scientists from the Florida campus of The Scripps Research Institute (TSRI) sheds light on a signaling circuit in
cells that drives therapy
resistance in prostate
cancer.
Currently, if breast
cancer cells develop
resistance to these therapies, patients are usually treated with toxic chemotherapy agents that have significant side effects.
Cancer stem cells can be considered the most dangerous type of cancer cells, as they appear to have an inherent resistance to the chemotherapeutic drugs used
Cancer stem
cells can be considered the most dangerous type of
cancer cells, as they appear to have an inherent resistance to the chemotherapeutic drugs used
cancer cells, as they appear to have an inherent
resistance to the chemotherapeutic drugs used today.
The authors said their results, which they have made publicly available, constitute an invaluable resource to help clinicians predict which chemotherapies will be most effective against tumor
cells with particular genetic mutations, and how to rationally combine therapies to prevent
cancers from developing
resistance.
In addition,
cancer cells» susceptibility to these agents varies widely, and tumors often develop
resistance to drugs that initially seem effective.
Cancer stem
cells, a type of self - renewing
cell found in tumors, are of particular interest because they are the main
cell type responsible for tumor progression and for
resistance to chemotherapy and radiotherapy, and therefore a major cause of tumor recurrence after treatment.
The common theory is that the
cancer cell develops «internal
resistance to treatment,» and overrides the toxic effects of the drug.