Sentences with phrase «dna in cancer cells»

The drug is formed from groups of molecules attached to a platinum atom, creating a compound that reacts with DNA in cancer cells.

They knew that they had found a new type of genetic defect, because the DNA in cancer cells from people with the altered gene was riddled with mutations.

Not exact matches

In the laboratory, steviol can be converted into a mutagenic compound — if cell DNA becomes mutagenic, cancer may ensue.

The increased mitochondrial DNA in the genomes of the cancer cells observed by the UAB team suggests somatic insertion of mitochondrial DNA occurred as the cancer developed.

Patients with colon and rectal cancer have somatic insertions of mitochondrial DNA into the nuclear genomes of the cancer cells, University of Alabama at Birmingham researchers report in the journal Genome Medicine.

Carcinogens may cause cancer by altering cellular metabolism or damaging DNA directly in cells, which interferes with normal biological processes.

A type of immune therapy known as PD - 1 blockade controlled cancer in 77 percent of patients with defects in DNA mismatch repair — the system cells use to spell - check and fix errors in DNA (SN Online: 10/7/15).

Scientists investigating the earliest stages of cancer development used an exquisitely sensitive sequencing method capable of detecting DNA mutations present in as few as 1.6 per cent of blood cells, to analyse 15 locations in the genome, which are known to be altered in leukemia.

The study found that carfilzomib and irinotecan have a potential synergistic effect in SCLC and other Irinotecan - sensitive cancers by allowing normal DNA damage repair and enabling normal cell - cycle death.

We know that they are under stress when they are fighting cancer or other diseases, so I wondered whether anything measureable could be seen if we put them under further stress with UVA light.We found that people with cancer have DNA which is more easily damaged by ultraviolet light than other people, so the test shows the sensitivity to damage of all the DNA — the genome — in a cell.»

Scientists at The Institute of Cancer Research, London, and the Wellcome Trust Sanger Institute used DNA sequencing to identify a panel of mutations present across thousands of cancer cells in three patients with leukCancer Research, London, and the Wellcome Trust Sanger Institute used DNA sequencing to identify a panel of mutations present across thousands of cancer cells in three patients with leukcancer cells in three patients with leukaemia.

According to Radu, «this new dual targeting approach shows that we can overcome the redundancy in DNA synthesis in ALL cells and identifies a potential target for metabolic intervention in ALL, and possibly in other hematological cancers.»

FRESH insight into prostate cancer has come in a study showing that the mitochondrial DNA of human prostate cancer cells is riddled with mutations.

PARP inhibitors also cause PARP to become trapped in the cancer cells» DNA, a process that is greatly enhanced when a DMNT inhibitor is added, Dr. Rassool says.

By promoting DNA demethylation, high - dose vitamin C treatment induced stem cells to mature, and also suppressed the growth of leukemia cancer stem cells from human patients implanted in mice.

When combined, these agents cause interactions that significantly disrupt cancer cells» ability to survive DNA damage, according to a preclinical study published in the journal Cancercancer cells» ability to survive DNA damage, according to a preclinical study published in the journal CancerCancer Cell.

Trifluridine, by contrast, does integrate into cancer cell DNA, but proved to be too toxic to patients when given in doses necessary to kill the cancer cells.

This suggests that random errors occurring during DNA replication in normal stem cells are a major contributing factor in cancer development.

First, the research demonstrates that RB status can be tracked using cell - free DNA samples, an approach referred to as «liquid biopsy,» in prostate cancer patient samples.

Now, results described in tomorrow's issue of Nature suggest that BRCA2 mutations could lead to cancer by interfering with cells» ability to repair damaged DNA.

Spearheaded by first author Christopher McNair, PhD, a graduate student in the laboratory of Dr. Knudsen, the study undertook an extensive analysis of tumor samples and cell - free DNA samples from patients with advanced, lethal - stage prostate cancer.

Being obese or having a higher body mass index (BMI) while carrying a BRCA (BReast CAncer gene) mutation is positively linked with higher levels of damage to the DNA in normal breast gland cells, new research suggests.

Working together, Johns Hopkins biomedical engineers and neurosurgeons report that they have created tiny, biodegradable «nanoparticles» able to carry DNA to brain cancer cells in mice.

Olaparib is good at killing cancer cells that have errors in genes that have a role in repairing damaged DNA such as BRCA1 or BRCA2.

«FDG PET shows tumor DNA levels in blood are linked to NSCLC aggressiveness: Insights derived from FDG PET could improve treatment selection for patients with advanced non-small cell lung cancer.»

«Despite the identification of circulating tumor cells (CTCs) and cell - free DNA (cfDNA) as biomarkers capable of providing clinically relevant information in cancer patients, at present their identification is not routinely used in clinical practice,» explains Silvia Morbelli, MD, PhD, of the IRCCS San Martino — IST National Cancer Research Institute and University of Genoa in Genoa, cancer patients, at present their identification is not routinely used in clinical practice,» explains Silvia Morbelli, MD, PhD, of the IRCCS San Martino — IST National Cancer Research Institute and University of Genoa in Genoa, Cancer Research Institute and University of Genoa in Genoa, Italy.

They found that cancer cells had acquired new genetic changes that cancelled out the original errors in DNA repair — particularly in the genes BRCA2 and PALB2 — that had made the cancer susceptible to olaparib in the first place.

«DNA repair helps thwart cancer and keep the cell in top shape — it is usually all in a day's work within each cell,» Dr. Durocher adds.

In a study presented in the featured clinical investigation article of the November issue of The Journal of Nuclear Medicine, they used 18F - fluorodeoxyglucose (FDG) PET / CT imaging to show that the amount of cell - free tumor DNA circulating in the bloodstream correlates with tumor metabolism (linked to cancer aggressiveness), not tumor burden (amount of cancer in the bodyIn a study presented in the featured clinical investigation article of the November issue of The Journal of Nuclear Medicine, they used 18F - fluorodeoxyglucose (FDG) PET / CT imaging to show that the amount of cell - free tumor DNA circulating in the bloodstream correlates with tumor metabolism (linked to cancer aggressiveness), not tumor burden (amount of cancer in the bodyin the featured clinical investigation article of the November issue of The Journal of Nuclear Medicine, they used 18F - fluorodeoxyglucose (FDG) PET / CT imaging to show that the amount of cell - free tumor DNA circulating in the bloodstream correlates with tumor metabolism (linked to cancer aggressiveness), not tumor burden (amount of cancer in the bodyin the bloodstream correlates with tumor metabolism (linked to cancer aggressiveness), not tumor burden (amount of cancer in the bodyin the body).

Klingelhutz and his team immortalized immature precursor fat cells by adding in two genes from HPV (the virus that causes cervical cancer) along with a gene for part of an enzyme that controls the length of cells» telomeres — the pieces of DNA that protect chromosome tips from deterioration.

In addition, they showed for the first time that these genes are often the same as those that are altered in breast tumours - when a tumour develops, the DNA within the cancer cells themselves mutateIn addition, they showed for the first time that these genes are often the same as those that are altered in breast tumours - when a tumour develops, the DNA within the cancer cells themselves mutatein breast tumours - when a tumour develops, the DNA within the cancer cells themselves mutates.

The size difference between tumor and healthy circulating DNA was initially discovered in animal tumor models created by inducing tumors with human cancer cells.

In previous research, this team of University of Alberta researchers found that PRC1 complex helps to repair DNA damage in cancer cellIn previous research, this team of University of Alberta researchers found that PRC1 complex helps to repair DNA damage in cancer cellin cancer cells.

«High concordance between EGFR mutations from circulating - free tumor DNA and tumor tissue in non-small cell lung cancer.»

Epidermal growth factor receptor (EGFR) mutations found in the circulating free tumor DNA (ctDNA) from the plasma of advanced non-small cell lung cancer (NSCLC) patients correlates well with the EGFR mutations from patient - matched tumor tissue DNA.

The proposed clinical trial, in which researchers would use CRISPR to engineer immune cells to fight cancer, won approval from the Recombinant DNA Advisory Committee (RAC) at the U.S. National Institutes of Health, a panel that has traditionally vetted the safety and ethics of gene therapy trials funded by the U.S. government and others.

«Potentially reversible changes in gene control «prime» pancreatic cancer cells to spread: Epigenetic changes, not DNA mutations, drive some metastasis.»

Dr. Ella Evron and Dr. Ayelet Avraham of the TAU - affiliated Assaf Harofeh Medical Center, together with Prof. Saraswati Sukumar of Johns Hopkins, have found that «gene regulation,» the process that shuts off certain parts of a cell's DNA code or blueprint in healthy breast tissue cells, may also play a critical role in the development of breast cancer.

Ali found that breast cancer cells that have high levels of RYBP are more sensitive to DNA damage after radiation or drug treatment, including PARP inhibitors (inhibitors of the enzyme poly ADP ribose polymerase used in cancer treatment).

Importantly, like cancer cells with other mutations in the HR repair pathway, CHD1 - depleted prostate cancer cells proved to be hypersensitive to chemotherapeutic drugs causing DNA breaks, such as Mitomycin C, Irinotecan and PARP inhibitors.

Min Huang, Jian Ding, and colleagues at the Shanghai Institute of Materia Medica, Chinese Academy of Sciences, discovered that inhibiting PGAM1 made cancer cells more sensitive to drugs that induce breaks in both strands of the cells» DNA.

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.

A team of researchers in Germany and Denmark led by Steven Johnsen, Professor at the University Medical Center Göttingen, Germany, used human prostate cancer cell lines and depleted them of the DNA - binding protein CHD1.

Previously, cancer researchers surmised that since chromosomal ends get swapped in ALT, mutation of genes that restrain DNA exchange, a process scientists call recombination, might actually cause the condition (or, to extend the ping - pong metaphor, make cells lose paddle control).

Mutagens are chemicals that can cause DNA damage in cells that in turn can cause cancer.

The technique typically homes in on circulating - tumor DNA (ctDNA), genetic material that routinely finds its way from cancer cells into the bloodstream.

Moreover, in some cases, pancreatic cancer cells can even repair damage to their DNA caused by the chemotherapy drugs that do get into the tumor, further protecting themselves.

Now his lab has found that Set2 is also a major player in DNA repair, a complicated and crucial process that can lead to the development of cancer cells if the repair goes wrong.

They work particularly well if the cancer cells they attack already have defects in the corresponding DNA repair pathways, as it frequently occurs in breast cancer and other tumors.

Dr. Vasmatzis» research on the «Quantification of Somatic Chromosomal Rearrangements in Circulating Cell - free DNA From Ovarian Cancers» is published in the July 20 edition of Scientific Reports.