Sentences with phrase «tumour dna»

Although the level of tumour DNA present in the blood is much lower during the early stages of these cancers, the program was still able to make a diagnosis demonstrating the potential of this method for the early detection of cancer, according to the researchers.

The DNA from cancer cells is mutated and this mutated DNA can get into the blood stream (circulating tumour DNA, ctDNA) and be detected by sequencing the DNA in blood.

Monitoring response to therapy in melanoma by quantifying circulating tumour DNA with droplet digital PCR for BRAF and NRAS mutations.

The sensitivity for detecting the presence of genomic changes in circulating tumour DNA (ctDNA) is limited by its low concentration in plasma.

It is hoped that these approaches will allow doctors to use circulating tumour DNA to tailor treatment for individual patients to get the best result.

In this early work they found they could see whether a patient was relapsing by tracking levels of circulating tumour DNA.

The researchers used a technique called «mutation tracking» — developing a digital PCR test that was personalised to the mutations found in an individual patient's cancer — to identify tumour DNA in the bloodstream.

Women who tested positive for circulating tumour DNA were at 12 times the risk of relapse of those who tested negative, and the return of their cancer was detected an average of 7.9 months before any visible signs emerged.

They found that it took longer for the disease to progress in patients whose tumour DNA count in the blood fell by more than a half after one cycle of chemotherapy, compared with patients whose DNA count did not drop.

They also showed that the level of tumour DNA in the blood reflects the amount of cancer seen on scans carried out before chemotherapy.

In a study of 40 patients with high grade serous ovarian cancer, the researchers monitored tumour DNA that could be detected in a blood sample taken before each chemotherapy treatment.

The researchers tested levels of this circulating tumour DNA in patients before and after treatment.

«The circulating tumour DNA values in the blood samples identified the metastases on average 11 months before they were diagnosed by standard clinical procedures.

Researchers then looked in the blood samples for circulating tumour DNA (ctDNA) with the same fingerprint.

Not exact matches

But the chemical has since 1995 been ruled as unsafe in food for human consumption because it is capable of causing damage to one's DNA which can potentially lead to the formation of malignant tumours.

Such keys could be used to unlock a cancer drug - filled DNA box at a tumour site.

We now have the first direct evidence that switching off certain genes — something that can be caused by our lifestyle or environment — can trigger tumours, without mutating the DNA itself.

In the body they form metabolites that react readily with DNA to produce mutations that in turn can cause tumours.

Now, the researchers have discovered an alternative in a mouse model: in the case of breast tumours with a specific defect in DNA repair, the animals can be cured using already established, cheap chemotherapy drugs, if enough DNA damage can be inflicted on the resting tumour cells.

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 mutates.

Prostate cancer researchers have mapped the impact of an acquired mutation that alters epigenetic identity, the make - up of DNA, in about 50 % of patient tumour samples.

So if biologists can discover how to disable cancer cells» DNA repair proteins, it may be possible to destroy tumours using lower doses of radiation or drugs.

RUNX3 is a tumour suppressor gene that prevents the formation of tumours by binding to DNA.

If these could be targeted to tumours — by attaching them to antibodies that recognise cancer cells, for instance — it would then be possible to destroy the malignant cells» DNA using lower doses of radiation or drugs.

In the retrospective study, the team sequenced the DNA of 299 tumours from 170 patients with breast cancer that either returned in the remaining breast — local relapse — or had spread — metastatic breast cancer.

Putting together their analyses of the mitochondrial DNA in each tumour cell line and the metabolic pathways at work, the team were able to deduce how each cell line's genetics directly affected its ability to multiply.

Such is the case for a DNA letter in the gene that encodes the protein called tumour necrosis factor receptor 1 (TNFR1).

The researchers demonstrated that this process requires FAK in order to work, and without it, these signals are never sent — making the tumour more vulnerable to DNA damaging therapy.

Cells lining the blood vessels send chemical signals, called cytokines, to the tumour to help it resist DNA damage and to recover.

In rats, tamoxifen causes liver tumours and appears to alter DNA in liver cells (This Week, 29 February and 14 March).

The response rate was much higher in patients whose tumours carried mutations to genes involved in repairing DNA.

The DNA of BKV has been discovered in several types of human cancers including prostate tumours, and mouse studies suggest the virus can trigger cancer.

Hart and Vile hooked up the switch gene to the marker gene and injected the DNA directly into two types of mouse tumour.

The study involved the researchers using powerful computers to conduct in - depth analysis of 700 billion DNA sequences from more than 4,000 tumours.

This point should be taken into consideration when studying DNA mutation and repair processes and in studies on evolution, whether in tumours or species,» López - Bigas says.

DNA shed from tumour cells has been identified as a non-invasive method of screening biomarkers for the early diagnosis and prognosis of cancer

In this film Professor Sir Mike Stratton (director of the Wellcome Trust Sanger Institute) describes how mutations in DNA can cause a cell to grow out of control and develop into a cancerous tumour.

In the genome of tumour cells of 11 patients, the scientists observed the insertion of a viral DNA segment from adeno - associated virus type 2, known as AAV2.

Recently, DNA shed from tumour cells has been identified as a non-invasive method of screening biomarkers for the early diagnosis and prognosis of cancer.

In this film she describes her day - to - day role in the laboratory, processing tumour samples and setting up experiments to analyse DNA.

BRCA1 is a tumour suppressor gene involved in DNA repair through homologous recombination and in preserving the integrity of the genome.

They thus confirmed their hypothesis: the integration of viral DNA was found more often in tumour cells than in healthy cells in these 11 patients.

However, not many reports are available regarding the mechanism of TRF2 mediated DNA damage response and its role in tumour stem cells.

«They have used an idea of making a carrier from DNA, like a little parcel, to carry thrombin to a tumour and this little «parcel» unfolds when it encounters the tumour site and releases the thrombin which will coagulate the local blood supply to the tumour causing it to die.

For example, whereas the p53 / p63 / p73 tumour suppressor family is holozoan - specific31, the HIPK kinase that phosphorylates p53 in the presence of DNA breaks is metazoan - specific, and the MDM2 ubiquitin ligase that regulates p53 appears as a eumetazoan feature.

The program works by looking for specific molecular patterns in cancer DNA that is free flowing in the patients» blood and comparing the patterns against a database of tumour epigenetics, from different cancer types, collated by the authors.

BRCA2 tumour suppressor protein has a recognized role in the repair of DNA double strand breaks by homologous recombination.

Kelley, lead investigator on the study published today in Nature Chemistry, explained how her team has advanced a completely new approach using magnetic nanoparticles with DNA capture probes on their surface that can target circulating tumour cells (CTCs) in blood samples to see if the cells contains biomarkers associated with drug resistance.

Differential protein expression, DNA binding and interaction with SV40 large tumour antigen implicate the p63 - family of proteins in replicative senescence.

The afternoon of the second day focused on somatic changes in melanoma, that is changes that occur in the tumour itself, and this session saw talks from ESR07 Sofia Chen on the mutational landscape of primary melanoma tumours; ESR08 Catarina Salgado on DNA hydroxymethylation (a form of regulation) in melanoma and naevi; and ESR10 Adriana Sanna on epigenetic regulation (reversible changes to the DNA which can turn genes on / off) of melanoma cell phenotypes.