Sentences with phrase «tumor cell mutation»

So far this year, American Veterinarian ® has reported on immunotherapies that may slow growth or even shrink gliomas in dogs and humans, a liquid biopsy assessment tool to detect tumor cell mutation, and a shared study between the American Kennel Club Canine Health Foundation and the V Foundation for Cancer Research on the treatment of bladder cancer.

Molecular testing: Some primary brain tumors, including some of the most common types of gliomas, are defined by their key molecular features resulting from tumor cell mutations.

Not exact matches

Their tumors also need to have a specific gene mutation that leads to the repair of cancerous cells.

As a cancer researcher, do you think the mechanisms of tumor growth are somehow changing to come into line with your perceptions, or is it possible that the process of our learning more about DNA mutations and cell architecture and nutrient exchange and epigenetic effects make it possible for us to inch ever closer to understanding that which is already going on under our noses?

Chan's laboratory uses genomic analyses to identify neoantigens — novel peptides found only in tumors that arise from mutations accumulated by cancerous cells.

In this special section of Science, expert contributors retrace the long and tortuous path leading to the mapping and identification of the BRCA1 gene; discuss the ways in which BRCA mutation status has been integrated into the clinical management of patients in high - risk families; and highlight the role of the BRCA proteins in preserving the structural and numerical integrity of chromosomes throughout the cell cycle, a function that may explain their tumor suppressor activity.

Cancer cells which arise due to genetic mutations are just such cells, and there are studies which suggest that microchimeric cells may stimulate the immune system to stem the growth of tumors.

Two genetic mutations in liver cells may drive tumor formation in intrahepatic cholangiocarcinoma (iCCA), the second most common form of liver cancer, according to a research published in the July issue of the journal Nature.

They found that depending on the cell of origin, mutations in PIK3CA and p53 induced very different types of tumors.

Bowel cancer, also called colorectal cancer, results from a series of genetic changes (mutations) that cause healthy cells to become progressively cancerous, first forming early tumors called polyps that can eventually become malignant.

«Just as normal cells with the same genome differentiate into many different cell types, a single tumor characterized by specific genetic mutations can contain many different types of cells — stem - like and more differentiated cells — with the difference being rooted in their epigenetic information.

Importantly, these three developmental signatures were found in distinct genetic clones — cells with identical patterns of genetic mutations — of tumor cells.

The drug causes tumor cells with a certain mutation — present in about 60 percent of melanomas — to commit suicide.

Mutations transform the genome of a tumor; its cells become genetic outlaws that spread, ignore normal stop - and - go signals and evade cancer - killing drugs or radiation.

Women with the KRAS - variant are also more susceptible to triple - negative breast cancer, tumors whose growth is not fueled by the hormones estrogen and progesterone, or by the presence of a particular genetic mutation known as HER2, which promotes cancer cell growth.

With a less efficient helicase and therefore less efficient DNA repair, Martin suggests, atherosclerotic lesions could arise like tumors from mutations in single cells, besides their well - known origin from chronic inflammation from high - fat diets.

«When cancer comes back, it's genetically very similar to the original tumor but often with additional mutations that may give cancer cells new strategies to survive attack by whatever drugs are thrown at them.

ON THE ROAD Breast cancer cells may break away from the main tumor in clumps, already bearing most of the mutations that will drive cancer recurrence, a study suggests.

How it spreads: Unlike normal cancers, where the disease - causing mutation is confined to one organism, devil facial tumor disease (DFTD) cells have evolved the ability to spread from devil to devil.

PTEN prevents tumor cells from growing uncontrollably, and mutations in the gene encoding this protein are commonly found in many different types of cancer.

The arithmetic is complex, but the consensus is that, to pose a health threat, cancers have to replicate at least 200 to 300 times, even though a clinically relevant tumor contains «only» a million million cells, which could be achieved by «only» 40 or so divisions if the originating cell had all the necessary mutations from the outset.

«One of the major and immediate downstream effects of myc activation is a dramatic increase in the capacity of affected cells to make protein,» Ruggero said «This, in turn, leads to increased cell survival and proliferation, and to unstable genomes that foster additional mutations that turn these abnormal cells into tumor cells.»

Yet, Hockemeyer says, telomerase levels are marginal, resulting is some unprotected chromosome ends in the surviving mutant cells, which could cause mutations and further fuel tumor formation.

The team integrated three, complementary gene sequencing approaches to look for mutations in tumor cells from SS patients: whole - genome sequencing in six subjects, sequencing of all protein - coding regions (exomes) in 66 subjects, and comparing variation in the number of copies of all genes across the genome in 80 subjects.

A mutation that helps make cells immortal is critical to the development of a tumor, but new research at the University of California, Berkeley suggests that becoming immortal is a more complicated process than originally thought.

«This finding has immediate clinical applications, because either mutation - PPM1D or TP53 — cause the tumor cells to be resistant to radiation,» said senior author Hai Yan, M.D., Ph.D., a professor of pathology at Duke University School of Medicine.

The researchers identified a genetic mutation in the tumor cells that plays a role in both the growth and the death of a cell.

The progression from gene mutation in the renal cells to the development of a tumor took eight to twelve months.

The researchers conducted genetic tests and found that many of the tumor cells had a mutation in a gene called PPM1D, which causes cells to proliferate and avoid natural death.

They tested these drugs one at a time for lethal interaction with 112 different tumor - suppressor gene mutations in human cancer cells growing in the lab.

In this mouse model, mutations in Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different colors.

«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.

Such genes help regulate cell division, and when they are missing or inactivated by mutations, cell division runs amok, resulting in tumors.

Researchers are creating organoids from tumor cells to mimic cancers and introducing specific mutations into organoids made from healthy tissue to study how cancer arises.

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.

«We know very little about how gene mutations in tumor cells can change how a tumor might respond or not to certain chemotherapy drugs.

For example, in colorectal cancer lab models, where a mutation in the beta - catenin gene drives MYC to cancerous levels, eliminating PVT1 from these cells made the tumors nearly disappear.

Rather than artificially triggering cancer by engineering genetic mutations, this model more closely mimics human liver cancer in that tumors develop as a natural consequence of non-alcoholic steatohepatitis (NASH), a chronic metabolic disorder that causes liver damage, fibrosis and numerous cell mutations.

«You can see they are very active and affect the DNA in the tumor tremendously, causing lots of mutations that may further the cells» uncontrolled growth, says Alon Keinan, a computational biologist at Cornell University.

Surprisingly, they found that although the patterns of gene expression — as shown by the RNA sequencing — differed between the hepatocellular carcinomas and the liver cancers with biliary phenotype and depended on the histological type, the overall pattern of mutations in the cells was actually similar between the tumors — of either type — that had emerged in patients who had had infections with either hepatitis C or B, and were different in patients without such infections.

About half of melanoma patients harbor an identical tumor - specific mutation in the BRAF gene, which encodes a protein kinase that helps drive cell growth.

In Wilms tumors, one set of mutations promotes abnormal and continued proliferation of the undifferentiated cells.

«While we expected to find some mutations in stem cell lines, we were surprised to find that about five percent of the stem cell lines we analyzed had acquired mutations in a tumor - suppressing gene called p53,» said Merkle.

Research from other scientists at Johns Hopkins, he says, had suggested that some tumors, particularly those that affect the nervous system, have mutations in the ATRX gene, which produces proteins that appear to maintain the length of telomeres, repetitive segments of DNA on the ends of chromosomes that typically shorten each time a cell divides.

Building on research recently published in Cell Reports, the researchers identified new mutations that appeared to be driving the strong drug resistance exhibited by these tumors.

The role of rebiopsy and repeat analysis in the setting of post-treatment relapse, along with testing of blood samples for mutations in circulating tumor cells, cell free tumor DNA, or exosomes will be considered.

While these mutations do not directly relate to the development or progression of a tumor, they can reveal its lineage — how individual tumor cells are related to each other.

Results of an initial study of tumors from patients with lung cancer or head and neck cancer suggest that the widespread acquired resistance to immunotherapy drugs known as checkpoint inhibitors may be due to the elimination of certain genetic mutations needed to enable the immune system to recognize and attack malignant cells.

DNA mutations cause tumor cells to grow out of control, but they also generate variety that enables organisms to adapt to their environments and evolve.