Sentences with phrase «mutation on their cancer cells»

Among patients who have this type of lung cancer, nearly one in three will carry a particular genetic mutation on their cancer cells.

Further, when TILs have been used for such purposes, the proportion of what Harari calls the «juiciest» T cells — those recognizing mutations on cancer cells — tends to decline significantly when the cells are expanded in culture.

Not exact matches

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?

Targeted cancer treatments are designed to attack molecules produced by mutations, but if the targeted mutation occurs on an evolutionary branch and not the trunk, the treatment will fail as other branches dominate and treatment resistant cells spread.

This mutation is on a particular receptor, or docking site, on the cancer cells that is crucial to the cell's growth and survival.

Although some cancers — particularly those that are rife with mutations like lung cancer or melanoma — create more tangible targets on the surface of cells for the immune system to recognize and attack, other malignancies such as prostate and pancreatic cancers have proved more intransigent.

Kornelia Polyak, an oncologist at Harvard Medical School in Boston, says that cancer researchers tend to focus on the mutations inside cells, and fail to consider how those mutated cells might influence the cells around them.

«We began with stem cells taken from cord - blood, which have fewer acquired mutations and little, if any, epigenetic memory, which cells accumulate as time goes on,» says Zambidis, associate professor of oncology and pediatrics at the Johns Hopkins Institute for Cell Engineering and the Kimmel Cancer Center.

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.

Previous studies of genetic alterations in lymphoma and lung cancer have found that certain genetic mutations — specifically when part of a gene breaks off and gets fused to another — can inappropriately switch on ALK, driving cancer cells to grow and divide.

However, on page 1391 in this issue, Yun et al. (5) show that high doses of vitamin C selectively kill colorectal cancer cells carrying activating mutations in the oncogenes KRAS or BRAF, which are often refractory to approved targeted therapies.

The runaway replication of cancer cells can also traced to genetic causes — mutations that remove the normal controls on cell growth.

Half of all melanomas harbor an activating mutation in the BRAF gene that turns on the cancer signaling pathway in cells known as the MAP kinase pathway.

The study builds on Polyak's earlier research finding that women already identified as having a high risk of developing cancer — namely those with a mutation called BRCA1 or BRCA2 — or women who did not give birth before their 30s had a higher number of mammary gland progenitor cells.

In addition to the afatinib - resistant NSCLC cells, the researchers tested the neratinib and valproic acid combination on cell lines derived from human pancreatic and ovarian cancers containing K - Ras mutations and N - Ras mutations, respectively.

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.

«We found that colorectal cancer cells survived under the condition of glucose depletion, and their resistance to such conditions depended on genomic alterations rather than on KRAS mutation alone.

Research fields are diverse, including basic research on cell proliferation, analysis of tumour cells and tissues to detect gene mutations, and identification of potential therapeutic targets in cancer.

The new DETECTR system, created at UC Berkeley based on CRISPR - Cas12a, can analyze cells, blood, saliva, urine and stool to detect genetic mutations, cancer and antibiotic resistance as well as diagnose bacterial and viral infections.

Students in the UBC program engage in a wide range of research: molecular mechanisms underlying cell proliferation in cancer or cell death in stroke; relating gene mutations to disease mechanisms; the social factors that determine access to health care for women living on the street.

Mutations in a gene that helps regulate when genes are switched on and off in cells have been found to cause rare cases of Wilms tumour, the most common kidney cancer occurring in children.

The researchers, including scientists from pharmaceutical company AstraZeneca, report in an advanced online publication in Nature Medicine on May 4, that their findings indicate «an underappreciated genomic heterogeneity» in mechanisms of resistance to tyrosine kinase inhibitor (TKI) drugs that target the Epidermal Growth Factor Receptor (EGFR) mutation that drive some cases of non-small cell lung cancer (NSCLC).

Because cancer cells acquire mutations in oncogenes — genes that can transform cells into cancer cells — to support their growth and survival, a great deal of research has focused on identifying oncogenes that could be targeted by cancer drugs.

Neoantigens are molecules on cell's surfaces that are produced by DNA mutations that are present in cancer cells but not in normal cells, making neoantigens ideal targets for immune therapy against cancer, say the scientists.

By contrast, the neoantigen vaccine is custom - made for each patient using antigens produced by mutations unique to the patient's cancer and only present on cancer cells, thus bypassing the nature immune tolerance process.

The aims of the CEMC are to define the step-wise molecular and cellular alterations that occur during the process of carcinogenesis; determine how environmental exposures cause key genetic mutations and epigenetic changes that underlie carcinogenesis; and discover the impact of environmental factors on the generation and maintenance of cancer stem cells.

On the other hand, genetic mutations that further promote the growth of intestinal stem cells are associated with uncontrolled organ regeneration and the development of colon cancer.

But in a study published April 5 in Cell, Kevan Shokat, PhD, a professor of cellular and molecular pharmacology, and postdoctoral researcher Qi Hu, PhD, discovered that another common cancer - causing mutation in a GTPase called Gαs (or G - alpha - s) subverts the model: it doesn't just jam the switch in the «on» position, but also disconnects the switch entirely.

Thus the search is on is to discover additional cancer - causing genes «downstream» of TET mutations that drive uncontrolled cell division in either context.

According to recent research, the most common solid tumors (that is, cancer that occurs as clusters of cells in or on organs, rather than in liquid form within the blood or lymphatic system) have up to 66 mutations that influence how the cancer cells operate — how fast they divide, whether they are susceptible to the signals that would normally cause a cell to die, when they detach from the main tumor to colonize another organ in the body, when and where they attach blood vessels to healthy tissues.

Understanding the effects of Eph receptor mutations in cancer cells will help shed light on the role of the Eph receptor / ephrin system in cancer cell transformation, malignant progression and drug resistance.

Fortunately, experiments done by Dr. Jan Vijg at the Albert Einstein College of Medicine and others on mutations (changes in base sequence in DNA) and additional studies commissioned by SENS Research Foundation on epimutations (changes in the arrangement of methyl groups) suggest that these latter kinds of alterations - the kind that accumulate in cells without triggering apoptosis or senescence or contributing to cancer - accumulate too slowly to make a difference with the current lifespan.

Areas of focus include: understanding how tumour - reactive T cells and B cells promote patient survival in cancer; defining the effects of standard treatments on tumor immunity; and using genomic approaches to identify novel tumour mutations that can serve as target antigens for immunotherapy.

Depending on their location in the genome and the proportion of cells they are present in, these mosaic mutations can cause a wide range of genetic disease syndromes and predispose carriers to cancer.

This dichotomy points out the importance of an indirect influence on proteins whose altered function is required during carcinogenesis but are too essential to be mutated (i.e., mutation of their encoding genes could decrease the viability of cancer cells).

The genesis of cancer has been typically been focused on DNA mutations leading to cell proliferation.

According to Lewis Cantley, director of the Cancer Center at Beth Israel Deaconess Medical Center at Harvard Medical School, as much as 80 percent of all cancers are «driven by either mutations or environmental factors that work to enhance or mimic the effect of insulin on the incipient tumor cells,» Gary Taubes reports, vii adding:

Some cancers develop mutations that serve the purpose of increasing the influence of insulin on the cell; others take advantage of the elevated insulin levels that are common to metabolic syndrome, obesity and type 2 diabetes.

What's worse, when free radicals wreak havoc on cell DNA they cause cell mutations that may result in skin cancer, including melanoma.

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 cCancer Research on the treatment of bladder cancercancer.