Sentences with phrase «such tumor cells»

In contrast to other cultured cells, such tumor cells can divide indefinitely and a cell line can therefore be cultured for many years.

However, such tumor cells display unusual antigens that are either inappropriate for the cell type or its environment, and can thus be recognized by the body's immune system.

Not exact matches

Immunotherapy differs from more traditional cancer treatments, such as surgery (cutting malignant cells out of the body), chemotherapy and radiation (poisoning the deadly mutants), and even the newer, more precise molecular drugs that attempt to jam the protein signals that tell tumor cells to keep dividing and conquering.

However, the impact of the two methylation - regulating enzymes was still seen at 10 to 15 months, when scientists found decreased expression of hundreds of genes — many of which are key tumor suppressor genes such as BMP3, SFRP2 and GATA4 — in the smoke - exposed cells and a five - or - more-fold increase in the signaling of the KRAS oncogene that is known to be mutated in smoking - related lung cancers.

«There was this initial thought that [circulating tumor cells] are only present at late stage,» says Sollier - Christen, but she notes that in the past year, several studies using more sensitive techniques have found such cells much earlier in tumor development, even before the tumor becomes visible by conventional imaging techniques.

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.

So far, researchers with the Allen Institute for Brain Science in Seattle have described the intricate shapes and electrical properties of about 100 nerve cells, or neurons, taken from the brains of 36 patients as they underwent surgery for conditions such as brain tumors or epilepsy.

Researchers used tissue and blood samples to show that the gammopathy (a precursor to myeloma) in both mice and patients with Gaucher disease is triggered by specific lipids, and that the antibodies made by tumor cells in nearly a third of myeloma patients are directed against such lipids.

Potti and his colleagues began by testing chemotherapy drugs on cultured cell lines from human tumors, such as from the lung, breast, or ovary.

«Our work strongly supports that cancer stem cells are the main source of growth in these tumors and, as such, should be considered promising targets for treatment,» says Mario Suvà, MD, PhD, of the MGH Department of Pathology, co-senior author of the Nature paper.

Several studies have supported a role for cancer stem cells in the aggressive brain tumors called glioblastoma, but those studies involved inducing human tumors to grow in mice, and as such their relevance to cancer in humans has been questioned.

These findings also have implications for treatment of cancer and other disorders, such as obesity, in which M2 macrophage cells play a regulatory role in tumor growth and fat deposition.

To acquire new insights into the biology and possible therapy of these tumors, Feigin et al. looked for aberrant expression of G protein — coupled receptors, cell signaling proteins that have been successfully targeted for treatment of other disorders such as depression.

The study published in Cancer Cell shows that exosomes from tumor cells of breast cancer (and other tumor types such as ovarian and endometrial) are different in size and composition than those of healthy cells.

Most cancer vaccines developed to date have been designed to recognize and attack a specific known molecule — such as a cell - surface receptor — that is likely to be found on cancerous cells in any patient with that type of tumor.

In principle, an attack by such T - cells on tumors should be particularly powerful as well as highly tumor - specific and thus sparing of healthy cells.

In cancer, these switches inappropriately activate or silence important genes, such as those that regulate cell growth and life cycle, ultimately leading to tumors.

The cells in such a brain tumor can display very different characteristics, such as varying cell size or number of cell nuclei.

Within a single tumor exists such an astonishingly varied population of cells, each with its own combination of normal and abnormal genes, that at least some cells nearly always have a way to survive any particular attack.

The ability of tumor - infiltrating lymphocytes (TILs) such as T cells to produce multitudes of clones that overwhelm and effectively control cancer cells has been demonstrated, but the significance of the composition of T - cell repertories is unknown.

Proliferation of such cells, which tend to resist chemotherapy and help tumors spread, are considered a major roadblock to successful cancer treatment.

«Our data strongly suggest that KIF1Bβ, which is localized on chromosome 1p36, might be such a neuroblastoma tumor suppressor gene,» says principal investigator Susanne Schlisio at the Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet and Assistant Member at the Ludwig Institute for Cancer Research in Stockholm, Swtumor suppressor gene,» says principal investigator Susanne Schlisio at the Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet and Assistant Member at the Ludwig Institute for Cancer Research in Stockholm, SwTumor and Cell Biology at Karolinska Institutet and Assistant Member at the Ludwig Institute for Cancer Research in Stockholm, Sweden.

Unaltered cells created tumors in all seven mice injected with such cells, but when cells missing ALKBH5 were used, they caused tumors in only 43 percent (six out of 14) of mice.

Each T cell, scientists believed, was programmed to recognize a particular snippet of protein, or peptide, unique to invaders such as bacteria, viruses or tumor cells.

They already knew of one such compound, a chemical called PD09859 that is one of 60,000 agents the NCI had screened for ability to block growth of human tumor cells.

«But mounting evidence confirming angiotropism and EVMM has revolutionized the knowledge of how cancer spreads through the body to the point that other scientists have confirmed the process in other solid tumor cell types such as pancreatic cancer.»

Rather than target a tumor - suppressor gene directly, Ideker and team took the approach of identifying genetic interactions between a tumor suppressor gene and another gene, such that simultaneous disruption of both genes selectively kills cancer cells.

Fine got federal approval this year to try such a drug screen on one patient whom he describes as «well - connected,» creating an organoid from her cells and adding bits of her tumor to it in hopes of throwing drug after drug at it until one vanquished the organoid's cancer.

«The treatment of multiple myeloma has improved significantly in recent years with the introduction of therapies such as proteasome inhibitors [which interfere with tumor cells» protein - disposal system] and potent immuno - modulatory agents,» said the paper's senior author and lead investigator, Paul Richardson, MD, clinical program leader and director of clinical research at Dana - Farber's Jerome Lipper Multiple Myeloma Center, and the R.J. Corman professor at Harvard Medical School.

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

Some types of innate immune cells, such as natural killer cells, can actually protect against tumor growth.

It was never known that endothelial tip cells have such unique secretion or deposition profiles, let alone shown that these profiles actually favor tumor growth.»

Inhibition of transcription (blockade of water) on tumor suppressor genes, such as p21, leads to cell transformation (growth of the cactus - like eremophytes instead of normal plants from the drought).

These reactive substances are toxic and damage the neighboring cells, such that e.g. tumors are decomposed.

The HER2 pathway is mutated in many cancers, which drives tumors, but inhibitors of this pathway, such as lapatinib, have only limited success because cancer cells quickly adapt.

As tumors grow and develop, they shed micro-metastases, clusters of a few cells that take up residence in far - flung organs such as the brain, liver and bone.

Next - generation NSG models that support human myeloid cell proliferation, such as the NSG - SGM3 mouse, can now provide in vivo conditions that better mimic the natural tumor environment.

We have shown that T cells can locally produce commercial therapeutics (such as antibodies) in a solid tumor.

The findings made by IMBA scientists now provide evidence that one can find key molecular brakes in innate immune cells that, when modified, allow such cells to seek out and destroy metastatic tumors.

The researchers picked one such experimental drug called RITA — Reactivation of p53 and Induction of Tumor cell Apoptosis — and used it to treat mice for a few days after cardiac injury.

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.

Mathew Garnett, a cancer biologist at the Wellcome Trust Sanger Institute near Cambridge, UK, says that HeLa cells could prove useful for studying aspects of the biology of cervical tumors, such as their response to cancer drugs.

They may also draw the attention of cells belonging to the innate immune system, such as natural killer cells, which can destroy tumor cells.

«The antibody - driven innate response creates an environment such that when the T cells come in, they can kill the tumor.

PDGFRα is a cell surface tyrosine kinase receptor involved in organ development and tumor progression, it is present in multiple cell types such as mesenchymal cells, neurons, astrocytes, megakaryocytes and oligodendrocyte progenitor.

HM - SNS allows researchers to sequence the genomes of single tumor cells and study multiple cells simultaneously, both lowering the cost and boosting data analysis for such studies.

A better approach, Monje said, would be to develop drugs that specifically block the tumor - stimulating activities of neuroligin - 3, such as a drug that stops the protein from being secreted into the area around the cancer cells.

These cells are on high alert for pathogens such as viruses, bacteria and even tumor cells, signaling the body's T - cell immune fighters into action when sensing harmful invaders.

Because diseases such as cancer tend to evade detection by T - cells» receptors, allowing a tumor to grow unchecked, scientists have long sought «intel» on this process as a means of developing therapies that target malignant cells, but leave healthy cells alone.

Immune sentries, known as T cells, are normally on the prowl for suspicious looking targets, such as bacterial invaders and potential tumor cells.