Sentences with phrase «when tumor cells»

The disseminated disease occurs when tumor cells spread beyond the local lymph nodes to the lung, liver, spleen, gastrointestinal system, eyes, central nervous system, skin, muscles, bone and / or the bone marrow.

When their tumor cells don't make osteoid and exclusively make cartilage, they have a condition that's referred to as chondrosarcoma.

«This is not its only effect, Thomas Matthes adds, H225 also significantly limited cell proliferation, even when tumor cells had already settled in the lymphatic system.

Lead author Dean Ho, a biomedical engineer at Northwestern University in Evanston, Illinois, says that one of the major challenges in chemotherapy is when tumor cells develop mechanisms to pump drugs right back out.

When tumor cells that no longer express CCR3 are implanted in the prostates of mice, tumor progression and dissemination are significantly reduced, especially in obese mice.

When tumor cells are present in an environment that lacks oxygen and nutrients, they receive a signal that it is time for the cells to move to a different part of the body.

Not exact matches

Or consider a vaccine that, when injected directly into a tumor, would not only destroy the malignant cells but also stimulate the body's immune system to go after similar tumor cells.

When a tumor is treated with chemo, the tumor may disappear but some cancer stem cells have the ability to survive, and they have the potential to regenerate the original tumor and spread the cancer elsewhere.

Similar to capsaicin, tumor necrosis factor is suspected to both induce and reduce cancer cell growth, and was shown to commit cells to survival when stimulating EGFR transactivation mechanisms, indicating that EGFR could act as a molecular switch determining the antiapoptotic effect of tumor necrosis factor (50).

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.

Similarly, when these cells were injected into mice, the cells in which SLC13A5 was suppressed formed barely discernable tumors compared to the unmanipulated cancer cells.

A successful test would therefore require isolating enough of these scarce cells to make statistically valid inferences about the tumor, often at a stage when the tumor itself is growing and changing rapidly.

In the upper panel, tumor cells formed colonization at day 14, while in the lower panel, when the mouse was treated with the compound edelfosine, most of the tumor cells disappeared at day 10 and failed to form colonization at day 14.

Here's why: when surgeons remove a tumor, they inevitably leave behind a few straggler cancer cells.

But when their functioning is altered, as the UCL researchers observed in tumor cells, the mitochondria can promote cell migration, thus leading to the formation of metastasis.

«Even when an entire tumor has been removed, it is common for a small number of tumor cells to remain behind.

A pre-clinical study of two drugs designed to boost T cell performance, has revealed the agents, when give in combination, may enhance the immune system's ability to kill melanoma tumors deficient in the tumor suppressor gene PTEN.

When the dendritic cells are activated, they train T cells — their allies in the adaptive arm of the immune system — to attack cancer cells anywhere in the body, whether at the site of the original tumor or distant metastases.

When Hong further boosted MAPK signals and DNA damage in the tumor cells, she found that she could intensify tumor cell death.

Also limiting the use of therapeutic stem cells to date, self - renewal, a quality so vital to a fast - growing fetus, can also be a source of cancer risk when haphazard, unlimited cell multiplication results in the abnormal tissue growth seen in tumors.

When researchers injected fresh breast cancer cells in the side opposite the original tumor site, the disease didn't recur in any of the mice, as the cancer was rejected by the immune system's memory.

By hitting breast cancer cells with a targeted therapeutic immediately after chemotherapy, researchers from Brigham and Women's Hospital (BWH) were able to target cancer cells during a transitional stage when they were most vulnerable, killing cells and shrinking tumors in the lab and in pre-clinical models.

Tumor cells become lethal when they spread.

When injected with cancer cells, animals housed there developed tumors 80 % smaller than those in control mice, or no tumors at all.

The investigators found that when working through an environment with no pre-existing tracks, tumor cells had to actively stick to the tissue, break it down and then move themselves forward.

Another challenge is producing stem - cell - derived tissues or organs that don't develop teratomas — tumors that contain a variety of tissues found in different organs — when transplanted.

But when islet cells begin turning into tumors, the FAK protein gets overproduced, researchers found.

The investigators utilized a targeting method called RNA interference (RNAi) which, when delivered via these natural nanoparticles or exosomes, zero in on mutant KRAS in pancreas cancer cells, impacting tumor burden and survival in multiple pancreas cancer models.

Studies in cancer patients indicate reduced rates of relapse when patients are pretreated with epigenetic drugs due to its far - reaching capabilities; killing progenitor cells at the site of the tumor, in circulation, or at a distant site.

These might make a cell hardier in a foreign environment — say, when a breast cell relocates to bone — or more able to escape the primary tumor and survive while rushed through the bloodstream.

When the scientists inserted human colorectal cancer cells into zebrafish embryos and allowed them to grow for 4 days, the resulting tumors showed three hallmarks of human solid tumors: rapid cell division, formation of blood vessels to supply nutrients, and the ability to spread to other locations in the body.

«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.

Reinhart - King's team discovered that tumor cells were less likely to spread when their stiff ECMs were replaced with ECMs softened by irradiation.

«Ionizing radiation found to soften tumor cell microenvironment: When irradiated, less stiff extracellular matrices reduced cancer growth and migration, bolstering the case to further understand fractionated radiation therapy.»

When researchers screened a library of more than 200 drugs and related compounds for activity against embryonal subtype tumor cells from three patients, the most promising results involved drugs that increased oxidative stress in tumor cells.

When the cells are reinfused, they stimulate T cells to attack the patient's tumors.

A study in this week's Neuron provides key evidence that DNA methylation — also known to occur as cancerous cells divide, when tumor suppressor genes are silenced — occurs in adult brains and can be triggered by environmental cues.

COLD SPRING HARBOR, N.Y. — When breast cancer spreads, it moves in gangs of ready - to - rumble tumor cells, a small genetic study suggests.

After more than six years of research, the research team led by María Soengas, head of CNIO's Melanoma Group, showed that RAB7 acts as an orchestra director, determining the fate of melanoma cells: at high concentrations of RAB7, cellular autodigestion is very active, and this allows tumor cells to obtain energy, prevent the accumulation of toxic components and thus divide and proliferate; when RAB7 is reduced, cells use endosomes to recycle metastatic proteins, favouring their dispersal throughout the body.

When researchers added the immune T cells to the fibroblasts, the tumor cells began to die off.

When present in tumors, both abnormal myc and abnormal mTOR are known to be able to rev up protein production and to foster cell growth.

EMT is crucial for normal embryonic development, but also operates in wound healing, and when abnormally switched on, can enable the spread of tumor cells.

When cancer cells start dividing rapidly to form tumors, these cells are actually reverting to an earlier time in their development when they were supposed to divide rapiWhen cancer cells start dividing rapidly to form tumors, these cells are actually reverting to an earlier time in their development when they were supposed to divide rapiwhen they were supposed to divide rapidly.

«Indeed, when we studied the mice at the embryonic stage, we saw the cells between the muscle fibers expanded explosively and formed tumors early in development,» Hatley said.

In addition, when a subcutaneous tumor began to recur two months after CAR T - cell therapy and a surgical biopsy was performed, the CAR T - cells spontaneously re-expanded and the tumor again went into remission, and phenomenon that had not previously been reported.

Damage occurs when metastatic tumor cells recruit pre-osteoclast cells to the bone and then induce their differentiation into mature bone - degrading cells, which results in the release of proteins from the bone matrix that promote tumor cell growth.

«In our study, we demonstrated that alpha - KGDH, when coupled with Gcn5, induces histone succinylation and promotes tumor cell proliferation and tumor development.»

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.

In earlier studies involving animal models and human cancer cell lines, researchers found that breast cancer spreads when three specific cells are in direct contact: an endothelial cell (a type of cell that lines the blood vessels), a perivascular macrophage (a type of immune cell found near blood vessels), and a tumor cell that produces high levels of Mena, a protein that enhances a cancer cell's ability to spread.

«We demonstrated that alpha - KGDH interacts with Gcn5 in the cell nucleus and found that tumor cell proliferation and tumor growth were inhibited when alpha - KGDH was blocked from entering the cell nucleus or by disruption of Gcn5's binding to succinyl - coenzyme A,» said Lu.