Sentences with phrase «cell tumors because»

Sometimes melanomas are categorized as a round cell tumor because they are typically round, raised, and darkly pigmented.

Not exact matches

Glioblastoma multiforme is the most common and deadliest of the glial tumors because the cells reproduce so rapidly.

«For pro-life folk, imagine a country where it was illegal to remove a tumor, even if the tumor might kill the host, because the tumor is its own collection of living cells.

Understanding how margin length decreases from surgery to pathology — because of how the removed tissue shrinks and tumor cells invade surrounding tissues — can lead to better surgical margin planning and in turn a better prognosis, said corresponding author Milan Milovancev, a board - certified veterinary surgeon at OSU's College of Veterinary Medicine.

These findings support that tumor cells prefer pre-formed tunnels because they allow the cells to move easier.

DIPGs are known as one of the most challenging tumors to treat because cancer cells are intimately intermingled with normal brain cells in a part of the brain that can not be surgically resected.

Because it treats the whole brain, the therapy is thought to control the spread of tumors by treating both identifiable and hidden cancerous cells.

We found that the inflammation unfortunately gets hijacked by tumor cells that are able to grow faster and penetrate deeper because the blood vessels in the brain are more permeable than in any other part of the body.

STRONGER TOGETHER Tumor cells (red) grown with bacteria (green) could stave off a common chemotherapy drug because some bacteria can inactivate the drug.

(Mackenzie notes that it shouldn't be a problem for her strategy, because she plans to use the same kind of cells as bone marrow transplants, which haven't caused tumors.)

The development of targeted therapies has significantly improved the survival of melanoma patients over the last decade; however, patients often relapse because many therapies do not kill all of the tumor cells, and the remaining cells adapt to treatment and become resistant.

«Because 85 percent of people in the study reported extending the antenna during calls, we might have expected to find a disproportionate cluster of tumors behind the eye and the ear on the side the cell phone was used since radiation emission is highest at the antenna,» says co-author Mark Malkin, a neuro - oncologist at Memorial Sloan - Kettering Cancer Center.

«About five percent of people have some kind of cartilage tumor in their bones, and in most cases it's because the growth - plate cartilage cells weren't fully replaced by bone tissue,» Alman said.

«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.

Sometimes, he speculated, it was because CTLA - 4 deactivated T cells before they could finish off a clump of tumor cells.

This is important because tumors are not all alike and some types of tumor cells may respond differently to a specific drug than others, Skala pointed out.

Metastasis, or cancer spread by the formation of tumors at new sites, is generally what makes cancers deadly because surgery and other treatments are unlikely to find and destroy every cancer cell.

Because of this lack of receptors, common cancer drugs can't «find» the cells, and doctors must treat the cancer with extremely aggressive and highly toxic treatment strategies,» said Salman Hyder, the Zalk Endowed Professor in Tumor Angiogenesis and professor of biomedical sciences in the College of Veterinary Medicine and the Dalton Cardiovascular Research Center.

Another is that the transplanted bits of tumor act nothing like cancers in actual human brains, Fine and colleagues reported in 2006: Real - life glioblastomas grow and spread and resist treatment because they contain what are called tumor stem cells, but tumor stem cells don't grow well in the lab, so they don't get transplanted into those mouse brains.

To see if PGD and the pentose phosphate pathway were tied to the epigenetic changes the researchers had detected in distant metastases, they treated tumor cells from different sites in a single patient with the drug 6 - aminonicotinamide (6AN), which is known to inhibit PGD but is not used in humans because of its severe side effects.

«This is why some cancers can be so difficult to treat with chemotherapy, because the cells can be in different states — some sensitive to treatment and some resistant to treatment, all in the same tumor,» says Sandro Santagata, a former visiting scientist in the lab of Whitehead Member Susan Lindquist.

«Pancreatic cancer cells are deadly because they program nearby immune cells to permit the tumors to survive and grow,» says study author George Miller, MD, head of the Cancer Immunology Program at Perlmutter and vice chair for research in the Department of Surgery at NYU Langone.

Cancer stem cells, a type of self - renewing cell found in tumors, are of particular interest because they are the main cell type responsible for tumor progression and for resistance to chemotherapy and radiotherapy, and therefore a major cause of tumor recurrence after treatment.

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.

But T cells typically can not attack tumors because the immunosuppressive microenvironment of tumors keeps APCs from turning these signals on.

There's a need for ways to find these cells and to study them, and importantly, to develop drugs that target them, because these cancer stem cells are resistant to chemotherapy drugs that target the main tumor.

Unfortunately, in most patients the melanoma recurs within a year because the tumor cells develop drug resistance.

Because it more effectively induces cancer cell apoptosis in p53 - deficient tumors, FL118 is especially effective against late - stage cancers, which usually lose functional p53 and are resistant to DNA - damage drugs.

«Natural killer cells are very attractive targets for immunotherapy because they are able to kill tumor cells,» said Si - Yi Chen, M.D., Ph.D., a faculty member of the USC Norris Comprehensive Cancer Center and senior author of the study.

«Myeloid cells are immune cells that are attracting attention because they can infiltrate a broad range of tumors.

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.

«But the antioxidant boosted the ability of the tumor cells to metastasize, an even more serious problem because metastasis is the cause of death in the case of melanoma.

However, these therapies often fail because insufficient numbers of T cells reach the tumor.

Malignant tumors pose a major threat to survival largely because they shed mobile cells that can form secondary tumors in other tissues.

Because the stem cells generate the brain cancer cells, killing off the stem cells might prevent tumors from recurring.

But the full potential of CARs for treating solid tumors has not been reached because they have targeted molecules found on the surface of both normal cells and cancer cells, resulting in serious side effects.

And because tumors typically have a leaky, ill - formed vasculature, the particles tend to leak out at the site of cancer tissue and be picked up and internalized inside tumor cells.

Because Zika targets the cells that generate tumor cells, it might prevent tumors from recurring.

The protein products of these genes, the authors note, «represent targets for immunotherapy, because inactivating mutations sensitize tumor cells to T - cell mediated attack.»

Polyploid cells, which carry additional copies of important tumor suppressor genes, are better protected and more resistant to cancer formation because they have these extra copies of the genome,» said Dr. Zhu, who is also an Assistant Professor of Pediatrics and Internal Medicine at UT Southwestern.

When researchers at Johns Hopkins University in Baltimore, Maryland, examined tumor tissue from the original man with colon cancer who responded to a PD - 1 inhibitor, they found a clue: His tumor had mutations in «mismatch repair» genes, so - called because their encoded proteins fix errors in DNA bases when cells replicate their DNA.

Tumors go mostly unmolested by the body's natural defenses, partly because cancer cells are descendents of normal body cells.

When using a well established model of colorectal cancer, the researchers observed that dietary emulsifier consumption was sufficient to make the animals more susceptible to developing colonic tumors because this created and maintained a pro-inflammatory environment associated with an altered proliferation / apoptosis (cell death) balance.

Because tumor cells in the brain frequently divide, normal brain cells would remain unaffected by the electric fields, the team reports online this week in the Proceedings of the National Academy of Sciences.

Matunis says the research may be useful for understanding cancer, because a lot of cancer involves cancer stem cells, also known as tumor - initiating cells.

Chakravarti further notes that because GBM cells take up methionine much faster than normal glioma cells, positron emission tomography that uses methionine as a tracer (MET - PET) might help map GBM tumors more accurately, allowing more precise surgical removal and radiation - therapy planning.

Treatment of brain tumors is particularly challenging because regulatory T - cells accumulate in brain tumors and suppress an immune attack.

«We kind of had this wild idea that because these tumor cells are just pouring [out microvesicles], maybe we can actually see it in the blood,» Breakefield says.

And because the immune system learns to recognize pancreas cancer cells, the drug may control tumors for a very long time.

Because tumor growth is a concern when cells are reprogrammed to an earlier stage of development, the researchers followed the mice in the Nature Cell Biology study for nearly a year to look for signs of tumor formation and reported finding none.