Sentences with phrase «cell tumors do»

Mast cell tumors do not have to involve the skin and can develop internally but most of the time there is skin involvement.

Mast cell tumors don't spread that often, but Quin» Cs was super-metastatic and had spread everywhere, peppering his body with tumors, especially in the liver, spleen, lymph nodes, and the brain.

Not exact matches

Since PSMA's limited on normal cells, the therapy should hammer away at tumors while letting healthy tissues do their job.

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?

While study results indicated that combining capsaicin with the chemicals «might promote cancer cell survival,» the report clearly stated that the control group of mice treated only with capsaicin ``... did not induce any skin tumors...» In addition, the study repeatedly cited other research studies in which the anti-cancer properties of capsaicin were solidly demonstrated.

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They did so by including factors like the mechanical forces acting on the cells and the tumor's cellular heterogeneity.

However, researchers have long thought that tumors don't release intact cells into the bloodstream until relatively late in the disease, and then only in vanishingly small numbers.

«To my great surprise, even injecting 10 million activated T cells specific to the P1A antigen did not affect tumor growth in this induced tumor model,» says Van den Eynde.

«This explained why they did not persist: The induced tumor behaves like a sink for these T cells.

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.

«It upholds our hypothesis that coalescence is so similar that there's got to be the same molecules and mechanisms that do it, and we may be able to find a drug that shuts tumor formation down without being toxic to healthy cells in the body,» says Soll, the paper's corresponding author.

Researchers at the University of Iowa did just that, documenting in real time and in 3 - D how melanoma cells form tumors.

Still, how melanoma cells join into tumors — whether by individual cells coming together or small or large clusters of cells doing so — follows the same pattern as breast tissue cancer cells: Cables are extended to reel in other cells or clusters.

«What our findings show is that the problems with iPS cells don't just involve one or two or a few abnormal iPS cells escaping into the body and forming tumors, but that the whole population of cells is screwed up,» Lanza says.

And how do occasional cells survive in this vulnerable state — sometimes hiding out in the brain for years — to eventually spawn new tumors?

If we can boost the immune system and allow microglia to do their job and control brain tumor stem cells, it would be like removing the seed from the soil — stopping the tumor growth before it starts to get out of control.»

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.

Our immune cells can destroy tumors, but sometimes they need a kick in the pants to do the job.

«We're still trying to figure out why these anti-tumor T - cells don't go into pancreatic tumors like they do for other malignancies,» Beatty said.

The team also compared the animals» responses to the therapy's effects in laboratory cell samples and found that in vitro studies did not predict how well the viral therapy and immune response would fight tumor cells in vivo.

The research team, led by senior author Timothy P. Cripe, MD, PhD, chief of the Division of Hematology / Oncology / BMT at Nationwide Children's Hospital, found that virotherapy doesn't always require a strong virus infection of cancer cells to cause tumors to shrink or die.

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.

Moderna is also doing animal safety tests of a personalized cancer vaccine that would code for immune - activating proteins unique to a person's cancer cells, based on genetic sequencing of their tumor.

Using tumor samples from a patient, they do lab tests to determine which substances can first make the different types of cancer cells uniform and then effectively kill them.

Another version, the CTC - iChip, rapidly isolates CTCs in a way that does not rely on preidentified tumor antigens, allowing capture of cells with gene expression patterns that may be missed by the antibodies used in the HBCTC - Chip.

Dana - Farber's Gordon Freeman, PhD, and his wife, Arlene Sharpe, MD, PhD, of Harvard Medical School, did some of the original research that resulted in the identification of PD - 1 on T cells, as well as the PD - L1 and - L2 protein «ligands» on tumor cells.

But the drug stayed bound to the diamond until it reached the tumor, so it didn't damage cells elsewhere in the body, and the animals survived.

Glutamine deprivation in these systems has been shown to be lethal to the cells — but does this also apply to naturally occurring tumors?

«But cancer cells in the lab don't necessarily indicate the response of human tumors,» Håkansson reminds the group.

«Hodgkin lymphoma is unusual among cancers in that it consists of a small number of tumor cells in a sea of inflammatory cells and immune system cells, including T cells that don't work very effectively.»

Bacteria had to be in direct contact with tumor cells to speed growth, but exactly how the bacteria do that isn't yet known.

Cheng and colleagues did experiments using human cells and identified hnRNPM's role in controlling the processes linked to tumor metastasis.

Any deviation in these processes could lead to cells that do not have the proper number of chromosomes, which could accelerate tumor initiation and progression.

«While these tumors appear to be muscle cells under the microscope, and clinicians had thought that they arose from muscle progenitor cells, that didn't explain why the tumors can occur in tissues that don't have skeletal muscle, like bladder, prostate and liver,» he continued.

If a given drug cocktail kills 90 percent of the cancer cells but doesn't affect the remaining 10 percent, the resistant tumor cells can take over and cause the tumor to grow back.

A multicenter team of researchers reports that a full genomic analysis of tumor samples from a small number of people who died of pancreatic cancer suggests that chemical changes to DNA that do not affect the DNA sequence itself yet control how it operates confer survival advantages on subsets of pancreatic cancer cells.

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.

Drugs like pembrolizumab boost the response in tumors where immune cells are present but don't work in tumors where there is no immune response to boost.

Niswander hopes her findings will provide insight into tumor formation, where cells don't die on cue.

The study showed that mice implanted with breast cancer cells lacking the protein developed small, self - contained tumors consisting of cells that didn't leave the tumor.

The tumor suppressor p53 does all it can to prevent oncogenes from transforming normal cells into tumor cells by killing defective cells or causing them to become inactive.

«The recent discovery of tumor - promoting milieus, referred to as metastatic niches, that are established at distant sites prior to or upon the arrival of disseminated tumor cells could explain cancer cells that relapse early, but in late relapsing populations, what tumor cells do from the time of dissemination to the time they become clinically detectable has been a big question.»

«Sometimes surgeons want to take out the tumor — and more — to avoid regrowth, in case there are some microscopic cells left behind, but they don't know how much they can safely cut off around it,» Yeom says.

«Not only did we find that LIGHT expression promoted tumor regression, upon further study we also identified the specific type of T - cell — CD8 — that was responsible for shrinking the tumor,» Maker said.

They found that the levels of two specific tRNAs were significantly higher in metastatic cells and metastatic tumors than in primary tumors that did not metastasize or healthy samples.

Moreover, in some cases, pancreatic cancer cells can even repair damage to their DNA caused by the chemotherapy drugs that do get into the tumor, further protecting themselves.

«Recent successes in cancer immunotherapy — in the form of immune checkpoint inhibitors and adoptive T cell transfer — demonstrate how activated immune cells can eradicate tumors, but until now we didn't fully appreciate immunosurveillance or the role of adaptive immunity in tumor formation,» said senior author Michael Karin, PhD, Distinguished Professor of Pharmacology and Pathology at UC San Diego School of Medicine.

Similarly, mice without immunosuppressive lymphocytes hardly had any tumors, even at 11 months, presumably since their absence left the cytotoxic T cells alone to do their tumor - fighting job.

NK cells require active STAT5 to kill tumor cells; however, when STAT5 is absent or inhibited, NK cells do the opposite: they accelerate cancer progression by promoting angiogenesis.