Sentences with phrase «tumor formation in»

In dogs, second - hand smoke has been linked to tumor formation in the lungs and an increase in nasal adenocarcinoma, particularly in long - nosed breeds.

Research with animals has suggested that raspberries have have the potential to inhibit cancer cell proliferation and tumor formation in various parts of the body, including the colon.

Parsley's volatile oils — particularly myristicin — have been shown to inhibit tumor formation in animal studies, and particularly, tumor formation in the lungs.

One study found that the compounds in Frankincense reduced cyst and tumor formation in the uterus after menopause.

In contrast to the transformation of HMEC - DD cells, one oncogenic event is sufficient to transform Rat1 - DD cells, indicated by both anchorage - independent growth in vitro and tumor formation in vivo (Ni et al., 2012).

Likewise, wild - type MELK cooperates with a second oncogene, for example NeuT, to induce tumor formation in vivo.

One host effector that may influence carcinogenesis in response to H. pylori is MMP - 7, a matrix metalloproteinase that enhances tumor formation in rodents, and is over-expressed in premalignant and malignant lesions within H. pylori - infected human mucosa.

Similarly, Cbl - b − / − mice and T cells lacking Cbl - b demonstrate improved control of s.c. - implanted tumors (23) and disseminated leukemia (32), along with decreased spontaneous tumor formation in ATM − / − mice (23) and UV B - treated mice (24).

Cancer researchers at Columbia have discovered three genes that undermine the DNA repair process and promote tumor formation in cells with BRCA mutations.

Knowing that insulin can stimulate the growth of blood vessels, «our expectation was that knocking out insulin signaling in these cells might slow the growth of blood vessels and reduce tumor formation in these mice,» Rask - Madsen says.

2) The two repeated experiments analyze the source of POSTN expression in the lung and whether it affects the number / size of primary and secondary tumor formation in a spontaneous mouse model of breast cancer (MMTV - PyMT).

In cell lines, the researchers first tested ruxolitinib, a general JAK inhibitor, but it did not block tumor formation in the JAK2 - amplified cells.

But most importantly, the researchers say, in three laboratory tests of tumor growth, the drug strongly blocked tumor formation in distant metastases and their precursors.

The researchers have identified a compound that reverses the reprogramming and prevents tumor formation in model systems.

Two genetic mutations in liver cells may drive tumor formation in intrahepatic cholangiocarcinoma (iCCA), the second most common form of liver cancer, according to a research published in the July issue of the journal Nature.

Not exact matches

Think about it, these single gene changes are usually what results in tumor formation, right?

A woman with previous breast surgery can get mastitis (infection of the breast tissues), galactocele formation (a milk filled tumor in your breast) and even galactorrhea (lactation that occurs without the occurrence of pregnancy or childbirth).

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.

By analysing the early steps that precede tumor formation, Alexandra Van Keymeulen and colleagues found that expression of oncogenic Pik3ca reactivates a multilineage differentiation program in adult stem cells that resembles to an immature embryonic state.

They discovered that the chemicals and radiation used to kill tumor cells damage the stem cell reservoir in the hippocampus and nearly halt the formation of new neurons in both children and adults.

«It was really surprizing to realize that oncogenic Pik3ca in basal cells induced the formation of luminal tumours, while its expression in luminal cells gave rise to heterogeneous and more aggressive tumors including basal - like tumors,» comments Alexandra Van Keymeulen, the first author of the paper.

The discovery of a treatment capable of blocking the mechanism responsible for the formation of metastasis and the existence of a family of promising compounds, is encouragement for their future assessment in a clinical study that aims to validate a preventive treatment against tumor metastasis.

Many more microchimeric cells are found in the blood of healthy women compared to those with breast cancer, for example, suggesting that microchimeric cells can somehow prevent tumor formation.

«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.

The group found the two cancers act similarly in the joining stages of tumor formation.

«When most people think about cancer genetics, they think about single key mutations that foster tumor formation — very specific things like the BRCA genes,» said Joe R. Delaney, PhD, a fellow in the Clinical Translation program at UC San Diego Moores Cancer Center and lead author of the paper published February 15 in Nature Communications.

Sure enough, 6 - HAP stopped DNA formation in different tumor cells grown in the lab.

This treatment prevented the formation of polyps, showing that bacteria are essential for early tumor development in this model.

MDSCs are immune cells originating from bone marrow stem cells that possess strong immunosuppressive abilities and are known to play a role in tumor formation and metastasis.

If the silencing occurred in a gene responsible for suppressing tumor formation, the result would appear the same as genetic mutations that predispose people to cancer.

For example, genes involved in suppressing tumor formation are turned off via epigenetic mechanisms, and genes involved in rapid growth and replication are turned on too high.

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.

This stress, which is notably induced in pre-cancerous lesions, is characterised by an increased DNA replication rate, which provokes DNA damage and genome instability, major drivers of tumor formation.

Different classes of MHC molecules exist and are involved in immunity against pathogens and tumor cells as well as the formation of immune tolerance to self - antigens.

Less suppression of the immune response and less blood vessel formation in the tumor leads to less tumor growth.

Indeed, tumors contain a lot of specific macrophages that play a decisive role in the formation of blood vessels.

Yet, Hockemeyer says, telomerase levels are marginal, resulting is some unprotected chromosome ends in the surviving mutant cells, which could cause mutations and further fuel tumor formation.

This study demonstrates that this endosome formation (via RAB7) is very active in tumor cells but not in normal cells.

«These findings underscore the significance of Gcn5 - regulated gene expression coupled with the metabolic enzyme alpha - KGDH in tumor cell proliferation and formation.»

«We saw the formation of new blood vessels in tumors reduced by 70 percent,» she says.

Scientists knew Apc was involved in stifling tumor formation because most colon cancers find a way to turn the gene off.

To better understand the formation of metastases in pancreatic cancer, Christine Iacobuzio - Donahue, M.D., Ph.D., professor of pathology at Memorial Sloan Kettering Cancer Center, collected tumor samples from eight patients with the most common form of pancreatic cancer (pancreatic ductal adenocarcinoma) immediately after their deaths.

In this mouse model, mutations in Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different colorIn this mouse model, mutations in Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different colorin Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different colorin the formation of individual tumor cell populations that were labeled with different colors.

In human cells as well, if Nbs1 and ATM function in the same way to ensure repair of DNA damage, tumor formation may be preventeIn human cells as well, if Nbs1 and ATM function in the same way to ensure repair of DNA damage, tumor formation may be preventein the same way to ensure repair of DNA damage, tumor formation may be prevented.

The drug Rituxan, a monoclonal antibody that represses B cells in rheumatoid arthritis and B cell lymphoma, might prevent the inflammatory response that fuels formation of solid tumors.

This group's achievement shows the possibility to clarify the mechanism of human tumor formation, especially the molecular mechanism responsible for in the initial stage of cell cancerization due to DNA damaged by radiation in the initial stage, by using the model of budding yeast, a primitive eukaryote.

This is important to avoid missegregation of the genetic material, which may result in cell death or tumor formation.

Although the researchers were predominantly interested in broccoli's impact on the formation and progression of cancerous tumors in the liver, Jeffery explained that they also wanted to observe the health of the liver and how the liver was metabolizing lipids because of the high - fat diet.

Using a fluorescent protein to detect Rgs16 expression, the investigators found that this gene is induced by pancreatic tumor formation starting from its earliest manifestation as ductal neoplasm all the way to advanced solid tumor in a spatially and temporally coincidental manner.

We then usually move onto xenograft models and then also, if available, try to test some of these compounds in genetically engineered mouse models that have particular mutations driving tumor formation.