Sentences with phrase «wilms tumor development»

High glycemic index foods affect insulin - like growth factors, which impact tumor development.36

«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.

In conclusion, this new study identifies the cellular origin of Pik3ca - induced tumours and reveals that oncogenic Pik3ca activates a multipotent genetic program, setting the stage for future intratumoural heterogeneity at the earliest stage of tumor development.

For this study, Guttridge, first author David J. Wang, who developed many of the study's concepts, and their colleagues monitored NF - kB activity during tumor development using mouse embryonic fibroblasts and two mouse models.

Moreover, experiments on an ovarian cancer murine model that investigated the effects of orally administered ONA resulted in longer lifespans and inhibited ovarian cancer tumor development.

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

Dr. Sergio Lira and his team at the Icahn School of Medicine at Mount Sinai, New York, asked if gut microbes have a hand in tumor development.

As not all cases of Barrett esophagus become malignant, it is important for the treating physician to know whether there are reliable indicators (so - called biomarkers) which allow the estimation of a tumor development in the still benign tissue.

After identifying FAK's role in tumor development, François started looking for ways to get it in check.

This complex mix of virus, host genes and tumor development may have relevance to a related human condition.

Our long - term goal is to translate this technology into clinical investigation of the pathological implication of exosomes in tumor development.

Although normal inflammation plays an important role in helping to fight off infections, there is mounting evidence that chronic inflammation is linked to increased risk of tumor development.

The work demonstrates that BRAF - mutated melanoma requires autophagy for tumor development and blocking autophagy could have therapeutic value, particularly in combination with BRAF inhibition.

The researchers used an example to demonstrate the mechanism: They identified the transcription factor STAT3, which regulates inflammatory processes and can promote tumor development, as a prominent target protein of one peroxiredoxin.

This lengthy period of time, compared to a mouse's lifetime, indicates that additional factors play a role in tumor development.

Investigators found that NPTX2 was expressed in all stages of kidney cancer, especially metastasis, which suggests it plays an important role in tumor development and progression.

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

To see whether Lin28 might be a factor in Wilms tumor development, Daley and an international team of collaborators measured the gene's expression in tumor samples from 105 Wilms patients.

Terbinafine, a U.S. Food and Drug Administration — approved antifungal drug targeting SQLE, markedly inhibited SQLE - induced NAFLD - HCC cell growth in NAFLD - HCC and HCC cells and attenuated tumor development in xenograft models and in Sqle transgenic mice.

Based on their results, Lu and her colleagues argue that the best strategy in such cases might be to use drug combinations that target multiple, parallel pathways involved in tumor development and maintenance.

«This is the best example that NF1 is a tumor suppressor,» says David Viskochil, a geneticist at the University of Utah, although he cautions that the case is not yet closed: There still could be other genes that play a role in NF tumor development.

When the researchers examined the cells and molecules involved in chronic contact allergy in mice, they identified several that already had been linked to tumor development.

Data from mice, too, suggested that the gene was necessary to prevent tumor development.

And these ITCs apparently destroy the products of the mutant p53 gene, but leave the healthy p53 proteins alone and free to suppress tumor development.

The researchers showed in mouse models that chronic skin inflammation caused by continuous skin contact with allergens contributes to tumor development.

They become factories for cytokines and growth factors that nurture tumor development.

Sometimes oncogenes manage to initiate tumor development in the presence of p53, but, even then, the tumor suppressor doesn't give up and focuses its efforts instead on limiting the tumor's ability to invade and metastasize.

This demonstrated that non-small-cell lung cancer selectively requires autophagy for tumor development and that therapeutically targeting autophagy may be an alternative to targeting Ras.

«The macrophage is migrating into a site and doing what we want it to do rather than driving tumor development in a normal way,» Lewis says.

This transformation recognizes that the immune inflammatory state serves as a key mediator of the middle stages of tumor development.

Recently, teaming up with co-investigator Associate Professor Dr. Rolf A. Brekken, they looked into its possible involvement in Pancreatic Ductal Adenocarcinoma (PDA), the most common form of pancreatic cancer, in a mouse model with an early onset aggressive form of tumor development.

miR - 184 is known to suppress tumor development by regulating a variety of genes involved in cancer growth, while SND1 has been shown to play a significant role in the development of breast, colon, prostate and liver cancers.

Dr. Yaffe's research focuses on the biology of the complex signaling pathways that cells use to respond to DNA damage and inflammation, particularly the role of protein kinases and modular binding domains in tumor development and anti-cancer therapeutics.

With the help of various mouse models for pancreatic cancer, they have succeeded in elucidating the molecular pathways of tumor development in detail and have gained a better understanding of how various characteristics of the disease arise.

In experiments with cancer cell lines, the PIM1 inhibitors killed cells in a MYC - dependent manner, and in two different mouse models — one in which mice were implanted with patient tumors and the other in which a genetic alteration of MYC predisposes the mice to tumor development — the administration of PIM1 inhibitors resulted in significant tumor regression.

This webinar is the third in a series focusing on the cancer pathways that support tumor development, the emerging research in identifying and targeting these pathways, and innovations in the development of increasingly effective cancer therapy options.

This webinar is the second in a series (see Part 1 here) focusing on the cancer pathways that support tumor development, the emerging research in identifying and targeting these pathways, and innovations in the development of increasingly effective cancer therapy options.

«Our discovery of germline mutations in so many cases of Wilms tumor means that the children and family members of these patients may be at risk for tumor development,» said Perlman.

When cancer develops, the generated cells are not uniform in their biological properties and contribute differently to tumor development.

This model of dosage amplification during tumor development had not previously been considered,» says Sebastian Müller, lead author of the study.

The scientists discovered that TRPV1, once activated by the EGFR, initiates a direct negative feedback on the EGFR, dampening the latter to reduce the risk of unwanted growth and intestinal tumor development.

«However, if EGFR signaling is left unrestrained, the risk of sporadic tumor development increases.»

The authors note that there are two different models of metastasis — one in which an advanced primary tumor disseminates metastatic cells late in its development, which would predict little genetic difference between primary and metastatic cells, and another in which metastasis occurs early in tumor development, which would predict significant genetic differences in metastatic cells that have evolved separately from those in the primary tumor.

Answering important clinical questions — such as whether genetic diversity is a risk factor for aggressive tumor development or how it relates to treatment resistance — requires analyzing samples from many patients with different types of cancer.

They further investigated this phenotype in a skin tumor model system, provided by Maria Sibilia from the Institute for Cancer Research of the Medical University of Vienna, and found that deactivating HDAC1 actually accelerates tumor development, while HDAC2 deactivation has no effect.

By matching normal and cancer cells from a patient, we can now study the differences — what molecules are key to tumor development and growth, and, ultimately, match treatments that might disable this cancer,» says the study's senior investigator, associate professor of pathology, Xuefeng Liu, MD, a member of the Center for Cell Reprogramming (CCR) at Georgetown University Medical Center.

The findings, published in the journal Cancer Research, show regular consumption of dietary emulsifiers in mice exacerbated tumor development.

«Scientists drill down to genetic root of prostate tumor development.»

The researchers observed that enhanced tumor development was associated with an altered intestinal microbiota, characterized by an increased pro-inflammatory potential.

This study demonstrated that emulsifier - induced alterations in the microbiome were necessary and sufficient to drive alterations in intestinal epithelial cells» homeostasis, which is thought to govern tumor development.