Sentences with phrase «melanoma is a tumor»

Melanoma is a tumor that is recognized by the immunological system and mechanisms leading to an anti-tumor immune response of potential value in the adjuvant setting.

Not exact matches

«And then, when we put a melanoma tumor into those mice, they either were very slow to grow or were completely rejected,» says Wargo.

BMS's drug, ipilimumab (Yervoy), was the first checkpoint inhibitor (a kind of cancer immunotherapy drug that essentially helps the immune system release its brake and go after tumor cells it might normally miss) to get approved in the US in 2011 for melanoma.

When Jedd Wolchok, a cancer doctor and immunologist leading a Yervoy trial at Memorial Sloan Kettering, examined a melanoma patient's scan 12 weeks after he'd received his course of treatment, the results were utterly disappointing — just like those of any other metastatic patient in the final throes of the disease: The tumors had gotten bigger, and there were more of them.

MEG TIRRELL, NIGHTLY BUSINESS REPORT CORRESPONDENT: Since they were approved in 2014, drugs that stimulate the immune system have been giving new hope to patients with melanoma, kidney cancer, lymphoma and other cancers, including famously to President Jimmy Carter, who credited the drug called Keytruda with shrinking tumors that had spread to his brain.

After adjusting for age, tumor location, and stage, researchers from Cleveland Clinic's Dermatology & Plastic Surgery Institute discovered that women diagnosed with malignant melanoma during their pregnancy or within one year of giving birth were 5.1 - times as likely to die, 6.9 - times as likely to experience metastasis, and 9.2 - times more likely to have a recurrence.

In melanoma, they can be used to determine tumor stage, diagnosis, therapy selection and when to monitor for disease recurrence.

His team discovered that treatment - resistant melanoma tumors, in what is akin to drug addiction, develop a dependency on MAPK - targeted therapy to retain their fitness.

In a retrospective analysis of clinical trial data, they found that melanoma patients with highly aneuploid tumors were less likely to benefit from immune checkpoint blockade therapy than patients whose tumors showed fewer chromosomal disruptions.

The findings, which were demonstrated in several major subtypes of melanoma tumors (including BRAF and NRAS melanoma), could lead to drug development strategies that suppress the development of drug resistance.

To determine local immune control, where the invasive tissue interfaces with normal cells, post-birth placentas and stage - four melanoma tumors were examined.

Approximately 50 percent of advanced melanoma tumors are driven to grow by the presence of BRAF mutations and another 20 percent by the presence of NRAS mutations.

There is currently a PD - 1 antibody on the market that blocks T cell exhaustion in patients with solid tumors, like lung cancer and melanoma.

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.

The compound then was tested in an experimental model for melanoma and found to significantly inhibit tumor cell growth without appreciable toxicities.

Scientists have long suspected a genetic association with uveal melanoma because one of two gene mutations is present in approximately 70 percent of all tumors.

Mutations in the gene BRAF are the most common mutation found in melanoma, with up to 50 percent of tumors testing positive for the mutations.

«New targeted therapy schedule could keep melanoma at bay: Optimizing the timing of targeted therapies for melanoma reverses tumor growth, and resistance can be mitigated..»

«Finding which mechanisms determine why melanoma is so aggressive is very complex because more than 80,000 mutations have been described for this tumor,» says Direna - Alonso Curbelo, the article's first author.

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 tMelanoma 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 tmelanoma 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.

BRAF inhibitors are a first line of treatment for melanoma patients who harbor the BRAF mutation, which is an abnormal change in a gene that causes some melanoma tumors to grow and spread more aggressively.

«This discovery that ATG7 promotes the growth of melanoma tumors underscores that the development of agents targeting autophagy may effectively inhibit melanoma growth,» notes Dr. Mehnert, who is an associate professor of medicine at Rutgers Robert Wood Johnson Medical School.

CNIO's Bioinformatics Unit has been key in comparing 900 cell lines derived from up to 35 tumor types in order to identify unique aspects of melanoma.

One application is the prognosis of the melanoma: the authors show in tumor biopsies that the amount of RAB7 in a cutaneous tumor defines the risk of developing metastasis.

«Leukemia is a liquid, circulating tumor, while breast tumors and melanoma are solid tumors, so this is going to be a very broad technology.»

It is well established that melanoma cells can spread through the blood to accumulate and form new tumors (metastases) in other parts of the body away from the original tumor.

Heeke says the study would be open to people whose tumors have evidence of HRD like those found in this study, which includes bladder, breast, cervix, liver and bile duct, colorectal, endometrial, gastric / esophageal, head & neck, kidney, neuroendocrine, lung, ovarian, pancreas, prostate, sarcoma, and thyroid cancers, as well as gastrointestinal stromal tumors, glioma, melanoma and unknown primary cancers.

Using tumor biopsies from melanoma patients, the researchers could show that there is a positive correlation between the production of CCL5 and the infiltration of NK cells.

The researchers are now planning to address the impact of targeting autophagy either clinically and pharmacologically on the immune landscape of melanomas by phenotyping other immune cells in the melanoma tumor microenvironment.

«New combination of immunotherapy drugs is safe, shrinks tumors in metastatic melanoma patients.»

Sentinel nodes are the first lymph nodes to which cancer cells from a primary tumor like melanoma will spread.

The result was a significant reduction in the skin cancer lesions, as well as a sizable reduction in melanoma tumors that had spread to the lungs.

In addition to monitoring the response of injected melanoma tumors, we are also measuring the boost in the anti-tumor immune cells of patients after injection,» explained Amod A. Sarnaik, M.D., assistant member of Moffitt's Cutaneous Oncology Program.

The tumors of 109 of these patients had the normal form of the gene BRAF, which is frequently mutated in melanoma.

The Ogretmen laboratory screened previously reported microarray data sets of several human tumor tissues (metastatic head and neck squamous cell carcinoma, melanoma, and renal cell carcinoma) and showed that, in these samples, only the levels of CerS4 were significantly decreased.

The findings suggest that targeting newly discovered pathways could be an effective approach to improving the clinical outcome of patients with BRAF inhibitor - resistant melanoma tumors.

Approximately 50 percent of melanoma tumors are driven by mutations in the BRAF gene, and patients with these tumors are prescribed BRAF inhibitors.

The light - sensitive cells and nanoparticles, called opto - CRAC, were then delivered with the tumor antigen surrogate ovalbumin to mice with melanoma tumors in their lymph nodes to see if an immune response could be activated to target cancer cells.

«Immunotherapy, pembrolizumab, is active against mucosal melanoma tumors: And prolongs survival for patients with bladder cancer.»

A new optogenetic technology developed by scientists at the University of Massachusetts Medical School and Texas A&M Health Science Center Institute of Biosciences & Technology, called optogenetic immunomodulation, is capable of turning on immune cells to attack melanoma tumors in mice.

The authors conclude that FL118 - based therapy may be beneficial for a subgroup of cancer patients with tumors such as chronic lymphocytic leukemia and melanomas, in which MdmX overexpression confers treatment resistance.

Unlike other solid tumors, there has been limited progress in understanding the contribution of genetic risk factors to the development of uveal melanoma, researchers say, primarily due to the absence of comprehensive genetic data from patients as the large sample cohorts for this rare cancer type have not been available for research.

Melanoma is a malignant tumor resulting from the transformation of melanocytes, the cells that undertake to synthesize melanin, which protects us from the negative effects of solar radiation.

Joining forces with dermatologists and oncologists from the University Hospital in Zurich and backed by the University Research Priority Program «Translational Cancer Research,» Sommer's team was able to demonstrate that, in melanoma cells, the epigenetic factor EZH2 controls genes that govern tumor growth as well as genes that are important for the formation of metastases.

According to Herlyn, these slow - growing JARID1B cells represent only one to five percent of the cells in a tumor, yet readily divide into the fast - growing cells that are the hallmark of advanced melanoma.

«We have found that the individual cells within melanoma tumors are not all identical, and tumors contain a sub-population of cells that are inherently drug resistant, which accounts for the fact that advanced melanoma tumors return no matter how much the tumor is depleted,» said Meenhard Herlyn, D.V.M., D.Sc., professor and director of Wistar's Melanoma Researchmelanoma tumors are not all identical, and tumors contain a sub-population of cells that are inherently drug resistant, which accounts for the fact that advanced melanoma tumors return no matter how much the tumor is depleted,» said Meenhard Herlyn, D.V.M., D.Sc., professor and director of Wistar's Melanoma Researchmelanoma tumors return no matter how much the tumor is depleted,» said Meenhard Herlyn, D.V.M., D.Sc., professor and director of Wistar's Melanoma ResearchMelanoma Research Center.

Crews noted that RNA splicing - targeted agents have been shown to have activity in a variety of solid tumors so the findings may be relevant to a variety of cancers, such as breast and drug - resistant melanoma.

Melanoma tumors were, as they described, heterogeneous.

«Tumor size is defining factor to response from promising melanoma drug.»

«This was the first robust assessment to determine the impact of baseline tumor size on clinical endpoints in patients with metastatic melanoma — in particular — those receiving MK - 3475.