Sentences with phrase «of human melanoma»

Moreover, one compound substantially decreased the growth of human melanoma xenografts in nude mice without any apparent side effects.

«The impact was particularly dramatic in a mouse model of human melanoma,» Vignali said.

The analysis also found that a significant fraction of tumors contained rearrangements and mutations of a gene called PREX2, and experiments confirmed that cancer - associated mutations of PREX2 promoted the growth of human melanoma cells in mice.

In these experiments, Berger and colleagues show that somatic PREX2 mutations identified through whole - genome sequencing of human melanoma can contribute to enhanced lethality of tumor xenografts in nude mice (Figure 3B, S6B, and S6C; Berger et al., 2012).

Unexpectdly the expression of FES, which encodes a kind of protein better known for their ability to promote cancer development -, is lost in a large fraction of human melanoma.

Taking advantage of these «simplified» versions of melanoma, the researchers identified a dozen of new genes that are likely to play key roles in the initiation and / or progression of human melanoma.

Not exact matches

In 2000, Medarex began its first phase of human testing on its new «CTLA -4-blockade» — in patients who had either prostate cancer or metastatic melanoma, a deadly form of skin cancer.

Prof. Marine and his team generated a refined mouse model that faithfully reproduces the early stages of melanoma development in humans.

«It is anticipated that this novel compound will have significant efficacy in human melanomas and other cancers either as a stand - alone therapy or in combination with other targeted or immune - based therapies,» explained co-corresponding author Rhoda Alani, MD, the Herbert Mescon Chair of Dermatology at Boston University School of Medicine (BUSM).

Dr. Aplin and Jessica Teh, PhD, his senior postdoctoral researcher at Jefferson (Philadelphia University + Thomas Jefferson University), examined the effects of a combination of two FDA - approved targeted agents on human melanomas grafted onto mice.

To that end, in collaboration with the University of Zurich and MD Anderson Cancer Center, the researchers tested melanoma tumor samples from human patients undergoing treatment with the same targeted therapies.

In experiments with mice, the UC San Diego - led team showed that verteporfin also suppresses the growth of uveal melanoma tumors derived from human tumors.

Beyond lung cancer, TiY is able to target TICs in 28 types of human cell lines derived from the central nervous system, melanoma, breast, renal, ovarian, colon, and prostate cancer.

The study, led by researchers at Boston University School of Medicine (BUSM), reports sporadic mutations in the APC / C protein complex, specifically in the essential protein component Cdh1, which may predispose humans to developing melanoma from the loss of the APC / C protein complex.

In one experiment this year, a team led by another CRISPR pioneer, Feng Zhang of the Broad Institute in Cambridge, Massachusetts, targeted the 20,000 or so known human genes, turning them on one by one in groups of cells to identify those involved in resistance to a melanoma drug.

One of these, UJ3, is as effective as the industry - standard drug Cisplatin in killing cancer cells in laboratory tests done on human esophageal cancer, breast cancer and melanoma.

The rarity is very similar in both humans and fish, which suggests that the underlying process of melanoma formation is probably much the same in humans.»

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.

«What's cool about this group of genes is that they also get turned on in human melanoma,» says Zon, who is also a member of the Harvard Stem Cell Institute and a Howard Hughes Medical Institute investigator.

B - raf gene mutations have known roles in the development of many human cancers including melanoma, lung and thyroid cancer.

To test their hypothesis, the researchers carried out experiments on human melanoma cells, a line of cancer cells they chose for their ability to grow easily and quickly.

After exploiting a technology that allowed them to activate each of nearly 16,000 genes individually in human melanoma cell lines containing mutant BRAF, the authors then treated the panel of cells with the drugs and monitored which cells showed altered drug sensitivity.

As a result, the researchers were able to prevent the growth and malignant spread of the cancer in the animal model and human melanoma cells.

Their preliminary findings indicate that MUS81 - induced movement of DNA to the cytosol also occurs in human cancer cells, including prostate cancer, breast cancer, colorectal cancer, uterine cancer, leukemia, and melanoma cells.

Prof. Marine and his research team also identified a pharmacological way of restoring the expression of FES in human melanoma.

The lesions and dark patches are a scalier version of what melanomas look like on humans, but it's unclear whether they make the animals unsafe to eat.

While past attempts to treat melanoma failed to meet expectations, an international team of researchers are hopeful that a compound they tested on both mice and on human cells in a petri dish takes a positive step toward creating a drug that can kill melanoma cancer cells without harming nearby healthy cells.

The Reproducibility Project did not attempt to replicate this finding, but subsequent studies have reported the frequency of PREX2 mutations in human melanoma (Hodis et al., 2012; Krauthammer et al., 2012; Marzese et al., 2014; Ni et al., 2013; Turajlic et al., 2012), including meta - analysis of 241 melanomas (Xia et al., 2014).

In a series of studies led by Dr. Arun Sharma, associate professor of pharmacology and Dr. Shantu Amin, professor of pharmacology, both of Penn State College of Medicine, researchers designed and synthesized a compound called napthalamide - isoselenocyanate — NISC - 6 — to inhibit both the Akt1 pathway and human topoisomerase IIα — topo IIα — activity, which contribute to melanoma tumor growth.

In 2012, as part of efforts to better understand the causes of melanoma, researchers at the Broad Institute, the Dana - Farber Cancer Institute and a number of other institutes reported the results of whole genome sequencing of 25 human metastatic melanomas (Berger et al., 2012).

Second, mutation of PREX2 can accelerate human melanoma growth.

Analysis of antigens recognized on human melanoma cells by A2 - restricted cytolytic T lymphocytes (CTL).

Cloning of the gene coding for a shared human melanoma antigen recognized by autologous T cells infiltrating into tumor.

Up - regulated expression of zonula occludens protein - 1 in human melanoma associates with N - cadherin and contributes to invasion and adhesion.

Mukherji B, Chakraborty NG, Yamasaki S, Okino T, Yamase H, Sporn JR, Kurtzman SK, Ergin MT, Ozols J, Meehan J, Mauri F. Induction of antigen - specific cytolytic T cells in situ in human melanoma by immunization with synthetic peptide - pulsed autologous antigen presenting cells.

A new family of genes coding for an antigen recognized by autologous cytolytic T lymphocytes on a human melanoma.

Our team was instrumental in the development of talimogene laherparepvec, the first in human oncolytic virus therapy for patients with melanoma.

Traversari C, van der Bruggen P, Van den Eynde B, Hainaut P, Lemoine C, Ohta N, Old L J, Boon T. Transfection and expression of a gene coding for a human melanoma antigen recognized by autologous cytolytic T lymphocytes.

In 1999, Wolchok received a grant from CRI to conduct a clinical trial of a xenogenic vaccine in humans with melanoma.

Further research uncovered a broad spectrum of cell surface stem cell markers (e.g., CD133, CD44, and CD24) that allow the identification of CSCs in human solid tumors, including brain, breast, prostate, pancreas, liver, ovary, skin, colon cancers, and melanoma (3 - 6)(Figure 1 based on 7).

Expression of the melanoma cell adhesion molecule in human mesenchymal stromal cells regulates proliferation, differentiation, and maintenance of hematopoietic stem and progenitor cells.

Intracellular retention of the NKG2D ligand MHC class I chain - related gene A in human melanomas confers immune privilege and prevents NK cell - mediated cytotoxicity.

The terms «Malignant melanoma of skin» returned 0 free, full - text review articles on human participants.

Germline mutations of the CDKN2 gene in UK melanoma families, in Human Molecular Genetics.

Published in Human Molecular Genetics Ghiorzo P, Gargiulo S, Pastorino L, Nasti S, Cusano R, Bruno W, Gliori S, Sertoli MR, Burroni A, Savarino V, Gensini F, Sestini R, Queirolo P, Goldstein AM, Scarrà GB.Impact of E27X, a novel CDKN2A germ line mutation, on p16 and p14ARF expression in Italian melanoma families displaying pancreatic cancer and neuroblastoma Hum Mol Genet.

Published in American Journal of Human Genetics Gillanders, E.; Hank Juo, S. H.; Holland, E. A.; Jones, M.; Nancarrow, D.; Freas - Lutz, D.; Sood, R.; Park, N.; Faruque, M.; Markey, C.; Kefford, R. F.; Palmer, J.; Bergman, W.; Bishop, D. T.; Tucker, M. A.; Bressac - de Paillerets, B.; Hansson, J.; Stark, M.; Gruis, N.; Bishop, J. N.; Goldstein, A. M.; Bailey - Wilson, J. E.; Mann, G. J.; Hayward, N.; Trent, J. Localization of a novel melanoma susceptibility locus to 1p22 Am J Hum Genet.

At the National Human Genome Research Institute, she's studying drug resistance in melanoma and in the lab performs Western blots on the gene products of SOX10 and PTEN.

They went on to show that Sox10, a factor needed for the formation of skin pigment cells from neural crest stem cells during development, was present at high levels in naevi and melanoma samples obtained from both the mouse model and human patients.

Knocking out or blocking the activity of Nrp1 on regulatory T cells in mouse models of several human cancers, including the deadly skin cancer melanoma, led to reduced, delayed or complete elimination of the tumors.

Both mutations affect the function of CDKN2A, a tumor suppressor gene associated with melanoma in humans.