We also confirmed the expression of OR2C3
in human melanomas, but not in normal melanocytes.
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.
«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).
«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.
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.
The researchers also identified a pharmacological way through which FES expression can be restored
in human melanoma.
Prof. Marine and his research team also identified a pharmacological way of restoring the expression of FES
in human melanoma.
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).
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.
ab85137 staining S100
in a human melanoma cell line by Flow Cytometry.
A p16INK4a - insensitive CDK4 mutant targeted by cytolytic T lymphocytes
in a human melanoma.
Metabotropic glutamate receptor 1 and glutamate signaling
in 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 cance
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 cance
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.
So what is the association between melanocortin - 1 (MC1R) receptor and
melanoma risk
in humans after controlling for sun exposure?
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 dru
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 dru
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 dru
in groups of cells to identify those involved
in resistance to a melanoma dru
in resistance to a
melanoma drug.
However, it has not been possible to test whether sunscreens prevent
melanoma, because these are generally manufactured as cosmetics and tested
in human volunteers or synthetic skin models.
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.
In one published study, where we put
melanoma cells into mice, we published it with mouse
melanoma cells, but we repeated it with
human cells.
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.
These DNA elements have epigenetic functions that are similar
in zebrafish and
human melanoma and could potentially be targeted with drugs to stop a mole from becoming cancerous.
The research team analyzed BRAF inhibitor resistance
in melanoma cell lines, mice bearing
human melanoma tumors, and
in human tumor biopsy samples.
B - raf gene mutations have known roles
in the development of many
human cancers including
melanoma, lung and thyroid cancer.
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.
Betulinic acid also shrank
human melanomas induced
in mice.
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.
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.
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.
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.
In the study, the compound caused human melanoma cells to die and inhibited tumor growth by about 69 percent in a mouse mode
In the study, the compound caused
human melanoma cells to die and inhibited tumor growth by about 69 percent
in a mouse mode
in a mouse model.
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 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
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
in nude mice (Figure 3B, S6B, and S6C; Berger et al., 2012).
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).
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.
Our team was instrumental
in the development of talimogene laherparepvec, the first
in human oncolytic virus therapy for patients with
melanoma.
In 1999, Wolchok received a grant from CRI to conduct a clinical trial of a xenogenic vaccine in humans with melanom
In 1999, Wolchok received a grant from CRI to conduct a clinical trial of a xenogenic vaccine
in humans with melanom
in humans with
melanoma.
Immunological factors
in human sarcomas and
melanomas: a rational basis for immunotherapy.
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).
A dominant negative Cx43 mutant differentially affects tumorigenic and invasive properties
in human metastatic
melanoma cells.
Expression of the
melanoma cell adhesion molecule
in human mesenchymal stromal cells regulates proliferation, differentiation, and maintenance of hematopoietic stem and progenitor cells.
Mucosal
melanomas with mutations
in CDK4 may respond to palbociclib or ribociclib, which have demonstrated activity
in advanced hormone receptor — positive,
human epidermal growth factor receptor 2 — negative breast cancer.
Germline mutations of the CDKN2 gene
in UK
melanoma families,
in Human Molecular Genetics.
Published
in Human Mutation Fung, D. C.; Holland, E. A.; Becker, T. M.; Hayward, N. K.; Bressac - de Paillerets, B.; Mann, G. J. eMelanoBase: an online locus - specific variant database for familial
melanoma Hum Mutat 21 (1): 2 - 7, 2003
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.