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.
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.
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 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.
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.
«Most importantly, we demonstrated in our study that blocking the pathway resulted in reduction of tumor growth in an experimental model of
human melanoma transplanted into mice,» Ballabio said.
In the study, the compound
caused human melanoma cells to die and inhibited tumor growth by about 69 percent in a mouse model.
Up - regulated expression of zonula occludens protein - 1 in
human melanoma associates with N - cadherin and contributes to invasion and adhesion.
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.
Moreover, one compound substantially decreased the growth of
human melanoma xenografts in nude mice without any apparent side effects.
Giorgio Parmiani and colleagues are the first to unequivocally demonstrate that
human melanoma antigens recognized by patient T cells include molecules belonging to the normal melanocyte lineage.
Analysis of antigens recognized
on human melanoma cells by A2 - restricted cytolytic T lymphocytes (CTL).
Prior studies had shown that the metastasis
of human melanoma cells in these mice is predictive of their metastasis in patients.
The work of Berger et al. supported the conclusion that cancer - associated PREX2 mutations can promote the growth of
human melanoma cells.
«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.
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 researchers also identified a pharmacological way through which FES expression can be restored in
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.
Human melanoma is a very aggressive skin cancer, but very little is known about the mechanisms that cause the disease to progress.
To further validate their findings, they studied the role of one of the genes, namely FES, and established its important contribution to the development of both mouse and
human melanoma.
Prof. Marine and his research team also identified a pharmacological way of restoring the expression of FES in
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.
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 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).
First, PREX2 was identified as a frequently mutated gene in
human melanoma.
ab85137 staining S100 in
a human melanoma cell line by Flow Cytometry.
Metabotropic glutamate receptor 1 and glutamate signaling in
human melanoma.
Furthermore,
human melanoma cells previously were shown to have higher levels of the long non-coding RNA (lncRNA), SPRINGTLY, compared to normal human melanocytes [48].
Olga Shakhova, Lukas Sommer and colleagues used a mouse model of melanoma that combined the presence of mutant Nras, a known melanoma - promoting factor, and deficiency of INK4a, which is often inactivated in
human melanoma.
«The impact was particularly dramatic in a mouse model of
human melanoma,» Vignali said.
In one of her most recent studies, she and her collaborators discovered that a mutation commonly found in
human melanoma and other cancers is also exceedingly common in an invasive form of canine bladder cancer.
The chemical compound lauroside B isolated from Laurus nobilis is an inhibitor of
human melanoma (skin cancer) cell proliferation at high concentrations in - vitro.
Phrases with «human melanoma»