Last year, Wittrup showed that delivering antibodies and IL - 2, a signaling molecule that helps to boost immune responses, could halt the growth of aggressive
melanoma tumors in mice for as long as the treatment was given.
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.
Not exact matches
Last fall, Bergö's group reported that ingestion of extra antioxidants drove the metastasis of
melanoma in a
mouse model, though they didn't have any effect on the primary
tumor.
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.
In a mouse model of melanoma, blocking this pathway resulted in reduction of tumor growt
In a
mouse model of
melanoma, blocking this pathway resulted
in reduction of tumor growt
in reduction of
tumor growth.
The research team analyzed BRAF inhibitor resistance
in melanoma cell lines,
mice bearing human
melanoma tumors, and
in human
tumor biopsy samples.
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.
In tests in mice with a very aggressive form of melanoma, the researchers found they could stop tumor growth by delivering this engineered form of IL - 2, along with antibody drugs, once a wee
In tests
in mice with a very aggressive form of melanoma, the researchers found they could stop tumor growth by delivering this engineered form of IL - 2, along with antibody drugs, once a wee
in mice with a very aggressive form of
melanoma, the researchers found they could stop
tumor growth by delivering this engineered form of IL - 2, along with antibody drugs, once a week.
The nanodisc technology was tested
in mice with established
melanoma and colon cancer
tumors.
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 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).
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.
James P. Allison and Matthew Krummel demonstrate that a monoclonal antibody directed against the CTLA - 4 molecule
in a
mouse model of
melanoma could result
in the rejection of
tumors and that this rejection also resulted
in immunity to a second exposure to
tumor cells.
In ligase deficient mice, growth of mouse melanoma cells in vivo is attenuated, while tumor infiltration by CD4 + / CD8 + T cells and dendritic cells is increase
In ligase deficient
mice, growth of
mouse melanoma cells
in vivo is attenuated, while tumor infiltration by CD4 + / CD8 + T cells and dendritic cells is increase
in vivo is attenuated, while
tumor infiltration by CD4 + / CD8 + T cells and dendritic cells is increased.
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.
Mouse studies confirmed the effect of high protein intake and GHR - IGF - 1 signaling on the incidence and progression of breast and
melanoma tumors, but also the detrimental effects of a low protein diet
in the very old.