They further investigated this phenotype in
a skin tumor model system, provided by Maria Sibilia from the Institute for Cancer Research of the Medical University of Vienna, and found that deactivating HDAC1 actually accelerates tumor development, while HDAC2 deactivation has no effect.
Not exact matches
Weeraratna's team used an artificial
skin reconstruct
model to recreate the interactions of melanoma cells with either a young or aged
tumor microenvironment.
«This
model supported cancer development so strongly that some mice developed invasive squamous cell
skin cancers similar to the patient's
tumor,» said lead author Shadmehr Demehri, MD, PhD, a dermatologist and postdoctoral fellow.
The researchers showed in mouse
models that chronic
skin inflammation caused by continuous
skin contact with allergens contributes to
tumor development.
Biocellion is being used to
model a variety of biological system behaviors, such as biofilm formation and wrinkling, microbial growth dynamics in complex soil structure, brain
tumor growth and invasion, formation of complex bacterial colonies, and changes in blood vessels and
skin cells.
Cutaneous SCC is a clinically aggressive cancer, and the inactivation of p21waf1 / cip1 has been shown to play a critical role in the formation of
skin tumor in knockout mice
models (14, 15).
Using melanoma cells and both young and old normal
skin cells as a
model, the lab is trying to unravel what these changes may be, and how they affect
tumor progression.
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.
Wistar researchers also create new tools for melanoma research, including three - dimensional «artificial
skin» that serves as a
model for studying how living
tumors behave, as well as a proving ground for new therapeutics.