Immunohistochemical of paraffin - embedded
human pancreas cancer using 10837 -1-AP (OPTN antibody) at dilution of 1:50 (under 10x lens)
Not exact matches
The scientists are testing the ability of drugs already on the market to reverse this cellular transformation in the
pancreas in mice models of
human pancreatic
cancer.
According to the National
Cancer Institute, more than a third of all
human cancers, including a high percentage of
pancreas, lung and colon
cancers are driven by mutations in a family of genes known as Ras.
Cancer of the
pancreas (scientifically known as pancreatic ductal adenocarcinoma or PaCa) is one of the most deadly forms of the disease in
humans.
Obesity in these mice resembles several important clinical features of
human obesity such as weight gain and disturbance of metabolism, and this mouse model was ideal for unraveling any underlying biological mechanisms of
pancreas cancer that are put in motion by obesity.
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).
Still, by the 1990s DuPont knew that the chemical caused cancerous tumors in the testes,
pancreases, and livers of lab animals, and there was even evidence of
human DNA damage and links to prostate
cancer in workers exposed to PFOA.
Studies of Gluts in
human tumors have shown a significant increase in the abundance of Glut1 and Glut3 mRNA in
cancers of the esophagus, colon, and
pancreas, overexpression of Glut1 and Glut3 mRNA and Glut1 protein expression in head and neck tumors and Glut1 protein overexpression in breast and renal cell carcinomas