Gene identified necessary for pancreatic cancer development!
Researchers from New York University and University of Michigan have identified a gene called Atdc (ataxia-telangiectasiagroup D-complementing) that is necessary for pancreatic cancer development.
Pancreatic ductaladenocarcinoma (PDA) is an aggressive form of pancreatic cancer that is driven by the oncogenic (cancer causing) KRAS. It is diagnosed in late stages and is resistant to therapy.
“We thought the deletion [of the Atdc gene] would slow cancer growth, not completely prevent it,” said Diane Simeone, director of the Pancreatic Cancer Center of NYU LangoneHealth’s PerlmutterCancer Center, and corresponding author of the study.
Pancreatic ductaladenocarcinoma (PDA) is an aggressive form of pancreatic cancer that is driven by the oncogenic (cancer causing) KRAS. It is diagnosed in late stages and is resistant to therapy.
“We thought the deletion [of the Atdc gene] would slow cancer growth, not completely prevent it,” said Diane Simeone, director of the Pancreatic Cancer Center of NYU LangoneHealth’s PerlmutterCancer Center, and corresponding author of the study.
The researchers have shown that deletion of the ataxia-telangiectasia group D-complementing (Atdc) gene, which is up-regulated (found in multiple copies) in the majority of pancreatic adenocarcinoma, completely prevented PDA development in the context of oncogenic KRAS. When the Atdc gene was present, 100% of the mice with KRAS and other mutations (gene abnormalities) developed PDA. Mice lacking ATDC are protected from developing PDA.
As for the mechanism, the researchers showed that ATDC promotes acinar–ductal metaplasia (ADM) to pancreatic intraepithelial neoplasia (PanIN) through the activation of β-catenin signaling and subsequent SOX9 up-regulation (over expression).
This breakthrough study revealed great hope for the development of potential new therapies for pancreatic cancer.
As for the mechanism, the researchers showed that ATDC promotes acinar–ductal metaplasia (ADM) to pancreatic intraepithelial neoplasia (PanIN) through the activation of β-catenin signaling and subsequent SOX9 up-regulation (over expression).
This breakthrough study revealed great hope for the development of potential new therapies for pancreatic cancer.
The study has been published today, May 2, 2019 in the scientific journal Genes & Development.
Corresponding author of this study is Dr. Diane Simeone: diane.simeone@nyulangone.org
Corresponding author of this study is Dr. Diane Simeone: diane.simeone@nyulangone.org
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