Publications by authors named "Anne M Lewis"

Article Synopsis
  • NQO1 plays a key role in protecting cells from oxidative damage by detoxifying harmful compounds and is found to be elevated in pancreatic cancer tissues and cell lines.
  • Immunohistochemistry studies show that both pancreatic cancer and precancerous lesions (PanIN) exhibit higher levels of NQO1 compared to normal pancreatic tissue.
  • The compound streptonigrin can effectively kill pancreatic cancer cells by exploiting high NQO1 levels, while inhibiting NQO1 reduces its effectiveness, suggesting NQO1 could be a potential target for pancreatic cancer treatment.
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The tumor microenvironment consists of tumor, immune, stromal, and inflammatory cells which produce cytokines, growth factors, and adhesion molecules that promote tumor progression and metastasis. Of particular interest in this setting is interleukin-1 (IL-1), a pleiotropic cytokine with numerous roles in both physiological and pathological states. It is known to be up regulated in many tumor types and has been implicated as a factor in tumor progression via the expression of metastatic and angiogenic genes and growth factors.

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NAD(P)H:quinone oxidoreductase (NQO1) functions as an important part of cellular antioxidant defense by detoxifying quinones, thus preventing the formation of reactive oxygen species (ROS). The aim of our study was to determine if NQO1 is elevated in pancreatic cancer specimens and pancreatic cancer cell lines and if so, would compounds previously demonstrated to redox cycle with NQO1 be effective in killing pancreatic cancer cells. Immunohistochemistry of resected pancreatic specimens demonstrated an increased immunoreactivity for NQO1 in pancreatic cancer and pancreatic intraepithelial neoplasia (PanIN) specimens versus normal human pancreas.

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