Tonia Jorgenson - Academia.edu (original) (raw)
Papers by Tonia Jorgenson
Supplementary Tables 1-4, Figures 1-2 from Identification of Susceptibility Loci in a Mouse Model... more Supplementary Tables 1-4, Figures 1-2 from Identification of Susceptibility Loci in a Mouse Model of KRASG12D-Driven Pancreatic Cancer
Cancer Research, 2013
We are investigating the role of reduction-oxidation (redox) state in human breast cancer progres... more We are investigating the role of reduction-oxidation (redox) state in human breast cancer progression. Physiologic levels of oxidants and antioxidants within subcellular compartments regulate and coordinate normal cell functions. Cells in a state of redox imbalance undergo adaptation and/or altered behavior. We propose to investigate the thioredoxin 1 (TRX1) redox couple in human breast cancer progression. This molecule is known to interact with several molecules involved in breast carcinogenesis, including redox-sensitive transcription factors and estrogen receptor (ER) alpha. We hypothesize human breast cancer tissues are in a state of redox imbalance favoring a more reducing environment, and post-translational redox modifications involving TRX1, thioredoxin reductase 1 (TRXR1), and thioredoxin interacting protein (TXNIP) are involved. Preliminary data demonstrated redox imbalance in comparisons of breast cancers to surrounding tissues. TRX1 protein levels were 1.5-fold increased,...
Cancer Research, 2013
For this article, we explore a hypothesis involving the possible role of reduction/oxidation (red... more For this article, we explore a hypothesis involving the possible role of reduction/oxidation (redox) state in cancer. We hypothesize that many modifications in cellular macromolecules, observed in cancer progression, may be caused by redox imbalance. Recent biochemical data suggest that human prostate cancer cell lines show a redox imbalance (oxidizing) compared with benign primary prostate epithelial cells; the degree of oxidation varied with aggressive behavior of each cell line. Our recent data suggest that human breast cancer tissues show a redox imbalance (reducing) compared with benign adjacent breast tissues. Accumulating data summarized in this article suggest that redox imbalance may regulate gene expression and alter protein stability by posttranslational modifications, in turn modulating existing cellular programs. Despite significant improvements in cancer therapeutics, resistance occurs, and redox imbalance may play a role in this process. Studies show that some cancer ...
Cancer Research, 2010
Genetic background affects susceptibility to pancreatic ductal adenocarcinoma in the Ela-KRASG12D... more Genetic background affects susceptibility to pancreatic ductal adenocarcinoma in the Ela-KRASG12D mouse model. In this model, KRAS oncogene expression is driven by an elastase promoter in acinar cells of the pancreas on an FVB/NTac (FVB) background [FVB-Tg(Ela-KRASG12D)] with the transgene carried on the Y chromosome. Through linkage analysis of crosses between the C57BL/6J (B6), BALB/cJ (BALB), and DBA/2J (D2) inbred strains of mice and resistant FVB-Tg(Ela-KRASG12D), we have identified six susceptibility loci that affect mean preinvasive lesion multiplicity. Markers on chromosome 2 segregated with high tumor multiplicity in all three strains; these loci were designated Prsq1-3 (pancreatic ras susceptibility quantitative trait loci 1-3; combined F2 and N2 LODW, 6.0, 4.1, and 2.7, respectively). Susceptibility loci on chromosome 4, designated Prsq4 and Prsq5, were identified in crosses between FVB transgenic mice and B6 or BALB mice (combined F2 and N2 LODW, 3.6 and 2.9, respectivel...
Supplementary Tables 1-4, Figures 1-2 from Identification of Susceptibility Loci in a Mouse Model... more Supplementary Tables 1-4, Figures 1-2 from Identification of Susceptibility Loci in a Mouse Model of KRASG12D-Driven Pancreatic Cancer
Cancer Research, 2013
We are investigating the role of reduction-oxidation (redox) state in human breast cancer progres... more We are investigating the role of reduction-oxidation (redox) state in human breast cancer progression. Physiologic levels of oxidants and antioxidants within subcellular compartments regulate and coordinate normal cell functions. Cells in a state of redox imbalance undergo adaptation and/or altered behavior. We propose to investigate the thioredoxin 1 (TRX1) redox couple in human breast cancer progression. This molecule is known to interact with several molecules involved in breast carcinogenesis, including redox-sensitive transcription factors and estrogen receptor (ER) alpha. We hypothesize human breast cancer tissues are in a state of redox imbalance favoring a more reducing environment, and post-translational redox modifications involving TRX1, thioredoxin reductase 1 (TRXR1), and thioredoxin interacting protein (TXNIP) are involved. Preliminary data demonstrated redox imbalance in comparisons of breast cancers to surrounding tissues. TRX1 protein levels were 1.5-fold increased,...
Cancer Research, 2013
For this article, we explore a hypothesis involving the possible role of reduction/oxidation (red... more For this article, we explore a hypothesis involving the possible role of reduction/oxidation (redox) state in cancer. We hypothesize that many modifications in cellular macromolecules, observed in cancer progression, may be caused by redox imbalance. Recent biochemical data suggest that human prostate cancer cell lines show a redox imbalance (oxidizing) compared with benign primary prostate epithelial cells; the degree of oxidation varied with aggressive behavior of each cell line. Our recent data suggest that human breast cancer tissues show a redox imbalance (reducing) compared with benign adjacent breast tissues. Accumulating data summarized in this article suggest that redox imbalance may regulate gene expression and alter protein stability by posttranslational modifications, in turn modulating existing cellular programs. Despite significant improvements in cancer therapeutics, resistance occurs, and redox imbalance may play a role in this process. Studies show that some cancer ...
Cancer Research, 2010
Genetic background affects susceptibility to pancreatic ductal adenocarcinoma in the Ela-KRASG12D... more Genetic background affects susceptibility to pancreatic ductal adenocarcinoma in the Ela-KRASG12D mouse model. In this model, KRAS oncogene expression is driven by an elastase promoter in acinar cells of the pancreas on an FVB/NTac (FVB) background [FVB-Tg(Ela-KRASG12D)] with the transgene carried on the Y chromosome. Through linkage analysis of crosses between the C57BL/6J (B6), BALB/cJ (BALB), and DBA/2J (D2) inbred strains of mice and resistant FVB-Tg(Ela-KRASG12D), we have identified six susceptibility loci that affect mean preinvasive lesion multiplicity. Markers on chromosome 2 segregated with high tumor multiplicity in all three strains; these loci were designated Prsq1-3 (pancreatic ras susceptibility quantitative trait loci 1-3; combined F2 and N2 LODW, 6.0, 4.1, and 2.7, respectively). Susceptibility loci on chromosome 4, designated Prsq4 and Prsq5, were identified in crosses between FVB transgenic mice and B6 or BALB mice (combined F2 and N2 LODW, 3.6 and 2.9, respectivel...