Journal
MODERN PATHOLOGY
Volume 23, Issue 1, Pages 98-104Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/modpathol.2009.139
Keywords
HMGA1; pancreatic ductal adenocarcinoma; oncogene; immunoreactivity
Categories
Funding
- Joseph C. Eggleston Award
- Eggleston family
- American Cancer Society Scholar Award, Alex's Lemonade Stand Foundation
- J.P. McCarthy Fund
- Flight Attendant Medical Research Institute Young Clinical Investigator Award
- Prevent Cancer Foundation
- Maryland Stem Cell Research Fund
- American Cancer Society Scholar Award [R01 CA092339, R03 CA139331-01]
- Alex's Lemonade Stand Foundation
- NIH [T32]
- NATIONAL CANCER INSTITUTE [R01CA092339, R03CA139331] Funding Source: NIH RePORTER
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Although pancreatic ductal adenocarcinoma is a common and almost uniformly fatal cancer, little is known about the molecular events that lead to tumor progression. The high-mobility group A1 (HMGA1) protein is an architectural transcription factor that has been implicated in the pathogenesis and progression of diverse human cancers, including pancreatic ductal adenocarcinoma. In this study, we investigated HMGA1 expression in pancreatic ductal adenocarcinoma cell lines and surgically resected tumors to determine whether it could be a marker for more advanced disease. By real-time quantitative RT-PCR, we measured HMGA1a mRNA in cultured pancreatic ductal adenocarcinoma cell lines and found increased levels in all cancer cells compared with normal pancreatic tissue. To investigate HMGA1 in primary human tumors, we performed immunohistochemical analysis of 125 cases of pancreatic adenocarcinoma and 99 precursor lesions (PanIN 1-3). We found nuclear staining for HMGA1 in 98% of cases of pancreatic adenocarcinoma, but only 43% of cases of PanIN precursor lesions. Moreover, HMGA1 immunoreactivity correlates positively with decreased survival and advanced tumor and PanIN grade. These results suggest that HMGA1 promotes tumor progression in pancreatic ductal adenocarcinoma and could be a useful biomarker and rational therapeutic target in advanced disease. Modern Pathology ( 2010) 23, 98-104; doi: 10.1038/modpathol.2009.139; published online 9 October 2009
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