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Ki-67 Immunostaining in Pancreatic Cancer and Chronic Active Pancreatitis: Does In Vivo FDG Uptake Correlate with Proliferative Activity?

Andreas C. Buck, Holger H. Schirrmeister, Carl-Albrecht Guhlmann, Christoph G. Diederichs, Changxian Shen, Inga Buchmann, Jens Kotzerke, Dieter Birk, Thorsten Mattfeldt and Sven N. Reske

Departments of Nuclear Medicine, Surgery, and Pathology, University of Ulm, Ulm, Germany



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FIGURE 1. Scattergram of FDG SUVs in patients with histopathologically confirmed ductal adenocarcinoma of pancreas (DPC) and CAP (CP).

 


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FIGURE 2. (A and B) Iteratively reconstructed FDG PET images (transaxial [A] and coronal [B] slices) of patient with histopathologically confirmed ductal adenocarcinoma of pancreatic head, which shows intense FDG accumulation. (C and D) Corresponding images of patient with histopathologically proven chronic active pancreatitis. Similar focal accumulation of FDG in pancreatic head region is apparent.

 


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FIGURE 3. Typical cross section of pancreatic adenocarcinoma stained with antihuman nuclear Ki-67 antibody MIB-1 and lightly counterstained with hematoxylin. Amount of Ki-67–positive tumor cells is approximately 60% in this cross section. (x200)

 


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FIGURE 4. Cross section of CAP stained with antihuman nuclear Ki-67 antibody MIB-1 and lightly counterstained with hematoxylin. Amount of Ki-67–positive tumor cells is approximately 2% in this cross section. Left upper part of figure shows newly formed reactive lymph node with lightly positive Ki-67 immunostaining. (x200)

 


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FIGURE 5. Scattergram of Ki-67 values in patients with histopathologically confirmed ductal adenocarcinoma of pancreas (DPC) and CAP (CP). pos. = positive.

 





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