Figure 1: Histopathological analysis of pancreata of PK and CPK mice and incidence of dysplastic lesions at increasing age. | Scientific Reports

Figure 1: Histopathological analysis of pancreata of PK and CPK mice and incidence of dysplastic lesions at increasing age.

From: K-Ras and cyclooxygenase-2 coactivation augments intraductal papillary mucinous neoplasm and Notch1 mimicking human pancreas lesions

Figure 1

(a) Representative pictures of HE-stained pancreatic sections at the ages of 1 month (1M), 3 months (3M), and 6 months (6M). (1M): PK mice developed tubular complexes (TC) and mucin-rich mPanIN-1A lesions. CPK mice developed multiple TC, mPanIN-1A and mPanIN-1B as well as mPanIN-2 lesions. (3M): PK mice displayed multiple TC and lesions graded mPanIN-1A and mPanIN-1B. CPK mice displayed multiple TC, mPanIN-1A, mPanIN-1B, and mPanIN-2. (6M): PK mice with multiple TC, mPanIN-1A, mPanIN-1B, and mPanIN-2 pancreatic lesions. CPK mice with multiple TC, mPanIN-1A, mPanIN-1B, mPanIN-2. Lesions start to acquire IPMN borderline features such as cellular budding into the lumen, and complete loss of cell polarity. (1M+CX): Lack of pathological changes in PK and CPK mice (n = 3, each) exposed to celebrex postnatally for 4 weeks. (b) Incidence of TC, mPanIN, and IPMN lesions in pancreata of PK and CPK mice as compared to C /CP/CK and WT/P/K mice of increasing age. Percentage of mice diagnosed with neoplastic pancreatic ducts by grade mPanIN-1A, mPanIN-1B, mPanIN-2, mPanIN-3, and IPMN-3 (borderline) as well as TC, and atypical flat lesions (AFL). Groups of 1M, 3M, and 6M-old mice of the indicated genotypes were analyzed. 1M: n = 25 WT/P/K, n = 19 C/CP/CK, n = 14 PK, n = 8 CPK; 3M: n = 5 WT/P/K, n = 7 C/CP/CK, n = 3 PK, n = 7 CPK; 6M: n = 15 WT/P/K, n = 4 C/CP/CK, n = 8 PK, n = 5 CPK. Tubular complexes (TC), mPanIN-1A (▲), mPanIN-1B (●), mPanIN-2 (↑), mIPMN-3 borderline (*). Magnifications: 10x (1M, 1M+CX); 40x (3M, 6M).

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