Histological Classification and Immunohistochemical Study of Feline Colorectal Epithelial Tumors

2020 ◽  
pp. 030098582097427
Author(s):  
Mizuho Uneyama ◽  
James K. Chambers ◽  
Ko Nakashima ◽  
Kazuyuki Uchida ◽  
Hiroyuki Nakayama

Among 113 feline gastrointestinal epithelial tumors diagnosed between 2006 and 2019, 78 (69%) were detected in the colorectum. Fifty colorectal tumors were selected for further pathological evaluations, of which 9 (18%) were histopathologically diagnosed as adenomas and 41 (82%) as carcinoma. The carcinomas included 33 tubular adenocarcinomas (TAC), 5 tubulovillous adenocarcinomas (TVAC), 2 mucinous adenocarcinomas, and 1 undifferentiated carcinoma. Histopathologically, TAC frequently showed vascular invasion (17/33 cases, 52%). In TAC cases, serosal infiltration (13/15 cases, 87%) and lymph node metastasis (8/9 cases, 89%) were common in bowel resection and lymphadenectomy samples, respectively. Immunohistochemically, the tumor cells of most cases were positive for cytokeratin (CK) 20 (50/50 cases, 100%) and CDX2 (48/50 cases, 96%). Focal immunopositivity for CD10 (11/50 cases, 22%) and CK7 (15/50 cases, 30%) was observed irrespective of the histological subtype. Only a few cases showed diffuse nuclear accumulation of β-catenin (2/50 cases, 4%) and p53 (5/50 cases, 10%). A lack of tubule formation, female sex, and low CDX2 labeling were statistically associated with carcinoma compared to adenoma (ρ = 0.615, P < .001; ρ = 0.279, P = .050; and ρ = −0.265, P = .063, respectively). Other features, including mucin profiles, Ki67 labeling index, and accumulation of β-catenin and p53, were not associated with malignancy. A sequence analysis revealed KRAS mutations in 3/7 TAC cases. These results suggest that KRAS mutations—rather than excessive Wnt/β-catenin signaling and the inactivation of TP53—contribute to the tumorigenesis of feline colorectal carcinoma.

2008 ◽  
Vol 13 (3) ◽  
pp. 172-176 ◽  
Author(s):  
Sang Wook Choi ◽  
Prodromos Hytiroglou ◽  
Stephen A. Geller ◽  
Sun Moo Kim ◽  
Kyu Won Chung ◽  
...  

1986 ◽  
Vol 10 (1) ◽  
pp. 26-33 ◽  
Author(s):  
Tetsuro Kodama ◽  
Shaw Watanabe ◽  
Yuichi Sato ◽  
Yukio Shimosato ◽  
Naoto Miyazawa

1991 ◽  
Vol 44 (8) ◽  
pp. 1206-1213
Author(s):  
T. Monden ◽  
H. Morimoto ◽  
H. Nakanishi ◽  
M. Fukunaga ◽  
T. Shimana ◽  
...  

2019 ◽  
Vol 70 (8) ◽  
pp. 2926-2933
Author(s):  
Pavel Onofrei ◽  
Elena Carmen Cotrutz ◽  
Ana Emanuela Botez ◽  
Vasile Bogdan Grecu ◽  
Carmen Solcan ◽  
...  

The results of the recent years researches support the need for personalized therapeutic of cancer by completing the clinical, imagistic and histopathological diagnosis with molecular studies to identify new useful biomarkers for diagnosis, prognosis and tumor progression. Maspin is a non-inhibitory serine protease having a proapoptotic activity, suppressor of tumor invasion, metastasis and angiogenesis. Ezrin is a member of Ezrin/Radixin/Moesin (ERM) family, involved in cellular adhesion mechanisms, motility and invasiveness of tumor cells. In colorectal tumors, there is a heterogeneity of research results regarding the clinical significance of the maspin due to a possible partnership with other molecules with which it interacts through the same signaling pathways. Our study investigated the two molecule�s immunoreactivity (IR) in 92 colorectal tumors highlighting an inverse correlation between ezrin�s and maspin�s expression, suggesting the fact that ezrin�s overexpression could influence maspin�s tumoral suppressor role. Furthermore there was observed a difference of the molecules IR within the same tumoral stage, suggesting their utility regarding the treatment protocol of these tumors.


2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 3632-3632 ◽  
Author(s):  
Van Karlyle Morris ◽  
Michael J. Overman ◽  
Cathy Eng ◽  
Eduardo Vilar Sanchez ◽  
Maria Morelli ◽  
...  

3632 Background: KRAS mutations in codons 12 and 13 are present in approximately 40% of all colon cancers and predict a lack of response to monoclonal antibodies to the EGFR among patients with metastatic disease. Activating mutations in codons 61 and 146 occur less frequently, and the clinicopathologic features of this subpopulation of KRAS-mutant colorectal tumors have not been clearly defined. Methods: Records of patients treated at MD Anderson Cancer Center between December 2000 and August 2012 for metastatic colorectal cancer whose tumors underwent testing for a KRAS mutation were reviewed for clinical characteristics, concurrent mutations, and survival outcomes. Associations between mutation status and clinic features were measured by calculation of odds ratios, and survival was estimated according to the Kaplan-Meier method. Results: Among the 487 records reviewed, 225 KRAS 12/13 mutations (47.2%) and 14 KRAS 61/146 mutations (2.9%) were detected. Liver metastases were less common for patients with KRAS 61/146 mutations than for patients with KRAS 12/13 mutations (OR 0.26, p-value=0.02). No difference in lung metastases was identified for KRAS 61/146 mutated patients when compared to those with KRAS wild-type tumors (OR=2.1, p-value=0.26), even though lung metastases were more common for patients with KRAS 12/13 mutations (OR 2.86, p-value=0.001). There was no association between the presence of a KRAS 61/146 mutation and gender, stage at presentation, site of primary tumor, body mass index, tobacco history, or concurrent PIK3CA mutation. Whereas a worse survival difference from the time of metastasis detection was noted for KRAS 12/13 patients when compared to those with KRAS wild-type tumors (HR 1.74, p-value= 0.002), patients with KRAS 61/146 mutations demonstrated no change in survival outcome (HR 1.10, p-value=0.87). Conclusions: Patients with KRAS 61/146 mutations have different patterns of metastases compared to KRAS 12/13, but do not appear to share the poor prognosis associated with the more common KRAS 12/13. These results suggest that clinical phenotypes for patients afflicted with colorectal cancer may differ based on the specific codon mutated within the KRAS oncogene.


2014 ◽  
Vol 3 (1) ◽  
pp. 179-184 ◽  
Author(s):  
HILMI KODAZ ◽  
ILHAN HACIBEKIROGLU ◽  
BULENT ERDOGAN ◽  
ESMA TURKMEN ◽  
HILMI TOZKIR ◽  
...  

1990 ◽  
Vol 14 (12) ◽  
pp. 1139-1147 ◽  
Author(s):  
Kazuya Kondo ◽  
Kiyoshi Mukai ◽  
Yuichi Sato ◽  
Yoshihiro Matsuno ◽  
Yukio Shimosato ◽  
...  

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