Non-ampullary–duodenal carcinomas: clinicopathologic analysis of 47 cases and comparison with ampullary and pancreatic adenocarcinomas

Abstract

Literature on non-ampullary-duodenal carcinomas is limited. We analyzed 47 resected non-ampullary-duodenal carcinomas. Histologically, 78% were tubular-type adenocarcinomas mostly gastro-pancreatobiliary type and only 19% pure intestinal. Immunohistochemistry (n=38) revealed commonness of 'gastro-pancreatobiliary markers' (CK7 55, MUC1 50, MUC5AC 50, and MUC6 34%), whereas 'intestinal markers' were relatively less common (MUC2 36, CK20 42, and CDX2 44%). Squamous and mucinous differentiation were rare (in five each); previously, unrecognized adenocarcinoma patterns were noted (three microcystic/vacuolated, two cribriform, one of comedo-like, oncocytic papillary, and goblet-cell-carcinoid-like). An adenoma component common in ampullary-duodenal cancers was noted in only about a third. Most had plaque-like or ulcerating growth. Mismatch repair protein alterations were detected in 13% (all with plaque-like growth and pushing-border infiltration). When compared with ampullary (n=355) and pancreatic ductal (n=227) carcinomas, non-ampullary-duodenal carcinomas had intermediary pathologic features with mean invasive size of 2.9 cm (vs 1.9, and 3.3) and 59% nodal metastasis (vs 45, and 77%). Its survival (3-, 5-year rates of 57 and 57%) was similar to that of ampullary-duodenal carcinomas (59 and 52%; P=0.78), but was significantly better than the ampullary ductal (41 and 29%, P<0.001) and pancreatic (28 and 18%, P<0.001) carcinomas. In conclusion, non-ampullary-duodenal carcinomas are more histologically heterogeneous than previously appreciated. Their morphologic versatility (commonly showing gastro-pancreatobiliary lineage and hitherto unrecognized patterns), frequent plaque-like growth minus an adenoma component, and frequent expression of gastro-pancreatobiliary markers suggest that many non-ampullary-duodenal carcinomas may arise from Brunner glands or gastric metaplasia or heterotopic pancreatobiliary epithelium. The clinical behavior of non-ampullary-duodenal carcinoma is closer to that of ampullary-duodenal subset of ampullary carcinomas, but is significantly better than that of ampullary ductal and pancreatic cancers. The frequency of mismatch repair protein alterations suggest that routine testing should be considered, especially in the non-ampullary-duodenal carcinomas with plaque-like growth and pushing-border infiltration.

Clinicopathological characteristics of non‐ampullary duodenal tumors and their phenotypic classification

“…However, this finding was not statistically significant. Categorization according to phenotype was found to be necessary because a higher rate of malignancy was observed in G‐type NADETs, suggesting a more aggressive behavior than I‐type NADETs . As reported by Ushiku et al and Xue et al , G‐type cases demonstrated a poor prognosis since most cases involved advanced cancers .…”

“…We excluded advanced invasive duodenal cancer from this study to refine the data quality. Ushiku et al and Zue et al demonstrated a poor prognosis of G‐type NADETs in the study population, mostly including advanced cancers . The predictive factors should be identified from the limited study population of the NADETs in the early stage because clinical decision making is crucial in the early stage.…”

“…Although the strong relationship between the tumor location, histologic grade, and its phenotype is highly anticipated, it is not well‐described. Furthermore, even though the malignant potential of G‐type NADETs has been reported, it remains controversial …”

“…Furthermore, even though the malignant potential of G-type NADETs has been reported, it remains controversial. 3,[13][14][15][16] Therefore, we conducted an immunohistological review to elucidate the clinicopathological features of NADETs according to the tumor location and phenotypic classification. Additionally, we searched for independent predictive factors associated with G-type NADETs.…”

Clinicopathological characteristics of duodenal epithelial neoplasms: Focus on tumors with a gastric mucin phenotype (pyloric gland-type tumors)

“…However, of these lesions, 70 (76.9%) showed focal intermingling of gastric-type mucin phenotypes positive for MUC5AC and for MUC6. During the process of mucosal healing, generative cell zones are formed in Brunner’s glands, and participate in gastric foveolar metaplasia and tumorigenesis [11–13,21]. We considered that this is the reason why many tubular-type tumors had focal gastric mucin.…”