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Clinicopathological and biomolecular characteristics of stage IIB/IIC and stage IIIA colon cancer: Insight into the survival paradox
Author(s) -
Kim Ho Seung,
Kim Kyeong Min,
Lee Sat Byol,
Kim Ga Ram,
Han Yoon Dae,
Cho Min Soo,
Hur Hyuk,
Lee Kang Young,
Kim Nam Kyu,
Min Byung Soh
Publication year - 2019
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.25515
Subject(s) - stage (stratigraphy) , medicine , colorectal cancer , oncology , confounding , overall survival , survival analysis , disease , cancer , gastroenterology , pathology , biology , paleontology
Background A survival paradox of stage IIB/IIC and IIIA colon cancer has been consistently observed throughout revisions of the TNM system. This study aimed to understand this paradox with clinicopathological and molecular differences. Methods Clinicopathological characteristics of patients with pathologically confirmed stage IIB/IIC or IIIA colon cancer were retrospectively reviewed from a database. Publicly available molecular data were retrieved, and intrinsic subtypes were identified and subjected to gene sets enrichment analysis (GSEA). Results Among the 159 patients included in the clinicopathological analysis, those at stage IIB/IIC had worse 3‐year disease‐free and overall survival than those at stage IIIA (59.3% vs 91.7%, P < 0.001 and 82.7% vs 98.5%, P < 0.001, respectively), even after adjusting for confounding factors. Data of 95 patients were retrieved from public databases, demonstrating a higher frequency of the microsatellite instable subtype in stage IIB/IIC. The consensus molecular subtype distribution pattern differed between the groups. The GSEA further suggested the protumor inflammatory reaction might be more prominent in stage IIB/IIC. Conclusions The survival paradox in colon cancer was confirmed and appears to be a multifactorial phenomenon not attributed to a single clinicopathologic factor. However, the greater molecular heterogeneity in stage IIB/IIC could contribute to the poor prognosis.