Various subtypes of nonconventional dysplasia have been recently described in inflammatory bowel disease (IBD). We hypothesized that goblet cell deficient dysplasia and serrated dysplasia may be the primary precursor lesions for goblet cell deficient (GCDAC) and serrated (SAC) variants of colonic adenocarcinoma, respectively. Clinicopathologic features of 23 GCDAC and 10 SAC colectomy cases were analyzed. All dysplastic lesions found adjacent to the colorectal cancers (n = 22 for GCDACs and n = 10 for SACs) were subtyped as conventional, nonconventional, or mixed-type dysplasia. As controls, 12 IBD colectomy cases with well to moderately differentiated adenocarcinoma that lacked any mucinous, signet ring cell, low-grade tubuloglandular, or serrated features while retaining goblet cells throughout the tumor (at least 50% of the tumor) were evaluated. The cohort consisted of 19 (58%) men and 14 (42%) women, with a mean age of 53 years and a long history of IBD (mean duration: 18 y). Twenty-seven (82%) patients had ulcerative colitis. GCDACs (57%) were more often flat or invisible than SACs (10%) and controls (25%; P= 0.023). The GCDAC and SAC groups were more likely to show lymphovascular invasion (GCDAC group: 52%, SAC group: 50%, control group: 0%, P= 0.001) and lymph node metastasis (GCDAC group: 39%, SAC group: 50%, control group: 0%, P= 0.009) than the control group. Notably, GCDACs and SACs were more frequently associated with nonconventional dysplasia than controls (GCDAC group: 77%, SAC group: 40%, control group: 0%, P< 0.001). Goblet cell deficient dysplasia (73%) was the most prevalent dysplastic subtype associated with GCDACs (P= 0.049), whereas dysplasias featuring a serrated component (60%) were most often associated with SACs (P= 0.001). The GCDAC group (75%) had a higher rate of macroscopically flat or invisible synchronous dysplasia compared with the SAC (20%) and control (33%) groups (P= 0.045). Synchronous dysplasia demonstrated nonconventional dysplastic features more frequently in the GCDAC (69%) and SAC (40%) groups compared with the control group (0%; P= 0.016). In conclusion, goblet cell deficient dysplasia and dysplasias featuring a serrated component could potentially serve as high-risk markers for GCDACs and SACs, respectively.

中文翻译：

---

非常规不典型增生经常与炎症性肠病中的杯状细胞缺陷和结肠腺癌锯齿状变体相关。

最近在炎症性肠病（IBD）中描述了非常规发育不良的各种亚型。我们假设杯状细胞缺陷型不典型增生和锯齿状不典型增生可能分别是杯状细胞缺陷型（GCDAC）和锯齿状（SAC）结肠腺癌变体的主要前体病变。分析23例GCDAC和10例SAC结肠切除病例的临床病理特征。所有与结直肠癌相邻的不典型增生病变（GCDAC 的 n = 22 例，SAC 的 n = 10 例）均被分类为传统型、非常规型或混合型不典型增生。作为对照，评估了 12 例具有高分化至中分化腺癌的 IBD 结肠切除病例，这些腺癌缺乏任何粘液、印戒细胞、低级别肾小管腺或锯齿状特征，同时保留整个肿瘤（至少 50% 的肿瘤）的杯状细胞。该队列由 19 名 (58%) 男性和 14 名 (42%) 女性组成，平均年龄 53 岁，有较长的 IBD 病史（平均病程：18 年）。二十七（82%）名患者患有溃疡性结肠炎。 GCDAC (57%) 比 SAC (10%) 和对照 (25%；P=0.023) 更经常平坦或不可见。 GCDAC组和SAC组更容易出现淋巴管侵犯（GCDAC组：52%，SAC组：50%，对照组：0%，P=0.001）和淋巴结转移（GCDAC组：39%，SAC组：50） %，对照组：0%，P=0.009)。值得注意的是，GCDAC 和 SAC 比对照组更频繁地与非常规不典型增生相关（GCDAC 组：77%，SAC 组：40%，对照组：0%，P < 0.001）。杯状细胞缺陷性发育不良 (73%) 是与 GCDAC 相关的最常见的发育不良亚型 (P = 0.049)，而具有锯齿状成分的发育不良 (60%) 最常与 SAC 相关 (P = 0.001)。与 SAC 组 (20%) 和对照组 (33%) 相比，GCDAC 组 (75%) 的宏观扁平或不可见同步发育不良发生率较高 (P=0.045)。与对照组（0%；P=0.016）相比，GCDAC（69%）和 SAC（40%）组中同步性发育不良表现出更频繁的非传统发育不良特征。总之，杯状细胞缺陷性发育不良和具有锯齿状成分的发育不良可能分别作为 GCDAC 和 SAC 的高风险标志物。