Tubular adenomas (TA) account for ~75 % to 85 % of all colorectal adenomas [1]. Accordingly, TA is the most prevalent histologic phenotype of all colon adenomas. Progression to invasive carcinoma occurs in <5 % of TA, a process that may take up to 20 years [2]. TA are histologically described as exhibiting nuclear hyperchromatism, nuclear crowding, elliptical to cigar-shaped nuclei with reduction or loss number of mucin-secreting goblet cells [3,4]. In addition, incidental morphologic parameters such as Paneth cell metaplasia, squamous metaplasia, neuroendocrine differentiation, signet-ring cell- like lesion, clear cell metaplasia and osseous metaplasia occasionally occur [5]. Gallupini et al. [3] defined tubular adenomas as polyps with largely conserved normal crypt architecture, with variable elongation of the crypts and an increased number of glands. The epithelium displays enlarged, hyperchromatic nuclei, with different degrees of nuclear atypia and stratification, with loss of nuclear polarity. There is a pseudo-stratification and a de-differentiation with decreased numbers of goblet cells. A small villous component (< 25 %) is acceptable in tubular adenomas [3]. Taherian et al. [6] described as colonic tubular adenomas those characteristically demonstrating nuclear hyperchromatism (i.e., dark purple nuclei), nuclear crowding (i.e., nuclei are bunched-up), elliptical/cigar-shaped nuclei, and loss or reduction in the number of goblet cells. Gibson and Odze [4] classified dysplasia in a two-tiered system (low- versus igh-grade) on the basis of both cytological and architectural features, such as high nuclear:cytoplasmic ratio, nuclear pleomorphism, loss of nuclear polarity and intraluminal cribriforming in at least two (or more) glands. The 2000 edition of the WHO, defines colorectal adenomas as precursor lesions typified by the presence of intraepithelial neoplasia, histologically classified by hypercellularity with enlarged hyperchromatic nuclei, varying degrees of nuclear stratification and loss of polarity [7]. The 2019 edition of the WHO colorectal adenomas were defined as benign, premalignant neoplasms composed of dysplastic epithelium [8]. Evidently, the occurrence of specific dysplastic crypt phenotypes has not been mentioned in any of the current definitions of colon adenomas [[3], [4], [5], [6], [7], [8]].

In a recent study, we found eight different nondysplastic crypt-associated anomalies in the colon mucosa with inflammation; one of them was called crypt-rings in tandem (CRT) epitomized by dysplastic cross-cut crypt rings in consecutive single files, preferentially found in well-oriented, vertical sections [9]. In a subsequent study we found CRT in inflammatory bowel disease (IBD). Since the material included infectious colitis, an inflammatory condition lasting only 7 to 14 days [10], it was inferred that CRT could be generated during the early stages of mucosal inflammation. Dysplastic CRT (DCRT) was also found in IBD-associated dysplasia [11]. It was assumed that dysplasia in DCRT evolved using CRT as scaffolds. More recently, DCRT were noticed interspersed in the dysplastic tissue of polypoid TA.

The purpose of the present study was to assess the frequency of DCRT in a cohort of endoscopically removed TA.