Colorectal cancer with gut-associated lymphoid tissue (GALT) carcinoma histopathology is particularly rare in very elderly patients. GALT is characterized by submucosal localization and prominent lymphoid infiltration with germinal center formation within tumor-infiltrating lymphocytes. This study aims to report a case of colorectal cancer with GALT carcinoma histopathology in a very elderly patient and to provide a comprehensive literature review. In this case, a 90-year-old female presented with an irregularly elevated tumor in the sigmoid colon, diagnosed via colonoscopy. Computed tomography revealed no lymph node or distant metastases. The patient underwent laparoscopy-assisted sigmoid colon resection with D3 dissection. Histopathological examination revealed well-differentiated adenocarcinoma in the submucosal layer with partial invasion into the muscle layer. Lymphocytes, along with lymph follicles, proliferated compressively in the stroma surrounding the tumor glands. Immunohistochemical analysis showed lost expression of mismatch repair proteins, MLH1 and PMS2, consistent with the tumor immunohistochemistry profile. B cells (CD20- and CD79a-positive) were generally distributed in and around the lymph follicles, while T cells (CD3-positive) were primarily located between the lymph follicles. This case highlights the rare histopathology of GALT carcinoma in colorectal cancer and underscores the importance of considering such diagnoses in elderly patients with colorectal tumors.

Tumors related to the gut-associated lymphoid tissue (GALT) have been recently described. GALT carcinomas (GCs) have a characteristic appearance: macroscopically, they appear as a "dome-type" lesion, whereas microscopically, they show dilated cystic glands in the submucosa, differentiated adenocarcinoma without goblet cells, and stromal lymphocytes with germinal centers. However, their origin and pathogenesis remain controversial. Here, we present the case of a 54-year-old man that presented with a protruding lesion in the upper rectum during colonoscopy and had no family or past medical history. Low anterior resection was performed, and the tumor was diagnosed as GC based on its typical morphology. The tumor cells were negative for Mucin 2 and other mucins and CD10. p53 showed null-type. The tumor was associated with rich lymphocyte infiltration and germinal centers. Next-generation sequencing detected EGFR missense and TP53 nonsense mutations. Although GCs are known as conventional colorectal carcinomas that invade the submucosa, this case showed no neoplastic lesion in the mucosal epithelium in situ. Moreover, we detected EGFR and TP53 mutations (no pathogenic APC or KRAS mutations), which are not conventional adenoma-carcinoma mutations. Further studies are warranted to confirm whether GC is a sporadic carcinoma that invades the GALT submucosa.

Colorectal cancer is the third most common cancer in both men and women in the United States, with most cases arising from precursor adenomatous polyps. Colorectal malignant polyps are defined as cancerous polyps that consist of tumor cells invading through the muscularis mucosae into the underlying submucosa (pT1 tumor). It has been reported that approximately 0.5-8.3% of colorectal polyps are malignant polyps, and the potential for lymph node metastasis in these polyps ranges from 8.5% to 16.1%. Due to their clinical significance, recognition of malignant polyps is critical for clinical teams to make treatment decisions and establish appropriate surveillance schedules after local excision of the polyps. There is a rapidly developing interest in malignant polyps within the literature as a result of an increasing number of identifiable adverse histologic features and recent advancements in endoscopic treatment techniques. The purpose of this paper is to have a focused review of the recent histopathologic literature of malignant polyps.

Colorectal epithelial neoplasm extending into the submucosal gut-associated lymphoid tissue (GALT) can cause difficulties in the differential diagnosis. Regarding GALT-associated epithelial neoplasms, a few studies favor the term "GALT carcinoma" while other studies have mentioned the term "GALT-associated pseudoinvasion/epithelial misplacement (PEM)".

The clinicopathologic characteristics of 11 cases of colorectal epithelial neoplasm associated with submucosal GALT diagnosed via endoscopic submucosal dissection were studied.

Eight cases (72.7%) were in males. The median age was 59 years, and age ranged from 53 to 73. All cases had a submucosal tumor component more compatible with GALT-associated PEM. Eight cases (72.7%) were located in the right colon. Ten cases (90.9%) had a non-protruding endoscopic appearance. Nine cases (81.8%) showed continuity between the submucosal and surface adenomatous components. Nine cases showed (81.8%) focal defects or discontinuation of the muscularis mucosae adjacent to the submucosal GALT. No case showed hemosiderin deposits in the submucosa or desmoplastic reaction. No case showed single tumor cells or small clusters of tumor cells in the submucosal GALT. Seven cases (63.6%) showed goblet cells in the submucosa. No cases showed oncocytic columnar cells lining submucosal glands.

Our experience suggests that pathologists should be aware of the differential diagnosis of GALT-associated submucosal extension by colorectal adenomatous neoplasm. Further studies are needed to validate classification of GALT-associated epithelial neoplasms.

Gut-associated lymphoid tissue (GALT) carcinoma is a rare colorectal tumour that arises in the epithelium covering GALT. GALT carcinoma is a differentiated tubular adenocarcinoma with dense lymphoid tissue with a characteristically well-demarcated margin. To date, 26 cases of GALT carcinoma, including the three cases discussed here, have been reported. Most (24 of 26) were discovered at early stages and none of the cases have documented any metastases. This suggests that GALT carcinoma may have a favourable prognosis. It is hypothesised that GALT carcinoma originates from M cells in specialised epithelia covering GALT. However, this hypothesis has yet to be confirmed.

In this study, we examined three cases of GALT carcinoma by immunohistochemistry detection of glycoprotein 2, a specific marker for M cells, and electron microscopy. Our findings showed that the tumour cells of GALT carcinoma in all three cases were negative for M cells. We thus concluded that GALT carcinoma may be a tubular adenocarcinoma arising by chance in the GALT. This unique carcinoma is a diferentiated adenocarcinoma that grows slowly with the development of GALT.

We propose that GALT carcinoma should be classified separately because of its histological setting and good prognosis.

Several types of colorectal cancers are associated with a prominent lymphoid component, which is considered a positive prognostic factor. We report a case of a dome-type carcinoma of the cecum in a 57 year old female. The sessile, non-polypoid lesion histologically consisted of a tubulovillous adenoma with low-grade dysplasia. The submucosal invasive component showed low-grade architectural features that included cystically dilated glands containing eosinohilic debris. Immunohistochemical studies displayed retention of the four mistmach repair proteins, consistent with a stable phenotype. After 3 years, the patient remains free of recurrence. A literature review highlighted striking similarities between dome-type carcinoma and the gut-associated lymphoid tissue carcinoma, the two sharing an intimate association with the gut associated lymphoid tissue.The two variants might therefore be grouped into a unified category.

Colonoscopic biopsies from 32 patients were studied at the ultrastructural level using a scanning electron microscope (SEM). Sixteen of the 32 patients had a previous diagnosis of total ulcerative colitis (UCR greater than 10 years) in protracted remission. The colonic mucosa was normal at endoscopic and histologic examinations (UCRN). The remaining 16 patients had normal colonic mucosa, but had an adenoma or an adenocarcinoma elsewhere in the colon. Several ultrastructural parameters were investigated, such as the number of crypts per area, the distance between the crypts, the outline of mucosal units, the number of mucous cells, the outline of absorptive cells, and the number of villi per area. Quantitative determinations of SEM structures (including measurements with an interactive digital image analyzer system; MOP 30, Zeiss Contron) were made. The results showed no significant differences between the various parameters (except for the number of crypts per area) between patients with UCRN and controls. The possibility of a total (or quasi-total) restitutio ad integrum of the colonic mucosa in certain patients with UCR is discussed. An international policy regarding the colonoscopic surveillance of patients with UCRN should be elaborated. It is suggested that the time interval between control colonoscopic biopsies in patients with UCRN should be increased substantially.

The presence of misplaced mucosal epithelium was studied in the colectomy specimens from 30 patients with Crohn's disease, 30 patients with ulcerative colitis, 15 patients with ulcerative colitis complicated by carcinoma and 30 patients with non-colitic colorectal carcinoma. Misplaced epithelium was present in 21 (70%) of the resection specimens with Crohn's disease, 20 (66.7%) with ulcerative colitis and 12 (80%) with ulcerative colitis complicated by carcinoma. None of the specimens with non-colitic colorectal adenocarcinoma showed misplaced foci of epithelium. Two pathogenetic mechanisms for epithelial misplacement are proposed: (1) the effects of mucosal inflammation and repair; and (2) muscular abnormalities in inflammatory bowel disease. The proposed mechanisms and patterns of epithelial misplacement are discussed and illustrated. The importance of its recognition is emphasized because, when associated with mucosal dysplasia, difficulties in interpretation arise in distinguishing it from 'early' invasive adenocarcinoma. Epithelial misplacement is common in patients with longstanding ulcerative colitis and may be a factor in increasing the significance of pre-existing mucosal dysplasia and promoting the development of adenocarcinoma. This may explain the unusual growth pattern encountered in ulcerative colitis, of submucosal cancer underlying a flat, non-dysplastic mucosa.