A Unique Coexistence of Colonic Collision and Synchronous Tumors!

Abstract

A true Bcollision^ tumor represents a coexistence of two adjacent but histologically different malignant neoplasms occurring in the same organ without histological admixture or zone of an intermediate cell population. Such tumors consist of components with different histogenesis and different tumorigenetic pathways representing a mosaic of two concurrent but independent tumors that have Bcollided^ with each other. Such tumors are difficult to diagnose preoperatively, and pathological identification of the dual components is often the only way to make a correct diagnosis [1]. The occurrence of collision tumors is rare in the colon. Reported cases include adenoma of the colon and carcinoid, adenocarcinoma of the colon and carcinoid, non-Hodgkin lymphoma, and adenocarcinoma of the colon [1]. On the other hand, synchronous colorectal cancers refer to two or more primary colorectal carcinomas detected in a single individual at the time of the first diagnosis of colorectal cancer. We present here a case representing a unique example of colonic collision and synchronous tumors. A 58-year-old man presented with diffuse abdominal pain. Colonoscopy revealed tumor growth in the right colon and another polypoid growth about 5–10 cm proximal from splenic flexure, which were confirmed on CT scan without signs of dissemination. The patient’s paternal aunt in her young age had colorectal cancer, and his father was operated for a large polypoid tumor in the colon. Clinically, there was a suspicion of Lynch syndrome. Therefore, subtotal colectomy was carried out. The colon segment measured 84 cm in length and showed synchronous tumors. The ascending colon showed a 30-mm sized adenosquamous carcinoma with a 3-mm spread beyond muscularis propria with evidence of keratinization. Adjacent to this was a focus of mucinous adenocarcinoma clearly separated from the adenosquamous carcinoma (Fig. 1; Table 1). p16 immunohistochemistry as well as high-risk and low-risk human papillomavirus in situ hybridization results were negative. Pathological staging was reported as T3 N0 V0, and there was retention of MLH1, MSH2, MSH6, and PMS2 protein expression by immunohistochemistry. The transverse colon showed a moderately differentiated adenocarcinoma with a 6-mm spread beyond the muscularis propria (Fig. 1; Table 1). Pathological staging was reported as T3 N0 V0, and there was retention of MLH1, MSH2, MSH6, and PMS2 protein expression by immunohistochemistry. There was no MLH1 promoter hypermethylation in any of the tumors. Microsatellite instability analysis with a panel of five markers showed variable instability in all the three carcinomas. Adenosquamous carcinoma showed instability in five out of five markers (BAT25, BAT26, NR21, NR24, and NR27). Mucinous adenocarcinoma showed instability in three out of five markers (BAT26, NR24, and NR27), while moderately differentiated adenocarcinoma showed instability in two out of five markers (BAT26 and NR27). DNA mutation analysis of all three carcinomas from formalin-fixed paraffin blocks showed no mutations in KRAS codons 12, 13, and 16 using real-time PCR (Cobas 4800) and KRAS codons 58, 59, 117, and 146 as well as NRAS codons 12, 13, 58, 59, 61, 117, and 146 using pyrosequencing. There was no BRAFmutation either with immunohistochemistry for V600E or with RTPCR-based mutation analysis (Cobas 4800). Although there is no satisfactory explanation for collision tumors, theories relating to the occurrence of such collision tumors include the following: (1) simultaneous proliferation of two different cell lines, (2) common * Parag Deepak Dabir drparagdabir@gmail.com