Target intelligence / Profile preview

Colonic adenocarcinoma cells

01

Overview

Colonic adenocarcinoma cells are the malignant epithelial cells that comprise colorectal adenocarcinoma, which accounts for approximately 85-90% of all colorectal cancers. These cells arise from the glandular epithelium of the colon and rectum and exhibit distinct molecular characteristics. The majority (~85%) exhibit chromosomal instability with changes in chromosome number and structure[3]. Approximately 16% of colorectal carcinomas are hypermutated, with three-quarters showing high microsatellite instability typically associated with MLH1 hypermethylation and silencing, while one-quarter harbor somatic mismatch repair gene and POLE mutations[4]. At the molecular level, these cells commonly harbor mutations in key genes including APC (found in ~90% of cases)[3], TP53 (59% of non-hypermutated cases)[4], KRAS, PIK3CA, and SMAD4[1][4]. The WNT/β-catenin signaling pathway is activated in nearly all cases, with APC mutation being the earliest event in colorectal carcinogenesis[3]. Additional significantly mutated genes include ARID1A, SOX9, and FAM123B[4]. These cells demonstrate alterations in MYC transcriptional targets in nearly 100% of tumors[4], and the TGF-β signaling pathway is deregulated in 27% of non-hypermutated and 87% of hypermutated cases[4]. Immunohistochemically, colonic adenocarcinoma cells typically express CDX2, CK20, and SATB2, which distinguish them from other carcinoma types[6].

Other names
Colorectal adenocarcinoma cellscolon cancer cellscolonic carcinoma cellscolorectal carcinoma cells
02

Biological functions

Uncontrolled proliferation and growthResistance to apoptosisInvasion and metastasis capabilitiesAngiogenesis promotionImmune evasionMetabolic reprogramming
03

Disease associations

Colorectal cancer (primary disease entity)Metastatic disease to liver, lung, and other organs
04

Interacting drugs

Chemotherapy agents (5-fluorouracil, oxaliplatin, irinotecan)

3 more in the full profile.

05

Biomarkers

Microsatellite instability status (MSI-H vs MSS)[1]Mismatch repair deficiency (dMMR)[1]KRAS, NRAS, and BRAF mutation status[1][4]PIK3CA mutations[1][4]APC mutations[1][3]TP53 mutations[1][4]CDX2, CK20, and SATB2 expression (positive markers)[6]Chromosomal instability (CIN) present in approximately 85% of cases[3]

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