Table 1. List of Various Identified Gene Mutations Responsible for the Incidence of Colorectal Cancer.

Gene	Significance of the Gene	Type of Mutation	Expression of the Gene	Effect on Colorectal Cancer linked Metabolic Pathway	Mechanism of Action	References
APC	Tumor Suppressor Gene	Truncating Mutation (e.g., Nonsense, Frameshift)	Underexpressed	Wnt/β-catenin pathway	Loss of APC leads to uncontrolled cell growth, as it fails to regulate β-catenin levels in the cell, resulting in increased cell proliferation.	(20)
KRAS	Oncogene	Point Mutation (e.g., G12D, G13A)	Overexpressed	MAPK Signaling Pathway	Mutations in KRAS lead to constitutive activation of the MAPK pathway, promoting uncontrolled cell proliferation and survival.	(21)
TP53	Tumor Suppressor Gene	Various Mutations (e.g., Missense, Nonsense, Frameshift)	Underexpressed	Cell Cycle Regulation	Loss of TP53 function allows for the unchecked growth of damaged cells, increasing the risk of tumorigenesis.	(22)
SMAD4	Tumor Suppressor Gene	Deletion, Missense, Nonsense, Frameshift	Underexpressed	TGF-β Signaling Pathway	Loss of SMAD4 disrupts the regulation of cell differentiation and growth in the TGF-β pathway, contributing to cancer development.	(23)
BRAF	Oncogene	Point Mutation (e.g., V600E)	Overexpressed	MAPK Signaling Pathway	Mutations in BRAF, such as V600E, lead to overactive MAPK signaling, driving uncontrolled cell division and tumor growth.	(24)
PIK3CA	Oncogene	Point Mutation (e.g., H1047R)	Overexpressed	PI3K/Akt Signaling Pathway	Mutations in PIK3CA enhance PI3K/Akt signaling, promoting cell survival and growth through the activation of downstream effectors.	(25)
PTEN	Tumor Suppressor Gene	Deletion, Missense, Nonsense, Frameshift	Underexpressed	PI3K/Akt Signaling Pathway	Loss of PTEN results in increased PI3K/Akt signaling, leading to enhanced cell survival and growth, and contributing to carcinogenesis.	(26)