[Colorectal carcinogenesis: update].

Area of Science:

• Molecular biology
• Oncology
• Genetics

Background:

• Colorectal cancer (CRC) pathogenesis involves distinct molecular mechanisms, including chromosomal instability (CIN) and genetic instability (GIN).
• Hereditary syndromes, such as familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC) syndrome, significantly increase predisposition to CRC.
• Understanding these molecular underpinnings is vital for advancing CRC research and clinical practice.

Purpose of the Study:

• To elucidate the molecular mechanisms driving colorectal carcinogenesis.
• To identify common signaling pathways involved in malignant transformation despite differing instability types.
• To highlight the importance of molecular classification for understanding tumor development and patient management.

Main Methods:

• Review of recent molecular biology findings on colorectal carcinogenesis.
• Identification of key molecular mechanisms: chromosomal instability and genetic instability.
• Analysis of hereditary syndromes predisposing to colorectal cancer.

Main Results:

• Two primary molecular mechanisms, chromosomal instability and genetic instability, are implicated in colorectal carcinogenesis.
• Familial adenomatous polyposis and hereditary non-polyposis colorectal cancer syndrome are key hereditary predispositions.
• Common signaling pathways, including APC/beta-catenin, TGFbeta, RAS, and TP53, are involved in malignant transformation, irrespective of the initial instability mechanism.

Conclusions:

• A unified understanding of signaling pathways is emerging in colorectal cancer, despite diverse initiating molecular events.
• Molecular classification of colorectal cancers offers critical insights into tumor development.
• This molecular understanding is essential for improving patient management strategies in colorectal cancer.