COLORECTAL CANCER
Click here to access a comprehensive colorectal cancer
study guide that breaks down the disease into easy-to-
understand sections, covering core concepts from the
adenoma-carcinoma sequence to clinical presentations
based on tumor location. It provides a clear framework
for learning risk factors, diagnostic methods, and the TNM
staging system, while explaining treatment options
across different stages. The guide includes high-yield
study tips and mnemonics like 'SCREEN the COLON' to
help with memorization, making it an efficient resource
for mastering key points needed for exams or clinical
practice in gastroenterology or oncology.
Colorectal Cancer (CRC) Study Guide
1. Core Concept: What is it?
Colorectal Cancer is a malignancy that arises from the in-
ner lining (mucosa) of the colon or rectum. It typically be-
gins as a non-cancerous growth called a polyp, which
over time (usually 10-15 years) can transform into can-
cer. This long pre-cancerous phase is why screening is so
effective.
Key Mnemonic for Major Points: "SCREEN the COLON"
• S - Screening is crucial
• C - CARCINOEMBRYONIC ANTIGEN (CEA) as a tumor
marker
• R - Risk factors (Age, Diet, Heredity)
• E - Early signs (Bleeding, Anemia, Change in bowel
habits)
• E - Evaluation via Colonoscopy
, • N - Neoplasms start as Polyps (Adenomas)
2. Pathophysiology & Progression (The "Adenoma-Carci-
noma Sequence")
This is the fundamental model for how most colorectal
cancers develop.
1. Normal Mucosa -> Aberrant Crypt Foci (microscopic
changes).
2. Small Adenomatous Polyp -> Large Adenomatous
Polyp. Driven by accumulated genetic mutations
(e.g., in the APC gene, which is the "gatekeeper").
3. Dysplasia (pre-cancerous cells) develops within the
polyp.
4. Invasive Carcinoma. The cancer breaks through the
basement membrane and can now spread.
Key Genes to Know:
• APC (Adenomatous Polyposis Coli): Tumor suppressor
gene; mutated in >80% of sporadic CRCs. Initiates
the process.
• KRAS: Oncogene; mutation causes uncontrolled cell
growth.
• p53: Tumor suppressor gene; mutation is a late
event, allowing for invasion and metastasis.
3. Risk Factors (Think Modifiable vs. Non-Modifiable)
Non-Modifiable:
• Age: >90% of cases are in people over 50 (though in-
cidence is rising in younger adults).
• Personal History: Previous CRC or adenomatous
polyps.
• Family History: Especially first-degree relatives.
• Inherited Syndromes:
Click here to access a comprehensive colorectal cancer
study guide that breaks down the disease into easy-to-
understand sections, covering core concepts from the
adenoma-carcinoma sequence to clinical presentations
based on tumor location. It provides a clear framework
for learning risk factors, diagnostic methods, and the TNM
staging system, while explaining treatment options
across different stages. The guide includes high-yield
study tips and mnemonics like 'SCREEN the COLON' to
help with memorization, making it an efficient resource
for mastering key points needed for exams or clinical
practice in gastroenterology or oncology.
Colorectal Cancer (CRC) Study Guide
1. Core Concept: What is it?
Colorectal Cancer is a malignancy that arises from the in-
ner lining (mucosa) of the colon or rectum. It typically be-
gins as a non-cancerous growth called a polyp, which
over time (usually 10-15 years) can transform into can-
cer. This long pre-cancerous phase is why screening is so
effective.
Key Mnemonic for Major Points: "SCREEN the COLON"
• S - Screening is crucial
• C - CARCINOEMBRYONIC ANTIGEN (CEA) as a tumor
marker
• R - Risk factors (Age, Diet, Heredity)
• E - Early signs (Bleeding, Anemia, Change in bowel
habits)
• E - Evaluation via Colonoscopy
, • N - Neoplasms start as Polyps (Adenomas)
2. Pathophysiology & Progression (The "Adenoma-Carci-
noma Sequence")
This is the fundamental model for how most colorectal
cancers develop.
1. Normal Mucosa -> Aberrant Crypt Foci (microscopic
changes).
2. Small Adenomatous Polyp -> Large Adenomatous
Polyp. Driven by accumulated genetic mutations
(e.g., in the APC gene, which is the "gatekeeper").
3. Dysplasia (pre-cancerous cells) develops within the
polyp.
4. Invasive Carcinoma. The cancer breaks through the
basement membrane and can now spread.
Key Genes to Know:
• APC (Adenomatous Polyposis Coli): Tumor suppressor
gene; mutated in >80% of sporadic CRCs. Initiates
the process.
• KRAS: Oncogene; mutation causes uncontrolled cell
growth.
• p53: Tumor suppressor gene; mutation is a late
event, allowing for invasion and metastasis.
3. Risk Factors (Think Modifiable vs. Non-Modifiable)
Non-Modifiable:
• Age: >90% of cases are in people over 50 (though in-
cidence is rising in younger adults).
• Personal History: Previous CRC or adenomatous
polyps.
• Family History: Especially first-degree relatives.
• Inherited Syndromes:
