Curriculum
Module 08 · 55 min
Wnt, Hedgehog & Notch
Three developmental pathways that re-emerge as drivers of cancer and stem-cell biology.
CoreClinicalResearch
Topics
What this module covers
- 01Canonical Wnt/β-catenin signaling
- 02Hedgehog: PTCH1, SMO, GLI
- 03Notch: ligand-receptor cleavage and NICD
- 04Drugs: vismodegib, gamma-secretase inhibitors
Learning objectives
By the end of this module you will be able to
- L01Explain how β-catenin escapes degradation when Wnt signaling is on.
- L02Map the Hedgehog pathway from SHH to GLI transcription.
- L03Describe Notch signaling as a ligand-induced regulated proteolysis cascade.
Expected takeaways
What you should walk away believing
- →APC mutations stabilize β-catenin → familial adenomatous polyposis & sporadic CRC.
- →PTCH1 loss drives basal cell carcinoma and medulloblastoma.
- →Notch is context-dependent: tumor suppressor in T-ALL, oncogene in some solid tumors.
Core summary
At the Core level
Wnt, Hedgehog, and Notch are ancient developmental pathways. They build embryos, maintain adult stem cells, and — when miswired — drive cancer.
Evidence-graded claims
Claims, scored A–F
A
APC loss is the most common initiating event in colorectal cancer
Vogelstein adenoma–carcinoma sequence.
D
Wnt agonists rejuvenate aging stem cells safely
Preclinical promise; tumor-promotion concerns.
Quiz
Check your understanding
Q1. In Wnt-OFF state, β-catenin is…
Flashcards
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Front
Vismodegib mechanism?
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