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Concept Breakdowns

Cell Cycle Checkpoints and Cancer Mutations

Cell cycle checkpoints and their associated cancer mutations are high-yield for USMLE Step 1, appearing in pathology and molecular biology sections. These flashcards cover G1/S, intra-S, and G2/M checkpoints, plus key tumor suppressors (p53, Rb) and oncogenes. Understanding checkpoint failure explains how cells become malignant and how targeted therapies work.

Interactive Deck

5 Cards
1
Front

What is the G1/S checkpoint?

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Back

The G1/S checkpoint (restriction point) is controlled by Rb (retinoblastoma protein). Rb is phosphorylated by CDK4/6–cyclin D, releasing E2F to drive S phase entry.

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Front

p53 role in cell cycle

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2
Back

p53 (TP53) is the guardian of the genome. DNA damage activates p53 → upregulates p21 → inhibits CDK2–cyclin E → halts G1/S transition for DNA repair or apoptosis.

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Front

What are CDKs and cyclins?

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Back

Cyclin-dependent kinases (CDKs) are activated by binding cyclins. They phosphorylate Rb and other targets to drive cell cycle progression. Cyclin levels fluctuate through the cycle.

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Locked

Li-Fraumeni syndrome mutation

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Locked

Rb gene and retinoblastoma

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Frequently Asked Questions

What is the difference between tumor suppressors and oncogenes?

Tumor suppressors (e.g., Rb, p53) normally inhibit cell growth; loss-of-function mutations (recessive) drive cancer.

Oncogenes (e.g., RAS, MYC) are gain-of-function mutations (dominant) that accelerate proliferation.

  • Tumor suppressor: both alleles must be lost
  • Oncogene: one mutant copy is sufficient

How does p53 loss lead to cancer?

When p53 is lost, cells with DNA damage bypass the G1 checkpoint and continue dividing. This allows accumulation of further mutations, genomic instability, and malignant transformation. TP53 is the most commonly mutated gene in human cancers.

What cancers are associated with CDK inhibitor loss?

Loss of p16 (CDKN2A), which normally inhibits CDK4/6, is associated with melanoma and pancreatic cancer. Without p16, CDK4/6 remain active, continuously phosphorylating Rb and driving uncontrolled G1/S progression.