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Cell Cycle Control
Ensures proper progression through stages; prevents uncontrolled division.
Checkpoints
G₁ (master), G₂, and M-phase checkpoints regulate cell cycle progression.
Cyclins & Cdks
Proteins that drive transitions between phases; cyclin binds Cdk to activate it.
Proto-Oncogenes
Normal genes that promote cell cycle when stimulated; mutations → oncogenes.
Tumor Suppressor Proteins
Halt cell cycle if DNA damage detected, e.g., p53.
p53
Master tumor suppressor: arrests cell cycle, activates DNA repair or triggers apoptosis.
Oncogenes
Mutated proto-oncogenes causing uncontrolled cell division; examples: HER2, Ras, ABL.
Tumor Suppressor Loss
Non-functional proteins allow damaged DNA to replicate; examples: p53, RB1, BRCA1/2, APC.
Mutagens
Agents that damage DNA (e.g., UV radiation causes thymine dimers).
Telomerase Activation
Enables indefinite cell division in cancer cells.
Benign Tumor
Localized, differentiated cells; slow-growing; few mutations.
Malignant Tumor
Poorly differentiated cells; metastasize; many mutations; cause cancer.
Angiogenesis
Cancer cells release signals to grow blood vessels nearby.
Growth Factor Loop
Cancer cells release growth factors to stimulate their own division.
Chromosomal Instability
Increased abnormalities with uncontrolled division.
Chemotherapy
Inhibits DNA replication or cell division.
Radiation
Causes severe DNA damage to kill cancer cells.
Targeted Therapy
Blocks specific oncogenic signals (e.g., Herceptin for HER2).
Immunotherapy
Uses immune system to attack cancer cells.
Surgery
Removes primary tumor.