tumor suppressor genes in human cancer
Tumor Suppressor Genes in Human Cancer
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Tumor Suppressor Genes in Human Cancer

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The Broken Brake: Tumor Suppressor Genes in Human Cancer

Every cell in the human body possesses internal genetic brakes designed to trigger self-destruction (apoptosis) if the DNA becomes too damaged to repair. When these brakes fail, the cell becomes immortal, and cancer is born. Tumor Suppressor Genes in Human Cancer is the fiercely detailed, highly molecular master text detailing the exact mechanisms of this biological catastrophe. This volume provides the precise genetic blueprints required to understand how a single missing protein can cause an organ to literally consume itself.

Mastering the Guardian of the Genome

The core philosophy of this text is the catastrophic deletion. The authors aggressively detail the mechanics of the p53 gene. It dictates exactly how this single protein physically binds to damaged DNA and forces the cell to repair it, and mathematically proves how the mutation of p53—found in over 50% of all human cancers—instantly removes the only barrier preventing the explosive, chaotic replication of malignant cells.

Navigating the Two-Hit Hypothesis

The book provides a masterclass in inherited vulnerability. It dictates the exact genetic pathways of Knudson’s hypothesis. It rigorously explores the terrifying reality of retinoblastoma, detailing how a child inherits one broken copy of the RB1 gene, meaning a single, random mutation in the remaining healthy gene will immediately trigger a lethal tumor in their eye before they even learn to walk.

Frequently Asked Questions (FAQs)

Is this a clinical manual detailing standard chemotherapy dosing?
Absolutely not. It is a strictly specialized *molecular biology, cancer genetics, and translational oncology textbook* focused entirely on the fundamental biochemical origin of the disease.

Who is the primary audience?
It is the absolute, mandatory definitive reference for Cancer Biologists, Molecular Pathologists, Genetic Counselors, and Academic Oncologists.