explain how uncontrolled cell division can result in the formation of a tumour

Replication and Division of Nuclei and Cells

Key Processes

In eukaryotic organisms the nucleus and the cell undergo distinct but coordinated cycles:

• Interphase – DNA replication (S‑phase) and preparation for division.
• Mitosis (M‑phase) – Division of the nucleus.
• Cytokinesis – Physical division of the cytoplasm to produce two daughter cells.

Stages of Mitosis

Control of the Cell Cycle

The cell cycle is regulated by:

1. Cyclins – proteins whose concentration rises and falls each cycle.
2. Cyclin‑dependent kinases (CDKs) – enzymes activated by cyclins to phosphorylate target proteins.
3. Checkpoints – surveillance mechanisms (G1, G2, and spindle checkpoints) that ensure conditions are suitable before progression.

Uncontrolled Cell Division and Tumour Formation

What Is a Tumour?

A tumour is an abnormal mass of tissue resulting from excessive cell proliferation. Tumours can be:

• Benign – localized, non‑invasive, usually harmless.
• Malignant – invasive, capable of metastasis, and potentially life‑threatening.

How Loss of Regulation Leads to Uncontrolled Division

Normal regulation ensures that cells only divide when required. Disruption of this control can occur through:

• Mutations in genes that encode cyclins or CDKs.
• Damage to tumour‑suppressor genes (e.g., p53, RB) that normally halt the cycle or trigger apoptosis.
• Activation of oncogenes (e.g., RAS, MYC) that drive the cell cycle forward.
• Failure of checkpoint mechanisms, allowing cells with DNA damage to continue dividing.

Sequence of Events Leading to a Tumour

1. DNA damage occurs (e.g., from U \cdot radiation, chemicals).
2. Repair mechanisms are defective or overwhelmed.
3. Mutations accumulate in genes controlling the cell cycle.
4. Cell‑cycle checkpoints become ineffective; the cell proceeds through G1/S or G2/M despite abnormalities.
5. Uncontrolled proliferation produces a clonal population of abnormal cells.
6. Additional mutations confer abilities such as tissue invasion and angiogenesis, converting a benign growth into a malignant tumour.

Key Molecular Changes (Illustrative Example)

Consider the pathway involving the tumour‑suppressor protein p53:

\$\text{DNA damage} \;\xrightarrow{\text{activate}} \; p53 \;\xrightarrow{\text{transcribe}} \; p21 \;\xrightarrow{\text{inhibit}} \; \text{CDK–cyclin complexes} \;\Rightarrow\; \text{Cell‑cycle arrest}\$

If the TP53 gene is mutated, p53 cannot be activated, p21 is not produced, CDK–cyclin activity remains unchecked, and the cell proceeds through the cycle with damaged DNA, increasing tumour risk.

Comparative Table: Normal vs. Uncontrolled Division

Summary

Uncontrolled cell division arises when the intricate network of cyclins, CDKs, checkpoints, and tumour‑suppressor genes is disrupted. The resulting loss of regulation allows cells with damaged DNA to proliferate, forming a tumour. Understanding these molecular mechanisms is essential for developing targeted therapies that restore normal control or specifically eliminate tumour cells.