---
title: "Cancer as Clonal Evolution: Drivers, Passengers and Selection in a Tissue"
description: "A tumour is a cell population under selection inside a body, so population genetics applies to it directly. This stop separates driver from passenger mutations and reads a tumour's history out of its "
canonical: https://lightmysky.com/learn/science/cancer-as-clonal-evolution-drivers-passengers-and-selection-in-a-tissue-mt_3qIJZwD0m5
source: https://lightmysky.com/learn/science/cancer-as-clonal-evolution-drivers-passengers-and-selection-in-a-tissue-mt_3qIJZwD0m5.md
retrieved: 2026-09-12
---

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# Cancer as Clonal Evolution: Drivers, Passengers and Selection in a Tissue

A tumour is a cell population under selection inside a body, so population genetics applies to it directly. This stop separates driver from passenger mutations and reads a tumour's history out of its mutation data.

Subject: Science · Area: Genetics & Evolution · Ages 22 to 23
Page: https://lightmysky.com/learn/science/cancer-as-clonal-evolution-drivers-passengers-and-selection-in-a-tissue-mt_3qIJZwD0m5

## Ready when they can

- Argue from recurrence and mutation frequency whether a gene is a plausible driver
- Explain what subclonal structure in a sequenced tumour says about the order of events
- Apply selection and drift arguments to a growing population of somatic cells

## Lesson: A tumour as evolution inside one tissue

You read a tumour as a cell population under selection inside a body. Mutations that speed growth are favored, their carrier cells expand into clones, and fresh mutations arise within those clones. Sequencing a tumour reads out an evolutionary tree written in somatic mutations.

You separate drivers from passengers with recurrence, not single tumour frequency. A gene hit repeatedly across independent patients, at the same functional sites, has almost certainly been selected. A gene mutated once at a random spot is likely a passenger carried along by a fast dividing clone.

**Example.** You compare two mutations in one patient. One sits in every tumour cell, so it came before the last clonal expansion. The other sits in a fraction of cells, so it came later within one branch. Their nesting reconstructs the order from founding lesion to latest aggressive subclone.

**Tip.** You apply selection and drift arguments to somatic cells directly. A driver is a beneficial allele sweeping its clone upward, while passengers are neutral alleles hitchhiking beside it. Therapy is fresh selection, so resistance often expands a rare subclone that already existed.

**Recap.** You call drivers by recurrence across tumours, you date events by subclonal nesting, and you expect selection to act on every clone.

## Practice

8 questions on this page, each with its working shown.

## Needs first

- [Selection Coefficients and Predicting Allele Frequency Change](https://lightmysky.com/learn/science/selection-coefficients-and-predicting-allele-frequency-change-mt__JS2XJxOXV)

## Opens up

- [What a Cell Has to Break to Become a Tumour](https://lightmysky.com/learn/science/what-a-cell-has-to-break-to-become-a-tumour-mt_cjg3DtLHQL)
