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📖 Lesson 17 ⏱ ~25 min Year 9 · Unit 1 ⚡ +115 XP

Cancer: When Cells Go Wrong

You'll be able to compare normal cell division with uncontrolled division in tumours.

What happens when cell division loses its controls, and why some risk factors matter far more than others.

Today's hook: Cells have several safeguards against uncontrolled growth: DNA repair, controls on cell division, programmed cell death and immune surveillance. These safeguards are not perfect. How can accumulated changes allow a cell to bypass controls and contribute to cancer?
0/5QUESTS
Warm-up
Think First
+5 XP each

Cancer is cells gone rogue. How does your body usually stop this from happening?

Why do you think cancer is called a 'disease of accumulated mutations'?

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Learning objectives
What you'll master
3 areas

● Know

  • Define cancer as a non-infectious disease caused by accumulated mutations
  • Identify how apoptosis and cell checkpoints normally remove faulty cells
  • Distinguish benign tumours from malignant tumours and metastasis

● Understand

  • Explain why several mutations must build up before a cell becomes cancerous
  • Describe common risk factors and how reducing them lowers risk
  • Understand how screening and early detection improve treatment outcomes

● Can do

  • Compare normal cell division with uncontrolled division in tumours
  • Interpret cancer statistics accurately and in context
  • Explain how lifestyle and screening choices support prevention and detection
Cross-lesson links: Cancer is a non-infectious condition discussed in Lesson 15: the cancer itself is not spread through ordinary contact as an infection is. Some infections, including persistent infection with certain HPV types, can contribute to cancer development. This connects to Lesson 4 on pathogens and Lesson 10 on vaccination: HPV vaccines prevent relevant infections and reduce the risk of associated cancers, rather than treating an existing cancer.
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Vocabulary · tap to flip
Words You Need
6 terms
Core term Concept Skill Reference
Cancer
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Cancer
A group of diseases in which cells divide uncontrollably and can invade other tissues.
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Mutation
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Mutation
A change in the DNA sequence of a cell that can disrupt how the cell grows and divides.
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Benign tumour
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Benign tumour
An abnormal growth of cells that stays in one place and does not spread to other tissues.
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Malignant tumour
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Malignant tumour
A cancerous growth whose cells can invade nearby tissue and spread to other parts of the body.
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Metastasis
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Metastasis
The spread of cancer cells from the original tumour to form new tumours elsewhere in the body.
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Carcinogen
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Carcinogen
An agent capable of causing cancer, such as tobacco smoke or UV radiation. Carcinogens can act through different biological mechanisms.
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The quantitative side of disease
Key Equations and Relationships
+5 XP

Your body produces billions of new cells every day. Occasionally, a cell acquires mutations, changes in its DNA that disrupt normal control mechanisms. Cells may repair DNA damage, pause division or undergo apoptosis, a process of programmed cell death. Apoptosis helps remove damaged cells, but no safeguard is perfect. If changes allow a cell to bypass growth controls and avoid cell death, it may survive and divide inappropriately, contributing to a tumour.

Not all tumours are cancerous. Benign tumours are non-cancerous and do not invade nearby tissues or spread to distant sites, although their size or location can still cause harm. Malignant tumours are cancerous: they invade nearby tissues and can spread to distant parts of the body through the bloodstream or lymphatic system in a process called metastasis. Growth speed alone does not distinguish benign from malignant tumours. Cancer involves failures in the body's control of cell growth and survival.

Normal cell division vs cancer cell division comparisonNormal DivisionSTOPContactinhibitioncells sense crowding, stop dividingNormal features• Controlled mitosis• Apoptosis when damaged• Responds to stop signalsCancer DivisionTumourmassmeta-stasisOncogene activationTumour suppressor failureCancer features• Uncontrolled division• Ignores stop signals• Can invade and metastasise
Normal cell division and cancer cell division.
Text description
  • Normal division: one cell divides into two, then stops (contact inhibition: cells sense crowding and stop dividing).
  • Normal features: controlled mitosis, apoptosis when damaged, responds to stop signals.
  • Cancer division: 1 → 2 → 4 cells and on into a tumour mass, which can spread (metastasis). Causes: oncogene activation, tumour suppressor failure.
  • Cancer features: uncontrolled division, ignores stop signals, can invade and metastasise.
Example

Skin cells exposed to UV radiation from the sun can develop DNA damage. Cells can repair damage or be removed through processes such as apoptosis. If further changes allow a damaged pigment-producing cell to bypass controls and survive, it may contribute to melanoma, a malignant skin cancer that can metastasise to other organs. One DNA mutation does not inevitably produce cancer.

Real-world anchor

Cancer Australia funds research into apoptosis-triggering therapies that force cancer cells to self-destruct, offering a gentler alternative to chemotherapy and radiation that damage healthy tissue as well as tumours.

Flashcards+5 XP

Tap each card to flip. Mark Got it when you can recall the answer without flipping.

0 / 4 mastered
AP tap to flip
Apoptosis
When?
USE FOR
Programmed cell death. The body normal way of removing damaged or unwanted cells before they multiply.
BE tap to flip
Benign tumour
When?
USE FOR
A non-cancerous growth that stays in one place and does not invade surrounding tissues.
MA tap to flip
Malignant tumour
When?
USE FOR
A cancerous growth that invades nearby tissues and can spread to other parts of the body.
ME tap to flip
Metastasis
When?
USE FOR
The spread of cancer cells from the original tumour to distant organs through blood or lymph.
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Stop & Check, Planning Your Depth Study
Quick Check
+5 XP

Cancer is not a single disease but a category of over 100 related diseases. What they share is uncontrolled cell division. Several factors increase cancer risk. Genetic factors include inherited mutations in genes like BRCA1 and BRCA2, which sharply increase breast and ovarian cancer risk. Environmental factors include exposure to tobacco smoke, asbestos, UV radiation, and certain viruses like HPV. Lifestyle factors include diet, physical activity, and alcohol consumption.

Importantly, most cancers result from a combination of these factors, not just one. A person with a genetic predisposition may never develop cancer if they avoid environmental triggers, while someone with no family history may develop lung cancer after years of smoking. Understanding risk factors helps guide prevention strategies, but it does not allow perfect prediction.

Example

HPV infection causes nearly all cervical cancers. The HPV vaccine prevents infection with the high-risk strains, which is why Australia national vaccination program has dramatically reduced cervical cancer rates in young women.

Real-world anchor

The Cancer Council Australia runs SunSmart campaigns and anti-smoking programs because modifiable lifestyle and environmental factors cause the majority of cancers diagnosed in Australia each year.

What is the key difference between a benign and a malignant tumour?
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Explore
Explore
+5 XP

Cancer prevention involves reducing exposure to risk factors and detecting cancer early when treatment is most effective.

Avoiding risk factors:

  • Tobacco: Causes about 20% of all cancer deaths. Quitting reduces risk over time.
  • UV radiation: Causes 95% of melanomas. Slip-slop-slap-seek-slide.
  • Alcohol: Increases risk of mouth, throat, liver, and breast cancers. Even moderate consumption increases risk.
  • Diet and exercise: Maintaining a healthy weight reduces risk of 13 cancer types.

Australian screening programs:

  • BreastScreen Australia: Free mammograms every 2 years for women 40-74. Detects cancers before they can be felt.
  • National Cervical Screening Program: HPV test every 5 years for women 25-74. Has reduced cervical cancer by 50% since 1991.
  • National Bowel Cancer Screening Program: Available to eligible people aged 45–74. People aged 45–49 can request their first free kit; people aged 50–74 are mailed a kit every 2 years. The test detects blood in stool.

Early detection saves lives: Most cancers are far more treatable when detected early. Bowel cancer caught at stage I has 99% survival; at stage IV, 13%.

Example

Australia has the highest skin cancer rates in the world due to its predominantly fair-skinned population, outdoor lifestyle, and high UV levels. The SunSmart campaign, launched by the Cancer Council in 1981, introduced the iconic "Slip! Slop! Slap!" message (slip on a shirt, slop on sunscreen, slap on a hat). Decades of public health messaging have shifted social norms: sunscreen is now standard at schools and sporting events, and sunbeds are banned nationwide. These efforts have contributed to declining melanoma rates in Australians under 40. However, melanoma remains the third most common cancer in Australia, with over 16,000 new cases annually. Continued vigilance through sun protection, self-examination, and dermatologist checks is essential.

Real-world anchor

Australia cancer control: Cancer Australia is the federal government national cancer control agency, coordinating research, prevention, and treatment. The Australian Cancer Plan 2023-2033 sets targets for reducing cancer incidence and improving survival. Australia has world-leading cancer survival rates for many cancers, partly due to universal healthcare (Medicare) ensuring access to treatment regardless of income. The Peter MacCallum Cancer Centre in Melbourne is Australia largest cancer research and treatment centre, pioneering immunotherapy and targeted treatments. Indigenous Australians have higher cancer mortality rates due to later diagnosis and reduced access to care, Closing the Gap initiatives aim to address these disparities through culturally appropriate screening and treatment services.

Which Australian cancer screening program uses a home test to look for tiny traces of blood in stool?
Heads-up · common traps
Spot the Trap
3 myths
✗

Wrong: "A depth study is just a long essay about a disease." No, a depth study is an investigation. It requires you to ask a question, gather evidence, analyse data, and draw conclusions. It is active science, not just research.

✓

Right: A depth study is an active scientific investigation that requires asking a question, gathering evidence, analysing data, and drawing conclusions. It is not just a research essay.

✗

Wrong: "The different topics in this unit have no connection to each other." No, they are deeply connected. Pathogens cause disease, which the immune system fights, which vaccines train, which antibiotics treat, which resistance limits, which public health prevents. Every topic links to others.

✓

Right: All topics in this unit are deeply connected: pathogens cause disease, which the immune system fights, which vaccines train, which antibiotics treat, which resistance limits, which public health prevents.

✗

Wrong: "Once you memorise facts about disease, you understand it." No, true understanding means being able to explain connections, apply concepts to new situations, and evaluate evidence. Facts are tools; understanding is the ability to use them.

✓

Right: True understanding means being able to explain connections between concepts, apply them to new situations, and evaluate evidence. Facts alone are not enough without the ability to use them.

Australian Context

Australian Scientists Fighting Disease

Professor Fiona Stanley (AC): An Australian epidemiologist who founded the Telethon Kids Institute in Perth. Her research on birth defects, Indigenous health, and population health methods transformed Australian public health. She championed the use of population data to guide health policy.

Professor Ian Frazer: Co-developer of the HPV vaccine at the University of Queensland. His work has prevented countless cases of cervical cancer worldwide and put Australia on track to eliminate cervical cancer entirely.

Modern Australian research: Today, Australian scientists at WEHI, the Doherty Institute, CSIRO, and universities across the country continue to fight disease. During COVID-19, Australian researchers contributed to vaccine development, genomic surveillance, and long COVID research. Aboriginal and Torres Strait Islander researchers are increasingly leading health research that addresses community priorities with cultural authority.

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From the lesson
Copy Into Books

✍ Copy Into Your Books

▾

Unit Connections

  • Pathogen -> Transmission -> Defence -> Treatment
  • Infectious vs non-infectious disease
  • Local, national, and global perspectives

Key Formulas

  • Herd immunity threshold ≈ 1 - 1/R0
  • Incidence rate = (new cases/population) × multiplier
  • Case fatality rate = (deaths/cases) × 100%

Depth Study Steps

  • Choose topic -> Formulate question -> Research -> Hypothesis -> Method -> Data collection -> Analysis -> Conclusions -> Communication
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From the lesson
Diagram
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From the lesson
Activity 1
Activity 1

Explain How Cancer Develops

Use cellular mechanisms and evidence to distinguish normal control, tumours and spread.

1 Write a labelled cause-and-effect chain showing how several DNA changes affecting cell-division control and programmed cell death can allow a damaged cell lineage to grow uncontrollably. Explain what apoptosis normally contributes and why one mutation does not automatically mean a person has cancer.
Answer in your book.
2 Classify these tumour descriptions and justify your answers. A is confirmed non-cancerous, remains local and does not invade surrounding tissue. B invades nearby tissue but no distant spread has been found. C has spread from its original site to another organ. Which evidence distinguishes benign from malignant, and which description specifically shows metastasis?
Answer in your book.
3 The lesson identifies HPV infection as one factor that can increase the risk of certain cancers. Explain how that can be true while cancer itself is described as non-infectious. Distinguish transmission of a virus from the uncontrolled growth of a person’s own altered cells.
Answer in your book.
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From the lesson
Activity 2
Activity 2

Evaluate Cancer Risk and Screening Claims

Interpret fictional data carefully and distinguish risk reduction, early detection and guarantees.

1 Choose two modifiable cancer risk factors and one inherited or age-related factor from the lesson. Explain how reducing a relevant exposure may lower risk, then evaluate the claim, “People who avoid all lifestyle risks are guaranteed never to get cancer.”
Answer in your book.
2 Two fictional populations were observed for the same year using the same case definition. Population A had 10 new cases among 1,000 people initially at risk; population B had 30 among 3,000. Calculate the percentage with a new case in each population. Evaluate the claim, “B had three times as many cases, so each person there had three times the risk.” Give one further population characteristic that would matter before a real comparison.
Answer in your book.
3 Explain why screening before symptoms can sometimes improve cancer outcomes. Then evaluate both claims: “A positive screening result proves cancer is present” and “Screening itself cures cancer.” Include the role of follow-up and treatment, without giving personal medical advice.
Answer in your book.
Reflect
Revisit your thinking
reflect

At the start of this lesson, you considered how DNA repair, cell-division controls, programmed cell death and immune surveillance help limit uncontrolled growth. Explain how changes can bypass several safeguards without assuming that every damaged cell becomes cancerous.

Now that you've worked through the lesson, can you explain what normally stops cells from dividing uncontrollably, and what goes wrong to allow a cancer to slip through those safeguards? What was most surprising to you?

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Quick check
Cancer is best described as a disease in which:
+10 XP
2
Quick check
Apoptosis helps prevent cancer because it:
+10 XP
3
Quick check
The key feature that makes a tumour malignant rather than benign is that it:
+10 XP
4
Quick check
Which of the following is a carcinogen?
+10 XP
5
Quick check
Why does early detection through screening improve cancer treatment outcomes?
+10 XP
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From the lesson
Additional content
Short answer · explain in your own words
Show your reasoning
3 questions
Recall Core 2 marks

Q1. Distinguish between a benign tumour and a malignant tumour. (2 marks)

Explain Core 3 marks

Q2. Cancer is sometimes called a "disease of accumulated mutations". Explain why several mutations usually have to build up before a normal cell becomes cancerous. (3 marks)

Evaluate Core 3 marks

Q3. Using two examples, explain how reducing exposure to carcinogens and taking part in screening programs can lower a person's risk of dying from cancer. (3 marks)

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From the lesson
Revisit

Revisit Your Thinking

Go back to your Think First answer. Has your understanding changed?

  • How has your understanding of disease and health developed across this entire unit?
  • What connections between concepts do you find most powerful or surprising?
Update your thinking in your book.
Model answers (click to reveal)

Answers

▾

MCQ 1

C Cancer is a group of diseases in which cells divide uncontrollably after accumulating mutations in their DNA. It is not caused by a virus replacing cells, nor by cells shrinking.

MCQ 2

A Apoptosis is programmed cell death. It removes damaged or faulty cells before they can multiply, which normally stops a mutated cell from forming a tumour.

MCQ 3

D A malignant (cancerous) tumour can invade nearby tissue and spread to distant organs through the blood or lymph (metastasis). A benign tumour stays in one place.

MCQ 4

B A carcinogen is an agent capable of causing cancer. UV radiation from the sun is a carcinogen that can damage DNA and increase melanoma risk. Other carcinogens can contribute through different biological mechanisms.

MCQ 5

A Cancers detected early through screening are usually smaller and have not yet spread, so they can be removed or treated before metastasis. For example, bowel cancer caught at stage I has about 99% survival compared with 13% at stage IV.

Short Answer 1

Model answer: A benign tumour is non-cancerous and does not invade surrounding tissues or spread to distant sites, although its size or location can still cause harm. A malignant tumour is cancerous: it invades nearby tissue and can spread to distant organs through the bloodstream or lymphatic system in a process called metastasis. Invasion and the capacity to spread distinguish malignancy; growth speed alone does not. A malignant tumour need not already have formed distant metastases.

Short Answer 2

Model answer: Cells have several safeguards, including DNA repair, controls that pause division, and apoptosis that removes some damaged cells. Many mutations have little effect on these safeguards; a single mutation does not automatically create cancer. Cancer usually involves accumulated changes affecting several processes, allowing inappropriate survival and division. These changes can arise from errors during cell division, inherited variants or exposures such as tobacco smoke and UV radiation. Age can allow more time for changes to accumulate, and relevant exposures can increase risk, but repeated carcinogen exposure is not necessary in every case.

Short Answer 3

Model answer: Reducing exposure to carcinogens lowers the chance that mutations will build up in the first place. For example, using sun protection (slip, slop, slap) reduces UV damage to skin cells and lowers the risk of melanoma, and not smoking avoids the carcinogens in tobacco that cause about one fifth of cancer deaths. Screening programs lower the risk of dying by detecting cancer early, when it is most treatable. For example, the National Bowel Cancer Screening Program uses a home test to detect tiny traces of blood in stool; a positive result needs further assessment and is not a cancer diagnosis. The National Cervical Screening Program tests for high-risk HPV infection, with follow-up when needed to check for abnormal cells. Finding and treating precancerous changes can help prevent some cancers. Together, prevention (fewer mutations) and early detection (treatment before the cancer spreads) substantially reduce cancer deaths.

Activity 1: Explain How Cancer Develops

  1. Mutations can affect genes that regulate division and responses to damage. Normally, control mechanisms can stop inappropriate division, and apoptosis removes some damaged cells. If a cell accumulates changes that allow it to bypass these controls and avoid cell death, it may keep surviving and dividing when it should not. A single mutation does not automatically create cancer: many mutations have little relevant effect, and cancer usually involves multiple changes. The exact pathway differs among cancers.
  2. A is benign: the description confirms it is non-cancerous, local and non-invasive. B is malignant because it invades nearby tissue, even without observed distant spread. C is malignant and shows metastasis, meaning spread to a distant site. Invasion and spread distinguish malignancy; size or growth speed alone is not a sufficient classification. Benign does not mean a tumour can never cause harm, because its location or size can still affect normal function.
  3. HPV is an infectious virus that can be passed between people. Persistent infection with certain HPV types can contribute to changes that increase the chance of some cancers. The cancer is uncontrolled growth of the affected person’s own cells; ordinary contact does not pass that cancer to another person as it passes a pathogen. HPV infection does not mean cancer is inevitable. Prevention of relevant infections can therefore reduce some cancer risk without making all cancers infectious diseases.

Activity 2: Evaluate Cancer Risk and Screening Claims

  1. Examples include tobacco smoke, UV exposure and alcohol, with inherited variants or increasing age as other influences. Reducing a relevant exposure can reduce DNA damage or other processes that contribute to cancer, but it cannot remove every possible cause. Inherited susceptibility, errors during cell division and other exposures also matter. Risk is a probability, not a promise or a judgement about someone’s choices. Credit accurate factors without requiring current numerical estimates.
  2. A: 10/1,000 × 100 = 1%; B: 30/3,000 × 100 = 1%. The new-case proportions in the supplied data are equal, despite B’s larger raw count. This does not mean every individual has the same risk. Age distribution, relevant exposure patterns, follow-up completeness or testing/diagnosis practices would matter in a real comparison. The same year and case definition help comparability but do not remove every possible difference.
  3. Screening may identify cancer or relevant precancerous changes before symptoms, when further assessment and treatment may offer better options. A positive screening result signals that follow-up may be needed; it is not automatically a confirmed cancer diagnosis. Screening is not itself a cure, and benefits depend on the condition, test, appropriate follow-up and effective treatment. Not every cancer is detected early or cured. No screening age, interval or individual recommendation is required.