What Is Cancer? Why and How Does It Develop? The Biology of Cancer
In this article
When a Cell Breaks the Rules: A Plain-Language Journey Into Cancer Biology
Cancer is not a single disease. It is the shared name for hundreds of different diseases that arise when cells in our body lose the rules that govern how they grow and divide. Those rules are written in each cell's DNA, and as billions of cells divide every day, errors can creep into these instructions. The body's repair and surveillance systems correct almost all of them; cancer develops when a few critical errors pile up in the same cell over many years and that cell slips past the watch of the immune system. In this article, we explain in plain language the journey from a single cell to a disease that has spread, what causes cancer, and how this knowledge has been turned into today's treatments. We have previously covered 10 facts about the causes of cancer, the real causes of cancer and what metastasis means in separate articles.
- What is cancer? A group of diseases in which cells, starting from one of the body's own cells, divide out of control, invade the surrounding tissue and can spread to distant organs, as a result of changes that accumulate in that cell's DNA.
- How does it develop? A single mutation is not enough. The switching on of "accelerator" genes that push the cell to grow (oncogenes), the failure of "brake" genes (tumour suppressor genes) and breakdowns in the DNA repair systems build up step by step, often over 10–20 years.
- Why does it develop? Some mutations come from random copying errors when cells divide, some from environmental factors such as smoking, alcohol, excess weight, sunlight and infections, and a small share from an inherited predisposition passed down in families. Age is the strongest risk factor.
- Why does it matter? About 40% of cancers are linked to preventable risk factors. Understanding cancer biology is the foundation of today's treatments, such as targeted drugs, immunotherapy and genetic testing.
Why does this topic matter?
More than 20 million people worldwide are diagnosed with cancer every year; roughly one in five people will face cancer at some point in their lives. In Turkey, about 236,000 new cancer cases were estimated for 2024. As populations age, these numbers are rising: the number of new cases worldwide is expected to reach 34 million by 2050 (the rise of cancer at a young age).
The 5 most common cancers worldwide (2024)
New cases, millions. GLOBOCAN 2024 estimates.
In 2024, an estimated 20.6 million new cancer cases occurred worldwide, with cancer-related loss of life estimated at 9.8 million people; as populations grow and age, the number of new cases is expected to reach 34 million by 2050.
The 5 most common cancers in Turkey (2024)
Number of new cases, both sexes. GLOBOCAN 2024 estimates for Turkey.
A total of 235,949 new cancer cases; the most common is lung cancer in men (24%) and breast cancer in women (24.5%). Estimated cancer-related loss of life: 113,805.
For someone diagnosed with cancer, and for their loved ones, the first questions are often the same: "Why me?", "Did I cause this?", "Will my children get it?". The answers begin with understanding how cancer develops. Knowing the biology of cancer helps ease unnecessary guilt, recognise the risks that can be prevented, appreciate the value of screening and early diagnosis, and better understand the treatment options.
What is cancer, and why and how does it develop?
Cancer is a group of diseases that arise when the body's own cells, because of changes (mutations) that accumulate in their DNA, stop following the rules of growth and division, multiply out of control, invade the surrounding tissue and can spread to distant organs. These changes usually build up over years, through random errors during cell division, factors such as smoking, alcohol, excess weight, radiation and certain infections, and, less often, an inherited predisposition.
It all starts with a single cell
The body of an adult is made up of about 37 trillion cells, and about 330 billion cells are renewed every day. Skin, gut and blood cells are constantly being replaced, while nerve cells and heart muscle cells hardly divide at all. What keeps this order in place are the instructions written in the DNA inside each cell's nucleus: from them, a cell learns when to divide, when to stop, what to do when it is damaged, and how to remove itself when it grows old (the Human Genome Project).
Figure 1 · A normal cell and a cancer cell
A cancer cell is the same cell, now "breaking the rules"
Errors in DNA: the accelerator, the brakes and the repair crew
The DNA in every cell is damaged tens of thousands of times a day, and the cell's repair systems fix almost all of this damage. Permanent changes that escape repair and alter the cell's behaviour are called mutations. Most mutations are harmless; the ones that matter for cancer are those affecting three groups of genes that govern cell growth (cancer mutations).
Figure 2 · Three groups of genes involved in cancer
A simplified car analogy
Examples of accelerator genes are KRAS, EGFR and HER2, which today are among the targets of targeted drugs (what is HER2). The most important brake gene is TP53, also known as the "guardian of the genome": it is faulty in about half of all cancers. The best-known examples of repair-crew genes are BRCA1 and BRCA2, which are linked to hereditary breast and ovarian cancer. Changes can occur not only in the DNA sequence itself but also in the chemical tags that switch genes on and off (epigenetic changes) (epigenetics and biological age).
One mutation is not enough: cancer is a multistep process
Cancer usually develops not from a single mutation but from several critical changes that follow one another in the same cell lineage. In common solid tumours, the number of "driver" mutations steering the cancer is usually between 2 and 8; the dozens of other mutations found in a tumour are mostly "passengers". Each new driver mutation gives the cell a small advantage over its neighbours, and its descendants gradually multiply. This is why cancer is also described as a small process of evolution unfolding inside the body.
Figure 3 · How colorectal cancer develops, step by step
The best-studied example; the process usually takes 10–15 years
The length of this process is striking: a genetic analysis of pancreatic cancer estimated that about 15–20 years pass between the first critical mutation and the appearance of cells able to spread. Moreover, the normal tissues of healthy people also contain small groups of cells carrying cancer-related mutations, and very few of them ever turn into cancer. In other words, carrying a mutation is not the same as having cancer. This long process offers an important window of opportunity for screening and early diagnosis (screening with colonoscopy).
Figure 4 · Inherited and non-inherited cancer: two hits
Knudson's two-hit hypothesis
About 5–10% of cancers involve an inherited predisposition. Cancer at a young age in the family, more than one cancer in the same person, or the same type of cancer appearing frequently in a family are important clues for genetic counselling (hereditary cancers, risk-reducing surgery in BRCA carriers). An inherited predisposition does not mean that cancer will definitely develop; it raises the risk and calls for closer follow-up.
Where do mutations come from?
Mutations have three main sources: random errors in copying DNA when cells divide, environmental and lifestyle factors, and predisposition inherited from our families. The relative share of these three sources varies greatly from one type of cancer to another.
Where do the mutations in cancer cells come from?
Percent. A model estimate of the sources of driver mutations across 32 cancer types (Tomasetti et al., Science 2017).
Source of mutations
These proportions refer to mutations, not to cancer cases. Even if most of the mutations in a cancer come from copying errors, an environmental factor can set off the cancer by adding a single critical mutation; this is why prevention still matters. The proportions vary greatly by cancer type: in lung cancer, the environmental share is much higher.
The large share of copying errors shows that some cancers can develop through "bad luck", without any risk factor at all. This is valuable in easing the "What did I do wrong?" guilt that many people diagnosed with cancer carry. On the other hand, it does not mean that cancer cannot be prevented: factors such as smoking, alcohol, excess weight and certain infections markedly increase the risk by adding one of the critical steps on the road to cancer (can cancer be prevented?).
The preventable share: how many cancers in the US are linked to which factor?
2019 data in adults aged 30 and over, percent (Islami et al., CA Cancer J Clin 2024).
Other factors include the sun's ultraviolet rays, physical inactivity, diet and infections such as HPV. These factors were linked to 44% of cancer-related loss of life, with smoking accounting for 28.5%. Worldwide, about 13% of cancers are estimated to be caused by infections.
- Smoking: Tobacco smoke contains more than 70 cancer-causing substances; besides the lungs, it causes cancer in many organs, including the mouth, larynx, oesophagus, bladder, pancreas and kidney (quitting smoking).
- Alcohol: In the body, it is converted into acetaldehyde, which damages DNA directly; there is no safe lower limit (how alcohol damages DNA).
- Excess weight and physical inactivity: Through hormones, insulin and inflammation, fat tissue raises the risk of at least 13 types of cancer (obesity and cancer).
- Infections: HPV (cervix, head and neck), hepatitis B and C (liver) and Helicobacter pylori (stomach) account for about 13% of cancers worldwide; these can be prevented with vaccination and treatment (20 years of the HPV vaccine, Helicobacter pylori and stomach cancer).
- Age: The strongest risk factor. Because mutations accumulate over time and both repair and immune surveillance weaken with age, the vast majority of cancers occur after the age of 50 (why cancer is more common in men).
What all cancers have in common
Although hundreds of different types of cancer arise in different organs and through different mutations, the abilities that cancer cells acquire are remarkably similar. In 2000, Douglas Hanahan and Robert Weinberg described these shared abilities as the "hallmarks of cancer". The list was expanded with new knowledge in 2011 and 2022 and today includes 14 items.
Figure 5 · The 14 hallmarks of cancer
The abilities cancer cells acquire, and the conditions that make them possible
One of these hallmarks shows up directly in everyday practice: most cancer cells use sugar in a fast, "wasteful" way even when oxygen is available (the Warburg effect). This is why radioactive sugar (FDG) builds up intensely in tumours on a PET-CT scan (what FDG uptake means). However, this does not mean that "eating sugar feeds cancer": blood sugar is tightly regulated by the body, and cutting out sugar does not stop a tumour from growing.
A tumour is never alone: the microenvironment
A tumour is not made up of cancer cells alone. Cancer cells steer the normal cells around them to work in their favour, creating a complex ecosystem that functions much like an organ. Nor are the cancer cells within a tumour identical: subgroups carrying different mutations live side by side. This diversity (heterogeneity) means that while the cells that respond to a treatment disappear, the resistant ones can multiply, and resistance can develop over time (how cancer cells develop resistance).
Figure 6 · The tumour microenvironment
Cancer cells and the normal cells that support them
The bacterial communities in the gut and within tumours (the microbiome) are also part of this ecosystem; some bacteria can contribute to cancer through inflammation and DNA damage, while others can influence the response to immunotherapy (the microbiome and colorectal cancer).
The immune system and cancer
The immune system keeps constant watch against cancer, recognising abnormal cells and clearing them away. The fact that some cancers are more common in people whose immune system is suppressed (for example, after an organ transplant) is evidence of this. Cancer can progress only once it manages to slip past this surveillance (immune tolerance).
Figure 7 · Three phases between the immune system and cancer
The concept of "immunoediting"
Spread: metastasis
Most cancer-related loss of life is caused not by the original tumour but by spread to distant organs (metastasis). Metastasis requires a cancer cell to clear a series of difficult steps, which makes it a very "inefficient" process: fewer than one in ten thousand cancer cells that enter the bloodstream can form a new tumour (does a biopsy spread cancer?).
Figure 8 · The steps of metastasis
At each step, the vast majority of cells fall away
Each cancer tends to spread to particular organs: for example, breast and prostate cancer often spread to bone, and colorectal cancer to the liver. This depends both on the direction of blood flow and on how well the cancer cell "fits" the new tissue; the "seed and soil" analogy proposed in the 19th century still holds true today.
Types of cancer: by the cell of origin
| Main group | Tissue of origin | Examples |
|---|---|---|
| Carcinoma | Cells that line organs and surfaces (epithelium) | Lung, breast, colorectal, prostate, stomach; about 80–90% of all cancers |
| Sarcoma | Bone, muscle, fat and connective tissue | Osteosarcoma, liposarcoma |
| Leukaemia | Blood-forming cells in the bone marrow | Acute and chronic leukaemias |
| Lymphoma and myeloma | Cells of the immune system | Hodgkin and non-Hodgkin lymphoma, multiple myeloma |
| Brain and nervous system tumours | Supporting cells of the brain and spinal cord | Glioma, glioblastoma |
| Others | Germ cells, pigment cells, hormone-producing cells | Testicular tumours, melanoma, neuroendocrine tumours |
Even cancers of the same organ can behave very differently depending on their cell type and molecular features; this is why pathology and, when needed, molecular testing are decisive in diagnosis.
From biology to treatment
Most of the progress in cancer treatment over the past 25 years has grown out of understanding the biology described above. While classic chemotherapy and radiotherapy target rapidly dividing cells, today we can use treatments that target a tumour's own particular weak spots. Tests that examine the genetic makeup of a tumour are becoming increasingly important in deciding which patient will benefit from which treatment (next-generation sequencing, what the mutations in a genetic test report mean).
Figure 9 · From the hallmarks of cancer to treatments
A simplified matching
Treatments that activate the immune system (immunotherapies and cancer vaccines) and new technologies such as gene editing (CRISPR) are the latest examples of cancer biology being turned into treatment.
Common misconceptions
| Misconception | The scientific facts |
|---|---|
| Cancer is contagious. | Cancer does not pass from person to person. Some viruses that can cause cancer (HPV, hepatitis B and C) can be transmitted; these can be prevented with vaccination and protection. |
| Sugar feeds cancer, and cutting out sugar stops it. | All cells use sugar, and blood sugar is regulated by the body. Cutting out sugar does not shrink a tumour, although excess weight raises the risk indirectly. |
| A biopsy or surgery spreads cancer. | A biopsy performed with the proper technique does not spread cancer; it is essential for the correct diagnosis and treatment. |
| Cancer is always inherited. | Only 5–10% of cancers involve a strong inherited predisposition; most develop from mutations that accumulate over a lifetime. |
| Stress alone causes cancer. | Stress has not been shown to cause cancer directly; however, it can affect risk indirectly, through smoking, alcohol and physical inactivity. |
| Herbal products and "natural" methods cure cancer. | Methods with no proven effectiveness can delay effective treatment and lead to drug interactions (the risks of alternative products). |
According to GLOBOCAN 2024 estimates, about 236,000 people in Turkey are diagnosed with cancer each year. The most common cancers are lung, prostate and colorectal cancer in men, and breast, thyroid and colorectal cancer in women. The fact that lung cancer makes up about a quarter of all cancers in men shows how heavily smoking weighs on the cancer burden in our country. At the Ministry of Health's Cancer Early Diagnosis, Screening and Training Centres (KETEM), Turkey's free cancer screening centres, screening for breast, cervical and colorectal cancer is offered free of charge. We have covered preventable cancers in our article on the 8 most preventable cancers.
Protecting yourself
- Do not smoke: It is the single largest preventable cause of cancer; quitting lowers the risk at any age.
- Limit alcohol, or avoid it altogether: When it comes to cancer, there is no safe lower limit.
- Maintain a healthy weight and stay active: Regular physical activity and a diet rich in vegetables, fruit and whole grains lower the risk of many cancers.
- Vaccination and treating infections: HPV and hepatitis B vaccines, and treatment for hepatitis C and Helicobacter pylori, help prevent cancer.
- Protect yourself from the sun: Avoid the sun, especially around midday, and do not use sunbeds.
- Keep up with screening: Breast, cervical and colorectal cancer screening, and lung cancer screening for those who qualify, can catch cancer early or even before it forms (lung cancer screening).
- Know your family history: If there is cancer at a young age, or many cases of cancer, in your family, ask for genetic counselling.
Frequently asked questions
- What is cancer?
- Cancer is a group of diseases in which the body's own cells, because of changes that accumulate in their DNA, divide out of control, invade the surrounding tissue and can spread to distant organs. It is not a single disease: there are hundreds of different types, depending on the organ of origin, the cell type and molecular features.
- Why does cancer develop?
- Cancer develops when mutations accumulate in the genes that control cell growth. Some of these mutations come from random errors during cell division, some from factors such as smoking, alcohol, excess weight, sunlight and certain infections, and about 5–10% from an inherited predisposition. Age is the strongest risk factor.
- How long does it take for cancer to develop?
- Most cancers develop over years, even decades, from the first critical mutation to diagnosis. For example, colorectal cancer usually develops from a polyp over 10–15 years, and in pancreatic cancer it has been estimated that 15–20 years pass between the first mutation and the ability to spread. This long period offers an opportunity for screening and early diagnosis.
- Can cancer be prevented?
- A substantial share of cancers can be prevented. According to US data, about 40% of cancers are linked to modifiable factors such as smoking, excess weight, alcohol, physical inactivity, sunlight and infections. Vaccines, screening and healthy lifestyle habits markedly reduce the risk; however, some cancers can develop even without any risk factor.
Glossary
- Mutation
- A permanent change in the DNA sequence.
- Oncogene
- A gene that, when mutated, pushes the cell to divide continuously; the cell's "accelerator".
- Tumour suppressor gene
- A gene that puts the brakes on cell division; when it fails, the brakes come off. Example: TP53.
- Driver mutation
- A mutation that plays a direct role in the development of cancer; the others are called "passenger" mutations.
- Apoptosis
- Programmed cell death: the orderly self-destruction of a damaged or unneeded cell.
- Telomere
- The protective cap at the ends of chromosomes that shortens with each division; cancer cells get around this limit with the enzyme telomerase.
- Epigenetics
- Chemical tags that switch genes on and off without changing the DNA sequence.
- Tumour microenvironment
- The normal cells, blood vessels and extracellular material surrounding cancer cells.
- Metastasis
- The spread of cancer cells from their organ of origin to distant organs.
- Dysplasia
- A precancerous change in which cells have become disorganised but are not yet cancer.
DROZDOGAN Academy Commentary
Cancer is not an outsider that enters our body from somewhere else; it is our own cells losing their rules through errors that build up over the years. This perspective eases both fear and guilt, while also showing the value of prevention and early diagnosis.
⚡ Why it matters
Understanding cancer biology explains why some cancers can be prevented, why screening works, why two patients with the "same" cancer are treated differently, and why resistance to treatment sometimes develops.
✅ What we know today
The genetic and cellular foundations of cancer have been largely uncovered. This knowledge has been turned into many treatments and diagnostic methods, such as targeted drugs, immunotherapy, PARP inhibitors and tracking tumour DNA in the blood.
⚠️ What we do not yet know
Why dormant cancer cells wake up years later, how to control the diversity within a tumour, and how to prevent metastasis remain among the biggest questions.
🩺 In practice
When we explain to our patients "why" their cancer developed, we use language that does not assign blame; at the same time, we emphasise that changes such as quitting smoking, managing weight and staying active still bring benefits after diagnosis. In planning treatment, we assess the tumour's pathological and molecular features together.
❓ Open questions
Will it become possible to detect cancers with a simple blood test long before they cause symptoms? Will we be able to predict which normal cells carrying mutations will turn into cancer? Can we train the immune system to prevent cancer?
Bottom line: Cancer is a long process that begins when a cell loses its rules. Every step of this process is a new opportunity for prevention, early diagnosis and treatment.
- This article was prepared in October 2026.
- Statistics are taken from GLOBOCAN 2024 estimates (International Agency for Research on Cancer), and the preventable share from a 2024 analysis of US data; this proportion may differ for Turkey.
- The proportions for the sources of mutations (66%, 29%, 5%) are estimates from a mathematical model and are debated in the scientific community; they show the sources of mutations, not of cancer cases.
- Numerical values (number of cells, number of driver mutations, efficiency of metastasis, timescale in pancreatic cancer) are approximate and may be reported differently in different studies.
- This article is for general information only and is not personal medical advice. The diagrams are simplified. The Academy commentary is our own.
References
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- Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell 2011;144:646-674. doi:10.1016/j.cell.2011.02.013
- Vogelstein B, Papadopoulos N, Velculescu VE, et al. Cancer genome landscapes. Science 2013;339:1546-1558. doi:10.1126/science.1235122
- Tomasetti C, Li L, Vogelstein B. Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention. Science 2017;355:1330-1334. doi:10.1126/science.aaf9011
- Yachida S, Jones S, Bozic I, et al. Distant metastasis occurs late during the genetic evolution of pancreatic cancer. Nature 2010;467:1114-1117. doi:10.1038/nature09515
- Islami F, Marlow EC, Thomson B, et al. Proportion and number of cancer cases and deaths attributable to potentially modifiable risk factors in the United States, 2019. CA Cancer J Clin 2024. cancer.org
- GLOBOCAN 2024 Turkey fact sheet. International Agency for Research on Cancer (IARC). gco.iarc.who.int
- IARC releases GLOBOCAN 2024. UICC, July 2026. uicc.org
- American Cancer Society reports latest global cancer statistics. The ASCO Post, July 2026. ascopost.com
- de Martel C, Georges D, Bray F, et al. Global burden of cancer attributable to infections in 2018: a worldwide incidence analysis. Lancet Glob Health 2020;8:e180-e190. doi:10.1016/S2214-109X(19)30488-7
- Sender R, Milo R. The distribution of cellular turnover in the human body. Nat Med 2021;27:45-48. doi:10.1038/s41591-020-01182-9
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