What Is Cancer and How Does It Start?
What Is Cancer and How Does It Start?
Cancer begins when a cell develops changes that allow it to grow, survive, and divide outside the body’s normal controls. Further changes may help its descendants form a tumor, invade nearby tissue, or spread elsewhere. Cancer is therefore not caused by one universal defect. It develops through a series of genetic changes that differ among cancer types and even among cells within the same tumor.
By Chris Morais, MSc, MPhil, PhD
- What Is Cancer and Is It a Single Disease?
- How Do Normal Cells Control Their Growth and Division?
- How Does a Normal Cell Become a Cancer Cell?
- What Causes the Genetic Changes That Start Cancer?
- How Are Cancer Cells Different from Normal Cells?
- How Can One Cancer Cell Develop into a Tumor?
- Does Cancer Always Form a Tumor?
- What Is the Difference Between a Benign Tumor, a Precancerous Change and Cancer?
- Can Cancer Start Anywhere in the Body?
What Is Cancer and Is It a Single Disease?
Cancer is a large group of diseases characterized by abnormal cells that grow without proper control and possess the capacity to invade nearby tissues. Some cancer cells can also enter the bloodstream or lymphatic system to establish secondary growths in distant organs—a process known as metastasis.
Cancer is not a single disease:
- Hundreds of distinct types: There are hundreds of cancer types and subtypes, each with unique biological characteristics, behaviors, and clinical courses. Skin cancer, leukemia, and glioblastoma all involve dysregulated cell growth, but they arise from fundamentally different cell lineages and develop via distinct molecular alterations.
- Biological heterogeneity: Even two cancers arising within the exact same organ are rarely biologically identical. They may harbor different gene mutations, proliferate at different rates, and respond differently to therapeutics and microenvironmental cues.
Consequently, cancer is best understood as a diverse family of related diseases sharing common capabilities rather than a single uniform disorder.[1–4]
How Do Normal Cells Control Their Growth and Division?
Normal cells do not divide simply because nutrients and space are available; their division is carefully regulated by signals from outside the cell, conditions inside the cell, and the structure and needs of the surrounding tissue.
Inside each cell, a series of molecular checkpoints regulates entry into the cell cycle—the ordered sequence of events through which a cell grows, replicates its DNA, and divides into two daughter cells.
How Do Healthy Cells Know When to Stop Dividing?
Cells continuously interpret biochemical and physical cues from their microenvironment:
- Growth factors and inhibitory signals: Growth-promoting factors stimulate division when new cells are required for growth or tissue repair, while inhibitory factors signal the cell to rest.
- Cell contact and spatial cues: Normal cells communicate with neighboring cells and attach to the extracellular matrix. These interactions help restrain inappropriate growth when cells become crowded or lose the tissue contacts they normally require.
- Checkpoint control: Before DNA replication or cell division proceeds, checkpoint systems can detect DNA damage, incomplete DNA replication, or other problems. The cell cycle can then pause to allow repair or prevent damaged cells from continuing to divide.
While renewal tissues such as the skin and intestinal lining divide continuously, other specialized cells divide only in response to specific injury, and certain terminally differentiated cells such as mature neurons rarely divide after development.
What Happens to Cells That Are Old or Damaged?
When a normal cell experiences significant stress, DNA damage, or aging-related changes, specific physiological pathways may intervene:
- Cellular senescence: Persistent DNA damage or other forms of cellular stress can place a cell into a stable, long-lasting state in which it remains metabolically active but stops dividing.
- Apoptosis: Severely damaged cells can activate programmed cell death. During apoptosis, cellular components are packaged and removed in a controlled way that usually limits inflammation in the surrounding tissue.
- Immune surveillance: The immune system can recognize and eliminate some abnormal or stressed cells before they expand further.
Cancer development requires abnormal cells to overcome enough of these protective mechanisms to continue surviving and multiplying.
How Does a Normal Cell Become a Cancer Cell?
A normal cell transforms into a cancer cell through the accumulation of alterations that disrupt the expression or function of genes regulating cell growth, DNA maintenance, survival, and differentiation.
Three primary functional classes of genes are implicated in this transformation:
- Proto-oncogenes: Normal genes that promote cell division or survival under physiological control. Mutations, gene amplification, or chromosome rearrangements can convert them into oncogenes that produce excessive or persistent growth-promoting signals.
- Tumor suppressor genes: Genes that encode proteins involved in cell-cycle control, responses to DNA damage, apoptosis, and other growth-limiting processes. Loss or reduction of their function can weaken important restraints on abnormal cell growth.
- DNA repair genes: Genes that encode proteins involved in correcting DNA damage and replication errors. Loss of repair function can increase genomic instability and allow further mutations or chromosome changes to accumulate.
In addition to nucleotide mutations, epigenetic alterations—such as promoter DNA methylation and histone modifications—can inappropriately silence tumor suppressors or activate growth-promoting pathways without altering the primary DNA sequence.
Does Cancer Usually Begin in One Cell?
Many cancers are thought to arise from a single altered cell lineage. If an early cancer-promoting change gives a cell a growth or survival advantage, that cell may undergo clonal expansion, producing a population of descendants that carry the founding alteration.
As the clone expands, additional genetic or epigenetic changes can arise in different descendant cells:
- Clonal evolution: Cells with changes that provide greater growth or survival advantages may expand more successfully within the local tissue environment.
- Intratumoral heterogeneity: Over time, a tumor can contain multiple genetically and biologically distinct subclones, contributing to differences in growth, treatment response, and invasive behavior within the same cancer.
Why Are Several Cellular Changes Usually Needed?
A single genetic alteration is rarely sufficient to produce a malignant neoplasm because human cells possess robust, overlapping safeguards. A cell driven by an activated oncogene may still be restrained by intact tumor suppressor pathways, senescence, apoptosis, or other control systems.
During cancer development, a cell lineage commonly acquires a combination of capabilities such as:
- Sustained growth-promoting signaling.
- Reduced response to signals that normally restrain growth.
- Resistance to cell death.
- Maintenance of sufficient replicative capacity, often through telomere maintenance.
- Metabolic changes that support continued growth.
- The ability to invade surrounding tissue and, in some cancers, spread to distant sites.
Different cancers acquire these capabilities through different molecular changes and not necessarily in the same order.
Because these changes build up over years or decades, their gradual accumulation helps explain why the incidence of most human cancers increases markedly with age[2].
What Causes the Genetic Changes That Start Cancer?
Cancer-initiating alterations stem from three main origins: inherited germline mutations, intrinsic errors occurring during normal DNA replication, and damage caused by external carcinogens or oncogenic infections. In most clinical cases, multiple contributing factors interact over a person’s lifetime.
Most individual DNA changes have little or no effect on cancer development. Only a subset alters genes or regulatory regions in ways that provide a cancer-promoting advantage.
Can Cancer-Causing Changes Be Inherited?
An individual can inherit a pathogenic variant through parental gametes (egg or sperm), resulting in its incorporation into virtually all cells of the body:
- Elevated risk, not absolute certainty: Inherited cancer syndromes confer genetic susceptibility, not an automatic guarantee of malignant transformation.
- Additional changes are still required: A person who inherits a cancer-predisposing variant usually needs additional acquired changes in particular cells before cancer can develop. For some inherited tumor suppressor syndromes, this follows the classic “two-hit” pattern in which the remaining functional copy of the gene is later lost or disabled.
- Frequency: About 5% to 10% of cancers are thought to be caused by harmful genetic changes inherited from a parent. Most other cancers arise mainly through genetic changes acquired during life.
Can Mistakes Occur When Cells Copy Their DNA?
Yes. Before a cell divides, it must copy billions of DNA base pairs. Despite proofreading and post-replication repair systems, occasional copying errors escape correction.
If a replication error persists and is copied in subsequent DNA replication, it can become established as a mutation in that cell lineage. In tissues with high turnover, repeated cell division provides repeated opportunities for random mutations to arise.
How Can Carcinogens and Infections Damage DNA?
A carcinogen is an agent capable of causing cancer or increasing cancer risk:
- Chemical carcinogens: Some cancer-causing chemicals, including substances in tobacco smoke, can directly damage DNA or generate reactive molecules that produce DNA lesions.
- Radiation: Ultraviolet (UV) radiation from sunlight can produce DNA lesions such as pyrimidine dimers. Ionizing radiation, including X-rays and radon-related radiation, can cause several forms of DNA damage, including chromosome and DNA strand breaks.
- Oncogenic infections: Certain infectious agents promote cancer through different biological mechanisms. High-risk human papillomaviruses produce proteins that interfere with tumor suppressors such as p53 and RB. Chronic hepatitis B and C infections can promote liver cancer through persistent inflammation and repeated tissue injury, while hepatitis B can also have more direct effects on infected cells. Chronic Helicobacter pylori infection causes long-lasting stomach inflammation that can contribute to gastric cancer development.[1]
How Are Cancer Cells Different from Normal Cells?
Cancer cells evade or weaken many of the biological constraints that maintain cooperation between cells in normal tissues:
Normal Cells: Regulated Growth Signals → Tissue Growth Restraints → Limited Replicative Capacity in Many Somatic Cells → Controlled Responses to Damage
Cancer Cells: Abnormal or Sustained Growth Signaling → Reduced Growth Restraints → Telomere Maintenance in Many Cancers → Increased Resistance to Cell Death
Why Do Cancer Cells Ignore Signals to Stop Growing?
Cancer cells can become less dependent on normal extracellular growth controls through several mechanisms:
- Autocrine signaling: Producing their own growth factor ligands to stimulate their own surface receptors.
- Constitutive pathway activation: Harboring mutations in intracellular transducers such as RAS or BRAF that keep growth cascades abnormally active without the usual external signal.
- Altered cell-contact signaling: Changes in cell adhesion and contact-sensing pathways can weaken signals that normally restrain growth when cells become crowded.
- Inactivation of cell-cycle brakes: Disabling tumor suppressor pathways such as the RB pathway can make it easier for cells to progress from G1 into S phase despite normal growth restraints.
How Do Cancer Cells Avoid Being Destroyed?
Malignant cells can acquire several mechanisms that increase their chances of survival:
- Blocking apoptosis: Downregulating pro-apoptotic effectors such as BAX/BAK or overexpressing anti-apoptotic survival proteins such as BCL-2.
- Telomere maintenance: In many normal somatic cells, progressive telomere shortening helps limit the number of divisions. Most cancers activate telomerase, while a smaller proportion use Alternative Lengthening of Telomeres (ALT), allowing telomeres to be maintained and supporting continued proliferation.
- Immune evasion: Cancer cells can alter antigen presentation, express immune-checkpoint ligands such as PD-L1, or create an immunosuppressive local environment. These changes can reduce the ability of immune cells to recognize or eliminate them.
How Can One Cancer Cell Develop into a Tumor?
A transformed cell can undergo repeated rounds of division and produce an expanding clone. During this process, the cancer cells interact continuously with surrounding normal cells, blood vessels, immune cells, and extracellular matrix.
As the population expands, it engages in dynamic reciprocal signaling with the tumor microenvironment:
- Diffusion limitations: Small clusters of cancer cells can obtain oxygen and nutrients by diffusion from nearby blood vessels, but this becomes increasingly difficult as the tumor grows.
- Blood supply and angiogenesis: As some tumors enlarge, poorly oxygenated regions can develop. Many cancers release pro-angiogenic signals such as VEGF that stimulate new blood-vessel growth. Some tumors can also make use of existing vessels rather than relying entirely on newly formed ones.
- Stromal interactions: Cancer cells can recruit or alter nonmalignant host cells—including fibroblasts, endothelial cells, pericytes, and immune cells—which can remodel the extracellular matrix and influence tumor growth.
Does Cancer Always Form a Tumor?
No. Many cancers form solid tissue masses, but some malignancies—particularly leukemias—primarily involve the bone marrow and blood rather than forming a single solid tumor. Other blood and immune-system cancers, such as lymphomas, can form masses in lymph nodes or other tissues.
The term tumor usually refers to an abnormal mass of tissue produced by excessive cell growth or reduced cell death. Tumors may be benign or malignant.
What Are Solid Tumors?
Solid tumors are localized masses of abnormal tissue arising in organs or other tissues. They are commonly classified according to the type of cell or tissue from which they arise:
- Carcinomas: Malignancies originating in epithelial tissues, which cover external body surfaces and line internal organs and cavities. Carcinomas represent the most common human cancers, including major malignancies of the lung, breast, prostate, colon, and skin.
- Sarcomas: Tumors arising from connective or supportive tissues, including bone (osteosarcoma), cartilage (chondrosarcoma), skeletal muscle (rhabdomyosarcoma), fat (liposarcoma), and vascular tissues.
- Central nervous system tumors: Primary tumors of the brain and spinal cord include gliomas and several other tumor types arising from different cells or precursor populations within the central nervous system.
Which Cancers Do Not Form Solid Tumors?
- Leukemias: Cancers arising from blood-forming stem or progenitor cells, most often in the bone marrow. Abnormal blood cells can accumulate in the marrow and enter the circulation without typically forming a single localized solid tumor.
- Lymphomas: Malignancies of lymphoid lineage that frequently present as solid nodal or extranodal masses, though some lymphoma cells may also circulate in the blood.
- Multiple myeloma: A malignancy of plasma cells that commonly involves multiple sites within the bone marrow rather than forming a single isolated tumor mass[1].
What Is the Difference Between a Benign Tumor, a Precancerous Change and Cancer?
These conditions differ in their biological behavior. A benign tumor is a noncancerous neoplasm that does not invade nearby tissue or metastasize. A precancerous change is abnormal tissue with an increased risk of progressing to cancer but has not become invasive cancer. Cancer is malignant and has acquired the ability to invade surrounding tissue.
| Type of Growth | Invades Nearby Tissue? | Can Spread to Distant Sites (Metastasize)? | General Biological Meaning |
|---|---|---|---|
| Benign Tumor | No | No | An abnormal, non-invasive growth that does not invade nearby tissue or metastasize, although some benign tumors can grow large or compress surrounding structures. |
| Precancerous Change | No | No | Abnormal tissue, such as dysplasia or intraepithelial neoplasia, that carries an increased risk of progressing to invasive cancer. |
| Cancer (Malignancy) | Yes | Some cancers can metastasize, depending on their type and stage. | A malignant neoplasm capable of invading surrounding tissue. Some malignant cancers can also spread to distant sites. |
What Does Carcinoma in Situ Mean?
Carcinoma in situ (CIS) is a non-invasive epithelial lesion in which abnormal cells with cancer-like features remain confined to the site where they formed and have not invaded nearby tissue. In epithelial tissues, these cells remain on the epithelial side of the basement membrane.[1]
The basement membrane is a specialized extracellular matrix boundary separating epithelial tissue from the underlying stroma:
- Because an in situ carcinoma has not crossed the basement membrane into the underlying stroma, it has not gained direct access to stromal blood and lymphatic vessels through local invasion.
- Depending on the organ and type of lesion, carcinoma in situ may remain stable or may progress to invasive carcinoma if additional changes occur.
- Penetration of the basement membrane marks the transition from in situ disease to invasive carcinoma.
What Makes a Tumor Malignant?
A solid tumor is classified as malignant when its cells demonstrate the ability to invade surrounding tissue:
- Malignant cells can alter cell adhesion, remodel the extracellular matrix, and migrate into neighboring tissue compartments.
- Some malignant cells can enter blood or lymphatic vessels, survive transport through the circulation, leave vessels at distant sites, and establish metastatic growths.
- Local invasion is a defining feature of malignant solid tumors and distinguishes them from benign tumors. Metastasis may occur later and is not required to be present when a cancer is first diagnosed.
Can Cancer Start Anywhere in the Body?
Cancer can develop in almost any anatomical tissue containing cells capable of undergoing cancer-promoting changes and producing an abnormal cell lineage. However, cancer incidence varies widely among different tissues.
Tissues with ongoing cell turnover undergo many rounds of DNA replication, which can create opportunities for mutations to arise. However, cell division alone does not determine cancer risk. Environmental exposures, inherited susceptibility, hormones, chronic inflammation, tissue architecture, and other biological factors also influence how often cancers develop in different organs.
In contrast, tissues composed predominantly of terminally differentiated, non-dividing cells such as adult cardiomyocytes and mature central neurons rarely give rise to primary cancers. Malignancies associated with the central nervous system arise from mitotic glial cells, meningeal tissues, or precursor populations rather than mature neurons.
Why Are Cancers Named After Where They Begin?
Cancers are generally classified and named according to their primary site and the type of cell or tissue in which they originated:
- Retention of lineage identity: Even after malignant transformation, cancer cells often retain enough structural, molecular, or antigenic features of their tissue of origin to help identify where the cancer began.
- Metastatic classification: If a breast carcinoma metastasizes to the bone, brain, or liver, it remains biologically breast cancer. The metastatic lesions consist of abnormal breast epithelial cells and are treated according to their breast-cancer origin rather than as primary bone, brain, or liver cancers.
Morais C. What Is Cancer and How Does It Start? [Internet]. BiologyWithin.com; 2026 Jul 31. Available from: https://www.biologywithin.com/2026/07/what-is-cancer-and-how-does-it-start.html
- National Cancer Institute. What Is Cancer? National Cancer Institute.
- Hanahan D. Hallmarks of Cancer: New Dimensions. Cancer Discov. 2022;12(1):31-46.
- National Cancer Institute. The Genetics of Cancer. National Cancer Institute.
- National Cancer Institute. Carcinoma in Situ. NCI Dictionary of Cancer Terms.
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Chris is a biologist dedicated to making complex biological and physiological sciences clear, rigorous, and accessible.
Disclaimer: This article is for general educational purposes only and does not constitute medical advice, diagnosis, or treatment. Consult a qualified healthcare professional about personal health concerns.
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