What Causes Cancer? A Plain-English Overview of Risk Factors
Cancer is multifactorial: genetics, environment, and lifestyle interact over time. The American Cancer Society projects about 2,041,910 new U.S. cases in 2025, and ACS estimates roughly 42% of cancers involve potentially modifiable risk factors.
Cancer Statistics, in Context
The American Cancer Society projects about 2,041,910 new U.S. cancer cases and 618,120 deaths in 2025, with long-term mortality declining thanks to reduced smoking, earlier detection, and better treatment. Globally, WHO's International Agency for Research on Cancer (IARC) forecasts over 20 million diagnoses a year, a figure that could approach 35 million by 2050 as populations age. Breast cancer remains one of the most commonly diagnosed cancers worldwide, which is part of why screening is emphasized. The ACS counts more than 18 million U.S. cancer survivors today.
These are population-level projections from ACS and WHO/IARC, not predictions about any one person.
How Cancer Develops
Cancer begins when DNA damage accumulates and cells escape normal controls on growth. The widely used Hallmarks of Cancer framework (Hanahan, 2022) describes the recurring capabilities tumors acquire. Common contributing pathways include:
- Genetic mutations: Changes in DNA disrupt normal cell regulation. A minority are inherited (germline), for example TP53 or BRCA1/2 variants that raise susceptibility to breast, ovarian, and other cancers, while most are somatic, acquired over a lifetime through replication or repair errors, enabling sustained proliferation and genome instability.
- Tobacco and environmental carcinogens: Chemicals in tobacco smoke and pollutants (e.g., benzene, asbestos) form DNA adducts that can initiate cancer. ACS attributes a large share of lung cancers to smoking, and occupational exposures such as diesel exhaust add further risk through chronic low-dose damage.
- Chronic inflammation: Persistent inflammation from excess body weight, infections, or autoimmune conditions releases signaling molecules that can drive DNA damage, new blood-vessel growth, and immune evasion. ACS links excess body weight to a meaningful fraction of cancers, including a substantial share of colorectal cases.
- UV radiation: Ultraviolet light induces DNA damage in skin cells that can overwhelm repair. It is implicated in nearly all non-melanoma skin cancers and the large majority of melanomas, which is why sun protection is emphasized.
- Hormonal factors: Prolonged estrogen exposure (e.g., from some hormone therapy or earlier menarche) can promote proliferation in hormone-sensitive tissues and is studied in breast, endometrial, and ovarian cancers.
- Oncogenic infections: Viruses such as HPV (cervical cancer) and hepatitis B/C (liver cancer) can integrate into host DNA or inactivate tumor-suppressor pathways. WHO estimates infections account for a notable share of global cancers, and vaccination plus antiviral therapy make several of these largely preventable.
- Diet and lifestyle factors: Processed meats, excess body weight, and physical inactivity are studied as contributors, for example via nitrosamines and insulin-related growth signaling. ACS attributes a large fraction of colorectal cancers to modifiable factors, and alcohol is studied as a contributor through acetaldehyde and folate effects.
- Epigenetic changes: Non-mutational changes such as DNA methylation can silence tumor-suppressor genes (e.g., MGMT in some gliomas), letting cells evade normal differentiation, recognized as an enabling characteristic in the updated Hallmarks framework.
- Metabolic reprogramming: Many tumors shift toward aerobic glycolysis (the Warburg effect) to fuel rapid growth even in low-oxygen conditions, an active area of research, including metabolic-targeting therapies.
These mechanisms frequently overlap. Many environmental risks also intersect with everyday home exposures: see the room-by-room guide for practical ways to reduce them.
How Much Cancer Is Potentially Preventable?
The American Cancer Society estimates that roughly 42% of U.S. cancer cases are linked to potentially modifiable risk factors: most prominently tobacco, excess body weight and diet, and chronic infections. Age and inherited genetics are not modifiable, which is why screening (such as colorectal screening starting at 45 for average-risk adults) remains important, especially as early-onset cases rise. Infection-driven cancers like cervical and liver cancer are among the most preventable, through vaccination and screening.
The percentages below are overlapping population-level estimates of attributable risk, not a personal risk calculator. Individual risk depends on many interacting factors.
Areas Researchers Are Watching
Several themes recur in recent literature: gut-microbiome changes studied in relation to early-onset colorectal cancer in adults under 50; machine-learning tools studied to support earlier detection; the continued importance of sun protection for skin cancer; and global hepatitis vaccination as a lever against liver cancer. These are areas of active investigation, not settled conclusions.
Follow the latest on these topics in the research feed.
Sources
- American Cancer Society. Cancer Facts & Figures 2025. cancer.org
- WHO International Agency for Research on Cancer (IARC). Global Cancer Observatory (GLOBOCAN). gco.iarc.fr
- Hanahan D. Hallmarks of Cancer: New Dimensions. Cancer Discovery (2022). doi.org
- Islami F, et al. Proportion of Cancer Cases Attributable to Potentially Modifiable Risk Factors in the United States. CA: A Cancer Journal for Clinicians (2018). doi.org
- U.S. Centers for Disease Control and Prevention. Cancer Prevention and Control. cdc.gov
Disclaimer: Educational only, not medical advice. Statistics are population-level projections from the cited sources and do not estimate any individual's risk. Consult your care team for personal guidance. Figures reflect ACS/WHO data as of 2025.