Cancer is not an infection. It is a disease that starts inside your own cells when their DNA becomes damaged or mutated, causing them to grow and divide without the normal controls. An infection, by contrast, is caused by an outside invader like a bacterium, virus, or parasite entering your body. That said, the relationship between cancer and infection is more complicated than a simple “no,” because certain infections can cause cancer, and roughly 1 in 9 cancers diagnosed worldwide are triggered by an infectious agent.
Why Cancer Is Not an Infection
An infection happens when a foreign organism enters your body, multiplies, and causes harm. Cancer happens when your own cells malfunction. The DNA inside a cell accumulates mutations that disable its built-in safety checks, the ones that tell damaged cells to stop dividing or to self-destruct. Once those brakes fail, the cell keeps copying itself, eventually forming a tumor or flooding the bloodstream with abnormal cells in the case of leukemia.
Your immune system treats these two problems differently. It detects infections by recognizing molecular patterns on the surface of bacteria and viruses that clearly mark them as foreign. Cancer cells are harder to spot because they are, at their core, still your cells. They carry your DNA, display most of your normal surface markers, and often develop ways to hide from immune surveillance. This is why the immune system can usually clear a bacterial infection in days but may fail to catch a growing tumor for months or years.
How Infections Can Cause Cancer
About 2.3 million new cancer cases in 2020 were caused by infectious agents. That figure, published in the Journal of the National Cancer Institute, accounts for roughly 11% of all cancers diagnosed globally that year. A handful of specific pathogens do the bulk of the damage.
The bacterium that causes most stomach ulcers was responsible for an estimated 850,000 cancer cases in 2020, making it the single largest infectious contributor at 36% of all infection-related cancers. Human papillomavirus (HPV) accounted for 730,000 cases (31%), mostly cervical and throat cancers. Hepatitis B followed with 380,000 cases (16%), primarily liver cancer. Several parasitic worms, particularly those found in parts of East Asia and Africa, are also classified as confirmed human carcinogens by the International Agency for Research on Cancer.
These pathogens do not turn into cancer themselves. They create the conditions for cancer to develop in your cells through two main routes. First, long-term infection triggers chronic inflammation, which forces cells to divide repeatedly to repair damaged tissue. Each round of division is another opportunity for a copying error in the DNA. Second, some viruses insert their own genetic material directly into your cell’s DNA. HPV, for example, produces proteins that bind to and disable two of the cell’s most important tumor suppressors, the molecular brakes that normally prevent runaway growth. Hepatitis B works similarly, integrating into liver cell DNA and altering the expression of genes that control cell division. The result in both cases is that your own cells accumulate mutations and eventually become cancerous. The infection is the trigger, but the cancer itself is still a disease of your own mutated cells.
The H. pylori and Stomach Cancer Connection
The link between the common stomach bacterium H. pylori and gastric cancer is one of the clearest examples of infection-driven cancer. The bacterium infects the stomach lining and causes chronic inflammation that can persist for decades. Over time, the inflamed tissue progresses through a sequence: chronic gastritis, then a condition called intestinal metaplasia where stomach cells start resembling intestinal cells, then precancerous changes, and finally cancer.
H. pylori also carries specific toxins that directly damage the DNA of stomach lining cells and reduce those cells’ ability to repair the damage. This accelerates the accumulation of mutations. A large, long-term trial found that treating H. pylori infection with a 10-day course of antibiotics and acid-reducing medication cut gastric cancer risk by 13% overall. For people whose infection was fully eliminated, the reduction was 19%. The benefit was especially striking for people treated before age 45: those who successfully cleared the bacterium saw a 35% drop in gastric cancer incidence and a 43% reduction in death from it. For people 45 and older, the treatment did not significantly lower cancer risk, likely because decades of accumulated DNA damage had already set the stage.
Vaccines That Prevent Cancer
Because some cancers are triggered by infections, preventing those infections prevents the cancer. The HPV vaccine is the most dramatic example. CDC data tracking cervical precancers across the United States from 2008 to 2022 found that among screened women aged 20 to 24, the age group most likely to have been vaccinated, precancerous lesions dropped by 79%. The most serious precancers in that group fell by 80%. Among women aged 25 to 29, who had lower vaccination coverage, serious precancers still declined by 37%.
The hepatitis B vaccine works on the same principle, preventing the chronic liver infection that can lead to liver cancer. Both vaccines target the infection years or decades before any cancer would develop, which is why vaccination in childhood or adolescence is so effective.
Can You “Catch” Cancer From Someone?
You cannot catch cancer from another person through casual contact, kissing, sharing food, or breathing the same air. Cancer cells from one person almost always die immediately in another person’s body because the recipient’s immune system recognizes them as foreign and destroys them.
There are a few extraordinarily rare exceptions. About 26 cases have ever been documented of a mother’s cancer cells crossing the placenta and establishing themselves in her baby. That works out to roughly 1 in 500,000 pregnancies. Cancer has also been inadvertently transferred through organ transplants, where the recipient’s immune system is deliberately suppressed with medication to prevent organ rejection, creating a narrow window for transplanted cancer cells to survive.
In one notable case, melanoma cells from a patient were injected into her elderly mother as an experimental immune therapy. The mother died of disseminated melanoma 15 months later. These cases are tragedies, but they require either a suppressed immune system or direct cell-to-cell transfer, conditions that do not occur in everyday life.
Transmissible Cancers in Animals
Two animal species do have genuinely contagious cancers, and they help illustrate why this doesn’t happen in humans. Tasmanian devils spread a fatal facial tumor through biting. The cancer cells physically transfer from one animal to another and grow in the new host. This works because Tasmanian devils have extremely low genetic diversity. When researchers tested immune cells from 30 devils against each other, no immune response was triggered at all. Their immune systems simply cannot tell the difference between their own cells and another devil’s cells, including tumor cells.
Dogs have a sexually transmitted tumor that spreads during mating. This cancer lineage has been circulating for thousands of years. It survives by hiding its identity markers from the host’s immune system through extensive mutations in the genes responsible for displaying cell-surface tags.
Both cases depend on specific biological quirks: either a population with almost no immune diversity or a tumor that has evolved over millennia to evade detection. Human populations have far greater genetic diversity, and our immune systems are highly effective at recognizing and destroying foreign cells. A transmissible cancer in humans would have to overcome barriers that, outside of organ transplantation or placental transfer, have essentially never been breached.