Breast cancer starts when cells in the breast tissue develop changes in their DNA and begin growing out of control. About 13% of women will be diagnosed with breast cancer at some point in their lifetime, and the majority of cases aren’t inherited. They result from genetic damage that accumulates in breast cells over the course of a person’s life.
Where It Starts in the Breast
The breast contains two main structures where cancer typically originates: the ducts and the lobules. Ducts are tiny tubes that carry milk toward the nipple. Lobules are the small glands that actually produce the milk. The most common form, invasive ductal carcinoma, begins in the cells lining the milk ducts. Invasive lobular carcinoma starts in the lobules and makes up a smaller portion of cases.
In both types, the process begins the same way. A cell in one of these structures develops DNA changes that override the normal signals telling it when to grow and when to stop. That cell divides, producing more abnormal cells, which eventually form a mass. Early on, the abnormal cells may stay contained within the duct or lobule (called “in situ”), but over time they can break through the walls of that structure and spread into surrounding breast tissue, becoming invasive.
How Cells Become Cancerous
Most breast cancers are sporadic, meaning they aren’t caused by an inherited gene passed down from a parent. Instead, cells accumulate mutations over an individual’s lifetime in a process that resembles evolution at the cellular level. Every time a cell divides, there’s a small chance of a copying error in its DNA. Most of these errors are harmless or get repaired. But occasionally a mutation lands in a gene that controls cell growth, cell death, or DNA repair, and the cell gains a survival advantage over its neighbors.
This is why age is one of the biggest risk factors. The median age at diagnosis is 63, and more than half of all new cases occur in women 55 and older. The longer cells divide, the more chances there are for these errors to stack up. Only about 2% of cases are diagnosed before age 35.
Beyond direct DNA mutations, breast cancer also involves epigenetic changes. These are modifications that don’t alter the DNA sequence itself but change how genes are read. One well-studied mechanism is DNA methylation, where chemical tags attach to certain regions of a gene’s promoter and effectively silence it. In breast cancer, this silencing hits tumor suppressor genes, DNA repair genes (including BRCA1), and genes that regulate the cell cycle and programmed cell death. When these protective genes go quiet, cells lose critical safeguards against uncontrolled growth.
The Role of Estrogen
Estrogen is not a carcinogen in the traditional sense, but it acts as a powerful growth signal for breast tissue. When estrogen binds to its receptor inside a breast cell, the receptor changes shape, enters the cell’s nucleus, and switches on hundreds of genes involved in cell growth and division. Some of these genes have direct cancer-promoting potential, driving cells to multiply faster and increasing the window of opportunity for DNA damage.
This is why anything that increases a person’s lifetime exposure to estrogen raises breast cancer risk. Starting menstruation early, going through menopause late, never having a full-term pregnancy, and having a first pregnancy after age 30 all extend the total years of estrogen cycling. Hormone replacement therapy that combines estrogen and progesterone, when taken for more than five years during menopause, also raises risk. About two-thirds of breast cancers are “hormone receptor positive,” meaning they have estrogen receptors and rely on estrogen signaling to fuel their growth.
Inherited Genetic Risk
A family history of breast cancer is present in roughly 10 to 20% of patients, but inherited gene mutations account for a smaller fraction than most people assume. The two most well-known genes are BRCA1 and BRCA2, which normally function as tumor suppressors involved in repairing damaged DNA. When someone inherits a harmful variant in either gene, their cells are less able to fix double-stranded DNA breaks, and mutations accumulate more readily.
Women who carry a harmful BRCA1 or BRCA2 change have a lifetime breast cancer risk exceeding 60%, compared to 13% in the general population. These mutations also affect men, though far less commonly. About 10% of male breast cancer cases involve a BRCA2 variant, and the lifetime risk for male carriers is roughly 5 to 10%, compared to 0.1% for men overall. Other genes linked to increased risk include PALB2, CHEK2, and ATM, each of which also plays a role in DNA repair. A CHEK2 variant, for example, roughly doubles the risk in women but increases it tenfold in men.
Lifestyle and Environmental Factors
For the majority of breast cancers that aren’t driven by inherited mutations, lifestyle and environmental exposures play a measurable role. Alcohol is one of the most consistent risk factors: risk increases with the amount consumed, with no clearly safe threshold. Physical inactivity and carrying excess weight after menopause both raise risk as well, partly because fat tissue produces estrogen, adding to the hormonal exposure discussed above.
Smoking, exposure to certain cancer-causing chemicals, and working night shifts (which disrupts hormones tied to the body’s internal clock) are also linked to increased risk, though the evidence is less definitive than for alcohol and obesity. Some oral contraceptives have been associated with a modest increase in risk, though this tends to fade after stopping them.
Breast Cancer in Men
Men have a small amount of breast tissue, and cancer can develop in it through similar mechanisms. Male breast cancer is rare, accounting for less than 1% of all breast cancer diagnoses, but it is now recognized as molecularly distinct from female breast cancer. Genetic predisposition plays a proportionally larger role. In high-risk families, BRCA2 variants are responsible for 60 to 70% of male cases, a much higher share than in women. Unlike female breast cancer, where BRCA1 and BRCA2 contribute roughly equally, BRCA2 is far more frequently altered in men.
How Screening Catches It Early
Because breast cancer develops silently over years before producing symptoms, screening mammography is the primary tool for catching it at an earlier, more treatable stage. Current recommendations from the U.S. Preventive Services Task Force call for mammography every two years for women ages 40 to 74. Biennial screening offers a favorable balance of catching cancers early while reducing unnecessary follow-up tests and false alarms compared to annual screening. For women 75 and older, there isn’t enough evidence yet to make a firm recommendation either way, so the decision is more individual.
For people with known BRCA mutations or strong family histories, screening often starts earlier and may include breast MRI in addition to mammography. The specific plan depends on the level of genetic risk involved.