Hemangiomas are clumps of extra blood vessels that form in the skin, liver, or other organs, and their exact cause depends on the type. The common thread is abnormal growth of the cells lining blood vessels, but what triggers that growth varies. Infantile hemangiomas, liver hemangiomas, and cherry angiomas each have distinct risk factors and biological drivers.
How Infantile Hemangiomas Form
Infantile hemangiomas are the most common tumors of infancy, and they appear to start with a problem of oxygen supply. When tissue doesn’t get enough oxygen, cells activate a survival response. A protein called HIF-1α ramps up, and it triggers the release of signals that recruit new blood vessels to the area. In babies with proliferating hemangiomas, nearly 96% of cells in the tumor show elevated HIF-1α activity, compared to just 15% in hemangiomas that have already started shrinking. The blood of children with active hemangiomas also carries roughly five times the normal level of a key blood vessel growth signal (VEGF-A), flooding the area with instructions to build more vessels.
This cascade of vessel-building signals causes the cluster of blood vessels to grow rapidly during the first 12 months of life, a stage called proliferation. After that, the growth slows and the hemangioma begins to shrink on its own. About half of children see their hemangioma fully resolve by age 5, and roughly 9 out of 10 are done shrinking by age 9.
Risk Factors for Infantile Hemangiomas
Several factors make a baby more likely to develop a hemangioma. Low birth weight is the strongest predictor: for every 500-gram drop in birth weight (roughly one pound), the risk of developing a hemangioma rises by about 40%. Premature birth amplifies the risk dramatically. One cross-sectional study found that a deeper type of hemangioma appeared in 1.13% of preterm newborns versus 0.0001% of full-term babies.
Girls are affected about twice as often as boys. In one large study, 65% of infants with hemangiomas were female, a ratio that has fueled research into hormonal causes. Caucasian infants, babies from multiple pregnancies, and those with a family history of hemangiomas also face higher odds. Interestingly, maternal age and race have not consistently shown up as independent risk factors once other variables are controlled for.
The Role of Estrogen
The strong female skew in infantile hemangiomas points toward estrogen as a growth promoter. Tissue samples from hemangiomas show higher levels of estrogen receptors, and lab studies have demonstrated that 17β-estradiol (the body’s primary form of estrogen) binds to stem cells within the tumor and boosts the production of blood vessel growth signals. Estrogen also adjusts the balance of other factors that either encourage or suppress vessel formation, which may explain why the tumor behaves differently during its growth and shrinking phases.
This hormonal connection extends beyond infancy. Liver hemangiomas in adults grow larger during pregnancy, when estrogen levels surge. Women who use hormone replacement therapy after menopause are also more likely to develop liver hemangiomas than women who don’t, reinforcing the link between estrogen exposure and hemangioma growth throughout life.
Genetic Mutations Behind Hemangiomas
Hemangiomas are not inherited in a simple parent-to-child pattern. Instead, they involve somatic mutations, meaning genetic changes that happen randomly in a small group of cells after conception. The type of mutation depends on the type of hemangioma.
In congenital hemangiomas (the less common type present at birth), researchers have identified mutations in two genes, GNAQ and GNA11, that lock a growth signaling pathway into the “on” position. These mutations affect a single amino acid and are found exclusively within the blood vessel clusters of the tumor, not in the surrounding tissue. When scientists used laser dissection to isolate the vascular portion of a congenital hemangioma, the mutant cells made up about 13% of that region, while the tissue around it carried less than 2%. The same mutations appear in certain eye cancers, suggesting they are powerful drivers of cell growth when they occur in the right tissue at the right time.
For infantile hemangiomas, research has found frequent loss of genetic material on chromosome 5q. Scientists believe this region normally contains a gene that acts as a brake on blood vessel growth. When that brake is lost through a random deletion, the cells grow unchecked.
What Causes Liver Hemangiomas
Liver hemangiomas are thought to be present from birth, though they’re often discovered incidentally during imaging for something else. The precise trigger for their formation is unknown, but hormonal exposure is the clearest risk factor. Women who have been pregnant at least once are more likely to have them than women who have never been pregnant, and those on hormone replacement therapy face elevated risk as well. Existing liver hemangiomas can grow larger during pregnancy as estrogen levels climb, which is one reason they’re sometimes monitored more closely in pregnant women.
Most liver hemangiomas are small, cause no symptoms, and require no treatment. They are not cancerous and do not become cancerous.
What Causes Cherry Angiomas
Cherry angiomas are the small, bright red dots that commonly appear on the torso and limbs in adulthood. They are the most common type of hemangioma in adults and are essentially a normal part of aging. Their frequency increases steadily after age 30, and most people over 70 have at least a few.
Beyond aging, pregnancy hormones and genetic mutations can contribute to their appearance. Exposure to certain industrial chemicals, including bromides and butoxyethanol (a solvent found in some cleaning products), has also been linked to new cherry angiomas. Avoiding known chemical triggers is the only established way to reduce your chances of developing them, though for most people they simply show up with time and pose no health risk.
Why Oxygen Deprivation Matters
Across hemangioma types, the theme of oxygen deprivation and compensatory blood vessel growth keeps recurring. When cells sense low oxygen, they activate a repair program designed to bring in more blood supply. In a hemangioma, that program overshoots. The combination of genetic susceptibility (whether from somatic mutations or inherited traits), hormonal exposure, and local tissue conditions determines whether this overshoot happens, where it happens, and how large it gets. Premature and low-birth-weight babies may be especially vulnerable because their tissues experience more oxygen stress during and after delivery, creating fertile ground for that cascade to begin.