When Did Skin Cancer Start? A Look at Its History

Skin cancer is far older than modern medicine, older than written history, and almost certainly older than our species. The earliest physical evidence of metastatic cancer in a human skeleton dates to roughly 1200 BC, found in a young man from ancient Nubia in what is now northern Sudan. But the biological vulnerability that makes skin cancer possible goes back millions of years, to the period when early humans lost most of their body hair and became exposed to ultraviolet radiation in ways no other primate had been. The story of skin cancer is really the story of human skin itself, and how sunlight shaped us from the beginning.

The Archaeological Record

Finding evidence of cancer in ancient remains is surprisingly difficult. Soft tissue rarely survives, and most cancers start in organs that decompose long before anyone digs up the bones. What researchers look for instead are signs that cancer spread to the skeleton. In 2014, a team studying remains from the archaeological site of Amara West in northern Sudan described a young adult male whose bones were riddled with destructive lesions across his vertebrae, ribs, sternum, pelvis, and the heads of his upper arm and thigh bones. After radiographic and microscopic imaging, they concluded this was metastatic carcinoma, meaning cancer that had started in soft tissue and spread widely through his body.¹ The specific type of soft-tissue cancer that killed him remains unknown, but the case demonstrates that cancer, including the kind that might originate in the skin, was present in human populations thousands of years ago.

The ancient Greeks gave cancer its lasting name. Hippocrates, writing in the fifth and fourth centuries BC, described various abnormal growths including what he called “karkinos” (crab) and “karkinoma,” terms that survive today as “cancer” and “carcinoma.” He distinguished between superficial and deep-seated cancers, ulcerated and hidden ones, and tried to categorize them based on their behavior.² Whether any of the growths Hippocrates observed were specifically skin cancers is impossible to say, but his terminology laid the groundwork for later physicians who would eventually make that distinction.

Why Humans Were Vulnerable from the Start

To understand why skin cancer has plagued humans since the beginning, you have to look at what makes human skin unusual. Most mammals are covered in fur, which blocks UV radiation before it reaches the skin. Early in the history of our genus, probably around two million years ago, our ancestors lost most of their body hair. The leading explanation is thermoregulation: hairless skin allowed more efficient sweating during long-distance movement in hot African environments. But losing that protective covering created a serious problem. Naked skin is directly exposed to the DNA-damaging effects of ultraviolet radiation.³

The evolutionary solution was melanin. Dark, eumelanin-rich pigmentation evolved in our African ancestors as a biological sunscreen, absorbing and scattering UV rays before they could cause widespread DNA damage. This was not a single mutation but a gradual process involving many genes. As human populations later migrated to higher latitudes with less intense sunlight, a competing pressure emerged: the body needs UV exposure to produce vitamin D. The result was a trade-off. Populations in lower-UV environments evolved lighter skin to allow more vitamin D synthesis, at the cost of reduced protection against UV damage.⁴ That trade-off is a big part of why skin cancer rates vary so dramatically by geography and ancestry today.

The DNA damage itself happens in a specific way. When UV light hits skin cells, it causes chemical bonds to form between adjacent building blocks in the DNA strand, creating structures called pyrimidine dimers. Cells have repair machinery to fix these errors, but the system is imperfect. When a dimer slips through unrepaired, it can lead to permanent mutations, and enough of the right mutations in the right genes can start a cancer.⁵ People born with defects in their DNA repair pathways, such as those with the rare genetic condition xeroderma pigmentosum, develop skin cancers at dramatically elevated rates, sometimes beginning in childhood.⁶ Their experience is a stark illustration of what UV does to unprotected skin over time.

The First Clinical Descriptions

Physicians observed skin tumors for centuries without understanding their cause, but a few landmark descriptions stand out. In the early nineteenth century, the French physician René Laennec, better known for inventing the stethoscope, published what is considered the first description of metastatic melanoma. He called it “melanosis,” noting the characteristic dark pigmentation of the tumors.⁷ Before Laennec, dark tumors had certainly been seen, but his clinical account gave melanoma its first formal identity in Western medicine.

An even earlier breakthrough came from a completely different type of skin cancer. In the late eighteenth century, the English surgeon Percivall Pott noticed an alarming pattern: chimney sweeps were developing destructive tumors on the skin of their scrotums. Other physicians had been diagnosing these lesions as venereal disease, but Pott recognized that the cause was occupational. Soot from chimneys became trapped in the folds of scrotal skin, and over years of exposure, it triggered cancers that often spread and killed the patient.⁸ Pott’s observation is widely regarded as the first identification of an occupational cancer, and it established a crucial principle: that prolonged exposure to certain environmental agents could cause cancer. The leap from soot to sunlight as a carcinogen would take another century, but Pott laid the conceptual groundwork.

When Skin Cancer Became an Epidemic

For most of human history, skin cancer existed but probably at relatively low rates in most populations. People who lived and worked outdoors certainly accumulated UV damage, but the massive surge in skin cancer incidence is a distinctly modern phenomenon, driven largely by cultural shifts in the twentieth century. Researchers who analyzed artwork, advertisements, and fashion trends over the past century found that the amount of skin people routinely exposed to the sun increased dramatically, driven by changing clothing styles, the rise of outdoor leisure, and the cultural embrace of the suntan as a sign of health and attractiveness. When they compared these trends to data from national cancer registries, melanoma incidence rose in parallel.⁹

Before the 1920s, pale skin was the beauty standard in Western countries, associated with wealth and indoor living. Tanned skin signaled manual labor. That flipped remarkably quickly. By mid-century, a tan was aspirational, beach culture was booming, and swimwear was shrinking. The consequences showed up in cancer registries a few decades later, since skin cancer typically develops years or decades after the UV exposure that triggers it. The epidemic was essentially manufactured by fashion.

Ozone Depletion Added Another Layer

On top of behavioral changes, the atmosphere itself changed. Industrial chemicals called ozone-depleting substances, particularly chlorofluorocarbons used in refrigerants and aerosols, began thinning the stratospheric ozone layer that filters out the most damaging wavelengths of UV radiation. Surface UV levels rose, peaking in the 1990s before international action began to reverse the trend. The estimated health toll of this atmospheric damage is staggering: the U.S. Environmental Protection Agency modeled that without the Montreal Protocol, the 1987 treaty that phased out these chemicals, roughly 443 million additional skin cancer cases and about 2.3 million additional skin cancer deaths would occur among people born in the United States between 1890 and 2100.¹⁰

A more recent study comparing effects in Australia and the United States found that the health impacts of ozone-depleting substances peaked several decades after UV levels did, with estimated increases of around 1% for melanoma incidence and 5% for non-melanoma skin cancer incidence relative to 1980 levels.¹¹ The ozone layer is recovering, but the lag between exposure and cancer development means the consequences of twentieth-century atmospheric damage are still playing out.

Sunscreen and Public Health Campaigns

The history of actually fighting back against skin cancer is shorter than you might expect. Evidence-based sunscreens are a twentieth-century invention. The first UVB filters were produced in 1928, but proof that they worked and a standardized way to measure protection did not come until decades later: efficacy and safety evidence arrived in 1956, the Sun Protection Factor (SPF) system was developed in 1974, and UVA-filtering sunscreens followed in 1980.¹² For most of the century when tanning culture was exploding, people had little or no reliable sun protection available.

Public awareness campaigns came even later. Australia, which has some of the highest skin cancer rates in the world due to its high-UV environment and largely fair-skinned population, launched its famous “Slip! Slop! Slap!” campaign in the summer of 1980-81, urging people to slip on a shirt, slop on sunscreen, and slap on a hat. The campaign and its successors played a measurable role in changing Australian attitudes toward sun exposure, and melanoma rates have since declined in younger age groups.¹³¹⁴ That decline among younger Australians is one of the clearest success stories in cancer prevention, though older age groups, whose sun damage accumulated before the campaign, continue to bear a heavy burden.

The Genetics of Familial Skin Cancer

Not all skin cancer is about sun exposure. About 10% of melanomas occur in families where multiple members are affected, and the search for the genes behind this clustering has been one of the major genetic detective stories of the past few decades. In 1994, researchers identified CDKN2A as the first high-penetrance familial melanoma susceptibility gene, and CDK4 followed two years later.¹⁵ CDKN2A mutations have since been found in roughly 20% to 40% of melanoma families and are associated with multiple melanomas in the same person, early onset, and an elevated risk of pancreatic cancer.¹⁶

Familial predisposition is often associated with having many atypical moles, a condition sometimes called dysplastic nevus syndrome. Genetic analyses have mapped melanoma susceptibility to several chromosomal regions, with the 9p21 region where CDKN2A sits being the most consistently implicated.¹⁷ Additional rare susceptibility genes, including BAP1, TERT, and POT1, account for another estimated 10% of familial clustering.¹⁶ For the remaining families with clustering but no identified mutation, the genetic picture is still being worked out, likely involving combinations of common lower-risk variants rather than single dramatic mutations.

Skin Cancer Is Not Just a Human Problem

One of the more surprising chapters in skin cancer history came from coral reefs. Researchers studying coral trout on the Great Barrier Reef found that roughly 15% of fish sampled at two southern reef locations had dark skin lesions. After histological examination, the growths were identified as melanomas, making coral trout the first wild fish population known to develop the disease. The researchers noted that the lesions closely resembled UV-induced melanomas seen in laboratory fish, and they found no evidence of an infectious cause.¹⁸

Laboratory fish have actually been central to melanoma research for almost a century. Genetic crosses between platyfish and swordtails, two species of the genus Xiphophorus, have been used to study melanoma formation since the 1920s.¹⁹ When these species hybridize, certain offspring develop melanomas due to incompatible genetic combinations. More recent work has mapped specific genes driving this incompatibility and found that some of the same genes cause melanoma in hybrids between even more distantly related fish species.²⁰ The fish models demonstrate that melanoma has deep biological roots that predate anything uniquely human. The fundamental vulnerability of pigment-producing cells to becoming cancerous is shared across vertebrates.

How Diagnosis and Treatment Evolved

For centuries, the only option for a suspicious skin growth was crude surgical removal or cauterization. Modern approaches began taking shape in the early twentieth century with the introduction of radiation therapy for skin lesions. The field of superficial radiation therapy experienced a burst of innovation in its early decades and became a mainstay of dermatological treatment, though its prominence faded later in the century as surgical methods improved and radiation equipment aged. Newer technology has revived interest in radiation as a nonsurgical option for non-melanoma skin cancers.²¹

The most significant surgical advance came in the 1930s, when Dr. Frederic Mohs developed a technique he called chemosurgery. It involved applying zinc chloride paste to tissue and then removing and examining it layer by layer, checking each slice under a microscope for remaining cancer cells. The technique achieved high cure rates but could take days to complete. Over time, it was refined into the fresh-tissue technique now known as Mohs micrographic surgery, which remains the gold standard for treating certain skin cancers because it removes the least healthy tissue while verifying clear margins.²²

Diagnosis also underwent its own revolution. The concept of using magnification to examine skin lesions dates back further than most people realize. The origins of dermoscopy trace to the mid-seventeenth century, but the technique became clinically important for melanoma detection through the work of Dr. Ronald Mackie in 1971, who demonstrated its value in catching melanomas early, when they are most treatable. Modern digital dermoscopy and, more recently, artificial intelligence-assisted analysis have built on that foundation, but the basic idea of looking at a mole under magnification before deciding whether to biopsy it goes back centuries.