A carcinoma is a cancer that starts in epithelial cells, the cells that line the surfaces of your body inside and out. This includes your skin, the lining of your digestive tract, the surfaces of your lungs, and the tissue covering your organs. Carcinomas are the most common category of cancer, and nearly every organ in the body has epithelial tissue that can give rise to one.
Where Carcinomas Start
Epithelial tissue acts as a barrier and lining throughout the body. It covers your skin, lines your mouth and throat, wraps around your intestines, and forms the inner surfaces of your bladder, kidneys, and lungs. Because this tissue is so widespread and its cells divide frequently to replace worn-out layers, it’s especially vulnerable to the DNA errors that lead to cancer.
What separates carcinomas from other cancers is this cell of origin. Sarcomas start in bone, muscle, or connective tissue. Lymphomas arise in the immune system. Leukemias begin in blood-forming tissue. Carcinomas specifically develop from the epithelial layer, which is why they show up in so many different organs and account for such a large share of cancer diagnoses.
Major Types of Carcinoma
Carcinomas are divided into subtypes based on which kind of epithelial cell they grow from. The most common are:
- Adenocarcinoma: Develops in glandular epithelial cells, the ones that produce mucus, digestive fluids, or other secretions. This is the most common form of cancer in the breast, prostate, colon, pancreas, and lungs.
- Squamous cell carcinoma: Originates in the flat, thin cells that make up the outer surface of the skin and line the throat, esophagus, and cervix. Squamous cells in the skin are constantly shed and replaced, and cancers can develop when that turnover process goes wrong.
- Basal cell carcinoma: Starts in the deeper layer of the skin’s outer surface, where new cells are produced before they move upward and flatten into squamous cells. Basal cell carcinoma is the most common skin cancer and tends to grow slowly with a very low risk of spreading to other parts of the body.
- Transitional cell (urothelial) carcinoma: Forms in transitional cells, a stretchy type of epithelial cell that lines the bladder, the tubes connecting the kidneys to the bladder (ureters), and the inner part of the kidneys called the renal pelvis. These cells expand and contract as the bladder fills and empties.
The subtype matters because it shapes how the cancer behaves, how quickly it grows, and which treatments work best against it.
In Situ vs. Invasive Carcinoma
Beneath every layer of epithelial cells sits a thin sheet of tissue called the basement membrane, which acts as a boundary between the surface lining and the deeper tissues underneath. When abnormal cells are confined above this membrane, the condition is called carcinoma in situ. The cells look cancerous under a microscope, but they haven’t broken through the barrier. Carcinoma in situ is highly treatable and, in most cases, curable.
Invasive carcinoma means the abnormal cells have breached the basement membrane and begun growing into surrounding tissue. Once past that boundary, the cancer gains access to blood vessels and lymphatic channels, which opens the possibility of spreading to other parts of the body. This distinction between in situ and invasive is one of the most important factors in determining prognosis and treatment approach.
How Carcinomas Spread
Most epithelial cancers first spread by entering the lymphatic system, the network of vessels and small filtering stations (lymph nodes) that normally helps your immune system patrol for infections. For a long time, researchers believed lymphatic vessels were just passive channels that cancer cells happened to drift through. More recent evidence paints a different picture: tumors actively reshape the lymphatic system around them.
Carcinomas release growth signals that cause nearby lymphatic vessels to expand and multiply, a process called lymphangiogenesis. This creates more routes for cancer cells to reach the nearest lymph nodes. The lymphatic vessels may even produce chemical signals that actively guide cancer cells toward lymph nodes, hijacking the same pathways immune cells normally use to travel. This is why doctors often check the nearest “sentinel” lymph node first when evaluating whether a carcinoma has begun to spread. If a large enough deposit of cancer develops inside a lymph node, it can block normal drainage and reroute flow toward other nodes, potentially widening the area of spread.
What Causes Carcinomas
Carcinomas develop when DNA changes accumulate in epithelial cells until those cells begin dividing without the normal checks. These genetic changes come from three main sources: random copying errors that happen every time a cell divides, environmental damage from carcinogens, and inherited mutations passed down from a parent.
The environmental category includes some well-known culprits. Chemicals in tobacco smoke, ultraviolet radiation from the sun, and infections like HPV all directly damage DNA in epithelial cells. Heavy metals such as cadmium and viruses like Epstein-Barr can also alter how genes are switched on and off without changing the DNA sequence itself, a process called epigenetic change.
Inherited genetic mutations account for up to 10% of all cancers. A person who inherits a mutated BRCA1 or BRCA2 gene, for example, faces a significantly higher risk of breast cancer and several other carcinomas. Inherited changes in the APC gene cause familial adenomatous polyposis, a condition that leads to hundreds of polyps in the colon and a very high lifetime risk of colorectal cancer. But the majority of carcinomas arise from a combination of random cell division errors and environmental exposures accumulated over a lifetime, which is why cancer risk increases with age.
How Carcinomas Are Diagnosed and Staged
A biopsy, where a small sample of tissue is removed and examined under a microscope, is the standard way to confirm a carcinoma. Pathologists use a technique called immunohistochemistry to identify specific proteins on the surface of tumor cells. One key protein, cytokeratin, is a reliable marker for epithelial origin and helps confirm the cancer is a carcinoma rather than a sarcoma or lymphoma. Other markers help pinpoint the exact type or guide treatment decisions. In breast cancer, for instance, testing for estrogen and progesterone receptors and a protein called HER2 determines which therapies are most likely to work.
Once a carcinoma is confirmed, it is staged using the TNM system, the most widely used framework for describing how far a cancer has progressed. The T score reflects the size and local extent of the primary tumor, from T1 (small, contained) through T4 (large or growing into nearby structures). The N score indicates whether cancer has reached nearby lymph nodes and how many are involved. The M score records whether the cancer has metastasized to distant parts of the body: M0 means it has not, M1 means it has. Together, these three values combine into an overall stage (typically I through IV) that guides treatment planning and gives a clearer picture of prognosis. Higher numbers in any category generally indicate more advanced disease.
Certain blood tests can also help monitor carcinomas over time. PSA levels are tracked in prostate cancer, CA-125 in ovarian cancer, and CEA in colorectal cancer. These markers are more useful for watching whether a treated cancer is coming back than for making an initial diagnosis.