Kaposi Sarcoma: Understanding Your Pathology Report

by Brian A Keller MD PhD and Bibianna Purgina MD FRCPC
April 10, 2026

Kaposi sarcoma is a type of cancer made up of abnormal blood vessel cells. It is classified as a sarcoma — a cancer that starts in the body’s connective tissues, which include blood vessels, fat, muscle, and fibrous tissue. Kaposi sarcoma most often appears as red, purple, or brown patches or nodules on the skin, but it can also develop inside the mouth and anywhere along the digestive tract, including the small intestine, colon, rectum, and anus. In some cases, it spreads to the lymph nodes and the lungs.

This article will help you understand the findings in your pathology report — what the terms mean and why each piece of information matters for your care.

What causes Kaposi sarcoma?

Kaposi sarcoma is caused by infection with a virus called human herpesvirus 8 (HHV-8), also known as Kaposi sarcoma-associated herpesvirus (KSHV). HHV-8 infects a type of cell that lines the inside of blood and lymphatic vessels, called an endothelial cell, and drives it to grow abnormally. However, most people infected with HHV-8 never develop Kaposi sarcoma. A weakened immune system plays a critical role — when immune function is reduced, the virus is more likely to cause cancer. This is why Kaposi sarcoma develops primarily in people with compromised immunity, whether from HIV infection, immunosuppressive medications, or advanced age.

What are the symptoms?

The most common symptom is the appearance of painless skin lesions — flat or raised patches, plaques, or nodules that are typically red, purple, or brown. These lesions most often develop on the legs, feet, or face, but they can appear anywhere on the body, including the genitals, mouth, and eyelids. Multiple lesions are common, and new ones may develop over time.

When Kaposi sarcoma involves the digestive tract, it may cause nausea, vomiting, abdominal pain, diarrhea, or bleeding from the gut. Lung involvement can cause shortness of breath, cough, or chest pain. Lymph node involvement may cause painless swelling under the skin. In some patients — particularly those with AIDS-related Kaposi sarcoma — the disease may cause significant swelling of the legs or face due to blockage of lymphatic drainage.

What are the types of Kaposi sarcoma?

There are four recognized types of Kaposi sarcoma. The type is based on the clinical setting in which it develops, and this affects how the disease behaves and how it is treated.

• Classic type — The most common type worldwide. It typically develops in older men of Mediterranean or Central and Eastern European ancestry. Most patients develop multiple red or purple lesions on the feet or lower legs. The tumors often grow slowly at first and many patients do not seek medical attention for months or years. Classic Kaposi sarcoma is associated with a mild degree of immune suppression related to aging, not HIV infection.
• Iatrogenic type — This type occurs in people whose immune system has been deliberately suppressed by medical treatment, most often immunosuppressive drugs taken after an organ transplant to prevent rejection, or chemotherapy for another cancer. Reducing or changing the immunosuppressive medication can sometimes cause the tumors to shrink or disappear — a response pathologists call regression.
• African (endemic) type — Found predominantly in equatorial Africa, this type occurs in both young children and middle-aged adults and is not related to HIV infection. It tends to grow more rapidly than classic Kaposi sarcoma and can spread quickly to lymph nodes and internal organs, making it aggressive and potentially fatal.
• AIDS-related (epidemic) type — The most aggressive type. It develops in people who are infected with both HIV and HHV-8. The severely weakened immune system caused by HIV allows HHV-8 to drive rapid tumor growth and spread, involving the skin, mouth, throat, digestive tract, lymph nodes, and lungs. Restoring immune function through antiretroviral therapy — medication that controls HIV — significantly improves outcomes and may cause tumors to regress without additional cancer treatment.

How is the diagnosis made?

The diagnosis is made after a tissue sample is examined under the microscope by a pathologist. The sample is usually obtained through a biopsy — a small piece of a suspicious skin lesion or internal tumor removed with a needle or scalpel. In some cases, a more complete surgical excision is performed to remove the visible tumor.

Under the microscope, Kaposi sarcoma has a characteristic appearance. The tumor is composed primarily of spindle cells — long, thin cells — arranged in intersecting bundles, a pattern pathologists describe as fascicular. These spindle cells form small, irregular, slit-like spaces that resemble abnormal blood vessels. As the tumor grows, these spaces merge into larger blood-filled channels, and red blood cells frequently leak into the surrounding tissue. Pathologists describe these escaped red blood cells as extravasated. Deposits of a dark pigment called hemosiderin — the breakdown product of red blood cells — are commonly seen scattered throughout the tumor. When the skin is involved, the tumor is almost always located in the dermis, the layer of tissue just beneath the skin surface.

To confirm the diagnosis and rule out other tumors that can look similar — particularly angiosarcoma — the pathologist uses a technique called immunohistochemistry (IHC). IHC uses antibodies to detect specific proteins inside cells, making particular cell types visible under the microscope. The most diagnostically important test is for HHV-8 LANA-1 (latency-associated nuclear antigen 1), a viral protein produced within infected tumor cells. Positive cells show a distinctive dotted brown staining pattern in their nuclei. A positive HHV-8 LANA-1 result, combined with the characteristic spindle cell appearance, establishes the diagnosis of Kaposi sarcoma. Pathologists also typically test for vascular markers — including CD31, CD34, and ERG — which confirm that the tumor cells are of blood-vessel origin, and D2-40, a marker of lymphatic endothelial cells, which supports the current understanding that Kaposi sarcoma arises from lymphatic rather than blood-vessel endothelium. Once the diagnosis is confirmed, imaging studies are used to determine the full extent of the disease, including whether internal organs or lymph nodes are involved.

Histologic grade

Most sarcomas are assigned a histologic grade using a standardized scoring system that reflects the tumor’s likely aggressiveness. Kaposi sarcoma is not graded using these standard sarcoma grading systems. All forms of Kaposi sarcoma are considered malignant (cancerous), but the clinical behavior — how aggressive the disease is and how quickly it progresses — depends primarily on the type of Kaposi sarcoma and the patient’s immune status, not on microscopic grading. Your pathology report will therefore not include a tumor grade, and this is expected and normal for this diagnosis.

Lymphovascular invasion

Because Kaposi sarcoma arises from cells that line blood and lymphatic vessels, the tumor cells are by definition present within vascular spaces. For this reason, lymphovascular invasion — tumor cells found inside lymphatic channels or blood vessels — is an inherent feature of Kaposi sarcoma rather than a finding that is separately assessed and reported as it is for most other cancers. What your pathologist may describe instead is the extent to which the tumor involves the surrounding tissue and how widespread the lesions are within the specimen.

Surgical margins

A margin is the edge of the tissue removed during surgery. The pathologist examines the cut surfaces of the specimen to determine whether tumor cells are present at the edge.

• Negative margin — No tumor cells are present at the cut edge. This suggests the tumor was completely removed in that area.
• Positive margin — Tumor cells are present at the cut edge, raising concern that some tumor remains in the body. This increases the risk of the tumor growing back at the same location after surgery, which is called local recurrence.

It is important to note that for Kaposi sarcoma, margin status is most relevant when a single lesion has been surgically excised. Many patients have multiple simultaneous lesions, and Kaposi sarcoma is typically managed as a systemic disease rather than by surgical excision of each individual lesion. In these situations, margin status may be less central to treatment planning, and your oncologist will consider it alongside the overall extent of disease.

Lymph nodes

Lymph nodes are small immune organs found throughout the body. Kaposi sarcoma can spread to lymph nodes, particularly in patients with African (endemic) Kaposi sarcoma and AIDS-related Kaposi sarcoma. When lymph nodes are removed during surgery or sampled by biopsy, the pathologist examines them under the microscope to determine whether tumor cells are present.

Your report will state the total number of lymph nodes examined and whether any contain Kaposi sarcoma. Lymph node involvement indicates that the cancer has spread beyond its starting point and is used as part of staging in AIDS-related Kaposi sarcoma (see Staging section below). When Kaposi sarcoma is found in a lymph node, the report may describe the extent of involvement within the node.

Biomarker and molecular testing

For most patients with Kaposi sarcoma, the pathology report does not include biomarker tests that guide treatment decisions in the way they do for cancers such as breast or colorectal cancer. The diagnosis is established by the microscopic appearance and HHV-8 immunohistochemistry (described above under “How is the diagnosis made?”), and treatment is driven primarily by the type of Kaposi sarcoma and the patient’s immune status rather than by tumor molecular markers.

In patients with advanced or treatment-refractory disease, oncologists may consider immunotherapy with checkpoint inhibitor drugs in selected cases, though this is not yet a standard approach for Kaposi sarcoma. Research into molecular targets in HHV-8-driven disease is ongoing. For more information about biomarker testing in cancer, visit our Biomarkers and Molecular Testing section.

Pathologic stage

Unlike most other cancers, Kaposi sarcoma is not routinely staged using the AJCC TNM system that assigns pT, pN, and pM categories based on tumor size, lymph node spread, and distant metastasis. This is because Kaposi sarcoma almost always presents as multiple simultaneous lesions and because its behavior is so strongly linked to immune status, which TNM staging does not capture.

For AIDS-related Kaposi sarcoma, the most widely used staging system is the ACTG (AIDS Clinical Trials Group) staging system, which was developed specifically for this context. It assigns patients to a good-risk or poor-risk category based on three independent factors:

• Tumor extent (T) —
  • Good risk (T0) — Kaposi sarcoma is confined to the skin and/or lymph nodes, and/or there is only minimal involvement of the mouth.
  • Poor risk (T1) — Tumor-associated swelling (edema) is present, or there is involvement of the mouth beyond the palate, or the tumor involves the digestive tract or internal organs.
• Immune status (I) —
  • Good risk (I0) — CD4+ T-cell count is 150 cells/mm³ or higher. CD4+ T cells are the immune cells targeted by HIV; higher counts indicate better immune function.
  • Poor risk (I1) — CD4+ T-cell count is below 150 cells/mm³, indicating more severe immune suppression.
• Systemic illness (S) —
  • Good risk (S0) — No HIV-related symptoms (fever, night sweats, weight loss) and no history of opportunistic infections.
  • Poor risk (S1) — Presence of systemic symptoms or a prior history of opportunistic infections.

For the other types of Kaposi sarcoma (classic, iatrogenic, and African), formal staging systems are not standardized, and the extent of disease is described clinically based on the number and distribution of lesions, lymph node involvement, and presence of internal organ disease.

What is the prognosis for Kaposi sarcoma?

The prognosis varies widely depending on the type of Kaposi sarcoma and the patient’s overall immune status.

Classic Kaposi sarcoma typically follows an indolent (slow) course. Most patients live for many years with well-controlled skin disease, and the majority die of unrelated causes rather than Kaposi sarcoma itself. Occasional patients develop more aggressive disease with visceral involvement.

Iatrogenic Kaposi sarcoma often improves substantially — and may resolve completely — when immunosuppressive treatment is reduced or changed. The prognosis is generally favorable if immune function can be restored.

African (endemic) Kaposi sarcoma has a more variable prognosis. The predominantly skin-limited form in adults is often indolent, while the form that affects children and young adults and involves lymph nodes and internal organs is considerably more aggressive and potentially fatal.

AIDS-related Kaposi sarcoma has improved dramatically since the introduction of combination antiretroviral therapy (cART), which controls HIV and allows immune function to recover. In many patients, cART alone causes Kaposi sarcoma lesions to regress. Patients with good-risk disease (T0, I0, S0) by ACTG staging have an excellent prognosis with modern treatment. Poor-risk patients — particularly those with extensive internal disease or severely depleted CD4+ counts — have a more guarded outlook, though outcomes continue to improve as HIV treatment advances.

Important factors affecting prognosis in all types include the extent of tumor spread (skin only vs. lymph node or visceral involvement), the number and distribution of lesions, and the degree of immune suppression. In AIDS-related Kaposi sarcoma, the CD4+ T-cell count and HIV viral load are among the most important prognostic determinants.

What happens after the diagnosis?

Treatment depends on the type of Kaposi sarcoma, the number of lesions, whether internal organs are involved, and the patient’s immune status. No single treatment approach is used for all patients.

For AIDS-related Kaposi sarcoma, starting or optimizing antiretroviral therapy (cART) is almost always the first step. Restoring immune function frequently causes lesions to regress without additional cancer treatment. Patients with limited skin disease may also be treated with local therapies, including radiation therapy, intralesional chemotherapy injections, or topical agents. For patients with extensive skin disease, multiple internal lesions, or rapidly progressing disease, systemic chemotherapy — most commonly with liposomal doxorubicin or paclitaxel — is recommended. Immunotherapy with checkpoint inhibitors is an emerging area of interest, though not yet standard practice for Kaposi sarcoma.

For iatrogenic Kaposi sarcoma, reducing immunosuppression is often the first treatment and may be curative in transplant patients.

For classic Kaposi sarcoma with limited skin lesions, local treatments such as radiation or surgical removal may be used. More widespread or symptomatic disease is treated with systemic chemotherapy.

After treatment, regular follow-up is important to monitor for new lesions, assess treatment response, and manage any complications. In patients with AIDS-related Kaposi sarcoma, ongoing HIV management with regular monitoring of CD4+ counts and viral load is central to long-term care.

Questions to ask your doctor

Your pathology report contains important information that will guide your care. The following questions may help you prepare for your next appointment.

• What type of Kaposi sarcoma do I have — classic, iatrogenic, African, or AIDS-related?
• Was the HHV-8 test positive, confirming the diagnosis?
• Was the tumor removed with a negative margin, or were tumor cells present at the edge of the specimen?
• Were any lymph nodes sampled, and if so, did any contain Kaposi sarcoma?
• Is there evidence of internal organ involvement — for example, in the digestive tract or lungs?
• How many lesions do I have, and are they confined to the skin or more widespread?
• If I have AIDS-related Kaposi sarcoma, what is my ACTG stage, and what does that mean for treatment?
• Should I start or adjust antiretroviral therapy as part of managing my Kaposi sarcoma?
• What treatment do you recommend — local therapy, systemic chemotherapy, or both?
• Is this type of Kaposi sarcoma likely to go away on its own if my immune function improves?
• What follow-up tests and appointments will I need, and how often?
• Are there any clinical trials available for my type of Kaposi sarcoma?