Kaposi Sarcoma Treatment (PDQ®)–Health Professional Version

Epidemiology

Kaposi sarcoma (KS) was first described in 1872 by the Hungarian dermatologist, Moritz Kaposi. From that time until the HIV disease epidemic identified with AIDS, KS remained a rare tumor. While most of the cases seen in Europe and North America have occurred in elderly men of Italian or Eastern European Jewish ancestry, the neoplasm may also occur in patients receiving immunosuppressive therapy.[1] The disseminated, fulminant form of KS associated with HIV disease is referred to as epidemic KS to distinguish it from the classic and transplant-related varieties of the neoplasm.[2]

Histopathology

Although the histopathology of the different types of the Kaposi tumor is essentially identical in all of these groups, the clinical manifestations and course of the disease differ dramatically.[2] Human herpes virus type 8 , also known as Kaposi sarcoma herpes virus, was identified in KS tissue biopsies from virtually all patients with classic, transplant-related, and AIDS-associated KS but was absent from noninvolved tissue.[2]

Classic Kaposi Sarcoma

Considered a rare disease, classic KS occurs more often in men, with a ratio of approximately 10 to 15 men to 1 woman. In North Americans and Europeans, the usual age at onset is between 50 and 70 years. Classic KS tumors usually present with one or more asymptomatic red, purple, or brown patches, plaques, or nodular skin lesions. The disease is often limited to single or multiple lesions usually localized to one or both lower extremities, especially involving the ankles and soles.

Classic KS most commonly runs a relatively benign, indolent course for 10 to 15 years or more, with slow enlargement of the original tumors and the gradual development of additional lesions. Venous stasis and lymphedema of the involved lower extremity are frequent complications. In long-standing cases, systemic lesions can develop along the gastrointestinal tract, in lymph nodes, and in other organs. The visceral lesions are generally asymptomatic and are most often discovered only at autopsy, though clinically, gastrointestinal bleeding can occur. As many as 33% of patients with classic KS develop a second primary malignancy, which is most often non-Hodgkin lymphoma.[3]

Epidemic Kaposi Sarcoma (HIV-Associated Kaposi Sarcoma)

Highly active antiretroviral therapy (HAART) has delayed or prevented the emergence of drug-resistant HIV strains, profoundly decreased viral load, led to increased survival, and lessened the risk of opportunistic infections.[4] The use of HAART has been associated with a sustained and substantial decline in KS incidence in multiple large cohorts.[5-7] KS can still appear during HAART with complete suppression of HIV; most cases in the United States occur in patients with high CD4 counts and ongoing HAART.[8]

The lesions that develop may involve the skin; oral mucosa; lymph nodes; and visceral organs, such as the gastrointestinal tract, lung, liver, and spleen. Most patients with HIV disease who present with the mucocutaneous lesions of KS feel healthy and are usually free of systemic symptoms, as compared with HIV patients who first develop an opportunistic infection. The sites of disease at presentation of epidemic KS are much more varied than the sites seen in other types of this neoplasm. While most patients present with skin disease, KS involvement of lymph nodes or the gastrointestinal tract may occasionally precede the appearance of the cutaneous lesions. The disease often progresses in an orderly fashion from a few localized or widespread mucocutaneous lesions to more numerous lesions and generalized skin disease with lymph node, gastrointestinal tract, and other organ involvement. Pleuropulmonary KS is an ominous sign usually occurring late in the course of the disease, especially in patients whose death is directly attributed to KS.

References

1. Ruocco E, Ruocco V, Tornesello ML, et al.: Kaposi's sarcoma: etiology and pathogenesis, inducing factors, causal associations, and treatments: facts and controversies. Clin Dermatol 31 (4): 413-422, 2013 Jul-Aug. [PUBMED Abstract]
2. Uldrick TS, Whitby D: Update on KSHV epidemiology, Kaposi Sarcoma pathogenesis, and treatment of Kaposi Sarcoma. Cancer Lett 305 (2): 150-62, 2011. [PUBMED Abstract]
3. Safai B, Good RA: Kaposi's sarcoma: a review and recent developments. Clin Bull 10 (2): 62-9, 1980. [PUBMED Abstract]
4. Lodi S, Guiguet M, Costagliola D, et al.: Kaposi sarcoma incidence and survival among HIV-infected homosexual men after HIV seroconversion. J Natl Cancer Inst 102 (11): 784-92, 2010. [PUBMED Abstract]
5. Portsmouth S, Stebbing J, Gill J, et al.: A comparison of regimens based on non-nucleoside reverse transcriptase inhibitors or protease inhibitors in preventing Kaposi's sarcoma. AIDS 17 (11): F17-22, 2003. [PUBMED Abstract]
6. Carrieri MP, Pradier C, Piselli P, et al.: Reduced incidence of Kaposi's sarcoma and of systemic non-hodgkin's lymphoma in HIV-infected individuals treated with highly active antiretroviral therapy. Int J Cancer 103 (1): 142-4, 2003. [PUBMED Abstract]
7. Grabar S, Abraham B, Mahamat A, et al.: Differential impact of combination antiretroviral therapy in preventing Kaposi's sarcoma with and without visceral involvement. J Clin Oncol 24 (21): 3408-14, 2006. [PUBMED Abstract]
8. Yanik EL, Achenbach CJ, Gopal S, et al.: Changes in Clinical Context for Kaposi's Sarcoma and Non-Hodgkin Lymphoma Among People With HIV Infection in the United States. J Clin Oncol 34 (27): 3276-83, 2016. [PUBMED Abstract]

The staging evaluation of patients with classic Kaposi sarcoma (KS) should be individualized. The advanced age of most of the patients, localized nature of the tumor, rarity of visceral involvement, and usually indolent course of the disease should temper the extent of the evaluation. A careful examination of the skin and lymph nodes is sufficient in most cases. For the rare patient with rapidly progressive tumor or signs or symptoms of visceral involvement, appropriate evaluation is indicated. No universally accepted classification is available for epidemic KS. Staging schemes that incorporate laboratory parameters as well as clinical features have been proposed. Since most patients with epidemic KS do not die of the disease, factors besides tumor burden are apparently involved in survival.

The conventions used to stage KS and the methods used to evaluate the benefits of KS treatment continue to evolve because of changes in the treatment of HIV and in recognition of deficiencies in standard tumor assessment. The clinical course of KS, the selection of treatment, and the response to treatment are heavily influenced by the degree of underlying immune dysfunction and opportunistic infections.

The AIDS Clinical Trials Group (ACTG) Oncology Committee has published criteria for the evaluation of epidemic KS.[1] The staging system incorporates measures of extent of disease, severity of immunodeficiency, and presence of systemic symptoms. As shown in Table 1 below, the ACTG criteria categorizes the extent of the tumor as localized or disseminated, the CD4 cell number as high or low, and a systemic illness as absent or present.

A subsequent prospective analysis of 294 patients entered on ACTG trials for KS between 1989 and 1995 showed that each of the tumor, immune system, and systemic illness variables was independently associated with survival.[2] Multivariate analysis showed that immune system impairment was the most important single predictor of survival. In patients with relatively high CD4 counts, tumor stage was predictive. A CD4 count of 150 cells/mm³ may be a better discriminator than the published cutoff of 200 cells/mm³. A study is in progress to determine if viral load adds predictive information. None of the previous studies were conducted at a time when highly active antiretroviral therapy (HAART) was readily available. The impact of HAART on survival in KS requires continued assessment.

Table 1. AIDS Clinical Trials Group Staging Classification

	Good Risk (0)	Poor Risk (1)
KS = Kaposi sarcoma; OI = opportunistic infection.
aMinimal oral disease is non-nodular KS confined to the palate.
b"B” symptoms are unexplained fever, night sweats, >10% involuntary weight loss, or diarrhea persisting >2 weeks.
	(Any of the following)	(Any of the following)
Tumor (T)	Confined to skin and/or lymph nodes and/or minimal oral diseasea	Tumor-associated edema or ulceration
		Extensive oral KS
		Gastrointestinal KS
		KS in other non-nodal viscera
Immune system (I)	CD4 cells ≥ 200/µL	CD4 cells <200 per cubic mm
Systemic illness (S)	No history of OIs or thrush	History of OIs and/or thrush
	No “B” symptomsb	“B” symptoms present
	Performance status ≥70 (Karnofsky)	Performance status <70
		Other HIV-related illness (e.g., neurological disease or lymphoma)

References

1. Krown SE, Metroka C, Wernz JC: Kaposi's sarcoma in the acquired immune deficiency syndrome: a proposal for uniform evaluation, response, and staging criteria. AIDS Clinical Trials Group Oncology Committee. J Clin Oncol 7 (9): 1201-7, 1989. [PUBMED Abstract]
2. Krown SE, Testa MA, Huang J: AIDS-related Kaposi's sarcoma: prospective validation of the AIDS Clinical Trials Group staging classification. AIDS Clinical Trials Group Oncology Committee. J Clin Oncol 15 (9): 3085-92, 1997. [PUBMED Abstract]

Classic Kaposi sarcoma (KS) usually is limited to the skin and has an indolent course. Patients with this tumor are predisposed to the development of a second primary malignancy, and the treating physician should consider this factor when arranging a schedule of follow-up treatment for the patient.

Treatment Options for Classic Kaposi Sarcoma

Solitary lesions

Treatment options for solitary lesions include the following (options are equivalent):

1. Radiation therapy: For solitary lesions or lesions of limited extent, modest doses of radiation applied to the lesions with a limited margin provide excellent control of disease in the treated area. Usually, superficial radiation beams such as electron beams are used. Some authors believe disease recurrence in adjacent, untreated skin is common if only involved-field radiation therapy is used and claim better cure rates when extended-field radiation therapy is used.[1]
   • Low-voltage (100 kv) photon radiation: 8 Gy to 10 Gy given as a single dose or 15 Gy to 20 Gy given over 1 week because solitary lesions control nearly 100% of local disease, but recurrence in adjacent areas is common.
   • Electron-beam radiation therapy (EBRT): 4 Gy given once weekly for 6 to 8 consecutive weeks with a 4-MeV to 6-MeV electron beam. Ports should include the entire skin surface 15 cm above the lesion.
2. Surgical excision may be of benefit in some patients with small superficial lesions, but local recurrence is likely to be a problem. However, over the years, multiple small excisions can be performed to achieve good disease control.

Widespread skin disease

Treatment options for widespread skin disease include the following (options are equivalent):

1. Radiation therapy: Modest doses are effective in controlling disease. The type of radiation (i.e., photon vs. electron) and fields used must be tailored to suit the distribution of disease in the individual patient.[1]
   • Extended-field EBRT.
   • For disease limited to areas distal to the knee, subtotal-skin EBRT directed to skin below the umbilicus.
   • For disease that extends above the knee, total-skin EBRT.

   EBRT used in this manner gave long-term results that were superior to those obtained with radiation therapy administered to successive individual lesions as they appeared.[2]

   • EBRT: 4 Gy given once weekly for 6 to 8 consecutive weeks, and subtotal- or total-skin radiation therapy given for extensive disease.
2. Chemotherapy: Because classic KS is such a rare disease in the United States and is usually treated initially with radiation therapy, few patients have been treated with chemotherapy. No randomized prospective trials have compared one agent with another. Several authors have used single-agent vinblastine given as a weekly dose of approximately 0.1 mg/kg.[3-6] Almost all of the patients had good to excellent response. In most cases, patients required prolonged courses of therapy, for several years, to maintain a partial response. Doses of vinblastine were titrated in individual patients to maintain a white blood count of more than 3,000 leukocytes. Follow-up after completion of therapy was not presented. In a multicenter trial of 55 patients who were treated over a decade, a 71% overall response rate was seen using pegylated liposomal doxorubicin.[7][Level of evidence C3] In addition to the positive response rates of pegylated liposomal doxorubicin and the vinca alkaloids, response rates showing a greater than 50% decrease in lesions have also been reported in small, uncontrolled series for etoposide, taxanes, gemcitabine, and recombinant interferon alfa.[8][Level of evidence C3]

   One patient was treated repeatedly with intralesional injections of 0.25 to 0.50 mg of vincristine, which resulted in complete disappearance of the treated lesion.[9] Multiple courses of therapy were required because of the recurrence of disease in untreated areas.

Electroporation of the skin lesions was combined with intravenous bleomycin for 19 patients with classical KS. Most patients responded after one application, the rest after two or three applications, with a median duration of response of 16 months.[10][Level of evidence C3]

Lymph node and gastrointestinal tract involvement

Treatment options for lymph node and gastrointestinal tract involvement include the following (options are equivalent):

1. Chemotherapy: Several patients who had widespread skin disease and were treated with chemotherapy also had lymph node and gastrointestinal tract involvement. The disease in these sites also responded to vinblastine. Trials are required to define therapy. One such trial, MSKCC-04055 (NCT00096538), has been completed.
2. Local radiation therapy may be added to chemotherapy if individual lesions require urgent therapy.

Current Clinical Trials

Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.

References

1. Tsao MN, Sinclair E, Assaad D, et al.: Radiation therapy for the treatment of skin Kaposi sarcoma. Ann Palliat Med 5 (4): 298-302, 2016. [PUBMED Abstract]
2. Nisce LZ, Safai B, Poussin-Rosillo H: Once weekly total and subtotal skin electron beam therapy for Kaposi's sarcoma. Cancer 47 (4): 640-4, 1981. [PUBMED Abstract]
3. Solan AJ, Greenwald ES, Silvay O: Long-term complete remissions of Kaposi's sarcoma with vinblastine therapy. Cancer 47 (4): 637-9, 1981. [PUBMED Abstract]
4. Tucker SB, Winkelmann RK: Treatment of Kaposi sarcoma with vinblastine. Arch Dermatol 112 (7): 958-61, 1976. [PUBMED Abstract]
5. Scott WP, Voight JA: Kaposi's sarcoma. Management with vincaleucoblastine. Cancer 19 (4): 557-64, 1966. [PUBMED Abstract]
6. Klein E, Schwartz RA, Laor Y, et al.: Treatment of Kaposi's sarcoma with vinblastine. Cancer 45 (3): 427-31, 1980. [PUBMED Abstract]
7. Di Lorenzo G, Kreuter A, Di Trolio R, et al.: Activity and safety of pegylated liposomal doxorubicin as first-line therapy in the treatment of non-visceral classic Kaposi's sarcoma: a multicenter study. J Invest Dermatol 128 (6): 1578-80, 2008. [PUBMED Abstract]
8. Régnier-Rosencher E, Guillot B, Dupin N: Treatments for classic Kaposi sarcoma: a systematic review of the literature. J Am Acad Dermatol 68 (2): 313-31, 2013. [PUBMED Abstract]
9. Odom RB, Goette DK: Treatment of cutaneous Kaposi's sarcoma with intralesional vincristine. Arch Dermatol 114 (11): 1693-4, 1978. [PUBMED Abstract]
10. Di Monta G, Caracò C, Benedetto L, et al.: Electrochemotherapy as "new standard of care" treatment for cutaneous Kaposi's sarcoma. Eur J Surg Oncol 40 (1): 61-6, 2014. [PUBMED Abstract]

Treatment of epidemic Kaposi sarcoma (KS) may result in the following:

No data are available, however, to show that treatment improves survival.[1] In addition to antitumor treatment, essential components of an optimal KS treatment strategy include highly active antiretroviral treatment (HAART), prophylaxis for opportunistic infections, and rapid recognition and treatment of intercurrent infections.

Most patients with good-risk disease, defined by the AIDS Clinical Trials Group as T0, show tumor regression with HAART alone.[2-4] Patients with poor-risk disease, defined as T1, usually require a combination of HAART and chemotherapy with discontinuation of the chemotherapy after disappearance of the skin lesion.[2-4] The combination of HAART and liposomal doxorubicin resulted in a 5-year overall survival (OS) rate of 85% in 140 patients with T1 disease.[3][Level of evidence C3]

Treatment Options for Epidemic Kaposi Sarcoma

Treatment options for epidemic KS include the following:

1. Local modalities.
2. Chemotherapy.
3. Biological and targeted therapy.

Local modalities

Small localized lesions of KS may be treated by electrodesiccation and curettage, cryotherapy, or by surgical excision. KS tumors are also generally very responsive to local radiation therapy, and excellent palliation has been obtained with doses at 20 Gy or slightly higher.[5,6] Radiation therapy is generally reserved to treat localized areas of the skin and oral cavity. It is less often used to control pulmonary, gastrointestinal tract, or other sites of KS lesions. Localized KS lesions have also been effectively treated with intralesional injections of vinblastine.[7] Alitretinoin 0.1% gel provided local control in a randomized prospective multicenter trial.[8][Level of evidence B3]

Chemotherapy

In epidemic KS, the already profoundly depressed immunologic status of the patient limits the therapeutic usefulness of systemic chemotherapy. Systemic chemotherapy studies in patients with epidemic KS have used doxorubicin, bleomycin, vinblastine, vincristine, etoposide, paclitaxel, and docetaxel alone or in combination.[9-13][Level of evidence C3] The combination of HAART and liposomal doxorubicin resulted in a 5-year OS rate of 85% in 140 patients with T1 disease.[3][Level of evidence C3]

Randomized multicenter trials showed an improvement in response rate (45%–60% vs. 20%–25%) and a more favorable toxic effects profile for pegylated liposomal doxorubicin or liposomal daunorubicin, compared with the combination of doxorubicin, bleomycin, and vincristine or bleomycin and vincristine.[14-16][Level of evidence B3] During HAART, both pegylated liposomal doxorubicin and paclitaxel are active single agents with response rates close to 50%.[17][Level of evidence B3]

Biological and targeted therapy

The interferon alfas have also been widely studied and show a 40% objective response rate in patients with epidemic KS.[18,19] In these reports, the responses differed significantly according to the prognostic factors of extent of disease, prior or coexistent opportunistic infections, prior treatment with chemotherapy, CD4 lymphocyte counts lower than 200 cells/mm³, the presence of circulating acid-labile interferon alfa, and an increase in beta-2-microglobulin. Several treatment studies have combined interferon alfa with other chemotherapeutic agents. Overall, these trials have shown no benefit with the interferon-chemotherapy combinations as compared with the single-agent activities.

Recombinant interferon alfa-2a and recombinant interferon alfa-2b were the first agents approved for the treatment of KS. Approval was based on single-agent studies performed in the 1980s before the advent of antiretroviral therapy. The early studies demonstrated improved efficacy at relatively high doses. High-dose monotherapy is rarely used today, and instead, interferon is given in combination with other anti-HIV drugs in doses of 4 to 18 million units. Neutropenia is dose limiting, and trials of doses of 1 to 10 million units combined with less myelosuppressive antiretrovirals are in progress. Response to interferon is slow, and the maximum effect is seen after 6 or more months. Interferon should probably not be used in the treatment of patients with rapidly progressive, symptomatic KS.

Imatinib, a c-kit/PDGF (platelet-derived growth factor) receptor inhibitor, resulted in partial responses in 10 of 30 previously treated patients (HAART and chemotherapy).[20]

Bevacizumab, the humanized, antivascular, endothelial growth–factor monoclonal antibody, resulted in a response rate in 5 of 16 patients who did not improve after the use of HAART and chemotherapy.[21][Level of evidence C3]

Recombinant interleukin-12 resulted in a response rate of 71% (95% confidence interval, 48%–89%) among 24 evaluable patients in a phase I and phase II trial.[22][Level of evidence C3]

Current Clinical Trials

Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.

References

1. Safai B: Kaposi's sarcoma and acquired immunodeficiency syndrome. In: DeVita VT, Hellman S, Rosenberg S, eds.: AIDS: Etiology, Diagnosis, Treatment and Prevention. 4th ed. Lippincott-Raven Publishers, 1997, pp 295-318.
2. Krown SE: Highly active antiretroviral therapy in AIDS-associated Kaposi's sarcoma: implications for the design of therapeutic trials in patients with advanced, symptomatic Kaposi's sarcoma. J Clin Oncol 22 (3): 399-402, 2004. [PUBMED Abstract]
3. Bower M, Dalla Pria A, Coyle C, et al.: Prospective stage-stratified approach to AIDS-related Kaposi's sarcoma. J Clin Oncol 32 (5): 409-14, 2014. [PUBMED Abstract]
4. Krell J, Stebbing J: Broader implications of a stage-guided stratified therapeutic approach for AIDS-related Kaposi's sarcoma. J Clin Oncol 32 (5): 373-5, 2014. [PUBMED Abstract]
5. Singh NB, Lakier RH, Donde B: Hypofractionated radiation therapy in the treatment of epidemic Kaposi sarcoma--a prospective randomized trial. Radiother Oncol 88 (2): 211-6, 2008. [PUBMED Abstract]
6. Tsao MN, Sinclair E, Assaad D, et al.: Radiation therapy for the treatment of skin Kaposi sarcoma. Ann Palliat Med 5 (4): 298-302, 2016. [PUBMED Abstract]
7. Epstein JB, Lozada-Nur F, McLeod WA, et al.: Oral Kaposi's sarcoma in acquired immunodeficiency syndrome. Review of management and report of the efficacy of intralesional vinblastine. Cancer 64 (12): 2424-30, 1989. [PUBMED Abstract]
8. Bodsworth NJ, Bloch M, Bower M, et al.: Phase III vehicle-controlled, multi-centered study of topical alitretinoin gel 0.1% in cutaneous AIDS-related Kaposi's sarcoma. Am J Clin Dermatol 2 (2): 77-87, 2001. [PUBMED Abstract]
9. Evans SR, Krown SE, Testa MA, et al.: Phase II evaluation of low-dose oral etoposide for the treatment of relapsed or progressive AIDS-related Kaposi's sarcoma: an AIDS Clinical Trials Group clinical study. J Clin Oncol 20 (15): 3236-41, 2002. [PUBMED Abstract]
10. Saville MW, Lietzau J, Pluda JM, et al.: Treatment of HIV-associated Kaposi's sarcoma with paclitaxel. Lancet 346 (8966): 26-8, 1995. [PUBMED Abstract]
11. Lim ST, Tupule A, Espina BM, et al.: Weekly docetaxel is safe and effective in the treatment of advanced-stage acquired immunodeficiency syndrome-related Kaposi sarcoma. Cancer 103 (2): 417-21, 2005. [PUBMED Abstract]
12. Gill PS, Tulpule A, Espina BM, et al.: Paclitaxel is safe and effective in the treatment of advanced AIDS-related Kaposi's sarcoma. J Clin Oncol 17 (6): 1876-83, 1999. [PUBMED Abstract]
13. Di Lorenzo G, Konstantinopoulos PA, Pantanowitz L, et al.: Management of AIDS-related Kaposi's sarcoma. Lancet Oncol 8 (2): 167-76, 2007. [PUBMED Abstract]
14. Stewart S, Jablonowski H, Goebel FD, et al.: Randomized comparative trial of pegylated liposomal doxorubicin versus bleomycin and vincristine in the treatment of AIDS-related Kaposi's sarcoma. International Pegylated Liposomal Doxorubicin Study Group. J Clin Oncol 16 (2): 683-91, 1998. [PUBMED Abstract]
15. Northfelt DW, Dezube BJ, Thommes JA, et al.: Pegylated-liposomal doxorubicin versus doxorubicin, bleomycin, and vincristine in the treatment of AIDS-related Kaposi's sarcoma: results of a randomized phase III clinical trial. J Clin Oncol 16 (7): 2445-51, 1998. [PUBMED Abstract]
16. Gill PS, Wernz J, Scadden DT, et al.: Randomized phase III trial of liposomal daunorubicin versus doxorubicin, bleomycin, and vincristine in AIDS-related Kaposi's sarcoma. J Clin Oncol 14 (8): 2353-64, 1996. [PUBMED Abstract]
17. Cianfrocca M, Lee S, Von Roenn J, et al.: Randomized trial of paclitaxel versus pegylated liposomal doxorubicin for advanced human immunodeficiency virus-associated Kaposi sarcoma: evidence of symptom palliation from chemotherapy. Cancer 116 (16): 3969-77, 2010. [PUBMED Abstract]
18. Real FX, Oettgen HF, Krown SE: Kaposi's sarcoma and the acquired immunodeficiency syndrome: treatment with high and low doses of recombinant leukocyte A interferon. J Clin Oncol 4 (4): 544-51, 1986. [PUBMED Abstract]
19. Groopman JE, Gottlieb MS, Goodman J, et al.: Recombinant alpha-2 interferon therapy for Kaposi's sarcoma associated with the acquired immunodeficiency syndrome. Ann Intern Med 100 (5): 671-6, 1984. [PUBMED Abstract]
20. Koon HB, Krown SE, Lee JY, et al.: Phase II trial of imatinib in AIDS-associated Kaposi's sarcoma: AIDS Malignancy Consortium Protocol 042. J Clin Oncol 32 (5): 402-8, 2014. [PUBMED Abstract]
21. Uldrick TS, Wyvill KM, Kumar P, et al.: Phase II study of bevacizumab in patients with HIV-associated Kaposi's sarcoma receiving antiretroviral therapy. J Clin Oncol 30 (13): 1476-83, 2012. [PUBMED Abstract]
22. Little RF, Pluda JM, Wyvill KM, et al.: Activity of subcutaneous interleukin-12 in AIDS-related Kaposi sarcoma. Blood 107 (12): 4650-7, 2006. [PUBMED Abstract]

The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.

Editorial changes were made to this summary.

This summary is written and maintained by the PDQ Adult Treatment Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® - NCI's Comprehensive Cancer Database pages.

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of Kaposi sarcoma. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

This summary is reviewed regularly and updated as necessary by the PDQ Adult Treatment Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

Board members review recently published articles each month to determine whether an article should:

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Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

The lead reviewers for Kaposi Sarcoma Treatment are:

• Eric J. Seifter, MD (Johns Hopkins University)
• Minh Tam Truong, MD (Boston University Medical Center)

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PDQ® Adult Treatment Editorial Board. PDQ Kaposi Sarcoma Treatment. Bethesda, MD: National Cancer Institute. Updated . Available at: https://www.cancer.gov/types/soft-tissue-sarcoma/hp/kaposi-treatment-pdq. Accessed . [PMID: 26389335]

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