Kaposi Sarcoma Treatment & Management

  • Author: Lewis J Rose, MD; Chief Editor: Jules E Harris, MD   more...
 
Updated: Aug 5, 2011
 

Medical Care

All therapies for Kaposi sarcoma (Kaposi's sarcoma, KS) have been markedly influenced by HAART (highly active antiretroviral therapy), which has decreased the incidence and severity of this disease. What followed is primarily related to HIV associated KS.

Antiretroviral therapy

The introduction of HAART (highly active antiretroviral therapy) has significantly reduced the incidence of Kaposi sarcoma and changed its clinical course. Optimal control of HIV infection using HAART is an integral part of successful Kaposi sarcoma therapy. It should be the first step in therapy. Response to such therapy can be anywhere from 20-80% based on stage of disease and the amount of pretreatment.[58]

However, patients with poor-risk Kaposi sarcoma rarely respond to HAART alone. In addition, a flare phenomenon may be noted associated with HAART initiation consistent with a reactivation of the immune system and associated inflammatory response. This occurs in association with increase in CD4 counts and control of HIV viremia.[59, 56] The criteria of for Kaposi sarcoma immune reactivation inflammatory syndrome (IRISI) per the AIDS Clinical Trial Group are as follows:

  1. Starting, restarting, or altering HAART regimen
  2. Increase of CD4 by greater than or equal to 50 cell, mL or a 2-fold increase in CD4 count, and decrease in HIV-1 viral load of greater than 0.5 log
  3. Amore than expected progression of Kaposi sarcoma within 12 weeks of initiating HAAR

In this clinical situation, chemotherapy may be necessary to ameliorate and reverse the disease progression.

The choice of therapy beyond HAART must be individualized and depends on the extent of disease, the presence and nature of the symptoms, the rate of disease progression, and the overall therapeutic goals. Since its inception, HAART treatment has changed the goal in Kaposi sarcoma treatment from short-term palliation to long-term remission and control.

Effective combination antiretroviral therapy usually is comprised of a combination of either a protease inhibitor(PI) or non-nucleoside reverse transcriptase inhibitor (NNRTI) with 2 nucleoside reverse transcriptase inhibitors (NRTI). Some evidence suggests a direct antitumor effect on angioproliferative Kaposi sarcoma–type lesions. Yet presently, no level 1 evidence supports this clinically.[60] No difference is apparent between PI-based and NNRTI-based antiretroviral regimens in terms of response of Kaposi sarcoma.

HAART may be tried as the sole modality used in nonvisceral disease. For visceral disease, chemotherapy may be added. For locally symptomatic disease, radiation therapy may be introduced.[4]

Local therapy

Local therapy is best suited for individuals who require palliation of locally advanced symptomatic disease (eg, radiation) or for individuals who have cosmetically unacceptable lesions. This therapy is also well suited for individuals with significant comorbidities and disease refractory to systemic modalities. It can provide better cosmesis, control bulky lesions that cause bleeding, pain or, edema, and treat extensive skin disease. Local therapy fails to halt the development of new Kaposi sarcoma lesions.

Radiation therapy is the most widely used and effective local therapy. This can palliate bleeding, pain, or unsightly lesions. This may be given in the form of low-voltage (100 kv) photons or electron-beam radiotherapy. Responses occur in 80-90% of patients. A higher cumulative dose (40 Gy) results in better local control than lower doses (8 Gy or 20 Gy). Electron beam therapy is reserved for treatment of superficial lesions. This is usually giving once weekly in 4 Gy fractions. Recurrence may be common in adjacent, untreated areas, leading some authors to recommend extended- field radiotherapy to affect a higher cure rate. Patients with HIV are more prone to develop radiation-induced mucositis as well and hyperpigmentation, desquamation, and ulceration of treated lesions.[4, 61, 62]

In patients with widespread skin involvement, extended-field electron beam radiation therapy (EBRT) has been effective in controlling the disease. This approach appears to give better long-term control than piecemeal radiation of individual lesions. This type of therapy is also given in 4-Gy fractions weekly for 6-8 weeks.

Surgical excision may be of benefit for patients with small superficial lesions. The major problem is local recurrence. The presence of clear surgical margins does not mean that Kaposi sarcoma has been permanently controlled at a given anatomical site. Local recurrence is very common. Yet over the course of many years, multiple small excisions may be a reasonable approach to achieve good control of disease.

Intralesional therapy with vinca alkaloids with low-dose vincristine or vinblastine as well as bleomycin has been used in a limited fashion primarily for the classic form of Kaposi sarcoma where localized skin disease predominates. Responses occur in 60-90% of patients with little in the way of systemic side effects with duration of 4-6 months. Dosing is done at about one-tenth the systemic dose of drug with 3- to 4-week intervals between treatment. Side effects include changes in pigmentation, swelling, blistering, ulceration, and pain on injection as well as localized but usually transient neuropathic symptoms. Because the disease recurs in other areas, its use is relatively limited. Also, systemic vinca alkaloid therapy may be equally effective and cause less localized skin toxicity.

Cryotherapy entails liquid nitrogen applied topically and may be useful for small facial lesions less than 1 cm in dimensions. Cryotherapy may cause skin hypopigmentation. It induces response in more than 85% of cases. Cryotherapy has the advantage of short duration, minimal discomfort, and ability to be used repeatedly and in combination with other forms of treatment.[4] It has limited penetration and is not ideal for large, deep lesions.

Laser and surgical therapies can be used locally. Laser photocoagulation can shrink smaller lesions and be used to palliate bleeding and pain in larger lesions. Similar to cryotherapy, it has limited application to deep, bulky lesions. Surgery is usually limited to patients with a visceral crisis such as obstruction or bleeding or for very deep, localized, painful lesions. The risk of transmission of HIV to the operating room team limits its use as well.

Topical retinoids

IL-6 is a cytokine implicated in the pathogenesis of Kaposi sarcoma. In vitro, retinoic acid down-regulates IL-6 receptor expression. A 0.1% (alitretinoin [Panretin]) gel is available commercially and may be applied topically 2-4 times daily. This agent is generally well tolerated but may cause local erythema and irritation. It induces responses in one third to one half of the patients at a time interval of 2-14 weeks after initiation of therapy.[4] Common side effects of local inflammation and depigmentation.

Palliative systemic therapy is indicated for symptomatic or life-threatening visceral disease, rapidly progressive mucocutaneous disease with pain or ulceration, and symptomatic lymphedema. In this setting, few reliable estimates of response rate with HAART alone compared with combined HAART and chemotherapy are available. One trial from South Africa comparing HAART with HAAART and chemotherapy showed in the intent to treat patient’s 39% response in HAART alone compared with 66% in HAART plus chemotherapy. Also, 35% of patient in the HAART arm crossed over to require palliative chemotherapy or radiation within 12 months of randomization. These results support that chemotherapy and HAART should be used together in patients with high tumor volume (T1).[63]

No randomized prospective clinical trials compare one adjuvant therapy to the other for classic Kaposi sarcoma.

Endemic Kaposi sarcoma

What follows applies primarily to epidemic Kaposi sarcoma.

Immunomodulation with interferon-alfa has clinical activity in Kaposi sarcoma that may be mediated by its antiangiogenic, antiviral, and immunomodulatory properties. Time to clinical response is long (ie, 4-6 mo). Therefore, it should be reserved for patients who do not require a clinical response. Interferon-alfa is most effective when the CD4 count is greater than 150-200/mm3 or when administered in conjunction with antiretroviral therapy.

Objective response rates have been seen in about 40% of patients.[64, 65] Responses are dependent on extent of disease, immunocompetence of the patient, prior treatment with chemotherapy, presence of circulating acid-labile interferon alpha, and beta-2 microglobulin levels. Immunocompetent patients have about a 4-fold increase in response compared with those with poor prognostic features.

As a rule, combination interferon and chemotherapy has been no better than chemotherapy or interferon alone. This therapy entails subcutaneous administration daily or 3 times weekly. Response may occur with low (1 million U/m2), intermediate (3-10 million U/m2), or high doses (50 million U/m2).

These agents, interferon alpha-2a and interferon alpha-2b, were approved in the pre-HAART era. Interferon-alfa has activity against HIV by suppressing mRNA translation into protein preventing the assembly of intact viral particles. Thus, it has synergy with antiretroviral drugs. High-dose monotherapy was used then because there was little else to offer. High-dose therapy is rarely used today in the era of HAART.

Because HAART alone is quite effective, lower doses of interferon-alpha are now the rule. Dose-limiting toxicity is neutropenia. Phase I trials with interferon and zidovudine have been completed with doses of interferon in the range of 4-5 million units with 200 mg of zidovudine being tolerated.[66] Trials with moderate doses of 1-10 million units combined with less myelosuppressive antiretrovirals are in progress. Toxicity is more common and severe with higher doses; symptoms may include fatigue, flulike symptoms, myalgia, arthralgia, fever, myelosuppression, and hepatotoxicity.

Interleukin-12 has shown a response rate of 71% (95% confidence interval, 48-89%) among 24 evaluable patients in a phase I/II trial.[67]

Chemotherapy is used with palliative intent. Chemotherapy is indicated for symptomatic visceral or rapidly progressive mucocutaneous disease for which a rapid response is desirable. It is used in disseminated disease not amenable to local modalities.

Initially, vincristine-, vinblastine-, and bleomycin-containing regimens were used. Etoposide and doxorubicin regimens were the second-line standards. These agents are capable of achieving rapid tumor regression and palliation of tumor-related symptoms but at a cost of myelosuppression and risk of opportunistic infections.

Combination therapy with regimens such as ABV (actinomycin D, bleomycin, and vincristine) versus single-agent therapy such as doxorubicin cause higher response rates but similar time to progression and overall survival. Prior to the availability of growth factor support, toxicity due to myelosuppression was significant. Combination chemotherapy results in about double the response rate, 45-60% versus 20-25% for single agents.

Several single cytotoxic agents are approved by the Food and Drug Administration (FDA) for AIDS-related Kaposi sarcoma and include liposomal doxorubicin (Doxil) for previously treated patients, liposomal daunorubicin (DaunoXome) for first-line use, and paclitaxel (Taxol) or oral etoposide (Vepesid) for second-line use. The liposomal technology has resulted in higher response rates with less cardiac and myelotoxicity for both liposomal doxorubicin and liposomal daunorubicin because of their more targeted nature.[68, 69, 70] Response rates of up to 80% can be seen with either of these drugs. The same is true for paclitaxel, which can be safely administered to severely immunocompromised patients refractory to other chemotherapeutic agents.[55] Response rates have been seen from 50-71% in two phase II trials for untreated patients.[71, 72]

Studies comparing liposomal preparations to combination chemotherapy regimens such as ABV have not been done in the HAART era. A small multicenter study of only 20 patients with cutaneous Kaposi sarcoma randomized between HAART alone compared with HAART and liposomal doxorubicin showed 76% for the combination compared with 20% for HAART alone.[73] Relapse rate from this approach is about 10-15% a year. Based on this and other data, liposomal doxorubicin is now considered the first line standard of care for Kaposi sarcoma.

In AIDS-associated Kaposi sarcoma, the problem has been balancing the immunosuppressive effects of chemotherapy with its potential benefit. This has required a great deal of finesse in the era of HAART, which can itself cause regression of Kaposi sarcoma. Treatment duration should be to a response plateau with lengthening out of the interval to approximately 6 weeks, a period in which Kaposi sarcoma will progress if treatment is not being administered. Also, recurrence of Kaposi sarcoma after chemotherapy does not necessarily mean resistance, making retreatment with the same regimen a reasonable option.

Because chemotherapy can be given long-term, treatment-related toxicities may prevent its ongoing administration.

Potential new avenues of therapy are being investigated. Because of its highly vascular nature, Kaposi sarcoma has been thought of as a natural target for angiogenesis inhibition. A phase II study of thalidomide in 20 patients with Kaposi sarcoma with HIV serology resulted in a 40% response rate with median duration of response of 7 months. Most of the patients were on HAART.[4] Combination chemotherapy of antiangiogenic and cytotoxic agents is being considered.[67]

Studies are underway involving VEGF pathway with agents such as the VEGF-inhibitors bevacizumab and sorafenib as well as studies with inhibitors of m-TOR such as sirolimus. Lenolidamide, an immune modulating agent is also being studied.[74]

Other compounds such as fumagillin analogs and peptidoglycan analogs produced by bacteria, which are potent blockers of angiogenesis, have shown minimal benefit as single agents. Glufanide disodium, an antiangiogenic dipeptide from solubilized fraction of thymic extract, has shown benefit with response rates of 36% when used as a nasal formulation.[55] Because of its male predominance, another way of treating the disease may be through hormonal manipulation. Work is being done to look at the potential inhibitory effect of beta-HCG.

Because of its etiologic link to Kaposi sarcoma human herpesvirus (KSHV) (HHV-8), antiviral therapy with foscarnet and ganciclovir may be effective. A randomized clinical trial of oral ganciclovir versus ganciclovir ocular implants has shown a lower rate of Kaposi sarcoma.[67]

Further studies are needed in this area.[4] Yet, antiherpes drugs have been ineffective. Activation of drugs by KSHV-kinases is an approach that needs further investigation. Also, the c-kit oncogene is up-regulated by KSHV. This would make it a rational target for blockade.

A small study with imatinib mesylate (Gleevec) has shown response in 4 of 5 patients.[75]

Finally, evaluation of the multiple pathways of potential pathogenesis may lead to inhibitors of both autocrine and paracrine factors. An inhibitor of basic fibroblast growth factor (bFGF) has been studied. Also, newer antiangiogenic compounds such as inhibitors of matrix metalloproteinases and oligonucleotides may show promise.[76]

Despite effective therapies and promising activity of novel agents, the investigation of new targeted therapies continues.

See related CME at Co-receptor Inhibitors (Slides with Transcript); FDA Approvals: PrandiMed, Doryx, Doxil; and FDA Safety Changes: Levaquin, Nexavar, AndroGel.

Next

Consultations

Obtain a radiation oncology consultation when considering the use of radiation as definitive therapy for palliation of locally advanced symptomatic disease or a cosmetically disturbing cutaneous lesion.

Previous
Proceed to Medication
 
 
Contributor Information and Disclosures
Author

Lewis J Rose, MD  Clinical Associate Professor of Medical Oncology, Division of Regional Cancer Care, Kimmel Cancer Center, Thomas Jefferson University Hospital; Consulting Staff, LRCRZ Associates

Lewis J Rose, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Hematology, Pennsylvania Medical Society, Phi Beta Kappa, and Philadelphia County Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Ari D Fishman, MD  Fellow, Department of Medical Oncology, Albert Einstein Comprehensive Cancer Center, Albert Einstein College of Medicine

Ari D Fishman, MD is a member of the following medical societies: American College of Physicians, American Medical Association, and American Society of Hematology

Disclosure: Nothing to disclose.

Joseph A Sparano, MD  Professor of Medicine, Albert Einstein College of Medicine/Cancer Center; Program Director, Director of Breast Medical Oncology, Department of Internal Medicine, Division of Oncology, Montefiore Medical Center

Joseph A Sparano, MD is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, and American Society of Hematology

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael Perry, MD, MS, MACP  Nellie B Smith Chair of Oncology Emeritus, Professor, Department of Internal Medicine, Division of Hematology and Oncology, Ellis Fischel Cancer Center, University of Missouri-Columbia School of Medicine

Michael Perry, MD, MS, MACP is a member of the following medical societies: Alpha Omega Alpha, American Association for Cancer Research, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society of Clinical Oncology, American Society of Hematology, International Association for the Study of Lung Cancer, and Missouri State Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Rajalaxmi McKenna, MD, FACP  Southwest Medical Consultants, SC, Department of Medicine, Good Samaritan Hospital, Advocate Health Systems

Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis

Disclosure: Nothing to disclose.

Chief Editor

Jules E Harris, MD  Clinical Professor of Medicine, Division of Hematology/Medical Oncology, Department of Internal Medicine, University of Arizona College of Medicine; Consulting Staff, Arizona Cancer Center

Jules E Harris, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Immunologists, American Society of Hematology, and Central Society for Clinical Research

Disclosure: GlobeImmune Salary Consulting

References

  1. DeVita V. AIDS-related malignancies. In: DeVita V, Vincent T Jr, eds. Cancer: Principles and Practice of Clinical Oncology. Vol 8. 5th ed. Philadelphia, Pa: Lippincott, Williams, & Wilkins; 2008:2404-2407.

  2. Renwick N, Halaby T, Weverling GJ, et al. Seroconversion for human herpesvirus 8 during HIV infection is highly predictive of Kaposi's sarcoma. AIDS. Dec 24 1998;12(18):2481-8. [Medline].

  3. Jacobson LP, Jenkins FJ, Springer G, et al. Interaction of human immunodeficiency virus type 1 and human herpesvirus type 8 infections on the incidence of Kaposi's sarcoma. J Infect Dis. Jun 2000;181(6):1940-9. [Medline].

  4. Escalon MP and Hagemeister FB. AIDS-Related Malignancies. In: Kantarjian HM, Wolff Ra, and Koller CA. MD Anderson Manual of Medical Oncology. McGraw-Hill; 2006:903-910. [Full Text].

  5. Nawar E, Mbulaiteye SM, Gallant JE, Wohl DA, Ardini M, Hendershot T, et al. Risk factors for Kaposi's sarcoma among HHV-8 seropositive homosexual men with AIDS. Int J Cancer. Jun 10 2005;115(2):296-300. [Medline].

  6. Penn I. Cancer in the immunosuppressed organ recipient. Transplant Proc. Apr 1991;23(2):1771-2. [Medline].

  7. Penn I. Tumors after renal and cardiac transplantation. Hematol Oncol Clin North Am. Apr 1993;7(2):431-45. [Medline].

  8. Antman K, Chang Y. Kaposi's sarcoma. N Engl J Med. Apr 6 2000;342(14):1027-38. [Medline].

  9. Franceschi S, Geddes M. Epidemiology of classic Kaposi's sarcoma, with special reference to mediterranean population. Tumori. Sep-Oct 1995;81(5):308-14. [Medline].

  10. Sarid R, Olsen SJ, Moore PS. Kaposi's sarcoma-associated herpesvirus: epidemiology, virology, and molecular biology. Adv Virus Res. 1999;52:139-232. [Medline].

  11. Touloumi G, Hatzakis A, Potouridou I, et al. The role of immunosuppression and immune-activation in classic Kaposi's sarcoma. Int J Cancer. Sep 9 1999;82(6):817-21. [Medline].

  12. Stallone G, Schena A, Infante B, et al. Sirolimus for Kaposi's sarcoma in renal-transplant recipients. N Engl J Med. Mar 31 2005;352(13):1317-23. [Medline].

  13. Gutiérrez-Dalmau A, Campistol JM. The role of proliferation signal inhibitors in post-transplant malignancies. Nephrol Dial Transplant. May 2007;22 Suppl 1:i11-6. [Medline].

  14. Campistol JM, Eris J, Oberbauer R, et al. Sirolimus therapy after early cyclosporine withdrawal reduces the risk for cancer in adult renal transplantation. J Am Soc Nephrol. Feb 2006;17(2):581-9. [Medline].

  15. Kaloterakis A, Papasteriades C, Filiotou A, et al. HLA in familial and nonfamilial Mediterranean Kaposi's sarcoma in Greece. Tissue Antigens. Feb 1995;45(2):117-9. [Medline].

  16. Calabrò ML, Sheldon J, Favero A, et al. Seroprevalence of Kaposi's sarcoma-associated herpesvirus/human herpesvirus 8 in several regions of Italy. J Hum Virol. Mar-Apr 1998;1(3):207-13. [Medline].

  17. Iscovich J, Boffetta P, Winkelmann R, Brennan P. Classic Kaposi's sarcoma as a second primary neoplasm. Int J Cancer. Jan 18 1999;80(2):178-82. [Medline].

  18. Fiorelli V, Gendelman R, Sirianni MC, et al. gamma-Interferon produced by CD8+ T cells infiltrating Kaposi's sarcoma induces spindle cells with angiogenic phenotype and synergy with human immunodeficiency virus-1 Tat protein: an immune response to human herpesvirus-8 infection?. Blood. Feb 1 1998;91(3):956-67. [Medline].

  19. Monini P, Colombini S, Sturzl M, et al. Reactivation and persistence of human herpesvirus-8 infection in B cells and monocytes by Th-1 cytokines increased in Kaposi's sarcoma. Blood. Jun 15 1999;93(12):4044-58. [Medline].

  20. Goedert JJ, Vitale F, Lauria C, et al. Risk factors for classical Kaposi's sarcoma. J Natl Cancer Inst. Nov 20 2002;94(22):1712-8. [Medline].

  21. de-Thé G, Bestetti G, van Beveren M, et al. Prevalence of human herpesvirus 8 infection before the acquired immunodeficiency disease syndrome-related epidemic of Kaposi's sarcoma in East Africa. J Natl Cancer Inst. Nov 3 1999;91(21):1888-9. [Medline].

  22. Parkin DM FJ, Hamdi-Cherif M, Sitas F, et al. Kaposi's Sarcoma. In: Cancer in Africa: Epidemiology and Preventiion. 153. Lyon, France: International Agency for Research on Cancer: IARC Scientific Publiciations; 2003:286-294.

  23. Ziegler J, Newton R, Bourboulia D, et al. Risk factors for Kaposi's sarcoma: a case-control study of HIV-seronegative people in Uganda. Int J Cancer. Jan 10 2003;103(2):233-40. [Medline].

  24. Osman M, Kubo T, Gill J, Neipel F, Becker M, Smith G, et al. Identification of human herpesvirus 8-specific cytotoxic T-cell responses. J Virol. Jul 1999;73(7):6136-40. [Medline]. [Full Text].

  25. Sirianni MC, Vincenzi L, Topino S, et al. NK cell activity controls human herpesvirus 8 latent infection and is restored upon highly active antiretroviral therapy in AIDS patients with regressing Kaposi's sarcoma. Eur J Immunol. Oct 2002;32(10):2711-20. [Medline].

  26. Friedman-Kien AE, Saltzman BR, Cao YZ, et al. Kaposi's sarcoma in HIV-negative homosexual men. Lancet. Jan 20 1990;335(8682):168-9. [Medline].

  27. Uccini S, Ruco LP, Monardo F, Stoppacciaro A, et al. Co-expression of endothelial cell and macrophage antigens in Kaposi's sarcoma cells. J Pathol. May 1994;173(1):23-31. [Medline].

  28. Lennette ET, Blackbourn DJ, Levy JA. Antibodies to human herpesvirus type 8 in the general population and in Kaposi's sarcoma patients. Lancet. Sep 28 1996;348(9031):858-61. [Medline].

  29. Spira TJ, Lam L, Dollard SC, et al. Comparison of serologic assays and PCR for diagnosis of human herpes virus 8 infection. J Clin Microbiol. Jun 2000;38(6):2174-80. [Medline]. [Full Text].

  30. Nascimento, MC, Sumita, LM, Souza, VU, et al. Seroprevalence of Kaposi Sarcoma –associated herpes virus and other serologic markers in the Brazilian Amazon. Emerg Infect Dis. 2009;15:664-667.

  31. Wang X, He B, Zhang Z, et al. Human herpesvirus-8 in northwestern China: epidemiology and characterization among blood donors. Virol J. Mar 17 2010;7:62. [Medline]. [Full Text].

  32. Duprez R, Lacoste V, Brière J, Couppié P, Frances C, Sainte-Marie D, et al. Evidence for a multiclonal origin of multicentric advanced lesions of Kaposi sarcoma. J Natl Cancer Inst. Jul 18 2007;99(14):1086-94. [Medline].

  33. Montaner S, Sodhi A, Ramsdell AK, et al. The Kaposi's sarcoma-associated herpesvirus G protein-coupled receptor as a therapeutic target for the treatment of Kaposi's sarcoma. Cancer Res. Jan 1 2006;66(1):168-74. [Medline].

  34. Grisotto MG, Garin A, Martin AP, Jensen KK, Chan P, Sealfon SC, et al. The human herpesvirus 8 chemokine receptor vGPCR triggers autonomous proliferation of endothelial cells. J Clin Invest. May 2006;116(5):1264-73. [Medline]. [Full Text].

  35. Paulose-Murphy M, Ha NK, Xiang C, Chen Y, Gillim L, Yarchoan R, et al. Transcription program of human herpesvirus 8 (kaposi's sarcoma-associated herpesvirus). J Virol. May 2001;75(10):4843-53. [Medline]. [Full Text].

  36. Biggar, RJ, Chatuvedi, AK, Goedert, JJ, et al. AIDS-related cancer and severity of immunosuppression in persons with AIDS. J Natl Cancer Inst. 2007;99:969-972.

  37. Brown EE, Whitby D, Vitale F, et al. Virologic, hematologic, and immunologic risk factors for classic Kaposi sarcoma. Cancer. Nov 1 2006;107(9):2282-90. [Medline].

  38. Stratigos AJ, Malanos D, Touloumi G, et al. Association of clinical progression in classic Kaposi's sarcoma with reduction of peripheral B lymphocytes and partial increase in serum immune activation markers. Arch Dermatol. Nov 2005;141(11):1421-6. [Medline].

  39. Kimball LE, Casper C, Koelle DM, Morrow R, Corey L, Vieira J. Reduced levels of neutralizing antibodies to Kaposi sarcoma-associated herpesvirus in persons with a history of Kaposi sarcoma. J Infect Dis. Jun 1 2004;189(11):2016-22. [Medline].

  40. Campbell TB, Borok M, Ndemera B, et al. Lack of evidence for frequent heterosexual transmission of human herpesvirus 8 in Zimbabwe. Clin Infect Dis. Jun 1 2009;48(11):1601-8. [Medline]. [Full Text].

  41. Hladik W, Dollard SC, Mermin J, et al. Transmission of human herpesvirus 8 by blood transfusion. N Engl J Med. Sep 28 2006;355(13):1331-8. [Medline].

  42. Frances C, Marcelin AG, Legendre Ch, et al. The impact of preexisting or acquired Kaposi sarcoma herpes virus infection in kidney transplant recipients on morbidity and survival. Am J Transplant. Nov 2009;9(11):2580-6. [Medline].

  43. Chang Y, Cesarman E, Pessin MS, et al. Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi's sarcoma. Science. Dec 16 1994;266(5192):1865-9. [Medline].

  44. SEER Cancer Statistics Review authored by Reis LAG, Eisner MP, Kosary, CL et al [database online]. Bethesda, MD: National Cancer Institute; 2003.

  45. Scadden D. Acquired Immunodeficiency Syndrome. In: Holland JF, Frei E. Cancer Medicine. 6. Hamilton, London: BC Decker Inc; 2003:2259-2275.

  46. Eltom MA, Jemal A, Mbulaiteye SM, et al. Trends in Kaposi's sarcoma and non-Hodgkin's lymphoma incidence in the United States from 1973 through 1998. J Natl Cancer Inst. Aug 21 2002;94(16):1204-10. [Medline].

  47. Beral V, Peterman TA, Berkelman RL, et al. Kaposi's sarcoma among persons with AIDS: a sexually transmitted infection?. Lancet. Jan 20 1990;335(8682):123-8. [Medline].

  48. Cote TR, Howe HL, Anderson SP, et al. A systemic consideration of the neoplastic spectrum of AIDS: registry linkage in Illinois. AIDS. 1991;5(1):49-53.

  49. [Best Evidence] Stebbing J, Sanitt A, Nelson M, et al. A prognostic index for AIDS-associated Kaposi's sarcoma in the era of highly active antiretroviral therapy. Lancet. May 6 2006;367(9521):1495-502. [Medline].

  50. Maurer T, Ponte M, Leslie K. HIV-associated Kaposi's sarcoma with a high CD4 count and a low viral load. N Engl J Med. Sep 27 2007;357(13):1352-3. [Medline].

  51. Lee FC, Mitsuyasu RT. Chemotherapy of AIDS--related Kaposi's sarcoma. Hematol Oncol Clin North Am. Oct 1996;10(5):1051-68. [Medline].

  52. Hussein MA, Remzi B, DiFabrizio L, et al. Evaluation of Sequential Thallium and Gallium Scans of the Chest in AIDs Patients. The Journal of Nuclear Medicine. October, 1996;37, 10:1662-1667.

  53. About the 3 by 5 Initiative. World Health Organization. WHO website. Available at http://www.who.int/3by5/about/initiative/en/endex.html. Accessed September 6, 2004.

  54. Levine AM, Tulpule A. Clinical aspects and management of AIDS-related Kaposi's sarcoma. Eur J Cancer. Jul 2001;37(10):1288-95. [Medline].

  55. Tulpule A, Groopman J, Saville MW, et al. Multicenter trial of low-dose paclitaxel in patients with advanced AIDS-related Kaposi sarcoma. Cancer. Jul 1 2002;95(1):147-54. [Medline].

  56. 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. Feb 1 2004;22(3):399-402. [Medline].

  57. Chachoua A, Krigel R, Lafleur F, et al. Prognostic factors and staging classification of patients with epidemic Kaposi's sarcoma. J Clin Oncol. Jun 1989;7(6):774-80. [Medline].

  58. Cattelan AM, Calabro ML, De Rossi A, et al. Long-term clinical outcome of AIDS-related Kaposi's sarcoma during highly active antiretroviral therapy. Int J Oncol. Sep 2005;27(3):779-85. [Medline].

  59. Bower M, Nelson M, Young AM, et al. Immune reconstitution inflammatory syndrome associated with Kaposi's sarcoma. J Clin Oncol. Aug 1 2005;23(22):5224-8. [Medline].

  60. Sgadari C, Barillari G, Toschi E, et al. HIV protease inhibitors are potent anti-angiogenic molecules and promote regression of Kaposi sarcoma. Nat Med. Mar 2002;8(3):225-32. [Medline].

  61. Cooper A. Treating HIV-infected children: the surgeon's role. Bull Am Coll Surg. Jun 1991;76(6):13-7, 43. [Medline].

  62. Nobler MP, Leddy ME, Huh SH. The impact of palliative irradiation on the management of patients with acquired immune deficiency syndrome. J Clin Oncol. Jan 1987;5(1):107-12. [Medline].

  63. Mosam A, Shaik F, Uldrick T, Esterhuizen T, Friedlnad G, Scadden D, et al. The KAART Trial: A randomized controlled trial of HAART compared to the combination of HAART and chemotherapy in treatment naïve patients with HIV-associated Kaposi's Sarcoma (HIV-KS) in KwaZulu-Natal (KZN) South Africa NCT 00380770 in: 17th Conference on Retorviruses and Opportunistic Infections, San Francisco, CA . 2010.

  64. 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. Apr 1986;4(4):544-51. [Medline].

  65. 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. May 1984;100(5):671-6. [Medline].

  66. Krown SE, Gold JW, Niedzwiecki D, et al. Interferon-alpha with zidovudine: safety, tolerance, and clinical and virologic effects in patients with Kaposi sarcoma associated with the acquired immunodeficiency syndrome (AIDS). Ann Intern Med. Jun 1 1990;112(11):812-21. [Medline].

  67. Little RF, Pluda JM, Wyvill KM, Rodriguez-Chavez IR, Tosato G, Catanzaro AT, et al. Activity of subcutaneous interleukin-12 in AIDS-related Kaposi sarcoma. Blood. Jun 15 2006;107(12):4650-7. [Medline]. [Full Text].

  68. 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. Jul 1998;16(7):2445-51. [Medline].

  69. 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. Feb 1998;16(2):683-91. [Medline].

  70. 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. Aug 1996;14(8):2353-64. [Medline].

  71. Saville MW, Lietzau J, Pluda JM, et al. Treatment of HIV-associated Kaposi's sarcoma with paclitaxel. Lancet. Jul 1 1995;346(8966):26-8. [Medline].

  72. 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. Jun 1999;17(6):1876-83. [Medline].

  73. Martin-Carbonero L, Barrios A, Saballs P, Sirera G, Santos J, Palacios R, et al. Pegylated liposomal doxorubicin plus high active antiretroviral therapy verusus Highy active antiretroviral therapy alone in HIV patients with Kaposi's sarcoma. AIDS. 2004;18:410-417.

  74. Uldrick TS, Whitby D. Update on KSHV epidemiology, Kaposi Sarcoma pathogenesis, and treatment of Kaposi Sarcoma. Cancer Lett. Jun 28 2011;305(2):150-62. [Medline]. [Full Text].

  75. Koon HB, Bubley GJ, Pantanowitz L, et al. Imatinib-induced regression of AIDS-related Kaposi's sarcoma. J Clin Oncol. Feb 10 2005;23(5):982-9. [Medline].

  76. Cianfrocca M, Cooley TP, Lee JY, et al. Matrix metalloproteinase inhibitor COL-3 in the treatment of AIDS-related Kaposi's sarcoma: a phase I AIDS malignancy consortium study. J Clin Oncol. Jan 1 2002;20(1):153-9. [Medline].

  77. Infectious Agents, Immunologic Factors, Hereditary Neoplastic Syndromes, Soft Tissue Sarcoma. In: Schottenfeld D and Fraumen J eds. Cancer. Epidemiology and Prevention. 3rd ed. New York: Oxford University Press; 2006:522, 523, 552, 553, 561, 562, 960-962, 968.

  78. Centers for disease control. Surveillance for AIDS-defining opportunistic illnesses, 1992-1997. MMWR. 1999;48:SS2:1-22.

  79. de Sanjose S, Mbisa G, Perez-Alvarez S, et al. Geographic variation in the prevalence of Kaposi sarcoma-associated herpesvirus and risk factors for transmission. J Infect Dis. May 15 2009;199(10):1449-56. [Medline].

  80. Dezube BJ. Acquired immunodeficiency syndrome-related Kaposi's sarcoma: clinical features, staging, and treatment. Semin Oncol. Aug 2000;27(4):424-30. [Medline].

  81. Dezube BJ. Clinical presentation and natural history of AIDS--related Kaposi's sarcoma. Hematol Oncol Clin North Am. Oct 1996;10(5):1023-9. [Medline].

  82. Di Lorenzo G, Konstantinopoulos PA, Pantanowitz L, et al. Management of AIDS-related Kaposi's sarcoma. Lancet Oncol. Feb 2007;8(2):167-76. [Medline].

  83. 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. Aug 1 2002;20(15):3236-41. [Medline].

  84. Gao SJ, Kingsley L, Li M, Zheng W, Parravicini C, Ziegler J, et al. KSHV antibodies among Americans, Italians and Ugandans with and without Kaposi's sarcoma. Nat Med. Aug 1996;2(8):925-8. [Medline].

  85. 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. Jun 1999;17(6):1876-83. [Medline].

  86. Iscovich J, Boffetta P, Franceschi S, et al. Classic kaposi sarcoma: epidemiology and risk factors. Cancer. Feb 1 2000;88(3):500-17. [Medline].

  87. Krown SE, Lee JY, Dittmer DP. More on HIV-associated Kaposi's sarcoma. N Engl J Med. Jan 31 2008;358(5):535-6; author reply 536. [Medline]. [Full Text].

  88. 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. Sep 1989;7(9):1201-7. [Medline].

  89. Mbisa GL, Miley W, Gamache CJ, et al. Detection of antibodies to Kaposi's sarcoma-associated herpes virus: a new approach using K8.1 ELISA and a newly developed recombinant LANA ELISA. J Immunol Methods. Apr 30 2010;356(1-2):39-46. [Medline]. [Full Text].

  90. AIDS-Related Malignancies-Kaposi's Sarcoma. In: Kantarjian HM, Wolff RA, and Koller CA. MD Anderson Manual of Medical Oncology. McGraw Hill; 2006:903-910/34.

  91. Simpson GR, Schulz TF, Whitby D, et al. Prevalence of Kaposi's sarcoma associated herpesvirus infection measured by antibodies to recombinant capsid protein and latent immunofluorescence antigen. Lancet. Oct 26 1996;348(9035):1133-8. [Medline].

  92. Stebbing J, Gazzard B, Newsom-Davis T, et al. Nadir B cell counts are significantly correlated with the risk of Kaposi's sarcoma. Int J Cancer. Jan 20 2004;108(3):473-4. [Medline].

  93. Tulpule A, Scadden DT, Espina BM, et al. Results of a randomized study of IM862 nasal solution in the treatment of AIDS-related Kaposi's sarcoma. J Clin Oncol. Feb 2000;18(4):716-23. [Medline].

  94. Tulpule A, Scadden DT, Espina BM, et al. Results of a randomized study of IM862 nasal solution in the treatment of AIDS-related Kaposi's sarcoma. J Clin Oncol. Feb 2000;18(4):716-23. [Medline].

  95. Vogel J, Hinrichs SH, Reynolds RK, Luciw PA, Jay G. The HIV tat gene induces dermal lesions resembling Kaposi's sarcoma in transgenic mice. Nature. Oct 13 1988;335(6191):606-11. [Medline].

  96. Von Roenn J. Kaposi's sarcoma evaluation and treatment. In: American Society of Clinical Oncology (ASCO) Educational book. 1998:76-85.

  97. Yarchoan R, Broder S. Preliminary results on the use of dideoxynuclosides in the therapy of AIDS. In: Chanock, RM, Lerner Ra, Brown F, Ginsberg H. Vaccines 87: modern approaches to new vaccines: prevention of AIKDs and other viral, bacterial, and parasitic disease. Cold Spring Harbor, NY: Colc Spring Harbor Press; 1987.

 
Previous
Next
 
Endoscopic view of a Kaposi sarcoma lesion situated in the gastric antrum.
Epidemic Kaposi sarcoma (KS). Large violaceous truncal nodules with typical linear and symmetric distribution pattern.
Kaposi sarcoma (KS), facial. Confluent, violaceous nodules involving the chest wall; extensive facial involvement with accompanied edema.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.