Kaposi’s Sarcoma

– Christian Hoffmann, Stefan Esser –

Kaposi’s sarcoma (KS) is the most common malignancy in patients with HIV infection. In 1981, the simultaneous occurrence of KS with pneumocystis pneumonias in young MSM led to the first description of AIDS. This entity is designated after the Hungarian dermatologist Moritz Kaposi who had described well 100 years before for the first time the ”classical” KS. Classical KS predominantly occurs in elderly, but otherwise healthy people from the Eastern Mediterranean area. It affects often only the skin at the lower extremities and thereby, clearly differs from HIV-associated KS which will be the focus of the following chapter.

In contrast to classical KS, HIV-associated KS may affect all skin and mucous membranes. Lymph nodes and internal organs such as stomach, gut, lung or liver may also be involved. The progression of HIV-associated KS is very variable and reaches from small lesions, remaining stable for years, to extremely aggressive courses, in which rapid progression may lead to death within a few months.

Compared to the 1980’s and early 1990’s, when KS was one of the most common AIDS illnesses, prevalence of KS today is relatively low (Francesci 2010). Since the early years of AIDS epidemic, the incidence fell to less than a tenth (Grabar 2006, Simard 2011). In addition, the clinical course of KS has changed with the introduction of antiretroviral therapy. The refractory variants with an aggressive, devastating and often fatal course which were seen in the pre-HAART era have became a rarity today.


The cellular origin of the spindle cells (considered as the KS tumor cells) is still controversially discussed. Newer investigations suggested lymphatic, endothelial cells (Dupin 2006). Since 1994, it is well known that KS is induced by an infection with the human Herpesvirus 8 (HHV-8) or Kaposi sarcoma associated herpesvirus (KSHV). HHV-8 can be always detected in the tumor tissue, and the level of HHV-8-plasma viremia correlates quite well with KS progression (Laney 2007). In HIV-infected patients with KS, a significant HHV-8 viremia is frequently found (Marshall 2010). Transmission of HHV-8 occurs predominantly by saliva (Pauk 2000), but also sexually, vertically and via blood products (Pica 2008). In some regions, particularly in Italy and Central Africa, HHV-8 can be found in up to 50% of the general population. The exact role of HHV-8 in the KS pathogenesis is not clear. Infection with HHV-8 does not lead inevitably to KS. Interactions particularly with HIV-1 (Aoki 2004), possibly also with other viruses such as HHV-6 and HSV-1, changed signal transduction chains, an increased production of growth factors as well as cytokine dysregulations may play a role (McCormack 2005).

Among the HIV population, MSM are almost exclusively affected by KS; in HIV-infected women, children or hemophiliacs KS is a rare disease. An immune defect and/or low CD4 T cells promote emergence and growth of KS. However, severe immunodeficiency is not a prerequisite for the development of KS which is one of the few AIDS illnesses occurring in patients with a relatively preserved immune status. Approximately 29% of all patients, who participated in the US in the years 1996-2007 in KS studies, had more than 300 CD4 T cells/µl and a HIV plasma viremia below the detection limit (Krown 2008). In one study, the activation of the CD8 T cells correlated more strongly with the progression than the number of CD4 T cells (Stebbing 2006). Although uncommon, there are some cases of very aggressive progressions occurring only a few months after introduction of antiretroviral therapy. This so-called IRIS-associated KS often comes with rapid pulmonary lesions (Crane 2005). High HHV-8 and HIV viremia seem to be risk factors (Letang 2009).

Signs, symptoms and diagnosis

HIV-associated KS does not have a preferential pattern of localization. It can begin on any area of the skin, but may also appear on oral, genital, or ocular mucous membranes. Typical findings at manifestation are a few asymptomatic purple macules or nodules. These lesions have a predilection for distribution along relaxed skin tension lines. As mentioned above, the disease progression is very variable: the tumors can remain unchanged for months to years, or grow rapidly within a few weeks and disseminate. Rapid growth can lead to localized pain and a yellow-green discoloration of the area around the tumor as a result of hemorrhage. Further progression of the tumor can lead to central necrosis and ulceration. The tumors may bleed easily. Plaque-like and nodular KS lesions, often become confluent and can be accompanied by massive lymphoedema. In the oral cavity, the hard palate is frequently affected. Lesions begin with purplish erythema and progress to plaques and nodules that ulcerate easily. KS lesions may also involve the external genitalia including the foreskin and glans penis.

Regression of KS during is not only indicated by size reduction of the lesions but also by colour changes from dark to bright red. However, some lesions may persist even lifelong. These often dirty-grey-brown to light brown hyperpigmentations are caused by hemosiderin deposits and, possibly, increased stimulation of melanocytes due to the inflammation. Lymphoedema can also persist over years.


Diagnosis of cutaneous KS is usually made based on clinical findings. However, in all inconclusive or questionable cases a histologic diagnosis (excision or incision) is recommended. Differential diagnosis includes other neoplasia such as cutaneous lymphomas or angiosarcoma, but also infectious diseases such as syphilis and bacillary angiomatosis. Histological findings include spindle-shaped cells with vascular channels lined by abnormal endothelial cells. Extravasated erythrocytes, hemosiderin, and fibrosis can often be seen.

In every case of KS, clinical staging procedures are recommended, including:

  1. Complete inspection (oral and genital mucous membranes!)
  2. Abdominal ultrasound
  3. Gastroduodenoscopy and coloscopy (both procedures obligatory when mucous membranes are involved)
  4. Chest radiography (exclusion of a pulmonary KS)


If KS is newly diagnosed in an HIV-infected patient who is naïve to antiretroviral therapy, ART should be initiated: In early KS stages additional chemotherapy is only required in 20% of cases (Bower 2009). In all patients on ART but without sufficient suppression of HIV plasma viremia, ART should be optimized. Treatment interruptions should be avoided (Silverberg 2007). With decreasing HIV plasma viremia and immune reconstitution, many KS lesions stabilize or even resolve completely without any specific treatment. In one Italian study on 22 consecutive, ART-naïve KS patients, the overall clinical response rate to ART only was 91%: 18 complete and 2 partial responses were achieved, and only two patients experienced disease progression. CR was sustained in all 18 patients (Cattelan 2005).

Animal and in vitro experiments have suggested a direct anti-proliferative effects of PIs (Sgadari 2002, Gantt 2011). However, there is no ART combination of choice for KS patients. PIs are not required necessarily as NNRTI-based regimens are also effective with regard to KS regression (Grabar 2006, Martinez 2006). With ART, there is also an improvement of the humoral response against HHV-8 (Sullivan 2010). ART interruptions should be avoided in patients with current or previous KS. In the SMART study, KS was among the most frequent AIDS-defining illnesses during treatment interruptions, in particular among patients with a history of KS (Silverberg 2007).

ART as the only therapy is not recommended in all cases. In patients with rapidly progressive disease, with KS-related symptoms, or with visceral disease, ART should be combined with cytotoxic chemotherapy. There are different options which will be discussed in the following.

Chemotherapy: should be considered in all patients with rapid progression of KS, with visceral involvement, lymphoedema or with persistant lesions during ART, especially in those with IRIS associated KS. Pegylated liposomal doxorubicin hydrochloride (Caelyx® or Doxil®)  at a dosage of 20 mg/m² body surface is the treatment of choice (Di Trolio 2006). It has replaced older therapies such as the ABV regimen, a combination of adriamycine, bleomycine and vincristine. With Caelyx® complete remission rates of up to 80% are possible (Lichterfeld 2005). The infusions over 30-60 min every 2-3 weeks are ambulatory feasible and usually well tolerated. An antiemetic therapy is not necessary. Usually 6-8 cycles are required to achieve a good clinical response. Relapses during Caelyx® therapy occur rarely and particularly during the first year (Martin-Carbonero 2008). During treatment, myelotoxicity and cardiotoxicity of doxorubicin should be considered. Although the latter is rare and occurs only above cumulative doses of 450 mg, echocardiography (ejection fraction?) is recommend at the beginning of therapy as well as controls after six cycles. Another important side effect of Caelyx® is palmo-plantar erythrodysesthesia (PPE, “hand-foot-syndrome”), which becomes apparent as painful erythemas at hands and feet (Lorusso 2007). The incidence of PPE is increased in patients receiving Caelyx® compared with conventional doxorubicin.

In August 2011, Janssen-Cilag reported shortage of Caelyx® (Doxil®) due to production delays at a contract manufacturer. Intermittent capacity constraints are expected for the remainder of 2011. The company advised doctors not to start new patients on the drug. An alternative may be liposomal daunorubicine (DaunoXome®) which, however, appears to be less effective than Caelyx® (Cooley 2007). Of note, non-liposomal and non-pegylated forms of doxorubicin are not bioequivalent.

Beside doxorubicine and daunorubicine, paclitaxel (Taxol®) is also effective in KS (Tulpule 2002, Dhillon 2005, Stebbing 2006, Cianfrocca 2010). However, paclitaxel is more myelotoxic and leads almost always to complete alopecia, often already during the first cycle (patient must be informed!). Paclitaxel should be used only, if KS lesions show progression during therapy with Caelyx® or when Caelyx® or DaunoXome® are not available. Docetaxel (Taxotere®) is also effective according to uncontrolled studies (Autier 2005, Lim 2005). It should be mentioned that there may exist significant interactions between the taxanes and ART (Bundow 2004).

For the treatment of doxorubicin refractory cases, beside taxanes, oral etoposide (Evans 2002), irinotecan (Vaccher 2005) and the ABV regimen mentioned above may be considered. According to a retrospective study from Kenya, even gemcitabine has promising activity in KS (Strother 2010).

Immunotherapy: With interferons (IFN) acceptable remission rates are reached. However, CR rates seem to be lower than with pegylated liposomal doxorubicin (Kreuter 2005). The effect mechanism of IFN is KS is not fully clarified. Apart from an immune modulating effect, IFN probably induce the apoptosis in KS-cells. It is important to note that the effectiveness depends on the immune status. In patients with more than 400 CD4 T cells/µl, remission rates during IFN are at least 45%, compared with only 7% in patients with less than 200 CD4 T cells/µl. There may be some other factors predicting response to IFN such as endogenous IFN levels, which are increased in the advanced stage of the HIV infection.

There are currently no standardized IFN treatment regimens. Due to the considerable side effects, a high dose treatment (up to 30 million I.U./day) is not commonly administered. Daily doses of 3-6 million I.U. subcutaneously are usually given. After remission (tumour growth stopped, tumours flattened, loss of purple colour, change to brownish colour), interferon dosing can be reduced to 3x/week. Remission can be expected after 6-8 weeks of treatment (often significantly later). There is no sufficient data on the use of the pegylated IFN for HIV-associated KS. However, there are some promising case report in AIDS patients (Van der Ende 2007, Ueno 2007) and in patients with classical KS (Di Lorenzo 2008).

Table 1: Specific therapies for KS when ART is not sufficient




Pegylated liposomal doxorubicine (Caelyx or Doxil)

20 mg/mi.v. every 2 weeks

Treatment of choice, cave myelotoxicity, cardiotoxicity, hand-foot-syndrome

Liposomal daunorubicin (DaunoXone)

40 mg/m2 i.v. every 2-3 weeks.

Slightly less effective than Caelyx, seldom used during the past decade. However, as capacity constraints for Caelyx are expected for 2011/12, an important alternative

Interferon-a 2a (Roferon)

3-6 x 106 I.E. s.c. or i.m.

3 x / week

Considerable side effects, less efficacy than with doxorubicin. Use only when CD4-T cells are >200/µl and limited disease

Pegylated Interferon-a 2b (PegIntron)

50 µg s.c. weekly

Tolerability improved compared to conventional IFN-a (2a,b), but lack of data in AIDS-KS, Off Lable-Use!


100 mg/m² i.v. every 2 weeks or

135 mg/m2 i.v. every 3 weeks

Cave neutropenia, peripheral neuropathy, allergic reactions, alopecia

Off Lable-Use! Caution with ART-interactions

Local therapy: is well-tolerated and less costly. Many different methods are used depending on the size and location of tumors: cosmetic camouflage, cryosurgery, intralesional injections of vinca alkaloids or interferons, soft x-ray radiation, electron beam therapy, cobalt radiation (fractionated) or Imiquimod (Celestin Schartz 2008). Compressive therapy with elastic stockings is an important strategy for the treatment of KS associated lymphoedema (Brambilla 2006).

KS is a strikingly radiosensitive tumor (Becker 2006). Superficial macular or plaque-like KS lesions respond well to daily doses of 4-5 Gy (total dose 20-30 Gy, fractionated 3x/week) of soft x-ray radiation. In the case of large KS lesions with oedema, radiation with fast electron beams (5 x 2 Gy per week, total dose 40 Gy) is recommended.

As KS is a multifocal systemic disease, surgical treatment is limited to excisional biopsies for diagnosis and palliative removal of small tumors in cosmetically disturbing areas. Since tumors often extend further into the surroundings than is clinically visible and local trauma can lead to new tumors (Koebner phenomenon), local and regional recurrences can be expected. These can be prevented by radiation therapy: in order to reach the tumor cells spreading along the vascular channels, the field of radiation should be extended 0.5-1.0 cm beyond the edges of the tumor.

New therapeutic approaches: With regards to the KS pathogenesis, several new therapies have been suggested such as virustatic agents, cytokines and inhibitors of angiogenesis. They will be discussed briefly.

·   Valgancyclovir – promising approach as this antiviral agent significantly reduces the frequency and quantity of HHV-8 replication. This was recently shown by a randomized trial (Casper 2008). Better tolerability than foscarnet which had been discussed in the 90’s. However, there are no data on clinical efficacy in AIDS-KS published to date. As HHV-8 is involved in early steps of the KS pathogenesis, it is questionable if valgancyclovir has any effect on manifest lesions. In patients with classical KS, the drug remained inefficient (Krown 2011).

·   Interleukin-12 – high response rates in a phase II study, in which this cytokine was combined with liposomal doxorubicin (Little 2007). No randomized studies.

·   Sirolimus (and everolimus) – new immunosuppressive agents used in the transplantation setting. Good response rates in uncontrolled studies on HIV negative renal transplant recipients with KS (Stallone 2005, Campistol 2007). It is postulated that these drugs inhibit tumour angiogenesis through impaired vascular endothelium growth factor production.

·   Bevacizumab – an early study of this VEGF-antibody showed moderate response rates in 31% of 17 HIV-infected patients with KS progression on ART (Uldrick 2010). A study on combination with liposomal doxorubicine is ongoing.

·   Imatinib (Glivec®) – activation of the platelet-derived growth factor (PDGF) and c-kit receptors has been proposed as important in mediating the growth of AIDS- KS. Treatment with the PDGF receptor/c-kit inhibitor, imatinib mesylate, resulted in clinical and histologic regression of cutaneous KS lesions in 5/10 patients within 4 weeks (Koon 2005).

·   Sorafenib (Nexavar®) – is an oral Raf kinase inhibitor, approved for the treatment of advanced renal cancer. Case reports on KS (Ardavanis 2008). Phase I studies are underway.

·   Matrix metalloproteinases (MMPs) – are involved in tumour metastasis and are overexpressed in Kaposi’s sarcoma (KS) cells. MMP inhibitors such as COL-3 have shown activity in a phase II study on patients with advanced KS (Dezube 2006). However, clinical response rates were at best moderate with 41%. The most common adverse events were photosensitivity and rash. Encouraging phase II study with topical halofuginone (Koon 2011).

·   Retinoid compounds (tretinoin, isotretinoin, acitretin) – may inhibit the proliferation of KS cells. Many studies on different formulations have been conducted (Duvic 2000, Bodsworth 2001, Bernstein 2002, Aboulafia 2003). However, efficacy is only moderate. Thus, retinoids will face a difficult path attaining approval for treatment of KS.


Aboulafia DM, Norris D, Henry D, et al. 9-cis-retinoic acid capsules in the treatment of AIDS-related Kaposi sarcoma: results of a phase 2 multicenter clinical trial. Arch Dermatol 2003, 139:178-86.

Aoki Y, Tosato G. HIV-1 Tat enhances KSHV infectivity. Blood 2004; 104: 810-4

Ardavanis A, Doufexis D, Kountourakis P, Rigatos G. A Kaposi’s sarcoma complete clinical response after sorafenib administration. Ann Oncol 2008, 19:1658-9.

Autier J, Picard-Dahan C, Marinho E, et al. Docetaxel in anthracycline-pretreated AIDS-related Kaposi’s sarcoma: a retrospective study. Br J Dermatol 2005, 152:1026-9.

Becker G, Bottke D. Radiotherapy in the management of Kaposi´s sarcoma. Onkologie 2006; 29: 329-33.

Bernstein ZP, Chanan-Khan A, Miller KC, Northfelt DW, Lopez-Berestein G, Gill PS. A multicenter phase II study of the intravenous administration of liposomal tretinoin in patients with acquired immunodeficiency syndrome-associated Kaposi´s sarcoma. Cancer 2002; 95: 2555-61.

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 2001; 2: 77-87.

Bower M, Nelson M, Young AM, et al. Immune reconstitution inflammatory syndrome associated with Kaposi´s sarcoma. J Clin Oncol 2005; 23: 5224-8.

Bower M, Weir J, Francis N, et al. The effect of HAART in 254 consecutive patients with AIDS-related Kaposi’s sarcoma. AIDS 2009, 23:1701-6.

Brambilla L, Tourlaki A, Ferrucci S, Brambati M, Boneschi V. Treatment of classic Kaposi´s sarcoma-associated lymphedema with elastic stockings. J Dermatol 2006; 33: 451-6.

Bundow D, Aboulafia DM. Potential drug interaction with paclitaxel and highly active antiretroviral therapy in two patients with AIDS-associated Kaposi sarcoma.  Am J Clin Oncol 2004, 27: 81-4.

Campistol JM, Schena FP. Kaposi’s sarcoma in renal transplant recipients–the impact of proliferation signal inhibitors. Nephrol Dial Transplant 2007, 22 Suppl 1:i17-22.

Casper C, Krantz EM, Corey L, et al. Valganciclovir for suppression of human herpesvirus-8 replication: a randomized, double-blind, placebo-controlled, crossover trial. J Infect Dis 2008, 198:23-30.

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 2005; 27: 779-85.

Celestin Schartz NE, Chevret S, Paz C, et al. Imiquimod 5% cream for treatment of HIV-negative Kaposi´s sarcoma skin lesions: A phase I to II, open-label trial in 17 patients. J Am Acad Dermatol 2008, 58:585-91.

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 2010, 116:3969-77.

Corbeil J, Rapaport E, Richman DD, Looney DJ. Antiproliferative effect of retinoid compounds on Kaposi’s sarcoma cells. J Clin Invest 1994, 93:1981-6.

Crane HM, Deubner H, Huang JC, Swanson PE, Harrington RD. Fatal Kaposi’s sarcoma-associated immune reconstitution following HAART initiation.Int J STD AIDS 2005; 16:80-3.

Dezube BJ, Krown SE, Lee JY, Bauer KS, Aboulafia DM. Randomized phase II trial of matrix metalloproteinase inhibitor COL-3 in AIDS-related Kaposi´s sarcoma: an AIDS Malignancy Consortium Study. J Clin Oncol 2006; 24: 1389-94.

Dhillon T, Stebbing J, Bower M. Paclitaxel for AIDS-associated Kaposi’s sarcoma. Expert Rev Anticancer Ther 2005, 5:215-9.

Di Lorenzo G, Di Trolio R, Montesarchio V, et al. Pegylated liposomal doxorubicin as second-line therapy in the treatment of patients with advanced classic Kaposi sarcoma: a retrospective study. Cancer 2008, 112:1147-52.

Di Trolio R, Di Lorenzo G, Delfino M, De Placido S. Role of pegylated lyposomal doxorubicin (PLD) in systemic Kaposi´s sarcoma: a systematic review. Int J Immunopathol Pharmacol 2006; 19: 253-63.

Dupin N, Grange PA. Looking for the target cell of Kaposi’s sarcoma-associated herpesvirus. J Invest Dermatol 2006, 126:545-7.

Duvic M, Friedman-Kien AE, Looney DJ, et al. Topical treatment of cutaneous lesions of acquired immunodeficiency syndrome-related Kaposi sarcoma using alitretinoin gel: results of phase 1 and 2 trials. Arch Dermatol 2000; 136: 1461-9.

Evans SR, Krown SE, Testa MA, Cooley TP, Von Roenn JH. 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 2002, 20:3236-41.

Franceschi S, Lise M, Clifford GM, et al. Changing patterns of cancer incidence in the early- and late-HAART periods: the Swiss HIV Cohort Study. Br J Cancer 2010, 103:416-22.

Gantt S, Carlsson J, Ikoma M, et al. The HIV protease inhibitor nelfinavir inhibits Kaposi sarcoma-associated herpesvirus replication in vitro. Antimicrob Agents Chemother. 2011 Mar 14. [Epub ahead of print]

Grabar S, Abraham B, Mahamat A, Del Giudice P, Rosenthal E, Costagliola D. Differential impact of combination antiretroviral therapy in preventing Kaposi´s sarcoma with and without visceral involvement. JCO 2006; 24: 3408-14.

Koon HB, Bubley GJ, Pantanowitz L, et al. Imatinib-induced regression of AIDS-related Kaposi´s sarcoma. J Clin Oncol 2005; 23: 982-9.

Koon HB, Fingleton B, Lee JY, et al. Phase II AIDS Malignancy Consortium trial of topical halofuginone in AIDS-related Kaposi sarcoma. J AIDS 2011, 56:64-8.

Kreuter A, Rasokat H, Klouche M, et al. Liposomal pegylated doxorubicin versus low-dose recombinant interferon Alfa-2a in the treatment of advanced classic Kaposi’s sarcoma; retrospective analysis of three German centers. Cancer Invest 2005, 23:653-9.

Krown SE, Dittmer DP, Cesarman E. Pilot study of oral valganciclovir therapy in patients with classic Kaposi sarcoma. J Infect Dis 2011, 203:1082-6.

Krown SE, Lee JY, Dittmer DP; AIDS Malignancy Consortium. More on HIV-associated Kaposi’s sarcoma. N Engl J Med 2008, 358:535-6.

Krown SE, Li P, Von Roenn JH, Paredes J, Huang J, Testa MA. Efficacy of low-dose interferon with antiretroviral therapy in Kaposi’s sarcoma: a randomized phase II AIDS clinical trials group study. J Interferon Cytokine Res 2002, 22:295-303.

Krown SE. AIDS-associated Kaposi´s sarcoma: is there still a role for interferon alfa? Cytokine Growth Factor Rev 2007;18:395-402.

Laney AS, Cannon MJ, Jaffe HW, et al. Human herpesvirus 8 presence and viral load are associated with the progression of AIDS-associated Kaposi´s sarcoma. AIDS 2007; 21:1541-5.

Letang E, Almeida JM, Miró JM, et al. Predictors of Immune Reconstitution Inflammatory Syndrome-associated with kaposi sarcoma in Mozambique: A Prospective Study. J AIDS 2009 Oct 1. [Epub ahead of print]

Lichterfeld M, Qurishi N, Hoffmann C, et al. Treatment of HIV-1-associated Kaposi´s sarcoma with pegylated liposomal doxorubicin and HAART simulta-neously induces effective tumor remission and CD4+ T cell recovery. Infection 2005; 33: 140-7.

Lim ST, Tupule A, Espina BM, Levine AM. Weekly docetaxel is safe and effective in the treatment of advanced-stage acquired immunodeficiency syndrome-related Kaposi sarcoma. Cancer 2005; 103: 417-21.

Little RF, Aleman K, Kumar P, et al. Phase 2 study of pegylated liposomal doxorubicin in combination with interleukin-12 for AIDS-related Kaposi sarcoma. Blood 2007, 110:4165-71.

Lorusso D, Di Stefano A, Carone V, Fagotti A, Pisconti S, Scambia G. Pegylated liposomal doxorubicin-related palmar-plantar erythrodysesthesia (´hand-foot´ syndrome). Ann Oncol 2007;18:1159-64.

Marshall V, Martró E, Labo N, et al. Kaposi sarcoma (KS)-associated herpesvirus microRNA sequence analysis and KS risk in a European AIDS-KS case control study. J Infect Dis 2010, 202:1126-35.

Martin-Carbonero L, Barrios A, Saballs P, et al. Pegylated liposomal doxorubicin plus highly active antiretroviral therapy versus highly active antiretrovi-ral therapy alone in HIV patients with Kaposi´s sarcoma. AIDS 2004; 18: 1737-40.

Martín-Carbonero L, Palacios R, Valencia E, et al. Long-term prognosis of HIV-infected patients with Kaposi sarcoma treated with pegylated liposomal doxorubicin. Clin Infect Dis 2008, 47:410-7.

Martinez V, Caumes E, Gambotti L, et al. Remission from Kaposi´s sarcoma on HAART is associated with suppression of HIV replication and is inde-pendent of protease inhibitor therapy. Br J Cancer 2006; 94: 1000-6. A

McCormick C, Ganem D. The kaposin B protein of KSHV activates the p38/MK2 pathway and stabilizes cytokine mRNAs. Science 2005; 307: 739-41.

Pauk J, Huang ML, Brodie SJ, et al. Mucosal shedding of human herpesvirus 8 in men. N Engl J Med 2000, 343:1369-77.

Pica F, Volpi A. Transmission of human herpesvirus 8: an update. Curr Opin Infect Dis 2007:152-6.

Ramirez-Amador V, Esquivel-Pedraza L, Lozada-Nur F, et al. Intralesional vinblastine vs. 3% sodium tetradecyl sulfate for the treatment of oral Kaposi’s sarcoma. A double blind, randomized clinical trial. Oral Oncol 2002, 38:460-7.

Sgadari C, Barillari G, Toschi E, et al. HIV protease inhibitors are potent anti-angiogenic molecules and promote regression of Kaposi sarcoma. Nat Med 2002, 8: 225-32.

Silverberg MJ, Neuhaus J, Bower M, et al. Risk of cancers during interrupted antiretroviral therapy in the SMART study. AIDS 2007;21:1957-63.

Simard EP, Pfeiffer RM, Engels EA. Cumulative incidence of cancer among individuals with acquired immunodeficiency syndrome in the United States. Cancer 2011, 117:1089-96.

Stallone G, Schena A, Infante B, et al. Sirolimus for Kaposi’s sarcoma in renal-transplant recipients. N Engl J Med 2005, 352:1317-23.

Stebbing J, Wildfire A, Portsmouth S, et al. Paclitaxel for anthracycline-resistant AIDS-related Kaposi´s sarcoma: clinical and angiogenic correlations. Ann Oncol 2003; 14: 1660-6.

Strother RM, Gregory KM, Pastakia SD, et al. Retrospective analysis of the efficacy of gemcitabine for previously treated AIDS-associated Kaposi’s sarcoma in western Kenya. Oncology 2010, 78:5-11.

Sullivan SG, Hirsch HH, Franceschi S, et al. Kaposi sarcoma herpes virus antibody response and viremia following highly active antiretroviral therapy in the Swiss HIV Cohort study. AIDS 2010, 24:2245-52.

Tulpule A, Groopman J, Saville MW, et al. Multicenter trial of low-dose paclitaxel in patients with advanced AIDS-related Kaposi sarcoma. Cancer 2002, 95:147-54.

Ueno T, Mitsuishi T, Kimura Y, et al. Immune reconstitution inflammatory syndrome associated with Kaposi´s sarcoma: successful treatment with interferon-alpha. Eur J Dermatol 2007;17:539-40.

Uldrick T, Wyvill K, Kumar P. A phase II study targeting vascular endothelial growth factor with the humanized monoclonal antibody bevacizumab in the treatment of patients with HIV-associated kaposi sarcoma. Abstract 31, 17th CROI 2010, San Francisco.

Van der Ende M, Mulder JW, van den Berge M, Blok W, Schutten M.Complete clinical and virological remission of refractory HIV-related Kaposi’s sarcoma with pegylated interferon alpha. AIDS 2007;21:1661-2.

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