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Bruce J. Dezube - One of the best experts on this subject based on the ideXlab platform.
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Targeted Therapy for Kaposi Sarcoma
BioDrugs, 2009Co-Authors: Ryan J Sullivan, Liron Pantanowitz, Bruce J. DezubeAbstract:Kaposi Sarcoma (KS) occurs as a result of Kaposi Sarcoma-associated herpesvirus (KSHV) infection, typically in the context of one of several immunodeficient states. In the US, patients with KS may either be co-infected with HIV or receiving immunosuppressant therapy following solid-organ transplantation. Systemic treatment of KS has traditionally involved one of several chemotherapeutic agents administered either in combination or as single agents, which typically provide reasonable response rates and short-term control. However, recurrence of KS is common, and progression-free intervals are under 1 year. For these reasons, new therapies have been sought and with the elucidation of novel pathogenic mechanisms of KS infection, rational therapeutic targets have been identified. These include KSHV replication, restoration of immune competence, and signal transduction pathways utilized by KSHV in the propagation of KS. This review focuses on these emerging targets in the treatment of patients with KS and also highlights important clinicopathologic characteristics.
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epidemiology pathophysiology and treatment of Kaposi Sarcoma associated herpesvirus disease Kaposi Sarcoma primary effusion lymphoma and multicentric castleman disease
Clinical Infectious Diseases, 2008Co-Authors: Ryan J Sullivan, Liron Pantanowitz, Corey Casper, Justin Stebbing, Bruce J. DezubeAbstract:Kaposi Sarcoma-associated herpesvirus infection is associated with the development of 3 proliferative diseases: Kaposi Sarcoma, primary effusion lymphoma, and multicentric Castleman disease. These conditions are also intimately associated with human immunodeficiency virus infection, and important synergistic interactions between these 2 viruses have been described. Despite differences in viral gene expression patterns in each condition, Kaposi Sarcoma-associated herpesvirus encodes similar oncogenic proteins that promote the activation of sequential and parallel signaling pathways. Therapeutic strategies have been implemented to target these unique signaling pathways, and this sort of molecular targeting is the focus of many current research efforts. The scope of this review is to present contemporary knowledge about the epidemiology, virology, and immunology of Kaposi Sarcoma-associated herpesvirus and to highlight several key oncogene products that may be targets for chemotherapy.
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Kaposi Sarcoma in unusual locations
BMC Cancer, 2008Co-Authors: Liron Pantanowitz, Bruce J. DezubeAbstract:Kaposi Sarcoma (KS) is a multifocal, vascular lesion of low-grade malignant potential that presents most frequently in mucocutaneous sites. KS also commonly involves lymph nodes and visceral organs. This article deals with the manifestation of KS in unusual anatomic regions. Unusual locations of KS involvement include the musculoskeletal system, central and peripheral nervous system, larynx, eye, major salivary glands, endocrine organs, heart, thoracic duct, urinary system and breast. The development of KS within wounds and blood clots is also presented. KS in these atypical sites may prove difficult to diagnose, resulting in patient mismanagement. Theories to explain the rarity and development of KS in these unusual sites are discussed.
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lymphatic reprogramming of blood vascular endothelium by Kaposi Sarcoma associated herpesvirus
Nature Genetics, 2004Co-Authors: Youngkwon Hong, Bruce J. Dezube, Kimberly E Foreman, Jay W Shin, Satoshi Hirakawa, Christine L Curry, David R Sage, Towia A Libermann, Joyce D Fingeroth, Michael DetmarAbstract:Kaposi Sarcoma is considered a neoplasm of lymphatic endothelium infected with Kaposi Sarcoma-associated herpesvirus. It is characterized by the expression of lymphatic lineage-specific genes by Kaposi Sarcoma tumor cells. Here we show that infection of differentiated blood vascular endothelial cells with Kaposi Sarcoma-associated herpesvirus leads to their lymphatic reprogramming; induction of approximately 70% of the main lymphatic lineage-specific genes, including PROX1, a master regulator of lymphatic development; and downregulation of blood vascular genes.
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Advances in the pathobiology and treatment of Kaposi Sarcoma.
Current Opinion in Oncology, 2004Co-Authors: Liron Pantanowitz, Bruce J. DezubeAbstract:PURPOSE OF REVIEW Kaposi Sarcoma, which has reached epidemic proportions in parts of Africa and in the Western world, continues to pose a problem in patients with AIDS receiving highly active antiretroviral therapy (HAART). This article reviews the new and important information regarding the epidemiology, biology, and management of Kaposi Sarcoma that was published in the last year. RECENT FINDINGS Worldwide Kaposi Sarcoma herpesvirus/human herpesvirus 8 (HHV8) seropositivity has been found to exceed the incidence of Kaposi Sarcoma. Therefore, investigators have justifiably implicated other cofactors (eg, blood-sucking arthropods, angiotensin converting enzyme inhibitors, hemodialysis, and iron) in the development of Kaposi Sarcoma. In the transplant setting, Kaposi Sarcoma lesions have been shown to originate from the engraftment of donor tumor cells. The detection of HHV8 in Kaposi Sarcoma lesions has provided a new diagnostic tool to help differentiate Kaposi Sarcoma from its mimics. Kaposi Sarcoma lesional cells, now confirmed to be of lymphatic origin, have been shown to express several chemokine receptors, some of which may help explain the predilection for skin. Regression of Kaposi Sarcoma has been characterized histologically for the first time. The finding that some tumor cells can remain in an atrophic state even in completely regressed lesions suggests that they have the potential to recur. Protease inhibitor-based and nonnucleoside reverse transcriptase inhibitor-based HAART regimens have been verified to be similarly effective. Although antiretrovirals have been noted to favorably alter the clinical characteristics of Kaposi Sarcoma favorably, they seem not to alter the natural history of this disease. In the HAART era, because CD4 cell count was shown no longer to provide prognostic information about AIDS-related Kaposi Sarcoma, the traditional classification system for staging AIDS-related Kaposi Sarcoma has been refined. Also, a new staging system for classic Kaposi Sarcoma has been proposed. SUMMARY Numerous advances have emerged regarding Kaposi Sarcoma during the last year, many of which still need to be translated into clinically useful information. The results of new clinical trials involving antivirals purposely directed against HHV8 and antiretrovirals for HIV-uninfected people are anticipated. Finally, although investigators during this period did provide us with additional potential therapeutic targets, more novel approaches such as RNA interference and gene therapy have been also proposed as options in the future management of Kaposi Sarcoma.
Liron Pantanowitz - One of the best experts on this subject based on the ideXlab platform.
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Targeted Therapy for Kaposi Sarcoma
BioDrugs, 2009Co-Authors: Ryan J Sullivan, Liron Pantanowitz, Bruce J. DezubeAbstract:Kaposi Sarcoma (KS) occurs as a result of Kaposi Sarcoma-associated herpesvirus (KSHV) infection, typically in the context of one of several immunodeficient states. In the US, patients with KS may either be co-infected with HIV or receiving immunosuppressant therapy following solid-organ transplantation. Systemic treatment of KS has traditionally involved one of several chemotherapeutic agents administered either in combination or as single agents, which typically provide reasonable response rates and short-term control. However, recurrence of KS is common, and progression-free intervals are under 1 year. For these reasons, new therapies have been sought and with the elucidation of novel pathogenic mechanisms of KS infection, rational therapeutic targets have been identified. These include KSHV replication, restoration of immune competence, and signal transduction pathways utilized by KSHV in the propagation of KS. This review focuses on these emerging targets in the treatment of patients with KS and also highlights important clinicopathologic characteristics.
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epidemiology pathophysiology and treatment of Kaposi Sarcoma associated herpesvirus disease Kaposi Sarcoma primary effusion lymphoma and multicentric castleman disease
Clinical Infectious Diseases, 2008Co-Authors: Ryan J Sullivan, Liron Pantanowitz, Corey Casper, Justin Stebbing, Bruce J. DezubeAbstract:Kaposi Sarcoma-associated herpesvirus infection is associated with the development of 3 proliferative diseases: Kaposi Sarcoma, primary effusion lymphoma, and multicentric Castleman disease. These conditions are also intimately associated with human immunodeficiency virus infection, and important synergistic interactions between these 2 viruses have been described. Despite differences in viral gene expression patterns in each condition, Kaposi Sarcoma-associated herpesvirus encodes similar oncogenic proteins that promote the activation of sequential and parallel signaling pathways. Therapeutic strategies have been implemented to target these unique signaling pathways, and this sort of molecular targeting is the focus of many current research efforts. The scope of this review is to present contemporary knowledge about the epidemiology, virology, and immunology of Kaposi Sarcoma-associated herpesvirus and to highlight several key oncogene products that may be targets for chemotherapy.
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Histological variants of cutaneous Kaposi Sarcoma
Diagnostic Pathology, 2008Co-Authors: Wayne Grayson, Liron PantanowitzAbstract:This review provides a comprehensive overview of the broad clinicopathologic spectrum of cutaneous Kaposi Sarcoma (KS) lesions. Variants discussed include: usual KS lesions associated with disease progression ( i.e. patch, plaque and nodular stage); morphologic subtypes alluded to in the older literature such as anaplastic and telangiectatic KS, as well as several lymphedematous variants; and numerous recently described variants including hyperkeratotic, keloidal, micronodular, pyogenic granuloma-like, ecchymotic, and intravascular KS. Involuting lesions as a result of treatment related regression are also presented.
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Kaposi Sarcoma in unusual locations
BMC Cancer, 2008Co-Authors: Liron Pantanowitz, Bruce J. DezubeAbstract:Kaposi Sarcoma (KS) is a multifocal, vascular lesion of low-grade malignant potential that presents most frequently in mucocutaneous sites. KS also commonly involves lymph nodes and visceral organs. This article deals with the manifestation of KS in unusual anatomic regions. Unusual locations of KS involvement include the musculoskeletal system, central and peripheral nervous system, larynx, eye, major salivary glands, endocrine organs, heart, thoracic duct, urinary system and breast. The development of KS within wounds and blood clots is also presented. KS in these atypical sites may prove difficult to diagnose, resulting in patient mismanagement. Theories to explain the rarity and development of KS in these unusual sites are discussed.
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Advances in the pathobiology and treatment of Kaposi Sarcoma.
Current Opinion in Oncology, 2004Co-Authors: Liron Pantanowitz, Bruce J. DezubeAbstract:PURPOSE OF REVIEW Kaposi Sarcoma, which has reached epidemic proportions in parts of Africa and in the Western world, continues to pose a problem in patients with AIDS receiving highly active antiretroviral therapy (HAART). This article reviews the new and important information regarding the epidemiology, biology, and management of Kaposi Sarcoma that was published in the last year. RECENT FINDINGS Worldwide Kaposi Sarcoma herpesvirus/human herpesvirus 8 (HHV8) seropositivity has been found to exceed the incidence of Kaposi Sarcoma. Therefore, investigators have justifiably implicated other cofactors (eg, blood-sucking arthropods, angiotensin converting enzyme inhibitors, hemodialysis, and iron) in the development of Kaposi Sarcoma. In the transplant setting, Kaposi Sarcoma lesions have been shown to originate from the engraftment of donor tumor cells. The detection of HHV8 in Kaposi Sarcoma lesions has provided a new diagnostic tool to help differentiate Kaposi Sarcoma from its mimics. Kaposi Sarcoma lesional cells, now confirmed to be of lymphatic origin, have been shown to express several chemokine receptors, some of which may help explain the predilection for skin. Regression of Kaposi Sarcoma has been characterized histologically for the first time. The finding that some tumor cells can remain in an atrophic state even in completely regressed lesions suggests that they have the potential to recur. Protease inhibitor-based and nonnucleoside reverse transcriptase inhibitor-based HAART regimens have been verified to be similarly effective. Although antiretrovirals have been noted to favorably alter the clinical characteristics of Kaposi Sarcoma favorably, they seem not to alter the natural history of this disease. In the HAART era, because CD4 cell count was shown no longer to provide prognostic information about AIDS-related Kaposi Sarcoma, the traditional classification system for staging AIDS-related Kaposi Sarcoma has been refined. Also, a new staging system for classic Kaposi Sarcoma has been proposed. SUMMARY Numerous advances have emerged regarding Kaposi Sarcoma during the last year, many of which still need to be translated into clinically useful information. The results of new clinical trials involving antivirals purposely directed against HHV8 and antiretrovirals for HIV-uninfected people are anticipated. Finally, although investigators during this period did provide us with additional potential therapeutic targets, more novel approaches such as RNA interference and gene therapy have been also proposed as options in the future management of Kaposi Sarcoma.
Corey Casper - One of the best experts on this subject based on the ideXlab platform.
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clinical presentation and outcome of epidemic Kaposi Sarcoma in ugandan children
Infectious Agents and Cancer, 2010Co-Authors: Corey Casper, Soren Gantt, Abel Kakuru, Anna Wald, Victoria Walusansa, Lawrence Corey, Jackson OremAbstract:Background—Kaposi Sarcoma (KS) is one of the most common pediatric cancers in subSaharan Africa. Few data are available about the clinical presentation or response to treatment of children with epidemic (HIV-associated) KS. Methods—Medical records of all children with KS and HIV infection referred to the Uganda Cancer Institute in Kampala, Uganda from October 2004 to June 2007 were reviewed. Charts were
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clinical presentation and outcome of epidemic Kaposi Sarcoma in ugandan children
Pediatric Blood & Cancer, 2010Co-Authors: Corey Casper, Soren Gantt, Abel Kakuru, Anna Wald, Victoria Walusansa, Lawrence Corey, Jackson OremAbstract:Background Kaposi Sarcoma (KS) is one of the most common pediatric cancers in sub-Saharan Africa. Few data are available about the clinical presentation or response to treatment of children with epidemic (HIV-associated) KS. Methods Medical records of all children with KS and HIV infection referred to the Uganda Cancer Institute in Kampala, Uganda from October 2004 to June 2007 were reviewed. Charts were abstracted for age, sex, location of KS lesions at presentation, biopsy results, CD4 T-cell count and percentage, and KS treatment and outcome. Results Seventy-three children with epidemic KS were identified, 37 males and 36 females. The median age was 10.1 years (range 2–18). KS presented with lymph node (LN) involvement in 60% of cases. The median absolute and percentage CD4 T-cells at presentation were 210 cells/µl and 7.4%, respectively. Those children with lymphadenopathic KS were younger (mean difference 3.7 years; P = 0.01) and had higher CD4 T-cell counts (mean difference 242 cells/µl; P = 0.03) than those without LN involvement. Of 32 patients for whom outcome data were available, a complete response to chemotherapy and/or antiretroviral therapy was documented in 20 (62.5%) patients. Conclusions In comparison to cutaneous involvement, LN involvement of epidemic KS occurs at younger ages and at higher CD4 levels. This clinical presentation may reflect recent infection with human herpesvirus 8 followed by a rapid progression to malignancy. Favorable response to treatment was observed in the majority of cases, but prospective studies are needed to determine optimal management. Pediatr Blood Cancer 2010;54:670–674. © 2010 Wiley-Liss, Inc.
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epidemiology pathophysiology and treatment of Kaposi Sarcoma associated herpesvirus disease Kaposi Sarcoma primary effusion lymphoma and multicentric castleman disease
Clinical Infectious Diseases, 2008Co-Authors: Ryan J Sullivan, Liron Pantanowitz, Corey Casper, Justin Stebbing, Bruce J. DezubeAbstract:Kaposi Sarcoma-associated herpesvirus infection is associated with the development of 3 proliferative diseases: Kaposi Sarcoma, primary effusion lymphoma, and multicentric Castleman disease. These conditions are also intimately associated with human immunodeficiency virus infection, and important synergistic interactions between these 2 viruses have been described. Despite differences in viral gene expression patterns in each condition, Kaposi Sarcoma-associated herpesvirus encodes similar oncogenic proteins that promote the activation of sequential and parallel signaling pathways. Therapeutic strategies have been implemented to target these unique signaling pathways, and this sort of molecular targeting is the focus of many current research efforts. The scope of this review is to present contemporary knowledge about the epidemiology, virology, and immunology of Kaposi Sarcoma-associated herpesvirus and to highlight several key oncogene products that may be targets for chemotherapy.
Denise Whitby - One of the best experts on this subject based on the ideXlab platform.
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Kaposi Sarcoma
Nature Reviews Disease Primers, 2019Co-Authors: Ethel Cesarman, Blossom Damania, Susan E. Krown, Jeffrey Martin, Mark Bower, Denise WhitbyAbstract:Kaposi Sarcoma is a rare cancer that typically presents with multiple pigmented skin lesions, but may take an aggressive course characterised by lesion ulceration, oedema and visceral organ involvement. This Primer describes the epidemiology, clinical features, cellular mechanisms and management of the main forms of Kaposi Sarcoma. Kaposi Sarcoma (KS) gained public attention as an AIDS-defining malignancy; its appearance on the skin was a highly stigmatizing sign of HIV infection during the height of the AIDS epidemic. The widespread introduction of effective antiretrovirals to control HIV by restoring immunocompetence reduced the prevalence of AIDS-related KS, although KS does occur in individuals with well-controlled HIV infection. KS also presents in individuals without HIV infection in older men (classic KS), in sub-Saharan Africa (endemic KS) and in transplant recipients (iatrogenic KS). The aetiologic agent of KS is KS herpesvirus (KSHV; also known as human herpesvirus-8), and viral proteins can induce KS-associated cellular changes that enable the virus to evade the host immune system and allow the infected cell to survive and proliferate despite viral infection. Currently, most cases of KS occur in sub-Saharan Africa, where KSHV infection is prevalent owing to transmission by saliva in childhood compounded by the ongoing AIDS epidemic. Treatment for early AIDS-related KS in previously untreated patients should start with the control of HIV with antiretrovirals, which frequently results in KS regression. In advanced-stage KS, chemotherapy with pegylated liposomal doxorubicin or paclitaxel is the most common treatment, although it is seldom curative. In sub-Saharan Africa, KS continues to have a poor prognosis. Newer treatments for KS based on the mechanisms of its pathogenesis are being explored.
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clinical features and outcomes of patients with symptomatic Kaposi Sarcoma herpesvirus kshv associated inflammation prospective characterization of kshv inflammatory cytokine syndrome kics
Clinical Infectious Diseases, 2016Co-Authors: Mark N. Polizzotto, Thomas S. Uldrick, Denise Whitby, Karen Aleman, Vickie Marshall, Kathleen M Wyvill, Victoria Wang, Stefania Pittaluga, Elaine S Jaffe, Corina MilloAbstract:BACKGROUND Kaposi Sarcoma herpesvirus (KSHV) is the cause of Kaposi Sarcoma (KS), primary effusion lymphoma (PEL), and a form of Castleman disease (KSHV-MCD). Recently a KSHV-associated inflammatory cytokine syndrome (KICS) distinct from KSHV-MCD was reported. METHODS We prospectively characterized the clinical, laboratory, virologic and immunologic features of KICS by evaluating symptomatic adults with KSHV using a prespecified definition. These features and overall survival were compared with controls from 2 prospectively characterized human immunodeficiency virus (HIV)-infected cohorts, including 1 with KSHV coinfection. RESULTS All 10 KICS subjects were HIV infected males; 5 had HIV viral load (VL) suppressed <50 copies mL (median 72, range <50-74 375); all had KS and 2 also had PEL. All had multiple severe symptoms attributable to KICS: median number of symptoms 8 (6-11), median grade of worst symptom 3 (2-4). These included gastrointestinal disturbance (present in 9); edema (9); respiratory (6); and effusions (5). Laboratory abnormalities included anemia (all); hypoalbuminemia (all) and thrombocytopenia (6). None developed KSHV-MCD; 6 died with median survival from KICS diagnosis 13.6 months. KICS subjects compared with controls had more severe symptoms; lower hemoglobin and albumin; higher C-reactive protein; higher KSHV VL; elevated interleukin (IL)-6 and IL-10; and an increased risk of death (all P < .05). Anemia and hypoalbuminemia at presentation were independently associated with early death. CONCLUSIONS KICS subjects demonstrated diverse severe symptoms, a high rate of KSHV-associated tumors, high mortality, and a distinct IL-6/IL-10 signature. KICS may be an important unrecognized cause of morbidity and mortality, including symptoms previously ascribed to HIV. Exploration of KSHV-directed therapy is warranted.
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bone marrow findings in hiv positive patients with Kaposi Sarcoma herpesvirus associated multicentric castleman disease
American Journal of Clinical Pathology, 2013Co-Authors: Girish Venkataraman, Thomas S. Uldrick, Denise Whitby, Karen Aleman, Deirdre Omahony, Donald S Karcher, Seth M Steinberg, Mark Raffeld, Vickie Marshall, Richard F LittleAbstract:Kaposi Sarcoma herpesvirus (KSHV), also known as human herpesvirus-8, is associated with 1 form of multicentric Castleman disease (MCD) and is the etiologic agent for most MCD in human immunodeficiency virus (HIV)–infected patients. Diagnosis is usually determined by lymph node biopsy. Bone marrow findings in KSHV-MCD are not well characterized. We conducted histomorphologic and immunohistochemical evaluation of bone marrow biopsy specimens in HIV-infected patients with KSHV-MCD, including evaluation for KSHV latency-associated nuclear antigen. Findings were correlated with clinical features and KSHV viral load. Reactive plasmacytosis was the predominant feature. Lymphoid aggregates were less common and not diagnostic of KSHV-MCD. Forty-eight percent of cases contained scattered KSHV-infected mononuclear cells. Although patients were generally cytopenic, bone marrow biopsy specimens were normocellular to hypercellular except in patients receiving hematotoxic therapy. Bone marrow biopsy specimens in KSHV-MCD patients recapitulate findings of interleukin-6 excess. In patients with HIV, unexplained cytopenias, and bone marrow plasmacytosis, evaluation for KSHV-MCD is warranted.
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an interleukin 6 related systemic inflammatory syndrome in patients co infected with Kaposi Sarcoma associated herpesvirus and hiv but without multicentric castleman disease
Clinical Infectious Diseases, 2010Co-Authors: Thomas S. Uldrick, Karen Aleman, Deirdre Omahony, Seth M Steinberg, Vickie Marshall, Kathleen M Wyvill, Victoria Wang, Stefania Pittaluga, Irina Maric, Denise WhitbyAbstract:Background Kaposi Sarcoma-associated herpesvirus (KSHV) is the causal agent for Kaposi Sarcoma (KS) and multicentric Castleman disease (MCD) in human immunodeficiency virus (HIV)-infected patients. Patients with KSHV-MCD develop fevers, wasting, hypoalbuminemia, cytopenias, and hyponatremia that are related to overproduction of KSHV-encoded viral interleukin (IL)-6 (vIL-6) and human IL-6 (hIL-6). Methods We identified 6 HIV-infected patients with KS or serological evidence of KSHV infection who had severe inflammatory MCD-like symptoms but in whom we could not diagnose MCD, and we hypothesized that these symptoms resulted from vIL-6 overproduction. Serum vIL-6 levels were assessed in these 6 patients and compared with levels in 8 control patients with symptomatic KSHV-MCD and 32 control patients with KS. KSHV viral load, serum hIL-6 level, and human IL-10 level were also evaluated. Results Patients with inflammatory MCD-like symptoms but without MCD had elevated vIL-6 levels, comparable with levels in patients with symptomatic KSHV-MCD, and had levels that were significantly greater than those in control patients with KS (P = .003). Elevated hIL-6, IL-10, and KSHV viral loads were also comparable to patients with symptomatic KSHV-MCD and significantly greater than those with KS. Conclusions A subset of patients with HIV and KSHV co-infection, but without MCD, can develop severe systemic inflammatory symptoms associated with elevated levels of KSHV vIL-6, IL-6, and KSHV viral loads. Excess lytic activation of KSHV, production of the lytic gene product vIL6, and associated immunologic dysregulation may underlie the pathophysiology of these symptoms. This IL-6-related inflammatory syndrome is important to consider in critically ill patients with HIV and KSHV co-infection.
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risk factors for classical Kaposi Sarcoma in a population based case control study in sicily
Cancer Epidemiology Biomarkers & Prevention, 2008Co-Authors: Lesley A Anderson, Denise Whitby, Carmela Lauria, Nino Romano, Elizabeth E Brown, Barry I Graubard, Yan Li, Angelo Messina, Lorenzo Gafa, Francesco VitaleAbstract:Background: Classical Kaposi Sarcoma is a rare complication of Kaposi Sarcoma-associated herpes virus (KSHV) infection. We conducted a population-based, frequency-matched case-control study in Sicily to further investigate the reported inverse relationship between smoking and classical Kaposi Sarcoma and to identify other factors associated with altered risk. Methods: All incident, histologically confirmed classical Kaposi Sarcoma cases in Sicily were eligible. A two-stage cluster sample design was applied to select population controls. KSHV seropositivity was determined using four antibody assays (K8.1 and orf73 enzyme immunoassays and two immunofluorenscence assays). Using SAS-callable SUDAAN, we compared the characteristics of classical Kaposi Sarcoma cases and KSHV-seropositive controls. Odds ratios (OR) and 95% confidence intervals (CI) are presented. Results: In total, 142 classical Kaposi Sarcoma cases and 123 KSHV-seropositive controls were recruited. Current cigarette smoking was associated with reduced risk of classical Kaposi Sarcoma amongst males (OR, 0.20; 95% CI, 0.06-0.67). Edema was associated with classical Kaposi Sarcoma, but only when it presented on the lower extremities (OR, 3.65; 95% CI, 1.62-8.23). Irrespective of presentation site, diabetes and oral corticosteroid medications were associated with increased risk (OR, 4.73; 95% CI, 2.02-11.1 and OR, 2.34; 95% CI, 1.23-4.45, respectively). Never smoking, diabetes, and oral corticosteroid medication use were all independently associated with classical Kaposi Sarcoma risk. Discussion: We confirmed previous reports that cigarette smoking was associated with a reduced risk of classical Kaposi Sarcoma, and we found that risk was lowest among current smokers. We also found that classical Kaposi Sarcoma risk was strongly and independently associated with oral corticosteroid use and diabetes. Corroboration of these observations and investigation of possible underlying mechanisms are warranted. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3435–43)
Soren Gantt - One of the best experts on this subject based on the ideXlab platform.
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clinical presentation and outcome of epidemic Kaposi Sarcoma in ugandan children
Infectious Agents and Cancer, 2010Co-Authors: Corey Casper, Soren Gantt, Abel Kakuru, Anna Wald, Victoria Walusansa, Lawrence Corey, Jackson OremAbstract:Background—Kaposi Sarcoma (KS) is one of the most common pediatric cancers in subSaharan Africa. Few data are available about the clinical presentation or response to treatment of children with epidemic (HIV-associated) KS. Methods—Medical records of all children with KS and HIV infection referred to the Uganda Cancer Institute in Kampala, Uganda from October 2004 to June 2007 were reviewed. Charts were
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clinical presentation and outcome of epidemic Kaposi Sarcoma in ugandan children
Pediatric Blood & Cancer, 2010Co-Authors: Corey Casper, Soren Gantt, Abel Kakuru, Anna Wald, Victoria Walusansa, Lawrence Corey, Jackson OremAbstract:Background Kaposi Sarcoma (KS) is one of the most common pediatric cancers in sub-Saharan Africa. Few data are available about the clinical presentation or response to treatment of children with epidemic (HIV-associated) KS. Methods Medical records of all children with KS and HIV infection referred to the Uganda Cancer Institute in Kampala, Uganda from October 2004 to June 2007 were reviewed. Charts were abstracted for age, sex, location of KS lesions at presentation, biopsy results, CD4 T-cell count and percentage, and KS treatment and outcome. Results Seventy-three children with epidemic KS were identified, 37 males and 36 females. The median age was 10.1 years (range 2–18). KS presented with lymph node (LN) involvement in 60% of cases. The median absolute and percentage CD4 T-cells at presentation were 210 cells/µl and 7.4%, respectively. Those children with lymphadenopathic KS were younger (mean difference 3.7 years; P = 0.01) and had higher CD4 T-cell counts (mean difference 242 cells/µl; P = 0.03) than those without LN involvement. Of 32 patients for whom outcome data were available, a complete response to chemotherapy and/or antiretroviral therapy was documented in 20 (62.5%) patients. Conclusions In comparison to cutaneous involvement, LN involvement of epidemic KS occurs at younger ages and at higher CD4 levels. This clinical presentation may reflect recent infection with human herpesvirus 8 followed by a rapid progression to malignancy. Favorable response to treatment was observed in the majority of cases, but prospective studies are needed to determine optimal management. Pediatr Blood Cancer 2010;54:670–674. © 2010 Wiley-Liss, Inc.
