Relevant bibliographies by topics / Kaposi, Sarcoma de

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  1. Journal articles
  2. Dissertations / Theses
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  5. Conference papers

Academic literature on the topic 'Kaposi, Sarcoma de'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "Kaposi, Sarcoma de"

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Radu, Oana, and Liron Pantanowitz. "Kaposi Sarcoma." Archives of Pathology & Laboratory Medicine 137, no. 2 (2013): 289–94. http://dx.doi.org/10.5858/arpa.2012-0101-rs.

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Kaposi sarcoma (KS) is a low-grade vascular tumor associated with Kaposi sarcoma herpesvirus/human herpesvirus 8 (KSHV/HHV8) infection. Kaposi sarcoma lesions predominantly present at mucocutaneous sites, but may involve all organs and anatomic locations. Recognized epidemiologic-clinical forms of KS include classic, African (endemic), AIDS-associated (epidemic), and iatrogenic KS. New clinical manifestations have been described, such as antiretroviral therapy–related KS regression or flares. Kaposi sarcoma lesions evolve from early (patch stage) macules into plaques (plaque stage) that grow into larger nodules (tumor stage). Newer histologic variants include anaplastic, hyperkeratotic, lymphangioma-like, bullous, telangiectatic, ecchymotic, keloidal, pyogenic granuloma–like, micronodular, intravascular, glomeruloid and pigmented KS, as well as KS with sarcoidlike granulomas and KS with myoid nodules. Latency-associated nuclear antigen (HHV8) is the most specific immunohistochemical marker available to help distinguish KS from its mimics. Since KS remains one of the most common AIDS-defining malignancies, it is important that pathologists be able to recognize KS and its contemporary manifestations.
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MARTIN, ROBERT W., ANTOINETTE F. HOOD, and EVAN R. FARMER. "Kaposi Sarcoma." Medicine 72, no. 4 (1993): 245–61. http://dx.doi.org/10.1097/00005792-199307000-00004.

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Pantanowitz, Liron. "Kaposi sarcoma." Cancer 112, no. 5 (2008): 962–65. http://dx.doi.org/10.1002/cncr.23263.

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El-Ashmawy, Amal A., and Ghada A. El-Ayat. "Kaposi sarcoma." Journal of the Egyptian Womenʼs Dermatologic Society 9, no. 2 (2012): 77–85. http://dx.doi.org/10.1097/01.ewx.0000413296.62974.c3.

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Gupta, Kush, Aung Tun, Ashish Gupta, et al. "A case of classic Kaposi sarcoma in an immunocompetent human immunodeficiency virus–negative Dominican man." SAGE Open Medical Case Reports 8 (January 2020): 2050313X2093824. http://dx.doi.org/10.1177/2050313x20938249.

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Kaposi sarcoma is an uncommon tumor that primarily arises in the skin and mucosal surfaces, but may metastasize to the internal organs. Four main variants of Kaposi sarcoma are recognized as the following: classic Kaposi sarcoma, which occurs in middle-aged or elderly men; epidemic Kaposi sarcoma, associated with human immunodeficiency virus infection; iatrogenic Kaposi sarcoma seen in patients on immunosuppressive drug therapy; and endemic Kaposi sarcoma. This report is of a case of classic Kaposi sarcoma in 55-year-old immunocompetent and human immunodeficiency virus–negative Dominican man who had lived in the United States for 2 years, who presented with a 2-year history of skin lesions on his lower extremities and soft palate. Biopsy of the soft palate was consistent with Kaposi sarcoma. The patient was treated with paclitaxel with a good response. This case report demonstrates the importance of recognizing that classic Kaposi sarcoma, first described almost 150 years ago, can still present in immunocompetent middle-aged men of all ethnicities.
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Yasnitsky, N. N. "Sarcoma idiopathicum multiplex haemorrhagicum (Kaposi)." Kazan medical journal 17, no. 2 (2021): 247–51. http://dx.doi.org/10.17816/kazmj79465.

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The disease of the skin, described for the first time by Kaposi in 1872 under the name sarcoma idiopathicum pigmentosum and attributed by him to the true primary sarcomas of the skin, being relatively rare, attracted the attention of prominent dermatologists at the end of the last century, serving as the subject of a lively and lengthy controversy both in the literature and and at various congresses of dermatologists, including the XII International Congress in Moscow.
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Wolff, K., and W. Jurecka. "Is Kaposi Sarcoma a Sarcoma?" American Journal of Dermatopathology 19, no. 4 (1997): 424. http://dx.doi.org/10.1097/00000372-199708000-00030.

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Rebizak, Ewelina A., Jolanta Węgłowska, and Katarzyna Łuczak. "Pseudo-Kaposi sarcoma." Dermatology Review 105, no. 4 (2018): 554–57. http://dx.doi.org/10.5114/dr.2018.78077.

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Costa, Mariana, Diana Carvalho, Mariana Silva, et al. "UNUSUAL KAPOSI SARCOMA." European Journal of Internal Medicine 22 (October 2011): S22—S23. http://dx.doi.org/10.1016/s0953-6205(11)60090-3.

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Gottlieb, Michael. "Pulmonary Kaposi Sarcoma." CJEM 18, no. 5 (2015): 399–400. http://dx.doi.org/10.1017/cem.2015.72.

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Dissertations / Theses on the topic "Kaposi, Sarcoma de"

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Khammisa, Razia Abdool Gafaar. "Oral HIV-associated Kaposi sarcoma: A clinical study from theGa-Rankuwa area, South Africa." Thesis, University of Limpopo (Medunsa Campus), 2011. http://hdl.handle.net/10386/433.

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Thesis (M Med (Periodontics and Oral Medicine))--University of Limpopo, 2011.
Background: Kaposi sarcoma (KS) is the most common neoplasm diagnosed in HIV-seropositive subjects. HIV-associated KS (HIV-KS) may affect any body system and the disease may be slowly progressing or fulminant. Oral involvement is frequent and extensive oral HIV-KS is associated with poor prognosis. Methods: All cases of oral HIV-KS treated in the Department of Periodontology and Oral Medicine over a period of seven years were included in this retrospective study. A record was made regarding the clinical and laboratory features, and differences in these features between males and females were statistically tested. The differences between the percentages of the different clinical appearances of oral HIV-KS lesions; and between the features of oral HIV-KS in patients who contracted HIV infection before the diagnosis of oral KS and those who were diagnosed with HIV infection at the time of oral KS presentation were also tested. Results: Of the 37 patients included in the study, 54% were females and 46% were males and two patients (5%) were children. In 21 patients (57%) the initial presentation of HIV-KS was in the mouth. Seventeen patients (46%) were diagnosed with HIV infection and oral KS at the same time. At the time of oral HIV-KS diagnosis, 29 patients (78%) had multiple lesions affecting one or several sites. There were no statistically significant differences between males and females regarding the clinical and laboratory features of oral HIV-KS except for the size of the lesions. The percentage of lesions <10mm was significantly lower in females than males (chi-squared test: p=0.007), whereas the percentage of lesions ≥10mm≤50mm was significantly higher in females than in males (chi-squared test: p=0.0004). There were significantly more patients with multiple oral HIV-KS lesions than patients with single oral HIV-KS lesions (binomial distribution test: p=0.0003). At the time of oral HIV-KS diagnosis, the difference between ix the average CD4+ T cell counts of the patients who were concurrently diagnosed with HIV infection and oral KS (130cells/mm3), and those who contracted HIV infection before developing oral HIV-KS (90 cells/mm3) was not statistically different. Nine patients (24%) developed facial lymphoedema in association with multifocal exophytic oral HIV-KS lesions. The average CD4+ T cell counts of these patients at the time of oral HIV-KS diagnosis was 28 cells/mm3, and was statistically significantly lower (t-test: p= 0.01) than the average CD4+ T cell count (133 cells/mm3) of those who did not develop facial lymphoedema. All the patients with facial lymphoedema died, on average within two weeks from the occurrence of facial lymphoedema. One patient (2.7%) developed immune reconstitution inflammatory syndrome (IRIS) – associated oral HIV-KS, and his oral HIV-KS resolved following administration of highly active antiretroviral therapy (HAART) and systemic cytotoxic chemotherapy, and surgical excision. Out of the 28 patients who were not lost to follow-up, 21 (75%) died, on average within 13.6 weeks from the time of oral HIV-KS diagnosis and seven (25%) survived. At the time of oral HIV-KS diagnosis the difference in the average CD4+ T cell count of the patients who died (64 cells/mm3) and those who survived (166 cells cells/mm3) was statistically significant (t-test: p=0.016). The prognosis of the patients who received cytotoxic chemotherapy was better than the prognosis of those who received only HAART, or those who were HAART-naïve. Conclusions: Oral HIV-KS affects females more frequently than males (M:F = 1:1.2), and it is not uncommon in children. A lower CD4+ T cell count at the time of oral HIV-KS diagnosis is associated with a poor prognosis. Patients who develop facial lymphoedema during the course of HIV-KS disease, die soon thereafter. Oral HIV-KS can be successfully treated with systemic cytotoxic chemotherapy.
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Hansen, A. "Kaposi sarcoma herpesvirus microRNA function in lymphatic endothelial cells." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/133395/.

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Kaposi’s sarcoma herpesvirus (KSHV) is the causative agent of Kaposi’s sarcoma (KS), the most common AIDS-associated malignancy. KS lesions are comprised of poorly differentiated, spindle-shaped endothelial cells, the precursors of which are lymphatic endothelial cells (LEC). KSHV infection of LEC induces transcriptional reprogramming towards a phenotype more analogous to blood vessel endothelial cells BEC. KSHV encodes 17 mature miRNAs (miRNA), 14 of which are co-expressed as a cluster. miRNAs are small non-coding RNA molecules that act posttranscriptionally to negatively regulate gene expression. It was the aim of this thesis to investigate the function of the KSHV miRNAs through identifying viral miRNA targets in LEC. miRNAs silence their target genes by either blocking translation or inducing mRNA degradation. Gene expression microarray (GEM) analysis was used to quantify changes in mRNA abundance of LEC transcripts induced by the KSHV miRNA cluster. MAF, a leucine zipper transcription factor, was significantly down-regulated in the presence of the viral miRNAs. miRNA expression analysis of KS lesions identified those KSHV miRNAs which are expressed and therefore relevant to KS pathogenesis. In silico prediction analysis identified multiple KSHV miRNAs binding sites in the MAF 3’UTR, MAF silencing was mediated through specific interactions with these sites. In particular, KSHV miRNAs miR-K12-6 and miR-K12-11 were identified as individual miRNAs responsible for MAF down-regulation. MAF was silenced specifically by these miRNAs during primary KSHV infection of LEC. MAF has been previously characterised as a LEC-specific transcription factor, although its function and target genes were unknown. GEM profiling of LEC in which MAF was silenced by siRNA revealed an increase in expression of BEC markers. Therefore, in LEC, MAF acts a transcriptional repressor of BEC transcripts helping to maintain lymphatic identity. Gene set enrichment analysis of three GEM data sets revealed a significant concordant increase in BEC genes during primary KSHV infection, expression of the KSHV miRNA cluster and MAF silencing. The miRNA cluster-induced up-regulation of BEC markers was shown to be by way of MAF silencing. In this study I have identified and validated MAF as a LEC-specific KSHV miRNA target and have shown MAF to have a role in maintaining LEC identity through repression of BEC markers. Consequently, down-regulation of MAF following KSHV miRNA expression contributes to the mechanism behind the transcription reprogramming of LEC observed upon KSHV infection.
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Pyakurel, Pawan. "AIDS and endemic kaposi's sarcoma development comparison by histopathology, virology (HHV-8/KSHV) and cytogenetics /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-465-1/.

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Sprinz, Eduardo. "Tratamento sistêmico do Sarcoma de Kaposi associado a AIDS : estudo clínico e farmacológico com doses fracionadas de Etoposida por via oral." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2000. http://hdl.handle.net/10183/115325.

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Pak, Fatemeh. "HHV-8/KSHV association with tumor cells during development of Kaposi sarcoma /." Stockholm, 2006. http://diss.kib.ki.se/2006/20060202pak/.

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Kimball, Louise Elizabeth. "Humoral immune response to Kaposi's sarcoma-associated herpesvirus in persons with and without Kaposi's sarcoma /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/9284.

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Mendoza, Tania Regina Tozetto. "Análise da variabilidade genética do Herpesvirus 8 humano (HHV-8) em indivíduos infectados por HIV com e sem sarcoma de Kaposi." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/99/99131/tde-31012014-111943/.

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O HHV-8 (herpesvírus 8 humano) é o agente etiológico do sarcoma de Kaposi (SK). Diferentemente dos outros herpesvírus, o HHV-8 é distribuído de modo não ubíquo ao redor do mundo. São sete os principais genótipos de HHV-8, de acordo com o padrão de variabilidade da ORF K1: A, B, C, D, E, F e Z. Estudos da variabilidade genética do HHV-8 poderão trazer melhores interpretações sobre o potencial patogênico dos genótipos de HHV-8 e das variações genotípicas funcionais. Dados sobre a variabilidade genética do HHV-8 no Brasil, em que o SK é associado ao HIV, permanecem escassos. Pelo nosso conhecimento, esse é o primeiro estudo que compara a variabilidade genética de HHV-8 em indivíduos infectados por HIV com SK e sem SK no Brasil. Objetivo. O estudo visou analisar a variabilidade genética do HHV-8 entre indivíduos infectados por HIV com SK e sem histórico de SK. Métodos. Sequências de DNA de HHV-8 foram investigadas em amostras criopreservadas de células mononucleares do sangue periférico a partir de 37 indivíduos infectados por HIV com SK (grupo 1); e de amostras de saliva de indivíduos sem SK (grupo 2), as quais foram selecionadas por meio da detecção positiva de DNA/ORF73/HHV-8 a partir de um total de 751 indivíduos. Dados demográficos e clínicos do estadio e evolução do SK, assim como parâmetros laboratoriais foram caracterizados. As análises moleculares e reconstruções filogenéticas foram baseadas nas ORFs K1 e K12 do HHV-8. Resultados. Foram obtidas sequências de DNA dos loci K1 e/ou K12 de 75 indivíduos, 34 indivíduos do grupo 1 e 41 do grupo 2. O sistema de primers empregado foi capaz de detectar os genótipos A, B, C, F e amplo perfil de subgenótipos de K1/HHV-8. Os dados não mostraram associação de genótipos de HHV-8 com a presença de SK ou estadio de SK. Todavia, o subgenótipo B1 predominou naqueles em que não houve registro de piora de SK (p=0,04). Os subgenótipos B1 e C3 foram igualmente predominantes em ambos os grupos. As frequências do genótipos A foram de 24% e 12,2% e dos genótipos B e C foram de 34,1 e 35,3%, nos grupos 1 e 2, respectivamente. O genótipo F foi descrito pela primeira no Brasil, um caso de cada grupo. Um amplo perfil de subgenótipos de C no grupo 2 sem SK foi encontrado (C1, C2, C3, C5 e C7). Subgenótipos K1 C5 e C7, exclusivos do grupo 2 (7%), foram confirmados como recombinantes. Não houve variabilidade genotípica de HHV-8 em amostras biológicas diferentes do mesmo indivíduo em oito casos estudados. Sítios polimórficos (6/59) em regiões codificadoras de miRNA do locus K12 foram observados, sendo 70% presentes exclusivamente em sequências de HHV-8 do grupo com SK e protótipos de SK. Conclusão. Embora não houvesse associação entre genótipos de HHV-8 e presença ou estadio de SK, o subgenótipo B1 foi significativamente relacionado ao melhor prognóstico de SK. Alguns recombinantes foram observados no locus K1 de HHV-8 em indivíduos do grupo 2 sem SK. A presença de SNPs em regiões codificadoras de miR12-12 e miR12-10 predominou em sequências de HHV-8 de indivíduos com SK, grupo 1, e protótipos de SK epidêmico, endêmico e clássico. A escoha de primers foi importante para garantir a amplificação de todos os genótipos e amplo perfil de subgenotipos de HHV-8.
HHV-8 (Human Herpes Virus 8) is the etiological agent of Kaposi\'s sarcoma (KS). Unlike other herpesviruses, the distribution of HHV-8 is not so ubiquitous around the world. There are seven major HHV-8 genotypes, according to the variability pattern of the ORF K1: A, B, C, D, E, F and Z. Studies on the genetic variability of HHV-8 may help to better understand the pathogenic potential of HHV-8 genotypes and their functional genotypic variations. Data on the genetic variability of HHV-8 in Brazil, where KS is associated with HIV infected people, remain scarce. To our knowledge, this is the first study comparing the genetic variability of HHV-8 among HIV-infected individuals with KS and without KS in Brazil. Objective. The study aimed to analyze the genetic variability of HHV-8 among HIV-infected individuals with and without KS. Casuistry and Methods. HHV-8 DNA sequences were obtained from samples of cryopreserved peripheral blood mononuclear cells from 37 individuals infected with HIV-KS (group 1); and saliva from individuals without KS (group 2) who were selected by means of detection of positive DNA/ORF73/HHV-8 from a total of 751 individuals. Demographic and clinical data (stage and progression of KS), as well as laboratory parameters were characterized. Molecular analysis and phylogenetic reconstructions were based on sequences of the ORFs K1 and/or K12 of HHV-8. Results. K1 and/or K12 DNA sequences of HHV-8 were obtained from 75 subjects, 34 from group 1 and 41 from group 2. The primer system used was able to detect the genotypes A, B, C, F and a wide profile of HHV- 8 K1 subgenotypes. Data showed no association of genotypes with the occurrence of KS or with visceral KS either. However, subgenotype B1 predominated in individuals who did not report any progression of KS (p=0.04). Subgenotypes B1 and C3 were equally prevalent in both groups. Genotype A frequencies were 24 % and 12.2% and genotypes B and C were 34.1 and 35.3 % in groups 1 and 2, respectively. We also described here for the first time the genotype F of HHV-8 in Brazil. A wide profile of subgenotypes C (C1, C2, C3, C5 and C7) in the group without KS was found. HHV-8 K1 DNA sequences of group 2 (7%) belonging to subgenotypes C5 and C7 were confirmed as recombinants. Our findings did not show virus variability in the same patient in samples collected at different times or from different biological material in the eight cases studied here. There was no statistical difference regarding the presence/absence of a given SNP from locus K12 between groups with and without KS. However, there were a total of 6/59 polymorphic sites in coding regions of miRNA, 70% of which present only in the HHV-8 DNA sequence of group with KS and KS prototypes. Conclusion. Although there was no association between HHV-8 genotypes and the presence of KS and KS clinical stage, subgenotype B1 was significantly related to the absence of progression of KS. Some recombinants in K1/HHV-8 locus were observed in the group without KS. The presence of SNPs in coding regions of miR12-12 and miR12- 10 predominated in sequences of HHV- 8 of SK cases (group 1) and of epidemic, endemic and classic KS prototypes. The choice of primers was essential to ensure amplification of all HHV- 8 genotypes and wide profile de subgenotypes.
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Silva, Suzane Ramos da [UNESP]. "Patobiologia do hespervírus associado ao Sarcoma de Kaposi/Hespervírus Humano Tipo-8: genotipagem de isolados virais em lesões de Sarcoma de Kaposi e imunoevasão dependente da inibição da síntese e modulação da degradação da proteína viral LANA-1." Universidade Estadual Paulista (UNESP), 2008. http://hdl.handle.net/11449/104599.

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Made available in DSpace on 2014-06-11T19:33:25Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-04-29Bitstream added on 2014-06-13T19:44:12Z : No. of bitstreams: 1 silva_sr_dr_botfm.pdf: 1456327 bytes, checksum: a429186d37bfb5815b5f13088abac56f (MD5)
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Silva, Suzane Ramos da. "Patobiologia do hespervírus associado ao Sarcoma de Kaposi/Hespervírus Humano Tipo-8 : genotipagem de isolados virais em lesões de Sarcoma de Kaposi e imunoevasão dependente da inibição da síntese e modulação da degradação da proteína viral LANA-1 /." Botucatu : [s.n.], 2008. http://hdl.handle.net/11449/104599.

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Orientador: Deilson Elgui de Oliveira
Banca: José Vassallo
Banca: Luisa Lina Villa
Banca: Sandra Cecília Botelho Costa
Banca: Claudio Sérgio Pannuti
Resumo: Não disponível.
Abstract: Not available.
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Penín, Mosquera Rosa Maria. "Factores de progresión tumoral en el sarcoma de Kaposi: estudio inmunohistoquímico." Doctoral thesis, Universitat Autònoma de Barcelona, 2003. http://hdl.handle.net/10803/4223.

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El sarcoma de Kaposi (SK) es una enfermedad angioproliferativa con cuatro formas clínico-epidemiológicas: clásica (SK-C), africana endémica, relacionada con fármacos inmunosupresores y relacionada con el síndrome de inmunodeficiencia adquirida (SK-SIDA). La afectación del SK es generalmente cutánea, pero en los casos agresivos puede diseminarse a localizaciones extracutáneas. En la piel, las lesiones se clasifican clínicopatológicamente en máculas, placas y tumores de acuerdo con su progresión y severidad. El SK parece iniciarse como una proliferación vascular reactiva debida a una red de citocinas alterada, mientras que en estadios avanzados, se comporta como una neoplasia multifocal.
El diferente comportamiento biológico del SK de acuerdo con sus presentaciones epidemiológicas y estadios puede estar relacionado con la presencia de alteraciones específicas en los mecanismos que controlan el crecimiento y desarrollo tumoral, como la sobreestimulación de citocinas y de factores de crecimiento angiogénicos o alteraciones en las oncoproteínas que controlan la proliferación celular y la apoptosis. Estas alteraciones podrían ofrecer los estímulos neoplásicos necesarios para el desarrollo, progresión y, en definitiva, un comportamiento más agresivo del SK.
El factor de crecimiento hepatocitario (HGF) es una citocina angiogénica pleiotrópica que está sobreexpresada en cánceres humanos invasivos y puede actuar como factor de progresión tumoral, estimulando la angiogénesis y la invasividad de las células tumorales. Estas respuestas son transducidas a través del receptor c-Met. El HGF estimula la proliferación de las células fusiformes cultivadas de lesiones humanas de SK, y además las células del SK sintetizan y secretan HGF y expresan c-Met, creando un rizo de retroalimentación para la proliferación tumoral y la neovascularización. Hemos estudiado la expresión del c-Met en diferentes estadios histológicos de lesiones de SK-C y SK-SIDA, observando que la intensidad de tinción de c-Met fue mayor en los tumores que en las placas, de forma que el HGF se comporta como un factor de progresión en el SK.
EL HHV-8, el factor etiológico del SK, codifica la v-ciclina, que formando complejo con la cinasa dependiente de ciclina (CDK) 6, contribuye a la fosforilación y degradación mediada por proteasoma del inhibidor de las cinasas dependientes de ciclina p27KIP1. La p27KIP1 regula negativamente la proliferación celular uniéndose e inhibiendo a los complejos ciclina-CDK de fase G1. Por otro lado, la infrarregulación de la expresión de la p27KIP1 parece facilitar el desarrollo tumoral y la diseminación metastásica; por ello la p27KIP1 ha sido considerada como un factor pronóstico independiente en una gran variedad de neoplasias humanas. Aunque la naturaleza neoplásica del SK todavía es controvertida, se ha demostrado repetidas veces que en algunos pacientes el SK puede comportarse como una neoplasia maligna y seguir un curso ominoso. Para determinar si la disminución de los niveles de la p27KIP1 está también relacionada con un comportamiento más agresivo del SK, decidimos investigar la inmunoreactividad de la p27KIP1 en biopsias de SK. De este modo, intentamos determinar si la disminución de los niveles de expresión de la p27KIP1 está relacionada con la afectación extracutánea en el SK, como ocurre en otras neoplasias cuando metastatizan. La media de porcentajes de células positivas para p27KIP1 era significativamente mayor en las biopsias de lesiones cutáneas y en las máculas-placas que en las lesiones extracutáneas y en los tumores respectivamente. Estos resultados apoyan la hipótesis de que la disminución de los niveles de la p27KIP1, que pueden ser producidos por la infección por el HHV-8, facilitan la progresión del SK a través de sus estadios histopatológicos y su eventual extensión extracutánea
Estudios recientes han demostrado que la degradación de la p27KIP1 a través de la vía ubicuitin-proteasoma está mediada por el complejo SCF/ p45SKP2 y por su receptor específico de sustrato F-box p45SKP2. La p45SKP2 está frecuentemente sobreexpresada en células transformadas, induce la fase S en células quiescentes y se sospecha que es un protooncogen en tumores humanos. De hecho, se ha determinado una asociación entre el incremento de los niveles de la p45SKP2 y la disminución de los niveles de la p27KIP1 en neoplasias epiteliales. Hemos estudiado si la expresión de la p45SKP2 está alterada en las lesiones agresivas del SK y su relación con la infrarregulación de la p27KIP1, sexo e infección por el VIH. La sobreexpresión nuclear de la p45SKP2 estaba presente en todos los estadios del SK, estando significativamente incrementada en los tumores cutáneos y en las lesiones extracutáneas en comparación con la máculas y placas. No se identificaron diferencias estadísticamente significativas en relación con el sexo y estatus VIH de los pacientes, y el análisis de regresión no mostró correlación entre la p45SKP2 y la p27KIP1. Estos hallazgos sugieren que la p45SKP2 está involucrada en el SK, no sólo promoviendo la degradación de la p27KIP1, sino también a través de otros mecanismos todavía desconocidos.
Kaposi's sarcoma (KS) is an angioproliferative disease with four clinical-epidemiological forms: classic (C-KS), African-endemic, immunosuppressive drug-related and acquired immune deficiency syndrome-related (AIDS-KS). KS involvement is usually limited to the skin, but in aggressive cases it may disseminate to extracutaneous locations. In the skin, lesions are clinicopathologically classified into macules, plaques and tumours in agreement with their progression in severity. KS seems to begin as a reactive vascular proliferation due to an unbalanced cytokine network, whereas in advanced stages, it behaves as a multifocal neoplasm.
The different biological behavior of KS according to its epidemiological presentations and stages might be related to the presence of specific alterations in the mechanisms controlling tumor growth and development, such as cytokine or angiogenic growth factor overstimulation or alterations of the oncoprotein networks that control cell proliferation and apoptosis. These alterations would provide neoplastic stimuli for the development, progression, and aggressive behaviour of KS.
Hepatocyte growth factor (HGF) is a pleiotropic angiogenic cytokine that is overexpressed in invasive human cancers and may function as a tumor progression factor, stimulating tumour cell invasiveness and angiogenesis. These responses are transduced through the c-Met receptor. HGF stimulates proliferation of spindle cells cultured from human KS lesions, and KS cells synthesize and secrete HGF and express c-Met, thus providing an autocrine loop for tumour proliferation and neovascularization. We have studied the expression of c-Met in different histological stages of AIDS-associated and classic KS lesions. The staining intensity of c-Met was stronger in tumours than in plaques showing that HGF would be a progression factor in KS.
HHV-8, the KS'etiologic factor, encoded v-cyclin, through its complexing with cyclin-dependent kinase (CDK) 6, contributes to the phosphorylation and proteasome-mediated degradation of p27KIP1, a cyclin-dependent kinase inhibitor. P27KIP1 regulates negatively cell proliferation by binding and inhibiting G1 cyclin-CDK complexes. On the other hand, down-regulation of p27KIP1 expression seems to facilitate tumour development and metastatic dissemination; then p27KIP1 has been considerated as an independent prognostic factor in a variety of human neoplasms. Although the neoplastic nature of KS remains controversial, it has been repeatedly demonstrated that in some patients KS may behave as a malignant neoplasm and follow an ominous course. To determine whether decreased p27KIP1 levels are also related to more aggressive behaviour in KS, it was decided to investigate p27KIP1 immunoreactivity in KS biopsy specimens. Thereby, we sought to determine whether the decrease in p27KIP1 expression levels is related to extracutaneous involvement in KS, as is the case in several other types of neoplasms when they metastasize. The mean percentages of p27KIP1-positive cells were significantly higher in biopsy specimens from skin lesions and in macules-plaques than in those from extracutaneous locations and tumours respectively. These results lend support to the hypothesis that decreased levels of p27KIP1, which may have been brought about by HHV-8 infection, play a role in KS progression through its various histopathological stages, to its eventual extracutaneous spread.
Recent studies have demonstrated that p27KIP1 degradation through the ubiquitin-proteasome pathway is mediated by the SCF/p45SKP2 complex and by the substrate-specific receptor of this complex, the F-Box protein p45SKP2. P45SKP2 is frequently over-expressed in transformed cells, induces S phase in quiescent cells and is a suspected proto-oncogene in human tumours. In fact, there are recent reports of increased levels of p45SKP2 in association with reduced p27KIP1 levels in epithelial neoplasms. We have studied of whether p45SKP2 expression is altered in aggressive lesions of KS and its relation to p27KIP1 down-regulation, gender and HIV infection. P45SKP2 nuclear over-expression was present in all KS stages, being significantly increased in skin tumours and extracutaneous lesions as compared with macules and plaques. No statistically significant differences were found in regard to patients´ sex and HIV status and regression analysis failed to show a correlation among p45SKP2 and p27KIP1. These findings suggest that p45SKP2 is involved in KS, not only by promoting the degradation of p27KIP1 but also through other mechanisms still unknown.
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Books on the topic "Kaposi, Sarcoma de"

1

Dittmer, Dirk Peter, and Susan E. Krown. Molecular basis for therapy of AIDS-defining cancers. Springer, 2010.

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2

Penn, Israel. The etiology of Kaposi's sarcoma. U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1988.

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Penn, Israel. The etiology of Kaposi's sarcoma. U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1988.

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G, Giraldo, ed. Recent advances in AIDS and Kaposi's sarcoma. Karger, 1987.

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Lehnherr, Melinda. Kaposi's sarcoma in Illinois: A comparison of AIDS cases to classic cases. Illinois Dept. of Public Health, Division of Epidemiologic Studies, 1989.

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Humans, IARC Working Group on the Evaluation of Carcinogenic Risks to. Epstein-Barr virus and Kaposi's sarcoma herpesvirus/human herpesvirus 8. IARC, 1997.

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Shepherd, Frances A. Management of Kaposi's sarcoma associated with human immunodeficiency virus infection: Report. Health and Welfare Canada, 1991.

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Canada. Health and Welfare Canada. Management of Kaposi's Sarcoma associated with human immunodeficiency virus infection/ Francis A. Shepard. Health and Welfare Canada, 1991.

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1925-, Vaeth Jerome M., ed. Cancer and AIDS: 19th annual San Francisco Cancer Symposium, San Francisco Calif., March 2-4, 1984. Karger, 1985.

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Daniels, Victor G. SIDA, sindrome de immunodeficiencia adquirida. 2nd ed. Manual Moderno, 1988.

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Book chapters on the topic "Kaposi, Sarcoma de"

1

Strumia, Renata. "Kaposi Sarcoma." In Dermatological Cryosurgery and Cryotherapy. Springer London, 2016. http://dx.doi.org/10.1007/978-1-4471-6765-5_133.

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Yen, Michael T., and Michelle Butler. "Kaposi Sarcoma." In Encyclopedia of Ophthalmology. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-35951-4_287-3.

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Boshoff, Chris. "Kaposi Sarcoma." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3197.

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Mocellin, Simone. "Kaposi Sarcoma." In Soft Tissue Tumors. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-58710-9_142.

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Ferguson, Nkanyezi N. "Kaposi Sarcoma." In Inpatient Dermatology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-18449-4_36.

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Taverna, Cecilia, and Alessandro Franchi. "Kaposi Sarcoma." In Encyclopedia of Pathology. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41894-6_5003.

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Terhorst, Dorothea, Martina Ulrich, and Theodore Rosen. "Kaposi Sarcoma." In Managing Skin Cancer. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-79347-2_9.

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Yen, Michael T., and Michelle Butler. "Kaposi Sarcoma." In Encyclopedia of Ophthalmology. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_287.

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High, Whitney A. "Kaposi Sarcoma." In Evidence-Based Dermatology. John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118357606.ch36.

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Crowe, David R. "Kaposi Sarcoma." In Deadly Dermatologic Diseases. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31566-9_9.

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Conference papers on the topic "Kaposi, Sarcoma de"

1

Shah, K., and S. Gulati. "Disseminated Kaposi Sarcoma Presenting as Chylothorax." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3929.

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Bridges, K., K. Hill, and G. E. Abraham. "An Atypical Presentation of Pulmonary Kaposi Sarcoma." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6375.

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D'Amico, T. A., K. D. Stettmeier, and J. P. Kanaan. "Multi-System Kaposi Sarcoma with Bronchopulmonary Involvement." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5888.

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Josan, E., I. Lalani, S. Williams, and M. Ayache. "Pulmonary Kaposi Sarcoma: Bronchoscopy and Imaging Findings." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2318.

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Omar, A., H. Chi, V. Sheth, and L. Blackwell. "Chylothorax in Kaposi Sarcoma: A Rare Complication." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1953.

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Delgado, G. G., J. V. Ricci Alves, J. Marques Rebello, et al. "Diagnostic Challenges of Pulmonary Kaposi Sarcoma in AIDS Patients." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3925.

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Wadud, N., M. Krishna, and S. El Zarif. "Kaposi Sarcoma Lymphadenopathy in the Setting of HIV Infection." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3764.

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Almajthoub, Z., and M. AlNabulsi. "A Case of Disseminated Kaposi Sarcoma with Challenging Pleuropulmonary Complications." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5871.

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Munir, M. Z., G. Gupta, and S. Rehmani. "Kaposi Sarcoma: A Rare Presentation with Pulmonary and Osseous Involvement." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4880.

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Yun, Jeong H., Young K. Chae, and Claudia Dourado. "Rapidly Progressive Pulmonary Kaposi Sarcoma Associated With Immune Reconstitution Inflammatory Syndrome." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4613.

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