Kaposi's sarcoma: Advances and perspectives

Schwartz, Robert A.

doi:10.1016/s0190-9622(96)90018-3

Cited by 83 publications

(63 citation statements)

References 120 publications

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“…Historically, each form has been distinguished by numerous clinical parameters, including the extent of anatomic involvement, the aggressiveness of lesion formation, and associated morbidity and mortality, as well as by divergent patient risk factors, notably age, sex, and ethnogeographic origin (each of these is discussed individually below [452,549]). Despite these clinical differences, it is now well established that all four epidemiologic forms of KS have in common KSHV infection of the host (12,13,161,176,250,290,343,390,412,419,449,466), with the four forms of KS being histologically indistinguishable (1).…”

Section: Clinicoepidemiology Of Kshvmentioning

confidence: 99%

Molecular Genetics of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Epidemiology and Pathogenesis

Dourmishev

Palmeri

et al. 2003

Microbiol Mol Biol Rev

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309

367

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Kaposi's sarcoma had been recognized as unique human cancer for a century before it manifested as an AIDS-defining illness with a suspected infectious etiology. The discovery of Kaposi's sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus-8, in 1994 by using representational difference analysis, a subtractive method previously employed for cloning differences in human genomic DNA, was a fitting harbinger for the powerful bioinformatic approaches since employed to understand its pathogenesis in KS. Indeed, the discovery of KSHV was rapidly followed by publication of its complete sequence, which revealed that the virus had coopted a wide armamentarium of human genes; in the short time since then, the functions of many of these viral gene variants in cell growth control, signaling apoptosis, angiogenesis, and immunomodulation have been characterized. This critical literature review explores the pathogenic potential of these genes within the framework of current knowledge of the basic herpesvirology of KSHV, including the relationships between viral genotypic variation and the four clinicoepidemiologic forms of Kaposi's sarcoma, current viral detection methods and their utility, primary infection by KSHV, tissue culture and animal models of latent- and lytic-cycle gene expression and pathogenesis, and viral reactivation from latency. Recent advances in models of de novo endothelial infection, microarray analyses of the host response to infection, receptor identification, and cloning of full-length, infectious KSHV genomic DNA promise to reveal key molecular mechanisms of the candidate pathogeneic genes when expressed in the context of viral infection

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Section: Clinicoepidemiology Of Kshvmentioning

confidence: 99%

Molecular Genetics of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Epidemiology and Pathogenesis

Dourmishev

Palmeri

et al. 2003

Microbiol Mol Biol Rev

Self Cite

309

367

View full text Add to dashboard Cite

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“…Kaposi's sarcoma (KS) is an angioproliferative disease that has a complex pathogenesis involving a disordered cytokine network, immune alterations, and active infection with human herpesvirus 8 (HHV-8) (1)(2)(3)(4)(5)(6). Four epidemiologic forms of KS have been described: classic form (C-KS), affecting mainly elderly men of Mediterranean origin; African-endemic KS; immunosuppressive drug-related KS; and acquired immunodeficiency syndrome-related KS (AIDS-KS).…”

mentioning

confidence: 99%

“…Four epidemiologic forms of KS have been described: classic form (C-KS), affecting mainly elderly men of Mediterranean origin; African-endemic KS; immunosuppressive drug-related KS; and acquired immunodeficiency syndrome-related KS (AIDS-KS). The last one affects mainly human immunodeficiency virus (HIV)-infected homosexual men and typically is associated with an aggressive course (1). All forms of KS have the same histology, which is characterized initially by a prominent angiogenesis and subsequently by the proliferation of spindleshaped cells that are considered to be the tumor cells of KS.…”

mentioning

confidence: 99%

Immunohistochemical Detection of Bcl-2 in Kaposi's Sarcoma Lesions Varies According to Histopathologic Stage, Whereas Expression of Bcl-x and Mcl-1 Differs According to Human Immunodeficiency Virus Serologic Status of Patients

et al. 2000

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“…FGF4 and INT2 belong to the fibroblast growth factor family, members of which have been suggested to be involved in the pathogenesis of KS (10,24). Coamplification of FGF4 and INT2 has been reported in different human malignancies including melanoma, breast cancer, and oral squamous cell carcinoma, but the expression pattern varies (25)(26)(27).…”

Section: Discussionmentioning

confidence: 99%

FGF4 and INT2 Oncogenes Are Amplified and Expressed in Kaposi's Sarcoma

et al. 2000

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Kaposi's sarcoma (KS) is a vascular tumor, the pathogenesis of which has been suggested to include human herpesvirus 8 (HHV-8) as well as various cytokines and growth factors. Very little is known about cytogenetic and molecular genetic changes in KS. We studied DNA copy number changes in KS and found a recurrent gain at 11q13. We then analyzed the amplification and expression status of two known oncogenes, FGF4 and INT2, residing at 11q13. Comparative genomic hybridization, interphase fluorescence in situ hybridization with yeast artificial chromosome probes containing FGF4 and INT2, and immunoperoxidase immunostaining with anti-FGF4 and -INT2 antibodies were used on 12 KS samples. All samples tested were shown by polymerase chain reaction to be HHV-8 positive. A recurrent gain at 11q13 was shown by comparative genomic hybridization in 4 of 10 cases studied. Of six cases studied by interphase fluorescence in situ hybridization, four showed a 3-to 4-fold amplification with the probes containing FGF4 and INT2. Expression of FGF4 and INT2 was found in nine and three cases, respectively, of nine studied. Amplification and expression of these genes is particularly interesting in the context of oncovirus involvement, because INT2 is a homolog of mouse int2, which causes mammary carcinoma in mice when activated by integration of retrovirus mouse mammary tumor virus. This raises the question of whether HHV-8 represents an integrating oncovirus that causes amplification and activation of genomic oncogenes in humans.

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Kaposi's sarcoma: Advances and perspectives

Cited by 83 publications

References 120 publications

Molecular Genetics of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Epidemiology and Pathogenesis

Molecular Genetics of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Epidemiology and Pathogenesis

Immunohistochemical Detection of Bcl-2 in Kaposi's Sarcoma Lesions Varies According to Histopathologic Stage, Whereas Expression of Bcl-x and Mcl-1 Differs According to Human Immunodeficiency Virus Serologic Status of Patients

FGF4 and INT2 Oncogenes Are Amplified and Expressed in Kaposi's Sarcoma

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