Spindle cells from AIDS-associated Kaposi's sarcoma lesions express telomerase activity that is enhanced by Kaposi's sarcoma progression factors

Barillari, Giovanni; Franzese, Ornella; Comandini, Alessandro; Bonmassar, Enzo; Ensoli, Barbara

doi:10.3892/or_00000849

Cited by 2 publications

(1 citation statement)

References 22 publications

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“…This hypothesis is supported by our recent observation that both FGF-2 and Tat can increase in KS cells the activity of the telomerase, an enzyme allowing cells to escape replicative senescence and to proliferate indefinitely [43, 44]. …”

Section: Discussionmentioning

confidence: 66%

Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's Sarcoma

Sgadari

Barillari

Palladino

et al. 2011

International Journal of Vascular Medicine

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Kaposi's sarcoma (KS) is a vascular tumor frequently occurring in Human Immunodeficiency Virus- (HIV-) 1-infected individuals. Our previous work indicated that the angiogenic fibroblast growth factor (FGF)-2 and the Tat protein of HIV-1, both expressed in KS lesions of HIV-infected patients, synergize at inducing angioproliferative, KS-like lesions in mice. Here we show that the development of angioproliferative lesions promoted in mice by combined Tat and FGF-2 associates with an increase in the levels of expression of the antiapoptotic Bcl-2 protein. Upregulation of Bcl-2 expression by combined FGF-2 and Tat occurs also in vitro, and this protects human primary endothelial cells from programmed cell death. As Bcl-2 is expressed in human KS lesions in a fashion paralleling the progression of the disease, these findings suggest a molecular mechanism by which Tat and FGF-2 cooperate in KS maintenance and progression in HIV-infected individuals.

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Section: Discussionmentioning

confidence: 66%

Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's Sarcoma

Sgadari

Barillari

Palladino

et al. 2011

International Journal of Vascular Medicine

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Association of CD4+ T-cell Count, HIV-1 RNA Viral Load, and Antiretroviral Therapy With Kaposi Sarcoma Risk Among HIV-infected Persons in the United States and Canada

Dubrow

Qin

Lin

et al. 2017

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Background Kaposi sarcoma (KS) remains common among HIV-infected persons. To better understand KS etiology and to help target prevention efforts, we comprehensively examined a variety of CD4+ T-cell count and HIV-1 RNA viral load (VL) measures, as well as antiretroviral therapy (ART) use, to determine independent predictors of KS risk. Setting North American AIDS Cohort Collaboration on Research and Design. Methods We followed HIV-infected persons during 1996-2009 from 18 cohorts. We used time-updated Cox regression to model relationships between KS risk and recent, lagged, trajectory, and cumulative CD4 count or VL measures, as well as ART use. We used Akaike's information criterion and global p-values to derive a final model. Results In separate models, the relationship between each measure and KS risk was highly significant (p<0.0001). Our final mutually-adjusted model included recent CD4 count (hazard ratio [HR] for <50 vs. ≥500 cells/μL = 12.4; 95% confidence interval [CI]: 6.5-23.8), recent VL (HR for ≥100,000 vs. ≤500 copies/mL = 3.8; 95% CI: 2.0-7.3), and cumulative (time-weighted mean) VL (HR for ≥100,000 vs. ≤500 copies/mL = 2.5; 95% CI: 1.0-5.9). Each p-trend was <0.0001. After adjusting for these measures, we did not detect an independent association between ART use and KS risk. Conclusions Our results suggested a multifactorial etiology for KS, with early and late phases of development. The cumulative VL effect suggested that controlling HIV replication promptly after HIV diagnosis is important for KS prevention. We observed no evidence for direct anti-KS activity of ART, independent of CD4 count and VL.

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Spindle cells from AIDS-associated Kaposi's sarcoma lesions express telomerase activity that is enhanced by Kaposi's sarcoma progression factors

Cited by 2 publications

References 22 publications

Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's Sarcoma

Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's Sarcoma

Association of CD4+ T-cell Count, HIV-1 RNA Viral Load, and Antiretroviral Therapy With Kaposi Sarcoma Risk Among HIV-infected Persons in the United States and Canada

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