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AIDS-Related Malignancy
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Mark Bower, Elena Gervasi, Alessia Dalla Pria
A number of other malignancies occur more frequently in immunocompromised patients, and these are often associated with oncogenic virus infection. A few appear to be particularly associated with HIV infection, such as squamous cell carcinoma of the conjunctiva39 and leiomyosarcomas in childhood.40 In many cases small case series describe the management of these non-AIDS-defining malignancies along the same lines as used in the general population and often with comparable outcomes. Again the most important issue for the treating oncologist is to appreciate the importance of pharmacological interactions and the importance of opportunistic infection prophylaxis but also to recognize that these patients generally have similar outcomes and should not be denied appropriate therapy nor access to clinical trials because of their HIV status.
Oncogenic DNA Viruses
Published in Pimentel Enrique, Oncogenes, 2020
The following discussion is mainly focused on the molecular events involved in malignant transformation induced by DNA viruses and the possible relation between the genes of DNA oncogenic viruses and specific cellular genes, especially proto-oncogenes, both at the nucleic acid and protein levels. Among the possibilities to be considered a priori are: (1) derangement of cellular oncogene functions by the presence of unintegrated or integrated DNA viruses within the cell; (2) production of oncogene-like proteins by oncogenic DNA viruses; and (3) interaction between DNA viruses protein products and specific proto-oncogene protein products.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
Viruses are obligate intracellular parasites that rely on the host cell’s replicative machinery to reproduce themselves. Oncogenic viruses have therefore evolved to induce host-cell replication by activating genes for cell growth. This confers a survival advantage on the virus. However, it is when proliferation becomes uncoordinated and excessive that carcinoma results. Epstein–Barr (DNA) virus has been implicated in the pathogenesis of 3 human cancers: Burkitt’s lymphomaNasopharyngeal carcinomaHodgkin’s disease
Prevalence and trend of AIDS-defining cancers and non-AIDS-defining cancers and their association with antiretroviral therapy among people living with HIV in South Carolina: a population-based cohort study
Published in AIDS Care, 2023
Chigozie A. Nkwonta, Jiajia Zhang, Shujie Chen, Sharon Weissman, Bankole Olatosi, Xiaoming Li
The predictive factors for ADC observed in our study were consistent with prior studies (Cahoon et al., 2016; Koshiol et al., 2011; Rubinstein et al., 2014; Wang et al., 2017). Hepatitis coinfection has also been associated with an increased risk of developing many other cancers. These findings may be due to the oncogenic nature of Hepatitis B and C viruses, which is currently and consistently attributed to excess cancer cases among PLWH (Calabresi et al., 2013; de Martel et al., 2015; Meijide et al., 2017). NHL associated with HIV was found approximately twice higher in whites than African Americans in a study of more than 4million US veterans (Koshiol et al., 2011). This is similar to a nationwide study that demonstrated KS risk was significantly higher among whites than blacks (Cahoon et al., 2016). Cahoon et al. (2016) added that one possible explanation for their findings is that human herpesvirus 8 prevalence is higher in whites with HIV because they are about twice as likely to be MSM. Other observed predictive risk factors such as recent CD4 counts and time spent with VL <200copies/ml were supported by other studies on risk for ADC (Borges et al., 2016; Dubrow et al., 2017; Park et al., 2018). A retrospective cohort study of ADC among 42,441 veterans found that the risk of having ADC was lowest among persons with long-term suppression (Park et al., 2018). The poor HIV-induced immune suppression may hinder the control of oncogenic viruses, and less able to detect and destroy cancer cells (Bouvard et al., 2009).
How metabolism and metabolites shape immunity during disease
Published in International Reviews of Immunology, 2022
Cancer is caused by multiple factors both intrinsic and extrinsic. Intrinsic factors include irreparable DNA damage, loss of cell cycle regulation, dysregulation of immunity or metabolism etc. The extrinsic factors can be physical, chemical, biological or environmental. Additionally, some microbial infections by an oncogenic virus or bacterial infection can result in the development of cancer. In this issue, the article by Pirzadeh et al. discusses the role of Helicobacter pylori and a few amino acid metabolisms and metabolites in immune suppression, which subsequently results in gastric cancer. This article will be of interest to a broad readership in the fields of onco-immunology and infectious disease biology as well as researchers active at the junction between metabolism, immunology and cancer biology (Figure 1).
Spotlight on ocular Kaposi’s sarcoma: an update on the presentation, diagnosis, and management options
Published in Expert Review of Ophthalmology, 2021
Nandini Venkateswaran, Juan C. Ramos, Adam K. Cohen, Osmel P. Alvarez, Noah K. Cohen, Anat Galor, Carol L. Karp
Oncogenic viruses cause cancer by initiating a sequence of cellular events, which lead to the dysregulation of cell cycle checkpoints [21,22]. As a result, the infected cells become immortalized and proliferate in an uncontrolled fashion. Specifically, when considering the role of HHV8 in inducing KS, viral proteins arising from human gene homologues, such as v-cyclin and vFLIP, can lead to uncontrolled cellular proliferation, suppression of apoptosis, and blockage of cellular senescence [23–25]. HHV8 infection also induces expression of tyrosine-protein kinase Kit (cKit) leading to proliferation of tumor spindle cells [26]. Other important HHV8 genes involved in the pathogenesis of KS include latency-associated nuclear antigen (LANA-1), viral interleukin 6 (vIL-6), and viral G-protein coupled receptor (VGPCR) [27]. In addition, HHV8 infection may reprogram the host’s blood endothelial cells so that they resemble lymphatic endothelium, upregulating vascular endothelial growth factor receptor 3 (VEGFR3), platelet-derived growth factor receptor alpha (PDGFR-A), lymphatic vessel endothelial receptor 1 (LYVE1), and podoplanin [12,28].