Disseminated form of the Kaposi sarcoma in HIV-negative patient associated with Hodgkin’s lymphoma

Tutaeva, Victoria; Bobin, Arthur; Ovsiannikova, M R; Bulgakova, M V; Kuchma, Y M; Kryukov, E.V.; Rukavitsyn, O.

doi:10.1093/omcr/omaa069

Oxford Medical Case Reports

2020

DOI: 10.1093/omcr/omaa069

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Disseminated form of the Kaposi sarcoma in HIV-negative patient associated with Hodgkin’s lymphoma

Victoria Tutaeva

Arthur Bobin

M R Ovsiannikova

et al.

Abstract: We report a case of a 35-year-old, non-HIV-infected male diagnosed simultaneously with a disseminated form of Kaposi’s sarcoma (KS; skin, stomach and colon are involved) and Hodgkin’s lymphoma. There is no sign of changes in the immune status, but three herpes viruses were detected in the patient’s blood (EBV, HHV6 and HHV8). He received ABVD chemotherapy and achieved complete metabolic remission for Hodgkin’s lymphoma. Moreover, the signs of the disseminated KS were resolved. Our observations indicate that a … Show more

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“…28 This results in abnormal cell proliferation and can provoke metastasis. 28 Immunosuppression can be caused by various random events such as viral infection, 29,30 insufficient generation and CD8 T-cell exhaustion, 31 and tissue repair associated with M2 macrophage polarization. 32 Chromosomal instability is associated with an ability to move and interconnect different pieces of chromosomes.…”

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Clinically relevant fusion oncogenes: detection and practical implications

et al. 2022

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Mechanistically, chimeric genes result from DNA rearrangements and include parts of preexisting normal genes combined at the genomic junction site. Some rearranged genes encode pathological proteins with altered molecular functions. Those which can aberrantly promote carcinogenesis are called fusion oncogenes. Their formation is not a rare event in human cancers, and many of them were documented in numerous study reports and in specific databases. They may have various molecular peculiarities like increased stability of an oncogenic part, self-activation of tyrosine kinase receptor moiety, and altered transcriptional regulation activities. Currently, tens of low molecular mass inhibitors are approved in cancers as the drugs targeting receptor tyrosine kinase (RTK) oncogenic fusion proteins, that is, including ALK, ABL, EGFR, FGFR1-3, NTRK1-3, MET, RET, ROS1 moieties. Therein, the presence of the respective RTK fusion in the cancer genome is the diagnostic biomarker for drug prescription. However, identification of such fusion oncogenes is challenging as the breakpoint may arise in multiple sites within the gene, and the exact fusion partner is generally unknown. There is no gold standard method for RTK fusion detection, and many alternative experimental techniques are employed nowadays to solve this issue. Among them, RNA-seq-based methods offer an advantage of unbiased high-throughput analysis of only transcribed RTK fusion genes, and of simultaneous finding both fusion partners in a single RNA-seq read. Here we focus on current knowledge of biology and clinical aspects of RTK fusion genes, related databases, and laboratory detection methods.

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Clinically relevant fusion oncogenes: detection and practical implications

et al. 2022

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The p53 family member p73 in the regulation of cell stress response

et al. 2021

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During oncogenesis, cells become unrestrictedly proliferative thereby altering the tissue homeostasis and resulting in subsequent hyperplasia. This process is paralleled by resumption of cell cycle, aberrant DNA repair and blunting the apoptotic program in response to DNA damage. In most human cancers these processes are associated with malfunctioning of tumor suppressor p53. Intriguingly, in some cases two other members of the p53 family of proteins, transcription factors p63 and p73, can compensate for loss of p53. Although both p63 and p73 can bind the same DNA sequences as p53 and their transcriptionally active isoforms are able to regulate the expression of p53-dependent genes, the strongest overlap with p53 functions was detected for p73. Surprisingly, unlike p53, the p73 is rarely lost or mutated in cancers. On the contrary, its inactive isoforms are often overexpressed in cancer. In this review, we discuss several lines of evidence that cancer cells develop various mechanisms to repress p73-mediated cell death. Moreover, p73 isoforms may promote cancer growth by enhancing an anti-oxidative response, the Warburg effect and by repressing senescence. Thus, we speculate that the role of p73 in tumorigenesis can be ambivalent and hence, requires new therapeutic strategies that would specifically repress the oncogenic functions of p73, while keeping its tumor suppressive properties intact.

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Disseminated form of the Kaposi sarcoma in HIV-negative patient associated with Hodgkin’s lymphoma

Cited by 2 publications

References 9 publications

Clinically relevant fusion oncogenes: detection and practical implications

Clinically relevant fusion oncogenes: detection and practical implications

The p53 family member p73 in the regulation of cell stress response

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