Insertional Polymorphisms of Endogenous HERV-K113 and HERV-K115 Retroviruses in Breast Cancer Patients and Age-Matched Controls

Burmeister, Thomas; Ebert, Andreas D.; Pritze, W; Loddenkemper, Christoph; Schwartz, Stefan; Thiel, Eckhard

doi:10.1089/0889222042545081

Cited by 3 publications

(3 citation statements)

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“…To date there is evidence for HML‐2 activation in ovarian cancer, melanoma, breast, prostate, lymphomas, leukemias and sarcomas . In the 1980s, Ono et al .…”

Section: Herv‐k and Solid Tumorsmentioning

confidence: 99%

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Human endogenous retrovirus K and cancer: Innocent bystander or tumorigenic accomplice?

et al. 2014

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Harbored as relics of ancient germline infections, human endogenous retroviruses (HERVs) now constitute up to 8% of our genome. A proportion of this sequence has been co-opted for molecular and cellular processes, beneficial to human physiology, such as the fusogenic activity of the envelope protein, a vital component of placentogenesis. However, the discovery of high levels of HERV-K mRNA and protein and even virions in a wide array of cancers has revealed that HERV-K may be playing a more sinister role–a role as an etiological agent in cancer itself. Whether the presence of this retroviral material is simply an epiphenomenon, or an actual causative factor, is a hotly debated topic. This review will summarize the current state of knowledge regarding HERV-K and cancer and attempt to outline the potential mechanisms by which HERV-K could be involved in the onset and promotion of carcinogenesis.

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“…To date there is evidence for HML‐2 activation in ovarian cancer, melanoma, breast, prostate, lymphomas, leukemias and sarcomas . In the 1980s, Ono et al .…”

Section: Herv‐k and Solid Tumorsmentioning

confidence: 99%

“…(Note the lower prevalence than reported above for both. This suggests ethnic differences in frequency of inheritance) …”

Section: Polymorphic Hml‐2 Group Membersmentioning

confidence: 99%

Human endogenous retrovirus K and cancer: Innocent bystander or tumorigenic accomplice?

et al. 2014

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“…One of the most preserved and best studied of the (HML‐2) elements is HERV‐K113. Its integration into chromosome 19p12 occurred approximately 1 million years ago and has now achieved an average allelic frequency of 13–30%, depending on the ethnic group . Although the provirus has open reading frames for all viral proteins, those coding for RT and Env have suffered from severe point mutations, with two mutations in each having been sufficient to reduce or abrogate the function of these proteins .…”

Section: Inventory Of the Hml‐2 Archivementioning

confidence: 99%

HERV‐K(HML‐2), a seemingly silent subtenant – but still waters run deep

Hanke

Hohn

Bannert

2016

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A large proportion of the human genome consists of endogenous retroviruses, some of which are well preserved, showing transcriptional activity, and expressing retroviral proteins. The HERV‐K(HML‐2) family represents the most intact members of these elements, with some having open and intact reading frames for viral proteins and the ability to form virus‐like particles. Although generally suppressed in most healthy tissues by a variety of epigenetic processes and antiviral mechanisms, there is evidence that some members of this family are (at least partly) still active – particularly in certain stem cells and various tumors. This raises the possibility of their involvement in tumor induction or in developmental processes. In recent years, many new insights into this fascinating field have been attained, and this review focuses on new discoveries about coevolutionary events and intracellular defense mechanisms against HERV‐K(HML‐2) activity. We also describe what might occur when these mechanisms fail or become modulated by viral proteins or other viruses and discuss the new vistas opened up by the reconstitution of ancestral viral proteins and even complete HML‐2 viruses.

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HERVs New Role in Cancer: From Accused Perpetrators to Cheerful Protectors

et al. 2018

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Initial indications that retroviruses are connected to neoplastic transformation were seen more than a century ago. This concept has also been tested for endogenized retroviruses (ERVs) that are abundantly expressed in many transformed cells. In healthy cells, ERV expression is commonly prevented by DNA methylation and other epigenetic control mechanisms. ERVs are remnants of former exogenous forms that invaded the germ line of the host and have since been vertically transmitted. Several examples of ERV-induced genomic recombination events and dysregulation of cellular genes that contribute to tumor formation have been well documented. Moreover, evidence is accumulating that certain ERV proteins have oncogenic properties. In contrast to these implications for supporting cancer induction, a recent string of papers has described favorable outcomes of increasing human ERV (HERV) RNA and DNA abundance by treatment of cancer cells with methyltransferase inhibitors. Analogous to an infecting agent, the ERV-derived nucleic acids are sensed in the cytoplasm and activate innate immune responses that drive the tumor cell into apoptosis. This “viral mimicry” induced by epigenetic drugs might offer novel therapeutic approaches to help target cancer cells that are normally difficult to treat using standard chemotherapy. In this review, we discuss both the detrimental and the new beneficial role of HERV reactivation in terms of its implications for cancer.

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Insertional Polymorphisms of Endogenous HERV-K113 and HERV-K115 Retroviruses in Breast Cancer Patients and Age-Matched Controls

Cited by 3 publications

References 0 publications

Human endogenous retrovirus K and cancer: Innocent bystander or tumorigenic accomplice?

Human endogenous retrovirus K and cancer: Innocent bystander or tumorigenic accomplice?

HERV‐K(HML‐2), a seemingly silent subtenant – but still waters run deep

HERVs New Role in Cancer: From Accused Perpetrators to Cheerful Protectors

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