Viral infections and breast cancer – A current perspective

Gannon, Orla M.; Antonsson, Annika; Bennett, Ian C.; Saunders, Nicholas A.

doi:10.1016/j.canlet.2018.01.076

Cited by 39 publications

(20 citation statements)

References 143 publications

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“…Our observation is consistent with two different studies from China by Peng et al (2%) and Li et al (2%) (15,16). The variation in prevalence of HPV in breast cancer in different countries may relate to the existence of geographic differences in HPV infection (14,17). Lawson et al showed that countries with low rates of HPV associated cervical cancer appear to have high rates of breast cancer and vice versa.…”

Section: Discussionsupporting

confidence: 92%

Detection of high and low-risk HPV DNA in archived breast carcinoma tissues from Ethiopian women

Gebregzabher

Seifu

Tigneh

et al. 2020

Preprint

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Background: HPV have been implicated in the development of cancer of the cervix, mouth and throat, anus, penis, vulva, or vagina, but it has not been much considered as a cause of breast cancer. However, a growing number of investigations have linked breast cancer to viral infections. High-risk HPV types, predominantly (HPV-16, -18, -31, -33, -35, -39, -45, -51, -52, -56, -58, and -59) are established as carcinogens in humans, while HPV-68 is probably carcinogenic. In this study we aimed to detect 19 high risk and 9 low risk HPVs from archived breast tumor tissue among Ethiopian women.Methods: In this study, 75 breast cancer patients from Tikur Anbassa Specialized Hospital in Addis Ababa (Ethiopia) were included. HPV detection and genotyping were done using the novel Anyplex™ II HPV-28 Detection Assay at the Orebro University Hospital, Sweden. The AnyplexTMII PCR System detects 19 high-risk HPV types (16, 18, 26, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66, 68, 69, 73, 82) and 9 low-risk HPV types(6, 11, 40, 42, 43, 44, 54, 61, 70). IHC for p16 was done in automated system using the Dako Autostainer Link.Results: Out of the 75 valid tests 2 were found to be positive (2.7%) for HPV. One of the cases were positive for high risk HPV16 genotype while the other were positive both for high risk HPV39 and low risk HPV6. The cell cycle protein p16 was highly expressed in the case positive for the high risk HPV16 but it was not expressed in the case positive for HPV39.Conclusion: With limited number of cases positive for HPV in this study, it is our conclusion that cervical cancer prevention strategies may help protection of breast cancer only in small groups of patients. Due to limitation of the number of participants in the study as well as possible other mechanisms of carcinogenesis, our observation should be reconfirmed using a larger set of patients and in case-control design.

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Section: Discussionsupporting

confidence: 92%

Detection of high and low-risk HPV DNA in archived breast carcinoma tissues from Ethiopian women

Gebregzabher

Seifu

Tigneh

et al. 2020

Preprint

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“…Results from past publications investigating the presence of HCMV in breast or other cancers have been inconsistent, which was discussed by us in more detail in another recent review article [24]. These discrepancies can, to some extent, be explained by difficulties to detect viral DNA/RNA by PCR based techniques in clinical tumor samples or by other technical reasons [20,25,26]. The discussion of whether HCMV plays a role in cancer or not, has been further fueled by the lack of direct evidence of oncogenic transformation induced by HCMV, since most of the HCMV strains examined are unable to transform normal human cells in in vitro cultures.…”

Section: Hcmv In Breast Cancermentioning

confidence: 99%

A Review of the Potential Role of Human Cytomegalovirus (HCMV) Infections in Breast Cancer Carcinogenesis and Abnormal Immunity

Geisler

Touma

Rahbar

et al. 2019

Cancers

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Previously recognized classical human onco-viruses can regulate complex neoplastic events, and are estimated to play a role during carcinogenesis in 15–20% of cancer cases. Although the DNA and gene products of several viruses have been found in breast tumors, none of the classical onco-viruses have definitely been linked to the initiation of breast cancer. However, recent evidence shows that human cytomegalovirus (HCMV) gene products are found in >90% of tumors and metastases of breast cancers, and their increased expression can be correlated to a more aggressive breast cancer phenotype. Supporting the active role of HCMV in breast cancer, a specific HCMV strain, HCMV-DB, was recently shown to exert oncogenic transformational activity in breast epithelial cells in vitro, and to give rise to fast-growing, triple-negative breast tumors when injected into immune deficient mice. The same observation holds true for clinical studies implying increased HCMV protein expression in triple negative breast cancer biopsies. In addition to functionally being able to hijack tumor-promoting cellular events, HCMV is known to exhibit a wide range of immunosuppressive effects, which can have radical impact on the tumor microenvironment. HCMV infected cells can avoid recognition and elimination by the immune system by orchestrating polarization of immunosuppressive type II macrophages, preventing antigen presentation, by expressing T cell inhibitory molecules, and possibly, by the induction of regulatory T (Treg) cell responses. These actions would be especially deleterious for the antigenic activation and proliferation of tumor specific CD8+ cytotoxic T lymphocytes (CTLs), whose effector functions have recently been targeted by successful, experimental immunotherapy protocols. The recognition of alternative causes and drivers of breast cancer is a pivotal research topic for the development of diagnostics and novel, effective preventive and therapeutic strategies targeting both tumor cells and their microenvironments.

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“…Earlier studies showed that HPVs could be found in 2–86% of human breast cancer cases ( 24 , 82 , 92 , 103 – 105 ). However, a small number of investigations could not find HPVs in breast cancer and normal mammary tissues ( 106 – 108 ). In this regard, E6/E7 onco-proteins of HPVs have been identified in breast cancer ( 109 ); though, there is a low level of transcription of these onco-proteins ( 110 ).…”

Section: Ebv/hpvs Interaction and Emt In Human Cancermentioning

confidence: 99%

Epstein–Barr Virus and Human Papillomaviruses Interactions and Their Roles in the Initiation of Epithelial–Mesenchymal Transition and Cancer Progression

et al. 2018

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Oncoviruses are implicated in around 20% of all human cancers including both solid and non-solid malignancies. Epstein–Barr virus (EBV) and human papillomaviruses (HPVs) are the most common oncoviruses worldwide. Currently, it is well established that onco-proteins of EBV (LMP1, LMP2A, and EBNA1) and high-risk HPVs (E5 and E6/E7) play an important role in the initiation and/or progression of several human carcinomas, including cervical, oral, and breast. More significantly, it has been recently pointed out that viral onco-proteins of EBV and high-risk HPVs can be co-present and consequently cooperate to initiate and/or amplify epithelial–mesenchymal transition (EMT), which is the hallmark of cancer progression and metastasis. This could occur by β-catenin, JAK/STAT/SRC, PI3k/Akt/mTOR, and/or RAS/MEK/ERK signaling pathways, which onco-proteins of EBV and HPVs share. This review presents the most recent advances related to EBV and high-risk HPVs onco-proteins interactions and their roles in the progression of human carcinomas especially oral and breast via the initiation of EMT.

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Viral infections and breast cancer – A current perspective

Cited by 39 publications

References 143 publications

Detection of high and low-risk HPV DNA in archived breast carcinoma tissues from Ethiopian women

Detection of high and low-risk HPV DNA in archived breast carcinoma tissues from Ethiopian women

A Review of the Potential Role of Human Cytomegalovirus (HCMV) Infections in Breast Cancer Carcinogenesis and Abnormal Immunity

Epstein–Barr Virus and Human Papillomaviruses Interactions and Their Roles in the Initiation of Epithelial–Mesenchymal Transition and Cancer Progression

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