Epigenetic markers in basal cell carcinoma: universal themes in oncogenesis and tumor stratification? - a short report

Rao, Rajesh C.; Chan, May P.; Andrews, Chris; Kahana, Alon

doi:10.1007/s13402-018-0402-8

Cited by 8 publications

(11 citation statements)

References 16 publications

(45 reference statements)

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“…On the contrary, upregulated H3K27me3 and 5hmC were positively associated with a more benign phenotype. Finally, the authors were able to discriminate BCCs from non-malignant epidermal cells through the upregulated levels NSD2, MOF, H3K27me3, and 5hmC [124]. Harms et al investigated a series of MCCs and found that EZH2 was deregulated, inducing gene silencing via histone H3 lysine 27 trimethylation and was thus associated with unfavorable characteristics, such as disease progression and a poorer prognosis [117,125].…”

Section: Histone Methylation and Acetylationmentioning

confidence: 99%

Current and Future Trends in Molecular Biomarkers for Diagnostic, Prognostic, and Predictive Purposes in Non-Melanoma Skin Cancer

Νikolouzakis

Falzone

Lasithiotakis

et al. 2020

JCM

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Skin cancer represents the most common type of cancer among Caucasians and presents in two main forms: melanoma and non-melanoma skin cancer (NMSC). NMSC is an umbrella term, under which basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and Merkel cell carcinoma (MCC) are found along with the pre-neoplastic lesions, Bowen disease (BD) and actinic keratosis (AK). Due to the mild nature of the majority of NMSC cases, research regarding their biology has attracted much less attention. Nonetheless, NMSC can bear unfavorable characteristics for the patient, such as invasiveness, local recurrence and distant metastases. In addition, late diagnosis is relatively common for a number of cases of NMSC due to the inability to recognize such cases. Recognizing the need for clinically and economically efficient modes of diagnosis, staging, and prognosis, the present review discusses the main etiological and pathological features of NMSC as well as the new and promising molecular biomarkers available including telomere length (TL), telomerase activity (TA), CpG island methylation (CIM), histone methylation and acetylation, microRNAs (miRNAs), and micronuclei frequency (MNf). The evaluation of all these aspects is important for the correct management of NMSC; therefore, the current review aims to assist future studies interested in exploring the diagnostic and prognostic potential of molecular biomarkers for these entities.

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Section: Histone Methylation and Acetylationmentioning

confidence: 99%

Current and Future Trends in Molecular Biomarkers for Diagnostic, Prognostic, and Predictive Purposes in Non-Melanoma Skin Cancer

Νikolouzakis

Falzone

Lasithiotakis

et al. 2020

JCM

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“…These data suggest that EZH2 may possess oncogenic functions in MPNST outside the context of PRC2, a phenomenon observed in other cancers. In many contexts, EZH2 expression negatively correlates with H3K27me3 levels but positively correlates with cancer cell proliferation and poor disease prognosis (121)(122)(123). There are also numerous examples of specific noncanonical EZH2 targets and interactions that drive tumor development and metastasis.…”

Section: Loss Of Prc2 In Mpnstmentioning

confidence: 99%

Malignant Peripheral Nerve Sheath Tumors: From Epigenome to Bedside

Korfhage

Lombard

2019

Molecular Cancer Research

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Malignant peripheral nerve sheath tumors (MPNST) are aggressive sarcomas typically developing in the context of neurofibromatosis type 1 (NF-1). With the exception of surgical resection, these tumors are resistant to all current therapies, and unresectable, recurrent, or metastatic tumors are considered incurable. Preclinical studies have identified several novel candidate molecular targets for therapeutic intervention, but, to date, targeted therapies have proven ineffective. Recent studies have identified recurrent mutations in polycomb repressive complex 2 (PRC2) core components, embryonic ectoderm development protein (EED) and suppressor of zeste 12 homolog (SUZ12), in MPNST. These mutations result in global loss of the histone H3 lysine 27 trimethylation epigenetic mark, normally deposited by PRC2, and subsequent gain in acetylation at this residue. This altered chromatin state has been shown to promote MPNST malignancy; however, acetylation at this residue sensitizes MPNSTs to BRD4 and bromodomain and extra-terminal domain inhibition. Interestingly, the catalytic component of PRC2, enhancer of zeste homolog 2 (EZH2), is not mutated in MPNST, hinting that a noncanonical, PRC2-independent function of EZH2 may play a role in this cancer. This review examines the pathobiology of MPNST, the contribution of PRC2 subunits to this process, and the prospects for PRC2-related therapies for this cancer. Implications: Identification of mutations in the PRC2 components EED and SUZ12 in the majority of MPNSTs may imply noncanonical oncogenic activities of the intact component, EZH2, and provide new opportunities for therapeutic intervention.

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“…Finally, one recent study reported the association between advanced BCC and the histone methyltransferase EZH2 [ 94 , 95 ]. First, the authors tested the expression levels of EZH2 and the proliferation marker Ki67 in 30 cases of less aggressive BCC histologic subtypes and 30 cases of more aggressive histologic subtypes (morpheaform, infiltrative, and micronodular).…”

Section: Histone Methylation: Highly Mutated Modifiers In Kcsmentioning

confidence: 99%

“…EZH2 and Ki67 expression were significantly increased in the more aggressive BCCs as compared to that of the less aggressive BCCs, and positively correlated with the aggressiveness of BCC. They suggested that EZH2 may be a potential target to inhibit BCC progression [ 95 ]. In follow-up work, they tested the expression levels of H3K27me3, 5hmC, NSD2, MOF, JARID1B, EZH2, and Ki67 from the same BCC patients that they examined in the previous study, as well as matched non-malignant normal epidermal tissue to further explore the relationship of epigenetic modifiers to BCC.…”

Section: Histone Methylation: Highly Mutated Modifiers In Kcsmentioning

confidence: 99%

Methyltransferases in the Pathogenesis of Keratinocyte Cancers

Capell

2021

Cancers

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Recent evidence suggests that the disruption of gene expression by alterations in DNA, RNA, and histone methylation may be critical contributors to the pathogenesis of keratinocyte cancers (KCs), made up of basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (cSCC), which collectively outnumber all other human cancers combined. While it is clear that methylation modifiers are frequently dysregulated in KCs, the underlying molecular and mechanistic changes are only beginning to be understood. Intriguingly, it has recently emerged that there is extensive cross-talk amongst these distinct methylation processes. Here, we summarize and synthesize the latest findings in this space and highlight how these discoveries may uncover novel therapeutic approaches for these ubiquitous cancers.

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Epigenetic markers in basal cell carcinoma: universal themes in oncogenesis and tumor stratification? - a short report

Cited by 8 publications

References 16 publications

Current and Future Trends in Molecular Biomarkers for Diagnostic, Prognostic, and Predictive Purposes in Non-Melanoma Skin Cancer

Current and Future Trends in Molecular Biomarkers for Diagnostic, Prognostic, and Predictive Purposes in Non-Melanoma Skin Cancer

Malignant Peripheral Nerve Sheath Tumors: From Epigenome to Bedside

Methyltransferases in the Pathogenesis of Keratinocyte Cancers

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