Aberrant<scp>DNA</scp>Methylation of Tumor Suppressor Genes and Oncogenes as Cancer Biomarkers

Alshammari, Eid; Zhang, Yingxue; Sobota, Jacob; Yang, Zhe

doi:10.1002/9781119807704.ch12

Cited by 11 publications

(4 citation statements)

References 120 publications

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“…For example, Promoter hypermethylation repressed BRCA1 expression, resulting in breast cancer growth and metastasis ( 80 , 81 ). On the other hand, hypomethylation at the promoter region causes overexpression of genes ( 82 ). Hypomethylation at the promoter region of oncogenes and proto-oncogenes can stimulate cancer development and metastasis.…”

Section: Induction Of Tls: Current and Potential Strategiesmentioning

confidence: 99%

Epigenetic targets to enhance antitumor immune response through the induction of tertiary lymphoid structures

Omotesho,

Escamilla,

Pérez-Ruiz

et al. 2024

Front. Immunol.

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Tertiary lymphoid structures (TLS) are ectopic lymphoid aggregates found in sites of chronic inflammation such as tumors and autoimmune diseases. The discovery that TLS formation at tumor sites correlated with good patient prognosis has triggered extensive research into various techniques to induce their formation at the tumor microenvironment (TME). One strategy is the exogenous induction of specific cytokines and chemokine expression in murine models. However, applying such systemic chemokine expression can result in significant toxicity and damage to healthy tissues. Also, the TLS formed from exogenous chemokine induction is heterogeneous and different from the ones associated with favorable prognosis. Therefore, there is a need to optimize additional approaches like immune cell engineering with lentiviral transduction to improve the TLS formation in vivo. Similarly, the genetic and epigenetic regulation of the different phases of TLS neogenesis are still unknown. Understanding these molecular regulations could help identify novel targets to induce tissue-specific TLS in the TME. This review offers a unique insight into the molecular checkpoints of the different stages and mechanisms involved in TLS formation. This review also highlights potential epigenetic targets to induce TLS neogenesis. The review further explores epigenetic therapies (epi-therapy) and ongoing clinical trials using epi-therapy in cancers. In addition, it builds upon the current knowledge of tools to generate TLS and TLS phenotyping biomarkers with predictive and prognostic clinical potential.

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Section: Induction Of Tls: Current and Potential Strategiesmentioning

confidence: 99%

Epigenetic targets to enhance antitumor immune response through the induction of tertiary lymphoid structures

Omotesho,

Escamilla,

Pérez-Ruiz

et al. 2024

Front. Immunol.

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“…It is a common epigenetic alteration observed in various cancers, including OSCC [227][228][229]. Aberrant hypermethylation can result in the silencing of TSG or the activation of oncogenes, disrupting normal gene regulation and promoting tumor development and progression [230].…”

Section: Aberrant Hypermethylated Genes Involving Osccmentioning

confidence: 99%

Epigenetic Regulation in Oral Squamous Cell Carcinoma Microenvironment: A Comprehensive Review

Mesgari,

Esmaelian,

Nasiri

et al. 2023

Cancers

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Oral squamous cell carcinoma (OSCC) is a prevalent and significant type of oral cancer that has far-reaching health implications worldwide. Epigenetics, a field focused on studying heritable changes in gene expression without modifying DNA sequence, plays a pivotal role in OSCC. Epigenetic changes, encompassing DNA methylation, histone modifications, and miRNAs, exert control over gene activity and cellular characteristics. In OSCC, aberrant DNA methylation of tumor suppressor genes (TSG) leads to their inactivation, subsequently facilitating tumor growth. As a result, distinct patterns of gene methylation hold promise as valuable biomarkers for the detection of OSCC. Oral cancer treatment typically involves surgery, radiation therapy, and chemotherapy, but even with these treatments, cancer cells cannot be effectively targeted and destroyed. Researchers are therefore exploring new methods to target and eliminate cancer cells. One promising approach is the use of epigenetic modifiers, such as DNA methyltransferase (DNMT) inhibitors and histone deacetylase (HDAC) inhibitors, which have been shown to modify abnormal epigenetic patterns in OSCC cells, leading to the reactivation of TSGs and the suppression of oncogenes. As a result, epigenetic-targeted therapies have the potential to directly alter gene expression and minimize side effects. Several studies have explored the efficacy of such therapies in the treatment of OSCC. Although studies have investigated the efficacy of epigenetic therapies, challenges in identifying reliable biomarkers and developing effective combination treatments are acknowledged. Of note, epigenetic mechanisms play a significant role in drug resistance in OSCC and other cancers. Aberrant DNA methylation can silence tumor suppressor genes, while alterations in histone modifications and chromatin remodeling affect gene expression related to drug metabolism and cell survival. Thus, understanding and targeting these epigenetic processes offer potential strategies to overcome drug resistance and improve the efficacy of cancer treatments in OSCC. This comprehensive review focuses on the complex interplay between epigenetic alterations and OSCC cells. This will involve a deep dive into the mechanisms underlying epigenetic modifications and their impact on OSCC, including its initiation, progression, and metastasis. Furthermore, this review will present the role of epigenetics in the treatment and diagnosis of OSCC.

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“…Gene silences frequently result from DNA methylation, especially in promoter regions. The detection of DNA methylation alterations that (1) may promote tumor initiation and spread or (2) may function as accurate diagnostic, prognostic, or predictive biomarkers is among the objectives of these initiatives [32,33]. Localized prostate tumors show extensive alterations in the hyper-or hypomethylation of certain areas that affect gene expression.…”

Section: Epigenetic and Predictive Biomarkers For Pca 21 Dna Methylationmentioning

confidence: 99%

The Cellular and Molecular Immunotherapy in Prostate Cancer

et al. 2022

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In recent history, immunotherapy has become a viable cancer therapeutic option. However, over many years, its tenets have changed, and it now comprises a range of cancer-focused immunotherapies. Clinical trials are currently looking into monotherapies or combinations of medicines that include immune checkpoint inhibitors (ICI), CART cells, DNA vaccines targeting viruses, and adoptive cellular therapy. According to ongoing studies, the discipline should progress by incorporating patient-tailored immunotherapy, immune checkpoint blockers, other immunotherapeutic medications, hormone therapy, radiotherapy, and chemotherapy. Despite significantly increasing morbidity, immunotherapy can intensify the therapeutic effect and enhance immune responses. The findings for the immunotherapy treatment of advanced prostate cancer (PCa) are compiled in this study, showing that is possible to investigate the current state of immunotherapy, covering new findings, PCa treatment techniques, and research perspectives in the field’s unceasing evolution.

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AberrantDNAMethylation of Tumor Suppressor Genes and Oncogenes as Cancer Biomarkers

Cited by 11 publications

References 120 publications

Epigenetic targets to enhance antitumor immune response through the induction of tertiary lymphoid structures

Epigenetic targets to enhance antitumor immune response through the induction of tertiary lymphoid structures

Epigenetic Regulation in Oral Squamous Cell Carcinoma Microenvironment: A Comprehensive Review

The Cellular and Molecular Immunotherapy in Prostate Cancer

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