Theranostic Interpolation of Genomic Instability in Breast Cancer

Abstract

Breast cancer is a diverse disease caused by mutations in multiple genes accompanying epigenetic aberrations of hazardous genes and protein pathways, which distress tumor-suppressor genes and the expression of oncogenes. Alteration in any of the several physiological mechanisms such as cell cycle checkpoints, DNA repair machinery, mitotic checkpoints, and telomere maintenance results in genomic instability. Theranostic has the potential to foretell and estimate therapy response, contributing a valuable opportunity to modify the ongoing treatments and has developed new treatment strategies in a personalized manner. “Omics” technologies play a key role while studying genomic instability in breast cancer, and broadly include various aspects of proteomics, genomics, metabolomics, and tumor grading. Certain computational techniques have been designed to facilitate the early diagnosis of cancer and predict disease-specific therapies, which can produce many effective results. Several diverse tools are used to investigate genomic instability and underlying mechanisms. The current review aimed to explore the genomic landscape, tumor heterogeneity, and possible mechanisms of genomic instability involved in initiating breast cancer. We also discuss the implications of computational biology regarding mutational and pathway analyses, identification of prognostic markers, and the development of strategies for precision medicine. We also review different technologies required for the investigation of genomic instability in breast cancer cells, including recent therapeutic and preventive advances in breast cancer.

Comprehensive analysis of Linc01436 for neoadjuvant chemotherapy response and its potential enriched pathways in breast cancer

“…Genomic instability is a hallmark of breast cancer which was resulted from alteration in several mechanisms like cell cycle checkpoints, mitotic checkpoints, DNA repair machinery, or telomere maintenance, as they are known to maintain the integrity of the human genome [33,34]. As a result, functional loss of tumor-suppressor genes or oncogene function activation would occur nally [35]. We also observed Linc01436 expression is associated with m1A, m5C and m6A, which are three classical forms of epigenetic modi cation [36].…”

Identification of VWA5A as a novel biomarker for inhibiting metastasis in breast cancer by machine-learning based protein prioritization

“…VWA5A lies in the vicinity of CHEK1 , PIG8 , and ROBO3 loci, and this genomic region is known to be commonly deleted together 19 . Therefore, CHEK1 deletion coupled with VWA5A loss would result in impaired DNA damage response, contributing to genomic instability and resultant aggressive behavior of the BC cells 20 – 22 . Another possible explanation would include the interaction between tumor cells and extracellular matrix.…”

Breast Cancer Exposomics

“…Advances in molecular approaches and analytical techniques based on high-throughput sequencing and mass spectrometry (MS) have generated multi-omics data that can be successfully used to understand the underlying molecular mechanisms involved in BC exposomics [ 60 ]. BC is mainly caused by mutations in multiple oncogenes and tumor suppressor genes, accompanying epigenetic aberrations of genes and protein pathways [ 61 ]. Thus, first of all, environmental toxicogenomics aims to collect, analyze, and interpret data on the changes in genes or protein expression, resulting from exposure to xenobiotics, using high-throughput technologies [ 62 ].…”

“…Thus, first of all, environmental toxicogenomics aims to collect, analyze, and interpret data on the changes in genes or protein expression, resulting from exposure to xenobiotics, using high-throughput technologies [ 62 ]. Evidence suggests that various pollutants, such as particulate matter involved in air pollution, act as carcinogenic factors in humans, inducing high rates of genomic instability [ 63 ], which is known as an initiator of BC development [ 61 ]. In addition, environmental epigenomics focuses on environmental factors that induce aberrant DNA methylation of cancer-related genes, even in developing embryos, when result in epigenetic mosaicism that can increase the oncogenic risk later in life [ 64 ].…”