Journal of Carcinogenesis & Mutagenesis

The Mechanisms of Mutagenesis and Genomic Instability in Cancer

Shaohua Gou^* Department of Genetics, Hebrew University, Jerusalem, Israel
^*Correspondence: Shaohua Gou, Department of Genetics, Hebrew University, Jerusalem, Israel, Email:

Received: 01-May-2023, Manuscript No. JCM-23-21749; Editor assigned: 03-May-2023, Pre QC No. JCM-23-21749 (PQ); Reviewed: 17-May-2023, QC No. JCM-23-21749; Revised: 24-May-2023, Manuscript No. JCM-23-21749 (R); Published: 31-May-2023, DOI: 10.35248/2157-2518.23.S38.001

Description

Cancer, a complex and multifactorial disease, arises from the accumulation of genetic alterations in cells, leading to uncontrolled proliferation and the potential to invade surrounding tissues. One of the key factors contributing to the development of cancer is mutagenesis, the process by which mutations occur in the DNA sequence. These mutations can disrupt normal cellular functions and promote genomic instability, further fueling the progression of cancer. This article aims to explore the mechanisms underlying mutagenesis and genomic instability in cancer, shedding light on the molecular processes that drive this devastating disease [1-3].

Mutations can arise from various sources, including environmental factors, such as Ultraviolet (UV) radiation, chemicals, and lifestyle choices, as well as endogenous processes, such as errors in DNA replication and spontaneous DNA damage. These factors induce DNA lesions, including base modifications, DNA strand breaks, and crosslinks. However, cells have evolved intricate DNA repair mechanisms to counteract these insults and maintain genomic integrity. Failure or impairment of these repair systems can result in the accumulation of mutations and the onset of cancer.

During cell division, DNA replication is a critical process where the genetic information is faithfully duplicated. However, this process is not error-free, and inaccuracy can occur during DNA synthesis. DNA polymerases possess repair mechanisms to detect and accurate replication errors. Nonetheless, errors that evade the error-checking process can persist, resulting in the introduction of mutations into the daughter cells. Mutations in genes involved in DNA replication and DNA repair mechanisms can substantially increase the risk of cancer development.

Chromosomal Instability (CIN) is a hallmark of many cancers and refers to an increased rate of chromosomal alterations within cancer cells. It encompasses numerical alterations, such as gains or losses of whole chromosomes (aneuploidy), and structural abnormalities, including translocations, deletions, and inversions. CIN can result from defects in the machinery responsible for faithful chromosome segregation during cell division, leading to unequal distribution of genetic material. The resulting aneuploidy and chromosomal rearrangements can contribute to the development of cancer [5].

To counteract DNA damage and ensure accurate repair, cells activate a series of signaling pathways collectively known as the DNA Damage Response (DDR). DDR triggers cell cycle checkpoints, temporary halts in the cell division process, allowing time for DNA repair before proceeding to the next phase. However, if the DNA damage is severe and cannot be adequately repaired, cells may undergo programmed cell death or senescence. Dysregulation of the DDR and cell cycle checkpoints can lead to genomic instability and the acquisition of mutations associated with cancer.

Oncogenes and tumor suppressor genes

Oncogenes and tumor suppressor genes play crucial roles in maintaining genomic stability. Oncogenes are genes that promote cell growth and division when mutated or overexpressed, while tumor suppressor genes inhibit cell division or induce cell death when their activity is lost or reduced. Mutations in oncogenes and tumor suppressor genes can disrupt normal cellular processes, including DNA repair and cell cycle regulation, leading to genomic instability and cancer development. In addition to genetic mutations, epigenetic alterations contribute to cancer development. Epigenetics refers to changes in gene expression patterns that do not involve alterations in the DNA sequence itself but are heritable. These changes can affect DNA methylation.

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