Journal of Medical Oncology and Therapeutics

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Rapid Communication - Journal of Medical Oncology and Therapeutics (2025) Volume 10, Issue 2

The Molecular Basis of Carcinogenesis: From Genetic Mutations to Cancer

Alexander Schmitz *

Department of Psychosomatics, University of Cologne, Germany

*Corresponding Author:
Alexander Schmitz
Department of Psychosomatics, University of Cologne, Germany
E-mail: a.schmitz@uk-koeln.de

Received: 1-Mar-2025, Manuscript No. JMOT-25-162119; Editor assigned: 4-Mar-2025, PreQC No. JMOT-25-162119 (PQ) Reviewed:17-Mar-2025, QC No. JMOT-25-162119Revised:24-Mar-2025, Manuscript No. JMOT-25-162119; Published:31-Mar-2025, DOI: 10.35841/jmot- 10.2.254

Citation: Schmitz A. The molecular basis of carcinogenesis: From genetic mutations to cancer. J Med Oncl Ther. 2025;10(2):254

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Introduction

Cancer is a complex disease that arises from the uncontrolled growth and proliferation of cells. At the heart of this process is carcinogenesis, the molecular transformation of normal cells into malignant ones. This transformation is driven by genetic mutations, epigenetic alterations, and disruptions in key cellular pathways that regulate growth, differentiation, and apoptosis. Understanding the molecular basis of carcinogenesis is essential for developing effective prevention strategies and targeted therapies [1].

Genetic mutations are the primary drivers of carcinogenesis. These mutations can be inherited (germline mutations) or acquired (somatic mutations) due to environmental exposure, spontaneous errors in DNA replication, or defective repair mechanisms. The most common types of mutations involved in cancer include point mutations, insertions, deletions, and chromosomal rearrangements. These alterations can activate oncogenes, inactivate tumor suppressor genes, or affect DNA repair genes, leading to uncontrolled cellular growth [2].

Oncogenes are mutated forms of normal genes (proto-oncogenes) that promote cell proliferation. When these genes undergo activating mutations, they drive excessive cell division and survival. Examples of oncogenes include RAS, MYC, and EGFR. In contrast, tumor suppressor genes, such as TP53, RB1, and BRCA1, function to regulate cell growth and promote apoptosis. Mutations or deletions in these genes result in the loss of cell cycle control, allowing cancerous cells to thrive unchecked [3].

Apart from genetic mutations, epigenetic alterations also play a significant role in carcinogenesis. Epigenetic changes, such as DNA methylation, histone modifications, and microRNA regulation, can influence gene expression without altering the DNA sequence. Hypermethylation of tumor suppressor gene promoters can silence their expression, while hypomethylation of oncogenes can lead to their overexpression. These changes contribute to the initiation and progression of cancer [4].

Cells have sophisticated DNA repair mechanisms, such as mismatch repair (MMR), nucleotide excision repair (NER), and homologous recombination repair (HRR), to correct errors in DNA replication and damage caused by external factors. Defects in these pathways, as seen in conditions like Lynch syndrome (MMR deficiency) and BRCA1/2 mutations (HRR deficiency), lead to genomic instability and an increased risk of cancer. Accumulation of DNA damage allows cells to evade normal regulatory mechanisms and become malignant [5].

The cell cycle is tightly regulated by checkpoints that ensure proper cell division. Cyclins, cyclin-dependent kinases (CDKs), and their inhibitors coordinate this process. In cancer, dysregulation of the cell cycle due to overactive CDKs or loss of CDK inhibitors (such as p16 and p21) results in unchecked cellular proliferation. This allows cancer cells to divide uncontrollably, forming tumors [6].

To sustain rapid growth, tumors induce the formation of new blood vessels (angiogenesis) through the secretion of vascular endothelial growth factor (VEGF). Angiogenesis supplies oxygen and nutrients to the growing tumor, facilitating further expansion and metastasis. Targeting angiogenesis with drugs like bevacizumab (anti-VEGF therapy) has shown promise in cancer treatment [7].

Normal cells undergo apoptosis (programmed cell death) when they experience irreparable damage. However, cancer cells evade apoptosis by inactivating pro-apoptotic proteins (BAX, PUMA) and overexpressing anti-apoptotic proteins (BCL-2, MCL-1). Additionally, cancer cells activate telomerase, an enzyme that extends telomeres and prevents cellular aging, allowing them to divide indefinitely [8].

One of the most dangerous aspects of cancer is metastasis, where cancer cells migrate from the primary tumor to distant organs. This process involves epithelial-mesenchymal transition (EMT), during which cancer cells lose adhesion, gain mobility, and invade surrounding tissues. Once in the bloodstream or lymphatic system, these cells establish secondary tumors in new locations, making treatment more challenging [9].

Chronic inflammation plays a crucial role in carcinogenesis. Inflammatory mediators such as cytokines, chemokines, and reactive oxygen species (ROS) promote DNA damage and tumor progression. The tumor microenvironment, composed of immune cells, fibroblasts, and extracellular matrix, interacts with cancer cells, facilitating their survival and resistance to treatment. Targeting inflammation-related pathways, such as COX-2 inhibitors, is an emerging strategy in cancer prevention [10].

Conclusion

The molecular basis of carcinogenesis is a multifaceted process involving genetic mutations, epigenetic alterations, and disruptions in key cellular pathways. Understanding these mechanisms has revolutionized cancer diagnosis, treatment, and prevention strategies. As research continues, novel therapies targeting the molecular drivers of cancer hold promise for improving patient outcomes and ultimately achieving better control over this devastating disease.

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