Opinion Article, J Clin Exp Oncol Vol: 13 Issue: 2

Examining Oncogenes Methods and Their Impact on Health

David Allisen^*

¹Department of Medicine, University of Colorado Cancer Center, Denver, United States of America

*Corresponding Author: David Allisen,
Department of Medicine, University of Colorado Cancer Center, Denver, United States of America
E-mail: david_allisen@ucc11.edu

Received date: 25 March, 2024, Manuscript No. JCEOG-24-136970;

Editor assigned date: 27 March, 2024, PreQC No. JCEOG-24-136970 (PQ);

Reviewed date: 10 April, 2024, QC No. JCEOG-24-136970;

Revised date: 17 April, 2024, Manuscript No. JCEOG-24-136970 (R);

Published date: 24 April, 2024, DOI: 10.4172/2324-9110.1000402

Citation: Allisen D (2024) Examining Oncogenes Methods and Their Impact on Health. J Clin Exp Oncol 13:2.

Description

Oncogenes, a class of genes that have the potential to cause cancer, play a pivotal role in the development and progression of many malignancies. They are typically mutated or expressed at high levels in tumor cells. Understanding the mechanisms by which oncogenes function and their impact on human health is essential for developing targeted therapies and improving cancer treatment outcomes. It explores the methods by which oncogenes contribute to cancer and examines their broader implications on human health. Oncogenes are mutated or overexpressed versions of normal genes, known as protooncogenes, that are involved in cell growth, differentiation, and survival. When proto-oncogenes undergo mutations, they become permanently activated or express abnormally high levels of their protein products, leading to uncontrolled cell proliferation and tumor development.

These genetic alterations can be caused by various factors, including environmental carcinogens, radiation, viral infections, and inherited genetic predispositions. Single nucleotide changes in the DNA sequence of proto-oncogenes can convert them into oncogenes. For example, a point mutation in the RAS gene, which encodes a protein involved in cell signaling, can lead to its continuous activation, driving uncontrolled cell division. Gene Amplification process involves the increase in the number of copies of a proto-oncogene within the cell. The overexpression of the gene product can lead to enhanced cell proliferation. An example is the MYC gene, which is often amplified in various cancers, including breast and lung cancers. Chromosomal translocations in which the rearrangement of genetic material between chromosomes can develop fusion genes that produce oncogenic proteins.

A notable example is the BCR-ABL fusion gene resulting from the Philadelphia chromosome translocation in Chronic Myeloid Leukemia (CML), which leads to the production of an abnormal tyrosine kinase that drives cancer progression. Insertional mutagenesis it occurs when viral DNA integrates into the host genome near a proto-oncogene, leading to its activation. Human Papillomavirus (HPV) can insert its DNA into the host genome and activate oncogenes like MYC and RAS, contributing to cervical cancer. Oncogenes significantly impact human health by driving the initiation and progression of cancer. Their activation can lead to various physiological changes that support tumor growth and metastasis. Understanding these impacts is vital for developing effective cancer therapies. Oncogenes promote continuous cell division, bypassing the normal regulatory mechanisms that control cell growth. This leads to the formation of tumors and the potential spread of cancer cells to other parts of the body. Resistance to apoptosis in which many oncogenes confer resistance to apoptosis, the programmed cell death that eliminates damaged or abnormal cells.

For instance, the BCL-2 gene, when overexpressed, prevents apoptosis, allowing cancer cells to survive and proliferate despite DNA damage or other cellular stresses. Oncogenes can stimulate the formation of new blood vessels (angiogenesis) to supply the growing tumor with nutrients and oxygen. The VEGF gene, often upregulated in tumors, promotes angiogenesis, facilitating tumor growth and metastasis. Oncogenes can enhance the invasive properties of cancer cells, enabling them to spread to distant organs. The MET gene, for example, encodes a receptor tyrosine kinase that, when mutated or overexpressed, promotes cell motility and invasion, leading to metastasis. Cancer cells often exhibit altered metabolic pathways to support rapid growth and division. Oncogenes like MYC reprogram cellular metabolism to increase glucose uptake and biosynthesis of macromolecules, supporting the energetic and anabolic needs of proliferating cancer cells.

Conclusion

Oncogenes play a central role in the development and progression of cancer by promoting uncontrolled cell proliferation, resistance to apoptosis, angiogenesis, metastasis, and altered metabolism. Understanding the mechanisms of oncogene activation and their impact on human health has led to the development of targeted therapies that have revolutionized cancer treatment. Despite the difficulties that remain, ongoing studies in oncogenes holds potential for new and more effective cancer treatments, ultimately improving patient outcomes and reducing the burden of this devastating disease.