Journal of Clinical & Experimental OncologyISSN: 2324-9110

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Opinion Article,  J Clin Exp Onco Vol: 13 Issue: 1

Examining the Types and Impact of Oncogenes on Human Health

Laures Christiano*

1Department of Medicine, Pennsylvania State University College of Medicine, Pennsylvania, United States of America

*Corresponding Author: Laures Christiano,
Department of Medicine, Pennsylvania State University College of Medicine, Pennsylvania, United States of America
E-mail:
laures_christiano@psucm21.edu

Received date: 23 January, 2024, Manuscript No. JCEOG-24-130941;

Editor assigned date: 25 January, 2024, PreQC No. JCEOG-24-130941 (PQ);

Reviewed date: 08 February, 2024, QC No. JCEOG-24-130941;

Revised date: 15 February, 2024, Manuscript No. JCEOG-24-130941 (R);

Published date: 23 February, 2024, DOI: 10.4172/2324-9110.1000391

Citation: Christiano L (2024) Examining the Types and Impact of Oncogenes on Human Health. J Clin Exp Oncol 13:1.

Description

Oncogenes, a diverse group of genes with the potential to promote cancer development, play a significant role in shaping the landscape of human health. Understanding the different types of oncogenes and their impact on cellular processes is essential for comprehending the complexities of cancer biology and devising effective therapeutic strategies. It delves into the various types of oncogenes and examines their profound impact on human health. Proto-oncogenes are normal cellular genes that regulate key functions such as cell growth, differentiation, and survival. When mutated or activated by various mechanisms, such as point mutations, gene amplifications, or chromosomal translocations, proto-oncogenes can transform into oncogenes, promoting uncontrolled cell proliferation and tumorigenesis. Examples of proto-oncogenes include RAS, MYC, and ERBB family members.

Growth factor receptors are cell surface receptors that transmit signals from the extracellular environment to the cell's interior, regulating processes such as cell growth, survival, and differentiation. Mutations or overexpression of growth factor receptors can lead to constitutive activation of downstream signaling pathways, driving oncogenic transformation. Examples of growth factor receptor oncogenes include Epidermal Growth Factor Receptor (EGFR) and Human Epidermal Growth Factor Receptor 2 (HER2). Signal transduction proteins relay intracellular signals from activated receptors to downstream effector molecules, orchestrating cellular responses to extracellular stimuli. Mutations in signal transduction proteins can disrupt normal signaling pathways, leading to aberrant cell growth and proliferation.

Examples of signal transduction oncogenes include RAS, RAF, and PI3K, which play vital roles in regulating cell proliferation and survival. Transcription factors are proteins that regulate gene expression by binding to specific DNA sequences and modulating the transcription of target genes. Dysregulated expression or activity of transcription factors can promote oncogenesis by altering the expression of genes involved in cell cycle regulation, apoptosis, and differentiation. Examples of transcription factor oncogenes include MYC, MYCN, and E2F family members. Oncogenes drive the initiation of cancer by promoting uncontrolled cell proliferation and survival. Mutated or overexpressed oncogenes disrupt normal cellular processes, leading to the unchecked growth and division of malignant cells. The activation of oncogenic signaling pathways fuels the development of pre-malignant lesions and facilitates the transition to invasive cancer.

Oncogenes play a key role in tumor progression and metastasis by enhancing the aggressiveness and invasiveness of cancer cells. Dysregulated oncogene signaling promotes tumor growth, angiogenesis, and resistance to apoptosis, allowing cancer cells to proliferate unchecked and invade surrounding tissues. Metastasis, the spread of cancer to distant sites, is facilitated by oncogene-driven processes such as Epithelial-Mesenchymal Transition (EMT) and extracellular matrix remodeling.

Targeting oncogenes and their associated signaling pathways has emerged as a potentially strategy for cancer treatment. Targeted therapies, such as small molecule inhibitors and monoclonal antibodies, selectively inhibit oncogenic signaling cascades, leading to tumor regression and improved patient outcomes. Examples of successful targeted therapies include EGFR inhibitors in lung cancer and BRAF inhibitors in melanoma.

Conclusion

Oncogenes represent a diverse array of genetic alterations that contribute to cancer development and progression. By understanding the various types of oncogenes and their impact on cellular processes, analysts and clinicians can develop targeted therapeutic strategies to combat cancer more effectively. Continued studies into the molecular mechanisms underlying oncogene-driven tumorigenesis is essential for advancing the understanding of cancer biology and improving patient outcomes in the fight against cancer.

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