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Oncogenes and oncogenesis: origin, development, cause, and therapy

  • Varruchi Sharma , Vikas Kushwaha , Anil Panwar , Imran Sheikh , Anuprabha , Manoj Singh , Sushil Kumar Upadhyay , Seema Ramniwas , Priyancka Arora and Anil K. Sharma
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Anticancer Therapeutics
This chapter is in the book Anticancer Therapeutics

Abstract

Oncogenes can have different origins, such as fusion genes produced by chromosomal translocations, viral oncogenes integrated into the host genome, or normal cellular genes (called proto-oncogenes) that undergo alterations. Proto-oncogenes are genes that encode proteins necessary for cell division, growth, and proliferation; yet, they can become carcinogenic when they undergo a mutation. During this process, healthy cells develop into malignant ones. Activation of oncogenes stimulates unchecked cell proliferation, apoptosis avoidance, angiogenesis, and metastasis. Several events activate oncogenes in the body. Such events involve epigenetic modifications, viral infections, chromosomal rearrangements, genetic mutations, and environmental carcinogens. Chromosome translocations can produce fusion genes with carcinogenic characteristics, while mutations in proto-oncogenes can cause their constitutive activation. In today’s scientific era, targeting oncogenes and associated signaling pathways has become a cornerstone of cancer therapy. For the same process, various strategies have been adopted, mainly including molecular inhibitors and gene therapies. These are targeted to inhibit oncogenic proteins or block the downstream signaling cascade.

Abstract

Oncogenes can have different origins, such as fusion genes produced by chromosomal translocations, viral oncogenes integrated into the host genome, or normal cellular genes (called proto-oncogenes) that undergo alterations. Proto-oncogenes are genes that encode proteins necessary for cell division, growth, and proliferation; yet, they can become carcinogenic when they undergo a mutation. During this process, healthy cells develop into malignant ones. Activation of oncogenes stimulates unchecked cell proliferation, apoptosis avoidance, angiogenesis, and metastasis. Several events activate oncogenes in the body. Such events involve epigenetic modifications, viral infections, chromosomal rearrangements, genetic mutations, and environmental carcinogens. Chromosome translocations can produce fusion genes with carcinogenic characteristics, while mutations in proto-oncogenes can cause their constitutive activation. In today’s scientific era, targeting oncogenes and associated signaling pathways has become a cornerstone of cancer therapy. For the same process, various strategies have been adopted, mainly including molecular inhibitors and gene therapies. These are targeted to inhibit oncogenic proteins or block the downstream signaling cascade.

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