Ultraviolet Radiation Carcinogenesis

Cleaver, James E.; Mitchell, David L.

doi:10.1002/9781119000822.hfcm026

Cited by 3 publications

(1 citation statement)

References 132 publications

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“…However, these heavily damaged cells are unlikely to become cancerous. Lighter damage may leave a stable, partly functional cell that may be capable of proliferating and eventually developing into cancer, especially if tumor suppressor genes are damaged (Little, 2000;Cleaver and Mitchell, 2000;Gawkrodger, 2004;William and Timothy 2006). New research suggests that radiation's harm isn't always immediate.…”

Section: Mechanism Of Cancer Development Due To Ionizing Radiationsmentioning

confidence: 99%

Ionizing Radiations and Cancers

OMORUYI,

OYEM,

ODAGWE

2023

AJHSE

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Ionizing radiations are types of energies that have sufficient force to remove electrons from atoms, creating ions in the process. They include all electromagnetic waves from ultraviolet light to x-rays and gamma rays as well as alpha to beta particles. Ionizing radiations results in harmful effects on living organisms such as damage of cell structures and DNA due to their ability to ionize atoms and molecules. This paper seeks to review the effects of these radiations and how to be protected in real time. Exposure to high levels of ionizing radiations cause immediate symptoms, such as burns, nausea, and vomiting, also it can lead to serious health problems, including cancer, genetic mutations and death. Long-term exposure to lower levels of ionizing radiation can increase the risks of cancer and other diseases. Cancers have become a scourge in today’s world, with breast cancer, leukemia, cervical and prostate cancers being the most notable types. The development of cancer is a complex multistage process that usually takes many years. The contributions of ionizing radiations to its development cannot be overemphasized. However, ionizing radiation is also used for beneficial purposes, such as medical imaging, radiation therapy, and for energy production. The key is to use it safely and responsibly so as to reduce its debilitating effects.

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Section: Mechanism Of Cancer Development Due To Ionizing Radiationsmentioning

confidence: 99%

Ionizing Radiations and Cancers

OMORUYI,

OYEM,

ODAGWE

2023

AJHSE

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p53 suppression overwhelms DNA polymerase η deficiency in determining the cellular UV DNA damage response

et al. 2007

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Xeroderma pigmentosum variant (XP-V) cells lack the damage-specific DNA polymerase η and have normal excision repair but show defective DNA replication after UV irradiation. Previous studies using cells transformed with SV40 or HPV16 (E6/E7) suggested that the S-phase response to UV damage is altered in XP-V cells with non-functional p53. To investigate the role of p53 directly we targeted p53 in normal and XP-V fibroblasts using short hairpin RNA. The shRNA reduced expression of p53, and the downstream cell cycle effector p21, in control and UV irradiated cells. Cells accumulated in late S phase after UV, but after down-regulation of p53 they accumulated earlier in S. Cells in which p53 was inhibited showed ongoing genomic instability at the replication fork. Cells exhibited high levels of UV induced S-phase γH2Ax phosphorylation representative of exposed single strand regions of DNA and foci of Mre11/Rad50/Nbs1 representative of double strand breaks. Cells also showed increased variability of genomic copy numbers after long-term inhibition of p53. Inhibition of p53 expression dominated the DNA damage response. Comparison with earlier results indicates that in virally transformed cells cellular targets other than p53 play important roles in the UV DNA damage response.

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Photocarcinogenesis inXiphophorusHybrid Models

Mitchell

Nairn

2006

Zebrafish

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The poeciliid fish genus Xiphophorus provides important models for investigating the etiology and genetics of sunlight-induced melanoma. Interspecific hybrids generated among platyfish and swordtails have been used as genetic tumor models, particularly for cutaneous malignant melanoma (CMM), for more than 6 decades. Oncogene and tumor suppressor gene involvement in a variety of spontaneous and carcinogen-induced tumors has been and continues to be extensively studied. Select hybrids develop melanoma spontaneously or after acute or chronic exposure to ultraviolet radiation. Many scientists believe that the etiology of CMM and particularly its initiation is different from other types of sunlight-induced skin cancers, and may involve free radical chemistry rather than the direct absorption of UVB by DNA. Xiphophorus offers a unique platform to scrutinize this question and determine the types of DNA damage that are involved, the solar wavelength ranges that are important, and the role of DNA repair genes in early tumorigenesis. The diverse photochemical and photobiological responses observed in the different Xiphophorus species and interspecies hybrids suggest that heritable traits governing DNA damage induction and repair may be involved in the susceptibility of Xiphophorus hybrids to melanomagenesis.

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Ultraviolet Radiation Carcinogenesis

Cited by 3 publications

References 132 publications

Ionizing Radiations and Cancers

Ionizing Radiations and Cancers

p53 suppression overwhelms DNA polymerase η deficiency in determining the cellular UV DNA damage response

Photocarcinogenesis inXiphophorusHybrid Models

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