The molecular basis of nonmelanoma skin cancer: new understanding

Grossman, D.

doi:10.1001/archderm.133.10.1263

Cited by 87 publications

(75 citation statements)

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“…UVR especially prior to the age of 20 years is suggested to initiate a process of basal cell carcinogenesis (15). UVR has two major effects that influence BCC development, namely DNA damage and immunosuppression (16). Exposure to UVR, specifically UVB, induces covalent bonds in DNA between adjacent pyrimidines, generating photoproducts such as cyclodipyrimidine dimers (T ⁄T) and pyrimidine lesions which are mutagenic if not repaired.…”

Section: Extrinsic Factorsmentioning

confidence: 99%

An Overview on Basal Cell Carcinoma

Avcı¹

2011

Skin Cancer Overview

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Section: Extrinsic Factorsmentioning

confidence: 99%

An Overview on Basal Cell Carcinoma

Avcı¹

2011

Skin Cancer Overview

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“…However, to date the genetic mechanism and the precise effect of the UV radiation in the development of cutaneous melanoma has not been fully understood. UV radiation stimulates DNA mutations and causes local damage by several mechanisms and induces apoptosis through a production of growth factors from skin cells [26]. Moreover; ultra-violate radiation is known to reduce the immunity and stimulates formation of reactive oxygen species in melanocytes locally [27].…”

Section: Molecular Pathwaysmentioning

confidence: 99%

Melanoma from Molecular Pathways to Clinical Treatment: An Up to Date Review

Kosmıdis¹,

Baka²,

Sapalidis³

et al. 2017

J. Biomed

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Skin cancer is divided to melanoma and non-melanoma. Melanoma occurs due to deregulation of melanocytes. Melanoma is frequent in Caucasian population. During the last decade there is an increase in melanoma and in many cases there is a diagnostic challenge. Moreover; choosing the right treatment is a challenge for many patients. Malignant melanoma is known to be a lethal disease due to its aggressive capacity for metastasis and resistance to therapy. In the last decade, considerable efforts have gone into development of an effective immunotherapy for treatment of melanoma. The combination of macrophage activation and other treatments such as immunotherapy, surgery, chemotherapy, and radiotherapy, may provide an effective and comprehensive anti-melanoma strategy.

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“…In addition, exposure to UV radiation can cause multimerization, clustering, and activation of cell surface receptor proteins for growth factors and cytokines, with activation of receptor-associated tyrosine kinase activities (334 Exposure to UV radiation is associated with an increased skin cancer risk and premature aging of the skin, particularly among fair-skinned individuals with histories of being sunburned. A strong positive correlation also exists between skin cancer and proximity to the equator, indicating that higher UV doses to human populations result in higher incidences of skin cancer [for reviews, see (338)(339)(340)(341)(342)]. Enhanced removal of LW-induced pyrimidine dimers lowers skin cancer rates in mice, indicating that unrepaired dimers cause cancer in mammalian skin (343).…”

Section: The Spindle Checkpointmentioning

confidence: 99%

Cell cycle control, checkpoint mechanisms, and genotoxic stress.

Shackelford

Kaufmann

Paules

1999

Environ Health Perspect

183

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The ability of cells to maintain genomic integrity is vital for cell survival and proliferation. Lack of fidelity in DNA replication and maintenance can result in deleterious mutations leading to cell death or, in multicellular organisms, cancer. The purpose of this review is to discuss the known signal transduction pathways that regulate cell cycle progression and the mechanisms cells employ to insure DNA stability in the face of genotoxic stress. In particular, we focus on mammalian cell cycle checkpoint functions, their role in maintaining DNA stability during the cell cycle following exposure to genotoxic agents, and the gene products that act in checkpoint function signal transduction cascades. Key transitions in the cell cycle are regulated by the activities of various protein kinase complexes composed of cyclin and cyclin-dependent kinase (Cdk) molecules. Surveillance control mechanisms that check to ensure proper completion of early events and cellular integrity before initiation of subsequent events in cell cycle progression are referred to as cell cycle checkpoints and can generate a transient delay that provides the cell more time to repair damage before progressing to the next phase of the cycle. A variety of cellular responses are elicited that function in checkpoint signaling to inhibit cyclin/Cdk activities. These responses include the p53-dependent and p53-independent induction of Cdk inhibitors and the p53-independent inhibitory phosphorylation of Cdk molecules themselves. Eliciting proper Gl, S, and G2 checkpoint responses to double-strand DNA breaks requires the function of the Ataxia telangiectasia mutated gene product. Several human heritable cancer-prone syndromes known to alter DNA stability have been found to have defects in checkpoint surveillance pathways. Exposures to several common sources of genotoxic stress, including oxidative stress, ionizing radiation, UV radiation, and the genotoxic compound benzo[alpyrene, elicit cell cycle checkpoint responses that show both similarities and differences in their molecular signaling. -Environ Health Perspect 107(Suppl 1):5-24 (1999 (Figure 1) (6,8).The description of the cell cycle being divided into four phases led to many questions about the regulatory mechanisms cells employ to ensure an ordered and sequential progression from G1 to M phase, as well as the mechanisms ensuring DNA stability. Some of these questions were summarized as the "completion" and "alternation" problems (8,9). In the completion problem, the question is raised as to how cells ensure that specific events are completed before subsequent events are initiated. For example, cells must ensure that once DNA is condensed for segregation during cytokinesis, it remains condensed throughout M phase and does not prematurely decondense. In the alternation problem, the question is raised as to how cells ensure that once an event is completed, it is not inappropriately repeated. For example, cells must ensure that once DNA replication in S phase is completed, it is followed by DNA co...

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The molecular basis of nonmelanoma skin cancer: new understanding

Cited by 87 publications

References 0 publications

An Overview on Basal Cell Carcinoma

An Overview on Basal Cell Carcinoma

Melanoma from Molecular Pathways to Clinical Treatment: An Up to Date Review

Cell cycle control, checkpoint mechanisms, and genotoxic stress.

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