High-Risk Cutaneous Squamous Cell Carcinoma 2016
DOI: 10.1007/978-3-662-47081-7_3
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Genomics of SCC: Tumor Formation, Progression, and Future Therapeutic Implications for High-Risk Cutaneous Squamous Cell Carcinoma

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Cited by 3 publications
(5 citation statements)
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“…cSCCs have the highest tumor mutation burden among malignancies harboring, on average, ≈50 mutations per megabase pair (Mbp) of DNA [ 15 , 26 , 27 , 28 ]. It is hypothesized that most of these mutations are “passengers”, offering little-to-no growth advantage nor impact on tumor progression, while a subset represent “driver mutations” that promote tumorigenesis by regulating cell fate, growth, survival, or genomic maintenance [ 9 ]. Whole exome and targeted sequencing analyses of unremarkable skin, AKs, SCCIS, and cSCCs provide evidence that numerous driver pathways act preferentially at specific stages to promote tumorigenesis [ 20 , 29 , 30 , 31 , 32 , 33 , 34 ].…”
Section: Genetic Alterations In Csccmentioning
confidence: 99%
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“…cSCCs have the highest tumor mutation burden among malignancies harboring, on average, ≈50 mutations per megabase pair (Mbp) of DNA [ 15 , 26 , 27 , 28 ]. It is hypothesized that most of these mutations are “passengers”, offering little-to-no growth advantage nor impact on tumor progression, while a subset represent “driver mutations” that promote tumorigenesis by regulating cell fate, growth, survival, or genomic maintenance [ 9 ]. Whole exome and targeted sequencing analyses of unremarkable skin, AKs, SCCIS, and cSCCs provide evidence that numerous driver pathways act preferentially at specific stages to promote tumorigenesis [ 20 , 29 , 30 , 31 , 32 , 33 , 34 ].…”
Section: Genetic Alterations In Csccmentioning
confidence: 99%
“…However, in human patients with UV-induced DNA damage, GOF Ras alterations are exceedingly rare in AKs/SCCIS, and are encountered predominantly in a small subset of late-stage cSCCs [ 33 , 34 , 73 ]. As such, Ras genes are not generally regarded as oncogenes driving the early stages of cSCC development [ 9 ].…”
Section: Genetic Alterations In Csccmentioning
confidence: 99%
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“…CSCC results from genetic and epigenetic changes in cell replication during keratinosis. Over time, aggressive tumors accumulate and eventually form ( 5 ). When intracellular defensive abilities are impaired, the accumulation of genetic changes and the development of malignant and precancerous lesions are accelerated ( 6 , 7 ).…”
Section: Introductionmentioning
confidence: 99%