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| 001 | 143730 | ||
| 005 | 20240229112606.0 | ||
| 024 | 7 | _ | |a 10.3390/cancers11040584 |2 doi |
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| 100 | 1 | _ | |a Rong, Chao |b 0 |
| 245 | _ | _ | |a Differential Activation of ERK Signaling in HPV-Related Oropharyngeal Squamous Cell Carcinoma. |
| 260 | _ | _ | |a Basel |c 2019 |b MDPI |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a Human papillomavirus (HPV)-related oropharyngeal squamous cell carcinoma (OPSCC) forms a distinct tumor entity with better survival clinical outcome. Numerous underlying molecular mechanisms have been postulated for differences in treatment response, but the impact of MEK/ERK signaling, a main driver of carcinogenesis in various cancers including OPSCC and key player mediating therapy resistance remains elusive. In a retrospective experimental cohort study, primary tumor samples from OPSCC patients (n = 124) were available on tissue microarrays (TMAs) and expression levels of phosphorylated ERK1/2 (pERK1/2) were detected by immunohistochemical staining. Correlations of pERK1/2 expression patterns with clinicopathological features and clinical outcome were evaluated by statistical analysis. A low pERK1/2 expression was strongly associated with HPV-related OPSCC, while primary tumors with high pERK1/2 staining showed a distinctly worse survival outcome and were associated with higher cellular differentiation. Co-activation of both ERK1/2 and AKT was a common event and was associated with unfavorable prognosis in our cohort. However, the combinatorial analysis of pAKT (Ser473) and pERK1/2 did not strengthen the predictive power of pERK1/2, suggesting that pERK1/2 plays a more significant function in OPSCC. In summary, our data provide a compelling experimental and statistical evidence that low levels of tumor cell intrinsic ERK1/2 activation contribute at least in part to the favorable outcome of HPV-related OPSCC. On the other hand, presented findings indicate that non-HPV-related OPSCC with elevated ERK phosphorylation are at high risk for treatment failure and might benefit from targeted therapy of MEK/ERK signaling. |
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| 700 | 1 | _ | |a Muller, Marie |b 1 |
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| 700 | 1 | _ | |a Horn, Dominik |b 6 |
| 700 | 1 | _ | |a Plinkert, Peter |b 7 |
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| 700 | 1 | _ | |a Affolter, Annette |b 9 |
| 773 | _ | _ | |a 10.3390/cancers11040584 |g Vol. 11, no. 4, p. 584 - |0 PERI:(DE-600)2527080-1 |n 4 |p 584 |t Cancers |v 11 |y 2019 |x 2072-6694 |
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