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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Human papillomavirus infection increases the chemoradiation response of esophageal squamous cell carcinoma based on P53 mutation.
Radiotherapy and Oncology 2017 July
BACKGROUND AND PURPOSE: A retrospective study was carried out to analyze multiple prognostic predictors, including human papillomavirus (HPV) infection for chemoradiation treatment of esophageal squamous cell carcinoma (ESCC).
MATERIALS AND METHODS: DNA extracted from a total of 192 patients treated with chemoradiation for locally advanced ESCC was examined to determine HPV status by polymerase chain reaction (PCR) and P53 gene mutation by genetic sequencing. The relationships between the chemoradiation response (CRR) and overall survival (OS) rate with HPV status and P53 gene mutation were analyzed.
RESULTS: Thirty-two of the 108 patients with P53 mutated tumors were stained positive for HPV, while thirty-five of the 84 P53 wild-type tumors were HPV positive. P53 mutation and HPV infection were two independent events (p=0.083, Kappa=0.083). HPV infection increased the CRR (p=0.017) and 3-year OS (p=0.047) compared with the HPV negative group. This difference was more significant in the P53 mutation subgroup (CRR p=0.019; OS p=0.025). However, HPV infection led to no difference in the P53 wild-type subgroup (CRR p=0.802; OS p=0.468). The P53 mutation status was an independent prognostic factor (CRR p=0.034; OS p<0.001). Age was another significant prognostic factor for OS (p=0.001).
CONCLUSIONS: Depending on P53 mutation status, HPV infection can contribute to a higher tumor response and better prognosis of ESCC treated with chemoradiation therapy.
MATERIALS AND METHODS: DNA extracted from a total of 192 patients treated with chemoradiation for locally advanced ESCC was examined to determine HPV status by polymerase chain reaction (PCR) and P53 gene mutation by genetic sequencing. The relationships between the chemoradiation response (CRR) and overall survival (OS) rate with HPV status and P53 gene mutation were analyzed.
RESULTS: Thirty-two of the 108 patients with P53 mutated tumors were stained positive for HPV, while thirty-five of the 84 P53 wild-type tumors were HPV positive. P53 mutation and HPV infection were two independent events (p=0.083, Kappa=0.083). HPV infection increased the CRR (p=0.017) and 3-year OS (p=0.047) compared with the HPV negative group. This difference was more significant in the P53 mutation subgroup (CRR p=0.019; OS p=0.025). However, HPV infection led to no difference in the P53 wild-type subgroup (CRR p=0.802; OS p=0.468). The P53 mutation status was an independent prognostic factor (CRR p=0.034; OS p<0.001). Age was another significant prognostic factor for OS (p=0.001).
CONCLUSIONS: Depending on P53 mutation status, HPV infection can contribute to a higher tumor response and better prognosis of ESCC treated with chemoradiation therapy.
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