ライフサイエンスコーパス: OPSCC

1 Methods: We retrospectively analyzed 162 OPSCC patients treated with concurrent chemoradiotherapy

2 Among the 2021 OPSCC survivors included in the analysis of this cohort

3 s were validated in an independent set of 21 OPSCC patients.

4 -genome patterns of DNA methylation among 24 OPSCC primary tumors and 24 matched normal mucosal sampl

5 Among 240 OPSCCs, 144 (60%) were p16 positive (p16+), 115 (48%) we

6 ing the shape, intensity, and texture of 430 OPSCC primary tumors.

7 ion cohort study included disease-free adult OPSCC survivors who completed curative treatment from Ja

8 a good surrogate for ISH+ tumor status among OPSCC, but not a good surrogate for non-OP HNSCC.

9 Among OPSCCs, p16 had high sensitivity (100%), specificity (91

10 HPV infection and cancer and between HPV and OPSCC was associated with increased likelihood of having

11 d cancer: OR, 4.1 [95% CI, 1.8-9.5]; HPV and OPSCC: OR, 3.7 [95% CI, 1.8-7.6]).

12 d the relationship between HPV infection and OPSCC (63 of 271 [23.3%]) or that HPV-associated OPSCC i

13 f the relationship between HPV infection and OPSCC based on survey responses.

14 g the relationship between HPV infection and OPSCC, paired with point-of-care vaccination, may be an

15 resence of lymph node metastases in OSCC and OPSCC, was first re-evaluated and trained on 94 samples

16 process that drives oral HPV persistence and OPSCC, highlighting new developments in the establishmen

17 HOPX protein expression in these tumours and OPSCCs.

18 nderlying the pathobiology of HPV-associated OPSCC (designated HPV(+) OPSCC) remain unclear.

19 rimary surgical patients with HPV-associated OPSCC and node-positive disease confirmed on neck dissec

20 C) could select patients with HPV-associated OPSCC for reduced radiation dose as a means of sparing l

21 tes CETUX/RT-treated low-risk HPV-associated OPSCC into excellent and poor prognosis subgroups.

22 C (63 of 271 [23.3%]) or that HPV-associated OPSCC is the most common HPV-associated cancer type (9 o

23 ab (CETUX) for CIS with RT in HPV-associated OPSCC resulted in inferior efficacy.

24 ive tests among patients with HPV-associated OPSCC was a false negative.

25 ostic cohort, 152 (93.3%) had HPV-associated OPSCC while 11 (6.7%) had HPV-negative OPSCC.

26 e association of knowledge of HPV-associated OPSCC with likelihood of having been vaccinated was asse

27 d to identify a population of HPV-associated OPSCC with superior prognosis.

28 geal squamous cell carcinoma (HPV-associated OPSCC) treated with cisplatin and radiotherapy (CIS/RT).

29 favorable-risk patients with HPV-associated OPSCC.

30 -related oropharyngeal squamous cell cancer (OPSCC), leading to calls for a new staging system.

31 The incidence of oropharyngeal cancer (OPSCC) has escalated in the past few decades; this has l

32 al of oropharyngeal squamous cell carcinoma (OPSCC survivors).

33 iated oropharyngeal squamous cell carcinoma (OPSCC) and is an indication for adjuvant treatment escal

34 lated oropharyngeal squamous cell carcinoma (OPSCC) and the morbidity of increased adjuvant therapy a

35 iated oropharyngeal squamous cell carcinoma (OPSCC) arising from the palatine tonsil and base of the

36 ce of oropharyngeal squamous cell carcinoma (OPSCC) continues to rise in the US, an increasing number

37 ce of oropharyngeal squamous cell carcinoma (OPSCC) has been rapidly increasing.

38 g for oropharyngeal squamous cell carcinoma (OPSCC) has been recommended since 2012.

39 lated oropharyngeal squamous cell carcinoma (OPSCC) has been reported predominantly among middle-aged

40 lated oropharyngeal squamous cell carcinoma (OPSCC) has increased more than 200% in the past 20 years

41 iated oropharyngeal squamous cell carcinoma (OPSCC) has increased over the past 40 years, particularl

42 V(+)) oropharyngeal squamous cell carcinoma (OPSCC) has one of the most rapidly increasing incidences

43 ce of oropharyngeal squamous cell carcinoma (OPSCC) has risen rapidly, because of an epidemic of huma

44 ative oropharyngeal squamous cell carcinoma (OPSCC) has shown resistance to conventional concurrent c

45 on in oropharyngeal squamous cell carcinoma (OPSCC) identifying synergistic interplay with HPV E6/E7

46 ce of oropharyngeal squamous cell carcinoma (OPSCC) incidence has occurred throughout the developed w

47 Oropharyngeal squamous cell carcinoma (OPSCC) incidence is increasing at a nearly epidemic rate

48 iated oropharyngeal squamous cell carcinoma (OPSCC) is a lateral neck mass.

49 itive oropharyngeal squamous cell carcinoma (OPSCC) is a relatively rare but serious disease with lit

50 stage oropharyngeal squamous cell carcinoma (OPSCC) is challenging to diagnose using clinical examina

51 itive oropharyngeal squamous cell carcinoma (OPSCC) is disproportionately high among men, yet empiric

52 nt of oropharyngeal squamous cell carcinoma (OPSCC) is evolving toward risk-based modification of the

53 iated oropharyngeal squamous cell carcinoma (OPSCC) is treatment-responsive.

54 l and oropharyngeal squamous cell carcinoma (OPSCC) outcomes, yet most of these cancers are detected

55 Most oropharyngeal squamous cell carcinoma (OPSCC) patients receive standard cancer therapy.

56 with oropharyngeal squamous cell carcinoma (OPSCC) prognosis.

57 itive oropharyngeal squamous cell carcinoma (OPSCC) represents an emerging disease that differs from

58 HPV+ oropharyngeal squamous cell carcinoma (OPSCC) samples to identify differentially methylated reg

59 py in oropharyngeal squamous cell carcinoma (OPSCC) that was determined to be relevant to the America

60 rozen oropharyngeal squamous cell carcinoma (OPSCC) tissues and normal mucosa samples using microarra

61 with oropharyngeal squamous cell carcinoma (OPSCC) treated with primary surgery or radiotherapy.

62 with oropharyngeal squamous cell carcinoma (OPSCC) undergoing primary transoral robotic surgery (TOR

63 er in oropharyngeal squamous cell carcinoma (OPSCC), its prevalence and significance have not been we

64 on of oropharyngeal squamous cell carcinoma (OPSCC), we performed elemental quanitification by X-ray

65 iated oropharyngeal squamous cell carcinoma (OPSCC).

66 or in oropharyngeal squamous cell carcinoma (OPSCC).

67 with oropharyngeal squamous cell carcinoma (OPSCC).

68 with oropharyngeal squamous cell carcinoma (OPSCC).

69 lated oropharyngeal squamous cell carcinoma (OPSCC).

70 iated oropharyngeal squamous cell carcinoma (OPSCC).

71 with oropharyngeal squamous cell carcinoma (OPSCC).

72 s for oropharyngeal squamous cell carcinoma (OPSCC).

73 iated oropharyngeal squamous cell carcinoma (OPSCC).

74 with oropharyngeal squamous cell carcinoma (OPSCC).

75 Oropharyngeal squamous cell carcinomas (OPSCC) that are associated with human papilloma virus (H

76 tive oropharyngeal squamous cell carcinomas (OPSCC) we noticed that, while ATP5B expression levels di

77 e of oropharyngeal squamous cell carcinomas (OPSCCs) is attributable to human papillomavirus (HPV) in

78 ated oropharyngeal squamous cell carcinomas (OPSCCs) is unknown.

79 t of oropharyngeal squamous cell carcinomas (OPSCCs), and current evidence supports these tumors as h

80 n of oropharyngeal squamous cell carcinomas (OPSCCs), particularly in white men.

81 n of oropharyngeal squamous cell carcinomas (OPSCCs), particularly in white men.

82 is survey study were unaware that HPV causes OPSCC.

83 Comparing OPSCC and non-OPSCC, patients with p16-positive OPSCC ha

84 obal gene promoter methylation in HPV-driven OPSCCs and identifies a signature that predicts the clin

85 ommonly presenting at late stage, HPV-driven OPSCCs are associated with improved prognosis compared w

86 owever, was largely restricted to HPV-driven OPSCCs, which were associated with increased levels of t

87 d clinical behavior compared with HPV-driven OPSCCs.

88 For OPSCC, the pretreatment ALC is prognostic for OS and als

89 , a weaker inverse association was found for OPSCC that were HPV(+) and p16(INK4a) high (HR = 0.55, 9

90 of knowledge about premalignant lesions for OPSCC poses a significant challenge to early detection.

91 s that identify individuals at high risk for OPSCC may act as surrogate markers for precancer but the

92 Primary radiotherapy and surgery for OPSCC.

93 risk factors for readmission after TORS for OPSCC offers opportunities for evidence-based shared dec

94 All patients undergoing TORS for OPSCC were identified using International Classification

95 years; 4475 [80.7%] male) underwent TORS for OPSCC.

96 rtality in older patients undergoing TOS for OPSCC.

97 Patients treated for OPSCC from 2012 to 2019 were extracted, and patients dia

98 In this study, we analyzed 199 fresh-frozen OPSCC specimens for HPV DNA, viral load, RNA expression

99 several policy implications to guide future OPSCC prevention efforts to combat this disease.

100 oropharyngeal squamous cell carcinoma (HPV + OPSCC).

101 ent of a genetic progression model for HPV + OPSCC and in vivo models that mimic HPV + OPSCC pathogen

102 thylation and gene expression data for HPV + OPSCC samples to filter the candidate SEs to identify fu

103 us, we propose that gene expression in HPV + OPSCC may be controlled by epigenetic alterations in SE

104 50 nearby genes (211 SE-gene pairs) in HPV + OPSCC.

105 + OPSCC and in vivo models that mimic HPV + OPSCC pathogenesis.

106 y of HPV-associated OPSCC (designated HPV(+) OPSCC) remain unclear.

107 profile miRNA expression patterns in HPV(+) OPSCC to provide a more detailed understanding of pathol

108 The overall proportion of HPV(+) OPSCC between 2002 and 2011 was 51.8% [95% confidence in

109 ar biology and clinical management of HPV(+) OPSCC in an effort to highlight important advances in th

110 he UICC/AJCC staging system separates HPV(+) OPSCC from its HPV-negative (HPV(-)) counterpart to acco

111 ion, owing to the distinct biology of HPV(+) OPSCCs, targeted therapies and immunotherapies have beco

112 Detection of HPV(+)OPSCC is traditionally accomplished using p16 immunohist

113 ts with confirmed primary or recurrent HPV(+)OPSCC or HPV(-)OPSCC, testing of corresponding PPP sampl

114 lasma (PPP) samples from patients with HPV(+)OPSCC have proven useful for detection and quantitation

115 from an initial clinical cohort of HPV(+/-) OPSCC tumors by quantitative PCR-based miRNA profiling.

116 ed primary or recurrent HPV(+)OPSCC or HPV(-)OPSCC, testing of corresponding PPP samples (n = 32) by

117 cologic outcomes in OPSCC generally and HPV+ OPSCC more specifically.

118 oropharyngeal squamous cell carcinoma (HPV+ OPSCC) disease burden is unknown.

119 oropharyngeal squamous cell carcinoma (HPV+ OPSCC), efforts to de-escalate treatment intensity, whil

120 fying patients with pathology-confirmed HPV+ OPSCC was 84%.

121 hat could shift treatment paradigms for HPV+ OPSCC.

122 Patients with treatment-naive HPV+ OPSCC (p16-positive) and preoperative ctHPVDNA levels we

123 Our findings demonstrate that the HPV+ OPSCC clinical outcomes are strongly correlated with the

124 NTS: This cohort study of patients with HPV+ OPSCC and positive test results for pretreatment TTMV-HP

125 sectional study comprised patients with HPV+ OPSCC who underwent primary TORS between September 2021

126 ed with disease burden in patients with HPV+ OPSCC who underwent TORS.

127 outcomes of patients with HPV driven (HPV+) OPSCC, a significant subset of HPV tumors associated wit

128 d oropharyngeal squamous cell carcinoma (HPV-OPSCC) to achieve similar excellent oncologic outcomes w

129 eck masses in level 2 and 47 (34.1%) had HPV-OPSCC.

130 Cancer seventh edition stage III and IVa HPV-OPSCC treated with NECTORS and CCRT between February 201

131 nsecutive patients with stage III or IVa HPV-OPSCC treated with NECTORS in 2017 to 2022 who had compl

132 tion for patients with stage III and IVa HPV-OPSCC.

133 est characteristics for the detection of HPV-OPSCC.

134 rospective cohort study of patients with HPV-OPSCC treated with the NECTORS protocol in 2017 to 2022.

135 ents positive outcomes for patients with HPV-OPSCC who undergo this treatment regimen.

136 63 [58-67] years; 54 [80.6%] male) with HPV-OPSCC, the most frequent cancer subsites were palatine t

137 Importantly, OPSCC is often detected at an advanced stage owing to a

138 ever, evidence regarding this association in OPSCC is lacking.

139 nd Measures: The annual percentage change in OPSCC incidence from 2000 to 2012, stratified according

140 in tumor- and radiation-induced dysphagia in OPSCC and offer a comprehensive dataset on the neural la

141 ant decrease in expression of these genes in OPSCC primary tumors relative to adjacent mucosa.

142 treatment response and oncologic outcomes in OPSCC generally and HPV+ OPSCC more specifically.

143 E, tobacco exposure and clinical outcomes in OPSCC patients (n = 143) with extensive tobacco exposure

144 he impact of tobacco exposure on the TIME in OPSCC patients remains unclear.

145 Objective: To update the trends in OPSCC incidence using US cancer registry data, with an e

146 changes in incidence and survival trends in OPSCC with selected tobacco-related cancers (larynx, ora

147 xpression to identify HPV16-driven tumors in OPSCC patient populations.

148 nature that predicts the clinical outcome in OPSCCs.

149 roscopic diagnostic confirmation of invasive OPSCC diagnosed between 2010 and 2021.

150 Similar results were observed for ISH+ OPSCC (P </= .01 for all).

151 with HPV16 and/or p16-positive, stage III-IV OPSCC received three cycles of IC with cisplatin, paclit

152 ), with the majority having stage T1-3N0-N2b OPSCC and a history of </= 10 pack-years of cigarette sm

153 of patients with HPV-positive and -negative OPSCC and identified in HPV-positive cases increased zin

154 N1-2b pathologically confirmed HPV-negative OPSCC in 2010 to 2012 were identified using the National

155 rging disease that differs from HPV-negative OPSCC in natural history and prognosis.

156 S was similar for patients with HPV-negative OPSCC when treated with primary surgery vs CRT.

157 ith newly diagnosed cT1-2 N1-2b HPV-negative OPSCC when treated with primary surgical resection vs CR

158 proportion of HPV-positive and HPV-negative OPSCC within the United Kingdom.

159 e OPSCC, 68%-71%; patients with HPV-negative OPSCC, 31%-34%) than patients with a higher educational

160 e OPSCC, 81%-86%; patients with HPV-negative OPSCC, 43%-46%).

161 Among those with HPV-negative OPSCC, comorbidity (12%-22%) and treatment intent (16%-4

162 ith patient overall survival in HPV-negative OPSCC, there was a strong correlation within the HPV16-p

163 for HPV-positive OPSCC than for HPV-negative OPSCC.

164 iated OPSCC while 11 (6.7%) had HPV-negative OPSCC.

165 C while 1490 patients (37%) had HPV-negative OPSCC.

166 ve non-OPSCC, but patients with p16-negative OPSCC and non-OPSCC have similar outcomes.

167 but patients with p16-negative OPSCC and non-OPSCC have similar outcomes.

168 Comparing OPSCC and non-OPSCC, patients with p16-positive OPSCC have better PFS

169 son of HPV transcript-positive OPSCC and non-OPSCC.

170 ynx, or larynx, collectively referred as non-OPSCC, where HPV infection is less common than in the or

171 velopment of a p16 IHC scoring system in non-OPSCC and improvement of HPV detection methods are warra

172 rmine whether HPV plays a causal role in non-OPSCC and to investigate whether HPV confers a survival

173 s with OPSCC, patients with p16-negative non-OPSCC have worse outcomes than patients with p16-positiv

174 is also detectable in nonoropharyngeal (non-OPSCC), but its pathogenic role and clinical significanc

175 so have a role in outcome in a subset of non-OPSCC.

176 outcomes than patients with p16-positive non-OPSCC, and HPV may also have a role in outcome in a subs

177 S and OS than patients with p16-positive non-OPSCC, but patients with p16-negative OPSCC and non-OPSC

178 Notably, however, HPV-driven non-OPSCCs display a distinct immune microenvironment and cl

179 ing lymphocytes compared with HPV-driven non-OPSCCs.

180 6 expression and high-risk HPV status in non-OPSCCs from RTOG 0129, 0234, and 0522 studies were deter

181 (15 of 103), and 6.9% (seven of 101) of non-OPSCCs from RTOG 0129, 0234, and 0522 studies, respectiv

182 HPV-driven tumors accounted for 4.1% of non-OPSCCs.

183 usal role for HPV in transcript-positive non-OPSCCs throughout the head and neck.

184 udy, patients with HPV-related nonmetastatic OPSCC were identified in the National Cancer Database be

185 ned US veterans diagnosed with nonmetastatic OPSCC from 2000 to 2020.

186 ropharyngeal squamous cell carcinomas (OCSCC/OPSCC).

187 ation sites may provide biomarkers for OCSCC/OPSCC diagnosis and prognosis as well as novel avenues f

188 for study of their potential role in OCSCCs/OPSCCs.

189 ps of microbial signatures related to OCSCCs/OPSCCs.

190 f 40264 patients who received a diagnosis of OPSCC from 2000 to 2012 were included.

191 40 264 patients who received a diagnosis of OPSCC from 2000 to 2012, 13 313 (33.1%) were aged 65 yea

192 ormation on all patients with a diagnosis of OPSCC from the Danish Head and Neck Cancer Group databas

193 However, despite the increasing incidence of OPSCC in older patients, data regarding the safety and p

194 ever, over the same period, the incidence of OPSCC in the broader UK population underwent a 2-fold in

195 gue that the rapidly increasing incidence of OPSCC in the United Kingdom cannot be solely attributabl

196 Conclusions and Relevance: The incidence of OPSCC is increasing among elderly patients in the United

197 t increases in the age-adjusted incidence of OPSCC were observed during the study period for both you

198 rehensive dataset on the neural landscape of OPSCC.

199 est that HPV DNA is found in the majority of OPSCC diagnosed in patients 65 years or older.

200 rves to dysphagia in treated mouse models of OPSCC.

201 ssess early response and predict outcomes of OPSCC.

202 Among patients with regional recurrence of OPSCC, there is a high rate of successful salvage treatm

203 is model was proposed to stratify subsets of OPSCC patients with low and high risks for treatment fai

204 ystemic therapy following primary surgery of OPSCC, induction chemotherapy in the treatment of OPSCC,

205 Median survival of OPSCC among the 2021 eligible patients was 6.8 (range, 0

206 stionnaires were mailed to 1600 survivors of OPSCC identified from the Texas Cancer Registry, with 40

207 xas Cancer Registry to identify survivors of OPSCC treated definitively with primary radiotherapy or

208 ves and denervation patterns in survivors of OPSCC.

209 without systemic therapy in the treatment of OPSCC are outlined for a variety of disease stages and c

210 , induction chemotherapy in the treatment of OPSCC, and the appropriate dose, fractionation, and volu

211 definitive radiotherapy in the treatment of OPSCC, postoperative radiotherapy with and without syste

212 Although the number of OPSCCs diagnosed within the United Kingdom from 2002 to

213 During 1995 through 2012, the proportion of OPSCCs caused by HPV has increased significantly.

214 During 1995 through 2012, the proportion of OPSCCs caused by HPV has increased significantly.

215 ma of the oral cavity (OSCC) and oropharynx (OPSCC) in a large multicenter cohort, using a diagnostic

216 mours of the oral cavity (OSCC), oropharynx (OPSCC) and nasopharynx (NPC).

217 001) with decreased CD8 infiltration in p16+ OPSCC tumors.

218 2.0% for a patient with non-T4, non-N3, p16+ OPSCC to 11.2% for a patients with LAHNSCC with a T4N3 p

219 From 1995 to 2012, the proportion of p16+ OPSCC increased significantly among women (from 29% to 7

220 tics of both regions for predictions of p16+ OPSCC outcomes.

221 grouped as (1) p16-positive oropharynx (p16+ OPSCC) and (2) p16-negative oropharynx and all other sub

222 ient cohort comprised 811 patients with p16+ OPSCC (median age, 59.0 years [IQR, 47.4-70.6 years]; 68

223 cans were analyzed of 811 patients with p16+ OPSCC treated with definitive radiotherapy or chemoradio

224 adiotherapy treatment for patients with p16+ OPSCC.

225 4.00]; P = .01) among all patients with p16+ OPSCC.

226 ntent TORS for biopsy-proven HPV-16-positive OPSCC performed by a single attending surgeon (A.H.M.) a

227 ed during TORS resections of HPV-16-positive OPSCC were diagnostically challenging.

228 Of the 367 patients with HPV-positive OPSCC (mean [SD] age, 60.6 [9.2] years; 310 [84.5%] male

229 sequencing was performed on 46 HPV-positive OPSCC and 25 normal tissue samples.

230 Strikingly, patients with HPV-positive OPSCC are highly curable with ionizing radiation and hav

231 ssociated with nodal disease at HPV-positive OPSCC diagnosis.

232 1% of patients experienced true HPV-positive OPSCC disease recurrence, with most incidences of DM occ

233 Because HPV-positive OPSCC patients have a better clinical outcome, there is

234 showing for the first time that HPV-positive OPSCC patients have increased intratumoral Zn levels and

235 better prognosis and outcome of HPV-positive OPSCC patients would warrant imaging follow-up that is l

236 egies for elderly patients with HPV-positive OPSCC should be performed.

237 ase course during follow-up for HPV-positive OPSCC than for HPV-negative OPSCC.

238 relative to normal tissue from HPV-positive OPSCC tumor samples.

239 ed, and patients diagnosed with HPV-positive OPSCC were identified.

240 s), and 2563 patients (63%) had HPV-positive OPSCC while 1490 patients (37%) had HPV-negative OPSCC.

241 arefully selected patients with HPV-positive OPSCC without obvious clinical ENE undergoing primary su

242 , treatment-naive patients with HPV-positive OPSCC without obvious clinical extranodal extension (ENE

243 yngeal squamous cell carcinoma (HPV-positive OPSCC), the association of de-escalated therapy with pat

244 ere living alone (patients with HPV-positive OPSCC, 68%-71%; patients with HPV-negative OPSCC, 31%-34

245 habiting partner (patients with HPV-positive OPSCC, 81%-86%; patients with HPV-negative OPSCC, 43%-46

246 Among patients with HPV-positive OPSCC, a considerable part of this survival gap was esti

247 udied patterns of recurrence in HPV-positive OPSCC, but only one has studied truly recurrent disease

248 dults with stage I, II, and III HPV-positive OPSCC, patients were recruited from a high-volume head a

249 CT imaging in the management of HPV-positive OPSCC.

250 ensitivity to chemoradiation in HPV-positive OPSCC.

251 strong correlation within the HPV16-positive OPSCC patient group.

252 207 adults with newly diagnosed p16-positive OPSCC and pathology-confirmed single-node disease who un

253 nrolled patients with T1-T2N0-2 p16-positive OPSCC between February 13, 2018, and November 17, 2020.

254 CC and non-OPSCC, patients with p16-positive OPSCC have better PFS and OS than patients with p16-posi

255 ensive comparison of HPV transcript-positive OPSCC and non-OPSCC.

256 lation between HPV-negative and HPV-positive OPSCCs and identified a specific pattern of differential

257 nonmetastatic HPV-associated (p16-positive) OPSCC.

258 The primary OPSCC site for most patients was tonsil (67%, 109 of 162

259 and, if prospectively validated, may refine OPSCC patient selection for risk-adaptive therapy.

260 stasis in human papillomavirus (HPV)-related OPSCC is more favorable compared with patients who are H

261 study suggest that patients with HPV-related OPSCC and single-node disease undergoing surgical resect

262 final surgical margin status in HPV-related OPSCC are imperative.

263 underwent transoral surgery for HPV-related OPSCC between January 2015 and December 2021 who were id

264 Analysis of ASE in HPV-related OPSCC identified multiple alterations likely involved in

265 l objectively derived system for HPV-related OPSCC using a national database of patients primarily tr

266 final surgical margin status in HPV-related OPSCC, particularly for base of tongue primaries and dee

267 The optimal management of early-stage OPSCC with surgery or radiation continues to be a clinic

268 images of 70 patients with advanced T-stage OPSCC who had completed concurrent chemoradiotherapy, bi

269 al staging in patients with advanced T-stage OPSCC.

270 predictor in patients with advanced T-stage OPSCC.

271 Consecutive patients with suspected OPSCCs or neck metastases (without visible primary tumor

272 tion of molecular factors that contribute to OPSCC development, progression, and differential respons

273 multistep progression from HPV infection to OPSCC development.

274 der, and residing in Denmark 1 year prior to OPSCC diagnosis.

275 f whom 106 (65%) had an oropharyngeal tumor (OPSCC, 95 [59%]; lymphoma, 7 [4%]; other type, 4 [5%]).

276 ch biomarker(s) can reliably determine which OPSCC specimens are truly driven by HPV infection.

277 rom 1,602 patients previously diagnosed with OPSCC (2002-2011) were collated from 11 centers.

278 total of 70 911 patients were diagnosed with OPSCC (82.9% male and 17.1% female).

279 total of 64 845 patients were diagnosed with OPSCC (83.9% male and 16.1% female).

280 eried in 2024 for any patient diagnosed with OPSCC from 2013 to 2021, creating a retrospective cohort

281 tumor status among women and nonwhites with OPSCC and patients with nonoropharyngeal head and neck s

282 tumor status among women and nonwhites with OPSCC and patients with nonoropharyngeal head and neck s

283 e total population was 135 756 patients with OPSCC (7.3% Black, 3.9% Hispanic, 86.2% White, 2.6% othe

284 Patients with OPSCC diagnosed from 2018 to 2021 of Black (PR, 1.18; 95

285 After propensity matching, 726 patients with OPSCC met inclusion criteria.

286 y validated in a cohort of 153 patients with OPSCC randomly assigned to a third trial, NRG Oncology R

287 ort study included consecutive patients with OPSCC treated from January 2013 to December 2023 at a si

288 l prediction of OS and PFS for patients with OPSCC treated with primary radiation-based therapy.

289 All patients with OPSCC treated with transoral robotic surgery were assess

290 al and survival outcomes among patients with OPSCC who underwent primary TORS or RT/CRT in 2002 to 20

291 ve CECT studies in consecutive patients with OPSCC who underwent surgical resection between October 2

292 vational cohort study included patients with OPSCC who underwent TTMV-HPV DNA testing between April 2

293 In a multivariable analysis, patients with OPSCC who were diagnosed from 2018 to 2021 at community

294 sed a derivation cohort of 493 patients with OPSCC with known p16 tumor status (surrogate of human pa

295 Similar to results in patients with OPSCC, patients with p16-negative non-OPSCC have worse o

296 latively homogeneous cohort of patients with OPSCC, proton therapy was associated with a higher rate

297 es related to treating elderly patients with OPSCC, their limited enrollment in clinical trials, and

298 Patients with OPSCC, unmatched for cancer stage or human papillomaviru

299 al and had high specificity in patients with OPSCC.

300 ted and functional outcomes in patients with OPSCC.

301 d for both younger and elderly patients with OPSCC.