ライフサイエンスコーパス: HNSCC

1 HNSCC spheroids were co-cultured in vitro with periphera

2 HNSCC UM-SCC-1 and UM-SCC-47 cells were cultured in 2D m

3 Between November 2009 and June 2013, 180 HNSCC patients eligible for adjuvant chemotherapy after

4 nctional DNA repair defects in a panel of 25 HNSCC cell lines, we applied machine learning to define

5 ival in a PIK3CA-characterized cohort of 266 HNSCC patients and explored the mechanism in relevant pr

6 wnregulated PD-1/PD-L1 in a Tgfbr1/Pten 2cKO HNSCC mouse model.

7 we performed epigenomic deconvolution on 580 HNSCC samples from the TCGA dataset.

8 rcinoma (HNSCC), along with two accompanying HNSCC biomarkers from a single cell lysate of oral cance

9 differences in pathway dysregulation across HNSCC basal primary tumors.

10 RT in patients with locoregionally advanced HNSCC.

11 A total of 891 patients with advanced HNSCC from a phase 3 trial of cisplatin plus radiotherap

12 finitive chemoradiation for locally advanced HNSCCs underwent pretherapeutic biopsies and peritherape

13 One prominent feature of aggressive HNSCC is the presence of severely hypoxic regions in tum

14 n than patients with wild-type p53, but also HNSCC patients with TP53 mutations and high levels of FO

15 For PIK3CA-altered HNSCC, predicted 5-yr DSS was 72% for NSAID users and 25

16 to implement NSAID therapy in PIK3CA-altered HNSCC.

17 echanism for cross talk between the LECs and HNSCC tumors through the CXCR3-CXCL11 axis and elucidate

18 isk factor for HNSCC, and tobacco-associated HNSCCs have poor prognosis and response to available tre

19 Data in The Cancer Genome Atlas HNSCC database showed a significant inverse correlation

20 own of the dominant ALDH isoform in high AVS HNSCC depleted the CIC pool in vitro and in vivo.

21 on which ALDH isoform to target in high AVS HNSCC tumors to deplete the CIC population.

22 results have broad clinical relevance beyond HNSCC to other HPV-associated malignancies and reveal a

23 hts into the tumor microenvironments of both HNSCC subtypes and identify potential therapeutic target

24 dent secretion of tumor-promoting factors by HNSCC-associated CAFs may explain their role in malignan

25 ependent head and neck squamous cell cancer (HNSCC) cell lines and a synthetic lethal interaction wit

26 ties for head and neck squamous cell cancer (HNSCC) patients treated with concomitant cisplatin and r

27 rcinoma, head and neck squamous-cell cancer (HNSCC), non-small-cell lung cancer (NSCLC), and other so

28 ated and HPV-negative head and neck cancers (HNSCC).

29 Head and neck squamous cell carcinoma (HNSCC) accounts for nearly 90% of head and neck cancer.

30 time, head and neck squamous cell carcinoma (HNSCC) and at least one clinically N0 neck side for whic

31 anced head and neck squamous cell carcinoma (HNSCC) and biomarkers that predict altered immunity, the

32 Head and neck squamous cell carcinoma (HNSCC) arises through exposure to environmental carcinog

33 Head and neck squamous cell carcinoma (HNSCC) associated with high-risk human papilloma virus (

34 es in head and neck squamous cell carcinoma (HNSCC) cases.

35 human head and neck squamous cell carcinoma (HNSCC) cell lines (UM-SCC-47 and UM-SCC-22B, respectivel

36 on of head and neck squamous cell carcinoma (HNSCC) cell lines and patient tumors showed that HPV16+/

37 human head and neck squamous cell carcinoma (HNSCC) cell lines and report that nearly 20% are hyperse

38 hough head and neck squamous cell carcinoma (HNSCC) has in the past been largely associated with toba

39 itive head and neck squamous cell carcinoma (HNSCC) have better responses to radiotherapy and higher

40 Head and neck squamous cell carcinoma (HNSCC) includes epithelial cancers of the oral and nasal

41 Head and neck squamous cell carcinoma (HNSCC) is a common and debilitating form of cancer chara

42 Head and neck squamous cell carcinoma (HNSCC) is a disease of significant morbidity and mortali

43 itive head and neck squamous cell carcinoma (HNSCC) is biologically distinct from HPV-negative HNSCC.

44 Head and neck squamous cell carcinoma (HNSCC) is characterized by the frequent manifestation of

45 Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide, and se

46 Head and neck squamous cell carcinoma (HNSCC) is the sixth most common malignancy worldwide and

47 ia in head-and-neck squamous cell carcinoma (HNSCC) leads to an immunosuppressive microenvironment an

48 es of head and neck squamous cell carcinoma (HNSCC) may be derived from the presence of stem-like cel

49 topic head and neck squamous cell carcinoma (HNSCC) model.

50 cy in head and neck squamous cell carcinoma (HNSCC) patients despite its overexpression.

51 Head and neck squamous cell carcinoma (HNSCC) presents a major public health concern because of

52 from head and neck squamous cell carcinoma (HNSCC) primary tumors had significantly more heterogenei

53 V(+)) head and neck squamous cell carcinoma (HNSCC) samples.

54 rrent head and neck squamous cell carcinoma (HNSCC) than chest x-ray (CXR) plus head and neck MRI or

55 cient head and neck squamous cell carcinoma (HNSCC) UM-SCC-1 cells both in in vitro three-dimensional

56 r for head and neck squamous cell carcinoma (HNSCC), along with two accompanying HNSCC biomarkers fro

57 ncer, head and neck squamous cell carcinoma (HNSCC), can develop therapeutic resistance that complica

58 In head and neck squamous cell carcinoma (HNSCC), cell migration facilitates distant metastases an

59 tatic head and neck squamous cell carcinoma (HNSCC), its role in the management of locally advanced (

60 es of head and neck squamous cell carcinoma (HNSCC), the lateral border of the tongue and the oral ph

61 et in head and neck squamous cell carcinoma (HNSCC), where EGFR-blocking antibodies are approved for

62 ve in head and neck squamous cell carcinoma (HNSCC), with programmed cell death ligand 1 (PD-L1) expr

63 ne in head and neck squamous cell carcinoma (HNSCC).

64 y for head and neck squamous cell carcinoma (HNSCC).

65 nt of head and neck squamous cell carcinoma (HNSCC).

66 with head and neck squamous cell carcinoma (HNSCC).

67 with head and neck squamous cell carcinoma (HNSCC).

68 t for Head and Neck Squamous Cell Carcinoma (HNSCC).

69 with head and neck squamous cell carcinoma (HNSCC).

70 le in head and neck squamous cell carcinoma (HNSCC).

71 anced head and neck squamous cell carcinoma (HNSCC).

72 BI in head and neck squamous cell carcinoma (HNSCC).

73 in head and neck of squamous cell carcinoma (HNSCC).

74 ch in head and neck squamous cell carcinoma (HNSCC).

75 t for head and neck squamous cell carcinoma (HNSCC).

76 rrent head and neck squamous cell carcinoma (HNSCC).

77 ce in head and neck squamous cell carcinoma (HNSCC).

78 human head and neck squamous cell carcinoma (HNSCC).

79 ce in head and neck squamous cell carcinoma (HNSCC).

80 ly as head and neck squamous cell carcinoma (HNSCC).

81 ) for head and neck squamous cell carcinoma (HNSCC).

82 anced head and neck squamous cell carcinoma (HNSCC; stage III-IV according to the Union for Internati

83 nt of head and neck squamous cell carcinomas HNSCC from potentially premalignant lesions (PPOLS) to m

84 ) of head and neck squamous cell carcinomas (HNSCC) and other solid malignancies is a key determinant

85 Head and neck squamous cell carcinomas (HNSCC) exhibiting resistance to the EGFR-targeting drug

86 e of head and neck squamous cell carcinomas (HNSCC), including oral cavity and pharynx (OC/P) cancers

87 n in head and neck squamous cell carcinomas (HNSCC), which is associated with increased autocrine sec

88 t of head and neck squamous cell carcinomas (HNSCC), yet treatment failure and disease recurrence are

89 from head and neck squamous cell carcinomas (HNSCC).

90 d in head and neck squamous cell carcinomas (HNSCCs) and expressed as at least seven isoforms in huma

91 Most head and neck squamous-cell carcinomas (HNSCCs) are driven by p16(INK4A) inactivation and cyclin

92 Head and neck squamous cell carcinomas (HNSCCs) are refractory to therapeutic interventions.

93 s of head and neck squamous cell carcinomas (HNSCCs) suggest that integration may represent an additi

94 e of head and neck squamous cell carcinomas (HNSCCs) that can arise in the oral cavity, oropharynx, h

95 the head and neck squamous cell carcinomas (HNSCCs).

96 es from head and neck squamous cancer cells (HNSCC) that often develop resistance to therapy.

97 e effects of PI3K inhibition in pre-clinical HNSCC models.

98 All patients with histologically confirmed HNSCC treated at a specialist cancer centre with curativ

99 In vitro, only crosslink repair-defective HNSCC cell lines are highly migratory and invasive.

100 In this work, we submitted EGFR-dependent HNSCC cell lines to RNA interference-based functional ge

101 esponses of a large panel of patient-derived HNSCC cell lines to various combinations of PI3K and EGF

102 LSD1 inhibits orthotopic and patient-derived HNSCC xenograft growth-specific target genes and signali

103 Whether elevated HNSCC incidence generates survival disparities within Ap

104 , we observed a reduction in CAF-facilitated HNSCC progression after blocking CAF autophagy.

105 al of the first immunotherapeutic agents for HNSCC, and discuss the development of strategies to decr

106 es have not been conclusively determined for HNSCC.

107 Tobacco use is the main risk factor for HNSCC, and tobacco-associated HNSCCs have poor prognosis

108 advances have been made in immunotherapy for HNSCC.

109 within radioimmunotherapy interventions for HNSCC.

110 development of immunotherapeutic options for HNSCC.

111 The 5-y survival rate for HNSCC remains at ~50%, and improving these outcomes requ

112 t GLS1 is a promising therapeutic target for HNSCC treatment.

113 n the setting of immunotherapy treatment for HNSCC by focusing on published clinical and preclinical

114 Cancer Genome Atlas RNA-sequencing data from HNSCC patients also showed a positive correlation betwee

115 relation was seen also in TILs isolated from HNSCC patients.

116 lations from patients with HPV(-) and HPV(+) HNSCC and healthy donors.

117 une cells within tumors of HPV(-) and HPV(+) HNSCC displayed a spectrum of transcriptional signatures

118 ide mechanistic insights into WEE1i and HPV+ HNSCC therapies.

119 nd B-cells explains better prognosis in HPV+ HNSCC.

120 evated basal FOXM1 activity predisposes HPV+ HNSCC to WEE1i-induced toxicity and provide mechanistic

121 Patients with HPV+ HNSCC have a better prognosis; however, the 5-year survi

122 ranscriptional signature in HPV+ versus HPV- HNSCCs.

123 rovide a comprehensive data set of the human HNSCC-associated fibroblast matrisome.

124 to anti-PD-1 (<=20%) immunotherapy as human HNSCCs.

125 a reliable prognostic marker for identifying HNSCC patients with risk of progression.

126 d occurred at high frequency in the immortal HNSCC cell lines.

127 s, development of additional immunocompetent HNSCC mouse models, as well as engineering of more robus

128 approaches that sensitize poorly immunogenic HNSCCs to checkpoint blockade.

129 In HNSCC, genetic aberrations in phosphatidylinositol 3-kin

130 nhibitors showed limited activity (<=20%) in HNSCC, highlighting the need to identify new therapeutic

131 We investigated MK2 pathway activation in HNSCC and the interaction of MK2 and RT in vitro and in

132 nt ERK/AKT-p70S6K-S6 signaling activation in HNSCC cells, and addition of human recombinant FGF19 cou

133 ture 5, is positively associated with age in HNSCC from non-smokers and that larynx SCC from non-smok

134 files reveal a poor prognosis association in HNSCC.

135 ncogenic function for secretory autophagy in HNSCC stromal cells that promotes malignant progression.

136 cal role for the RAP1/RAC1 signaling axis in HNSCC cell migration.

137 y possible positive prognostic biomarkers in HNSCC as well as possible mechanisms of increased sensit

138 o use is a major driver of carcinogenesis in HNSCC and is a poor prognosticator that has previously b

139 of curative radiotherapy or chemotherapy in HNSCC.

140 i-PD1 and cisplatin enriched BMI1(+) CSCs in HNSCC while inhibiting HNSCC growth.

141 and p63 collaborate as oncogenic drivers in HNSCC.

142 knockout counteracts the observed effects in HNSCC cells carrying high endogenous FGF19, with knockou

143 R inhibitors to enhance clinical efficacy in HNSCC.

144 function of epigenetic regulator enzymes in HNSCC progression, including potential therapeutic appli

145 Central genomic events in HNSCC have been found to possess previously unknown role

146 a significantly elevated GLS1 expression in HNSCC, and patients with high expression levels of GLS1

147 ated CpG's for regulating gene expression in HNSCC.

148 liferation and soft agar colony formation in HNSCC cells with low FGF19 expression through activation

149 cancers, specific members have a function in HNSCC.

150 encoding LZK) is an amplified driver gene in HNSCC.

151 Moreover, DDB2 inhibits HIF1alpha in HNSCC cells.

152 er stem cells (CSCs) have been identified in HNSCC, and BMI1 expression has been linked to these phen

153 poxia that are also prognostic indicators in HNSCC.

154 for enhanced synergy with PI3K inhibitors in HNSCC patients and motivate further preclinical studies

155 combined use of PI3K and EGFR inhibitors in HNSCC, in-human studies have displayed limited clinical

156 arks and is co-expressed with CSC markers in HNSCC.

157 e role of the dysbiotic tissue microbiome in HNSCC.

158 at 3q resulted in increased MAP3K13 mRNA in HNSCC tumor samples and cell lines.

159 Here, we study patterns of mutations in HNSCC that are derived from the specific nucleotide chan

160 e best therapy for the clinically N0 neck in HNSCC.

161 cretion of FGF19 and poor patient outcome in HNSCC.

162 redicted treatment responses and outcomes in HNSCC patients undergoing chemoradiation and may help to

163 ctivation of the HER3-PI3K-AKT-S6 pathway in HNSCC cell lines and patient-derived xenografts (PDXs).

164 DSG3 is membrane-bound protein in HNSCC cells of invaded lymph nodes, vascular endothelial

165 tivation can mediate radiation resistance in HNSCC.

166 otential predictor for treatment response in HNSCC patients.

167 We mapped the evolution of SCNAs in HNSCC progression.

168 ls of Streptococcus which is what is seen in HNSCC.

169 ency upon FGF19/FGFR4 autocrine signaling in HNSCC, revealing a therapeutic target for this cancer ty

170 ascade that potentiates Ras/ERK signaling in HNSCC.

171 cinoma cells to invade surrounding stroma in HNSCC.

172 ll cycle checkpoints and is being studied in HNSCC regimens.

173 ted with longer progression-free survival in HNSCC patients.

174 ting it is a potential therapeutic target in HNSCC.

175 expression is inappropriately upregulated in HNSCC and an orthotopic HNSCC mouse model.

176 , we report that autophagy is upregulated in HNSCC-associated CAFs, where it is responsible for key p

177 important pharmacological vulnerabilities in HNSCC and support combining MEK and EGFR inhibitors to e

178 mutant p53s' gain-of-function activities in HNSCCs.

179 r immune responses in many cancers including HNSCC.

180 of these alterations in multiple independent HNSCC data sets and show that, along with previously des

181 tic enzymes and signaling pathways to induce HNSCC growth and metastasis.

182 ls cells' glutamine consumption, may inhibit HNSCC cell growth.

183 iched BMI1(+) CSCs in HNSCC while inhibiting HNSCC growth.

184 results support the idea that BPTES inhibits HNSCC growth by inducing apoptosis and cell cycle arrest

185 of dysplasia, ultimately leading to invasive HNSCC, most patients are diagnosed with late-stage HNSCC

186 recent advances on the identification of key HNSCC oncogenes that impair antitumor immunity and emerg

187 -based chemoradiotherapy in patients with LA HNSCC.

188 cer cells, MCF-7 breast cancer cells, and LU-HNSCC-25 head and neck squamous carcinoma cells in phosp

189 5, a representative cell type of mesenchymal HNSCC and its normal oral keratinocyte counterpart.

190 y, resulting in the inhibition of metastatic HNSCC and prevention of HNSCC relapses.

191 mab for treatment of recurrent or metastatic HNSCC and pembrolizumab as primary treatment for unresec

192 t-line treatment for recurrent or metastatic HNSCC and pembrolizumab monotherapy is an appropriate fi

193 ed locally incurable recurrent or metastatic HNSCC done at 200 sites in 37 countries.

194 lib and cetuximab in recurrent or metastatic HNSCC.

195 t for PD-L1-positive recurrent or metastatic HNSCC.

196 lumab in unselected patients with metastatic HNSCC.

197 n of an oropharyngeal SCC tissue microarray, HNSCC cell lines, and patient-derived xenograft (PDX) tu

198 Here, we report a mouse HNSCC model system that recapitulates the human tobacco-

199 y associated with p-STAT3 in human and mouse HNSCC.

200 uamous cell carcinomas of the head and neck (HNSCC) and lung (LUSC), and is associated with poor prog

201 uamous cell carcinomas of the head and neck (HNSCC) arise from mucosal keratinocytes of the upper aer

202 3% for those with HPV-positive and -negative HNSCC, respectively.

203 HPV-positive and p16-negative, HPV-negative HNSCC cell lines.

204 Compared to HPV-negative HNSCC genomes, HPV+ cases demonstrated a marked increase

205 regression in HPV-positive and HPV-negative HNSCC PDXs.

206 n combination with radiation in HPV-negative HNSCC where comorbidities prevent the use of cytotoxic c

207 val rates than do patients with HPV-negative HNSCC, but the mechanisms underlying this phenomenon are

208 l of 180 patients with advanced HPV-negative HNSCC, who were treated with cisplatin-based chemoradiot

209 ) is biologically distinct from HPV-negative HNSCC.

210 ed disease-specific survival in p16-negative HNSCC patients.

211 dancy for NSD family members in HPV-negative HNSCCs and suggest a potential role for impaired H3K36 m

212 atin regulators is warranted in HPV-negative HNSCCs driven by aberrant H3K36 methylation.

213 lation in the genesis of 13% of HPV-negative HNSCCs.

214 Remarkably, we find that >70% of HNSCC lesions respond to intratumoral anti-CTLA-4.

215 Immunohistochemical analysis of HNSCC tumor arrays showed enhanced expression of CXCR3 a

216 ore the impact of hypoxia on the behavior of HNSCC and define that the controlling function of phosph

217 e effects of radiation, and blocks growth of HNSCC PDXs by inhibiting CSCs.

218 dation of the molecular genetic landscape of HNSCC over the past decade has revealed new opportunitie

219 geted therapeutics and diagnostic markers of HNSCC are lacking due to the inherent heterogeneity and

220 in an in vivo orthotopic nude mouse model of HNSCC through a novel transcription-independent mechanis

221 tumor growth in an orthotopic mouse model of HNSCC.

222 reduce tumor growth in a xenograft model of HNSCC.

223 isoforms play a role in the pathogenesis of HNSCC.

224 better understanding of the pathogenesis of HNSCC.

225 bition of metastatic HNSCC and prevention of HNSCC relapses.

226 has an important role in the progression of HNSCC.

227 reduced cell viability and proliferation of HNSCC cells with 3q gain but not control cell lines.

228 then predicted and analyzed the responses of HNSCC to tocilizumab (TCZ) and cisplatin combination the

229 mographic groups and other anatomic sites of HNSCC is unclear.

230 Traditional staging of HNSCC using the tumour-node-metastasis system has been s

231 KLF4 levels sustains the oncogenic state of HNSCC by reactivating repressed chromatin domains at key

232 Studies of HNSCC using in vitro, ex vivo, and in vivo approaches pr

233 tors as a therapeutic approach in subsets of HNSCC.

234 a potential, attractive, and novel target of HNSCC.

235 markers and targets for precision therapy of HNSCC.

236 Treatment of HNSCC cell lines with BYL719 significantly reduced AKT a

237 that underlie the molecular tumorigenesis of HNSCC have been identified.

238 years emerged as the fastest growing type of HNSCC.

239 fforts aim to integrate our understanding of HNSCC biology and immunobiology to identify predictive b

240 112 had greater antiproliferative effects on HNSCC cells compared with the FDA-approved translation i

241 site, genera earlier shown to be enriched on HNSCC mucosa, Capnocytophaga, Fusobacterium, and Porphyr

242 l- and endothelial cell (EC)-secreted IL6 on HNSCC growth and the CSC fraction.

243 othia, which is found at depressed levels on HNSCC mucosa, was high.

244 ead and neck squamous cell carcinoma (non-OP HNSCC).

245 g OPSCC, but not a good surrogate for non-OP HNSCC.

246 Among 623 non-OP HNSCCs, a higher proportion were p16+ compared with ISH

247 In non-OP HNSCCs, p16 had lower sensitivity (83%) and positive pre

248 ately upregulated in HNSCC and an orthotopic HNSCC mouse model.

249 Using orthotopic HNSCC models, we show that radiation combined with anti-

250 of signature 5 mutations compared with other HNSCC sub-sites.

251 HPV16+/p53WT HNSCC but not in HPV-/p53HRmut HNSCC.

252 re associated with prognosis in HPV16+/p53WT HNSCC but not in HPV-/p53HRmut HNSCC.

253 separated into HPV-negative and HPV-positive HNSCC.

254 poor survival in patients with HPV-positive HNSCC.

255 Tobacco use, a primary HNSCC risk factor, was evaluated through the Behavioral

256 Combining radiotherapy, a primary HNSCC treatment modality, with immunotherapy has been sh

257 In the later stages of progression, HNSCC with and without nodal metastases showed some clea

258 fate from differentiation to proliferation, HNSCC are considered a heterogeneous group of tumors cat

259 Our study showed that LSD1 promotes HNSCC growth and metastasis.

260 trategies, PET/CT-based staging in recurrent HNSCC was able to significantly discriminate among the s

261 profiles for hundreds of tumors, we refined HNSCC subtypes by their malignant and stromal compositio

262 Cancers in the oral/head & neck region (HNSCC) are aggressive due to high incidence of recurrenc

263 that recapitulates the human tobacco-related HNSCC mutanome, in which tumors grow when implanted in t

264 ve strategy for treating erlotinib-resistant HNSCC tumors.

265 that the HPV16 E6/E7 oncoproteins sensitize HNSCC cells to single-agent WEE1i treatment through acti

266 Despite tumor response observed in some HNSCC patients, cetuximab alone or combined with radio-

267 most patients are diagnosed with late-stage HNSCC without a clinically evident antecedent pre-malign

268 nase coactivation signaling network supports HNSCC survival in the setting of EGFR blockade, and that

269 This syngeneic HNSCC mouse model provides a platform to accelerate the

270 /CT has high NPV for the N0 neck in T2 to T4 HNSCC.

271 stitution and The Cancer Genome Atlas (TCGA) HNSCC imaging data.

272 The HNSCC cohort of the TCGA database was used to define 3 T

273 as high-ranking essential kinase hits in the HNSCC cell lines.

274 ere positive controls overexpressed into the HNSCC culture medium.

275 Our results provide insight into the HNSCC ecosystem and define stromal interactions and a p-

276 that accurately mimic the complexity of the HNSCC mutational landscape and tumor immune environment

277 ng requires thorough characterization of the HNSCC regulators of innate immune sensors, development o

278 Like other solid tumors, the HNSCC growth rate results in the development of hypoxic

279 These HNSCC lesions have similar immune infiltration and respo

280 To address this, HNSCC survival data for 259,737 tumors from the North Am

281 Thus, HNSCC can be separated into HPV-negative and HPV-positiv

282 requency of SCNA in transition from PPOLs to HNSCC that correlated with their expression.

283 ty for each imaging modality with respect to HNSCC staging were compared using Kaplan-Meier analysis,

284 rrence-free survival (p = 0.029), similar to HNSCC cases from the TCGA (n = 499), where highest AZGP1

285 Twenty HNSCC patients scheduled for lymph node dissection under

286 sistant or cetuximab-resistant HPV-unrelated HNSCC, palbociclib and cetuximab results in promising ac

287 cetuximab-resistant (group 2) HPV-unrelated HNSCC.

288 /6 inhibitors are warranted in HPV-unrelated HNSCC.

289 Using HNSCC cells and LECs we determined the mechanisms mediat

290 cutive patients with histologically verified HNSCC recurrence were enrolled from September 2013 to Ma

291 riments involving human ECs coimplanted with HNSCC cell line xenografts.

292 ts a potential alternative for patients with HNSCC and could be particularly beneficial for patients

293 n the identification of ENE in patients with HNSCC and has the potential to be integrated into clinic

294 te remains relatively low, and patients with HNSCC eventually relapse.

295 op a durable response, <15% of patients with HNSCC respond to immune checkpoint inhibitors, underscor

296 th urothelial carcinoma, eight patients with HNSCC, 20 patients with NSCLC, and 23 patients with othe

297 an papillomavirus infection in patients with HNSCC.

298 e antitumor immune response in patients with HNSCC.

299 ted tomography (CT) imaging in patients with HNSCC.

300 from two external data sets of patients with HNSCC: an external institution and The Cancer Genome Atl