ライフサイエンスコーパス: HNSCC

1 HNSCC cells and xenografts (HPV/p16-positive and -negati

2 HNSCC cells with increased miR-375 expression have lower

3 HNSCC is not characterized by frequent kinase mutations,

4 HNSCC spheroids were co-cultured in vitro with periphera

5 HNSCC varied in mechanisms of cell death, as indicated b

6 perfusion and necrosis induction in SCC-026 HNSCC tumors.

7 lood and patient-matched tumor pairs from 13 HNSCC patients with synchronous lymph node metastases an

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

9 line by screening an additional panel of 39 HNSCC cell lines.

10 immune checkpoints were investigated in 402 HNSCC patients.

11 ion data were similarly used to classify 464 HNSCCs and these analyses were integrated with genomic,

12 s were used to predict the HPV status of 520 HNSCCs profiled by The Cancer Genome Atlas project.

13 A total of 550 HNSCC patients and 404 controls from twelve eligible stu

14 re immunohistochemically characterized in 73 HNSCC patients treated by definitive chemoradiotherapy a

15 PI3K/PDK1 and TGFbeta signaling in advanced HNSCC patients with PIK3CA amplification.

16 Single patient with locally advanced HNSCC who received erlotinib monotherapy in a window-of-

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

18 inases hyperphosphorylated at Tyr-321 in all HNSCC cell lines.

19 Genetic alterations that are common to all HNSCC types are likely to be important for squamous carc

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

21 Similarly, knockdown of Sema4D in an HNSCC cell line resulted in a loss of MDSC function as s

22 We analyzed HNSCC samples from TCGA and a separate dataset of HPV+ o

23 treatments for FGFR1-driven lung cancers and HNSCC may be achieved by combining MTOR inhibitors and F

24 ion between RASSF1A promoter methylation and HNSCC remains unclear and controversial.

25 ion between aberrant RASSF1A methylation and HNSCC.

26 te during standard chemotherapy in NSCLC and HNSCC.

27 erved between RASSF1A methylation status and HNSCC risk under a random-effects model (OR = 2.93, 95%

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

29 ction; and data from The Cancer Genome Atlas HNSCC project were analyzed.

30 lar inhibitor against DYRK1A in mice bearing HNSCC xenograft tumors induced regression of tumor growt

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

32 resected head and neck squamous cell cancer (HNSCC).

33 b is effective against head and neck cancer (HNSCC), but in only 15% to 20% of patients, and the vari

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

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

36 ed in head and neck squamous cell carcinoma (HNSCC) and has been shown to impart tumorigenic and inva

37 tween head and neck squamous cell carcinoma (HNSCC) and microbial dysbiosis, we profiled the microbio

38 ed in head and neck squamous cell carcinoma (HNSCC) and other cancers.

39 rs in head and neck squamous cell carcinoma (HNSCC) and whether specific mechanisms or genes could be

40 lated head and neck squamous cell carcinoma (HNSCC) are commonly attributed to unresected fields of p

41 targeting head neck squamous cell carcinoma (HNSCC) by NOTCH1 pathway inhibition and explore the syne

42 ng of head and neck squamous cell carcinoma (HNSCC) by upfront (18)F-FDG PET/CT (i.e., on the day of

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

44 ) and Head and Neck Squamous Cell Carcinoma (HNSCC) cell lines and was due to senescence rather than

45 uding head and neck squamous cell carcinoma (HNSCC) cell lines resistant to cetuximab (Erbitux).

46 rived head and neck squamous cell carcinoma (HNSCC) cells in vitro and in vivo.

47 Head and neck squamous cell carcinoma (HNSCC) has a variety of causes.

48 stage head and neck squamous cell carcinoma (HNSCC) has not improved significantly over the past deca

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

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

51 Head and neck squamous cell carcinoma (HNSCC) is a highly heterogeneous disease that develops v

52 Head and neck squamous cell carcinoma (HNSCC) is a leading cause of cancer deaths worldwide wit

53 Head and neck squamous cell carcinoma (HNSCC) is generalized term that encompasses a diverse gr

54 ic of head and neck squamous cell carcinoma (HNSCC) is that local invasion rather than distant metast

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

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

57 human head and neck squamous cell carcinoma (HNSCC) lines from oncolysis by vesicular stomatitis viru

58 stage head and neck squamous cell carcinoma (HNSCC) or recurrent disease is a reflection of an incomp

59 py in head and neck squamous cell carcinoma (HNSCC) patients frequently results in tumor resistance t

60 Head and neck squamous cell carcinoma (HNSCC) patients have a poor prognosis, with invasion and

61 om 18 head and neck squamous cell carcinoma (HNSCC) patients, including five matched pairs of primary

62 Head and neck squamous cell carcinoma (HNSCC) progression depends on various dysregulated pathw

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

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

65 el of head and neck squamous cell carcinoma (HNSCC) was shown to be polymer structure dependent.

66 es in head and neck squamous cell carcinoma (HNSCC) were assessed and changes in reactive oxygen spec

67 with head and neck squamous cell carcinoma (HNSCC) who undergo radiotherapy (RT).

68 n the head and neck squamous cell carcinoma (HNSCC) with lymph node metastasis, where it also predict

69 k tumors, including squamous cell carcinoma (HNSCC), adenoid cystic carcinoma (ACC), and other saliva

70 k tumors, including squamous cell carcinoma (HNSCC), adenoid cystic carcinoma (ACC), and other saliva

71 with head and neck squamous cell carcinoma (HNSCC), and these events pose the greatest threats to lo

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

73 uding head and neck squamous cell carcinoma (HNSCC), where STAT3 represents a promising therapeutic t

74 human head and neck squamous cell carcinoma (HNSCC)-secreted Sema4D on myeloid cell differentiation.

75 g the head and neck squamous cell carcinoma (HNSCC).

76 sk of head and neck squamous cell carcinoma (HNSCC).

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

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

79 uding head and neck squamous cell carcinoma (HNSCC).

80 ed in head and neck squamous cell carcinoma (HNSCC).

81 on of head and neck squamous cell carcinoma (HNSCC).

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

83 th of head and neck squamous cell carcinoma (HNSCC).

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

85 63 in head and neck squamous cell carcinoma (HNSCC).

86 lopment of head and neck squamous carcinoma (HNSCC)-in particular, oropharyngeal squamous cell carcin

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

88 that head and neck squamous cell carcinomas (HNSCC) harbor the most frequent genomic amplifications o

89 positive head neck squamous cell carcinomas (HNSCC) usually have a better prognosis than the HPV-nega

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

91 Head and neck squamous carcinomas (HNSCC) present as dense epithelioid three-dimensional (3

92 tive head and neck squamous cell carcinomas (HNSCCs) are deadly and common cancers.

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

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

95 d in head and neck squamous cell carcinomas (HNSCCs).

96 stasis in head and neck squamous carcinomas (HNSCCs), a finding that unveils new markers of poor outc

97 factor nature and the strategy for confining HNSCC invasion to facilitate local treatment is limited.

98 mote resistance of additional EGFR-dependent HNSCC and lung cancer cell lines to EGFR blockade, they

99 h Fanconi anemia have a high risk to develop HNSCC, we investigated whether and to which extent Fanco

100 sults: A total of 132 participants developed HNSCC during the follow-up period (103 men and 29 women;

101 suggested that progression of PIK3CA-driven HNSCC is facilitated by 3-phosphoinositide-dependent pro

102 nsight into how PIK3CA overexpression drives HNSCC invasion and metastasis, providing a rationale for

103 ED15 overexpression is a clonal event during HNSCC progression.

104 rcome resistance to treatments and eradicate HNSCC metastasis.

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

106 In the FaDu HNSCC xenograft model, we show that combined blockade of

107 ster chromatid cohesion was observed in five HNSCC cell lines.

108 es have not been conclusively determined for HNSCC.

109 advances have been made in immunotherapy for HNSCC.

110 viously demonstrate a specific mechanism for HNSCC local invasion: the epithelial-mesenchymal transit

111 s gamma-11 and gamma-12 species, had ORs for HNSCC that ranged from 2.64 to 5.45 (P < .01 for all com

112 nce selectivity of oncolytic VSV therapy for HNSCC by inhibiting VSV replication in normal cells with

113 -positive (HPV(+)) and HPV-negative (HPV(-)) HNSCCs represent distinct clinical entities, with the la

114 Regardless of anatomic site, HPV+ HNSCCs shared highly similar gene expression and DNA met

115 NOTCH1/HES1 elevation was found in human HNSCC, especially in tissue post chemotherapy and lymph

116 the most common genetic alterations in human HNSCC.

117 ers of the canonical NOTCH1 pathway in human HNSCC.

118 ted in both HPV-positive and -negative human HNSCC tumors relative to adjacent normal tissue.

119 Examination of human HNSCC clinical samples revealed that both PIK3CA and PDK

120 This model and primary human HNSCC samples contain highly tumorigenic, invasive, and

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

122 Chen et al. (2017) show that mouse and human HNSCCs and their metastases depend on Bmi1-expressing ca

123 Here, we identified HNSCC cell lines harboring FADD/BIRC2 amplifications and

124 In HNSCC cell lines as well as primary tumors, integration

125 plus radiation may be particularly active in HNSCC, which harbor frequent FADD/BIRC2 genomic alterati

126 ase 6 (HDAC6) expression and its activity in HNSCC cells significantly inhibited autophagy induction

127 ave characterized the genetic alterations in HNSCC and demonstrated that mutations confer resistance

128 ly enhancing bortezomib-induced apoptosis in HNSCC cells.

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

130 6c-3p expression and the RUNX2/INHBA axis in HNSCC specimens.

131 e prospectively as a predictive biomarker in HNSCC patients.

132 ns with irreversible ERBB family blockers in HNSCC.

133 ole in the development of chemoresistance in HNSCC and how autophagy is initiated when HNSCC cells un

134 anemia pathway inactivation underlies CIN in HNSCC of non-Fanconi anemia individuals.

135 CD33(+) cells cultured in HNSCC cell line-derived conditioned medium differentiate

136 and p63 collaborate as oncogenic drivers in HNSCC.

137 y reduce the antitumor efficacy of EGFRIs in HNSCC.

138 thway and increased apoptosis was evident in HNSCC cells following combined EphB4 downregulation and

139 nal role of DEK has not yet been explored in HNSCC.

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

141 We observed decreased survival fractions in HNSCC cells following EphB4 knockdown in clonogenic assa

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

143 PV-5 type suggest a broader role for HPVs in HNSCC etiology.

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

145 ated with sensitivity to STAT3 inhibition in HNSCC cells, suggesting that PTPRT promoter methylation

146 understanding of the components involved in HNSCC autophagy machinery that responds to EGFR inhibito

147 regulation of specific proteins involved in HNSCC invasion.

148 4 is expressed at high to moderate levels in HNSCC cell lines and patient-derived xenograft (PDX) tum

149 owever, the molecular autophagy machinery in HNSCC cells and potential biomarkers of patient response

150 ken together, our results implicate MED15 in HNSCC and hint that MED15 overexpression is a clonal eve

151 We investigated the implication of MED15 in HNSCC.

152 rtant than preventing systemic metastasis in HNSCC and other invasive-predominant cancers.

153 nregulation fosters lymph node metastasis in HNSCC.

154 e role of the dysbiotic tissue microbiome in HNSCC.

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

156 ade, might be novel target genes for pain in HNSCC patients.

157 WES study of patient-matched tumor pairs in HNSCC, we found synchronous lymph node metastases to be

158 ivated tyrosine kinase signaling pathways in HNSCC, we compared the phosphotyrosine profiles of a pan

159 ay alterations are present at a high rate in HNSCC, the identification of efficacious agents in patie

160 the antitumorigenic inflammatory response in HNSCC and other epithelial malignancies.

161 apoptosis, and the cell survival response in HNSCC.

162 te to improved chemoradiotherapy response in HNSCC.

163 hylation and gene silencing is reversible in HNSCC cells, leading to PTPRT-specific downregulation of

164 b significantly upregulated IL6 secretion in HNSCC cell lines, which our laboratory previously report

165 a novel immunosuppressive role for Sema4D in HNSCC through induction of MDSC, and it highlights Sema4

166 cinoma cells to invade surrounding stroma in HNSCC.

167 hat HOPX functions as a tumour suppressor in HNSCC and suggest a central role for HOPX in suppressing

168 YRK1A could be a novel therapeutic target in HNSCC.

169 Here we demonstrate that in HNSCC cells, a noncytotoxic dose of IB represses mesench

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

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

172 trategy to block TICs and drug resistance in HNSCCs.

173 PV detection in the oral cavity and incident HNSCC.

174 Main Outcomes and Measures: Incident HNSCC, which includes cancers of the oropharynx, oral ca

175 PV-16 detection was associated with incident HNSCC (OR, 7.1; 95% CI, 2.2-22.6), with positive associa

176 ypermethylated in several cancers, including HNSCC (60.1% of tumors analyzed) in association with dow

177 expressed in a variety of cancers, including HNSCC, but whether or not it plays different roles in HP

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

179 d transgenic mouse model of HPV16 E7-induced HNSCC, we demonstrate that Dek is required for optimal p

180 tro, FADD or BIRC2 siRNA knockdown inhibited HNSCC displaying amplification and increased expression

181 ression alone was not sufficient to initiate HNSCC formation, it significantly increased tumor suscep

182 Twenty patients with stage III-IVa HNSCC prospectively underwent (18)F-FDG PET/CT and DW MR

183 However, a patient with stage IVA HNSCC received 13 days of neoadjuvant erlotinib and expe

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

185 e potential use of immunotherapy in managing HNSCC.

186 lecular mechanisms through which it mediates HNSCC progression are not well understood.

187 a poor predictor for primary and metastatic HNSCC samples.

188 lating RUNX2 expression in highly metastatic HNSCC cells, where it was downregulated commonly.

189 terations that underlie recurrent/metastatic HNSCC.

190 ls (LEC) but not in oral epithelium and most HNSCCs.

191 mined with immunostaining of human and mouse HNSCC tissue sections.

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

193 t, a novel SMAC mimetic, sensitized multiple HNSCC lines to cell death by agonists TNFalpha or TRAIL

194 nhibition of PI3K signaling in PIK3CA-mutant HNSCC cell lines.

195 quamous cell carcinoma in the head and neck (HNSCC) is a common yet poorly understood cancer, with ad

196 quamous-cell carcinoma of the head and neck (HNSCC) progressing after first-line platinum regimens ha

197 uamous cell carcinomas of the head and neck (HNSCC), the increasing incidence of oropharyngeal squamo

198 quamous cell carcinoma of the head and neck (HNSCC).

199 ion in recurrent and metastatic HPV-negative HNSCC (13 of 30 tumors [43%]), cutaneous SCC (11 of 21 t

200 preferentially overexpressed in HPV-negative HNSCC and that this overexpression of TMEM16A is associa

201 erent roles in HPV-positive and HPV-negative HNSCC is unknown.

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

203 a potentially useful target in HPV-negative HNSCC.

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

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

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

207 21 (K-allele), which is expressed in >40% of HNSCC cases.

208 erate staining of DYRK1A in 97.5% (39/40) of HNSCC tissues analyzed.

209 icant upregulation of MUC4 in 78% (68/87) of HNSCC tissues compared with 10% positivity (1/10) in ben

210 in invasion and colony formation ability of HNSCC cell lines.

211 lete understanding of the molecular basis of HNSCC pathogenesis.

212 he RUNX2-mediated metastatic capabilities of HNSCC cells.

213 UNX2 promoted the metastatic capabilities of HNSCC, whereas RUNX2 silencing inhibited these features.

214 Incident cases of HNSCC (n = 132) were identified during an average 3.9 ye

215 s were confirmed in an independent cohort of HNSCC tumors by methylation-specific PCR and immunohisto

216 d to analyze the spatiotemporal evolution of HNSCC in individual patients and to identify potential t

217 A pathway is a negative prognostic factor of HNSCC patient survival.

218 sgenic epidermal cells and for the growth of HNSCC tumors.

219 replication stress, and hypersensitivity of HNSCC cells to CHKi monotherapy was found.

220 address the challenges in the management of HNSCC.

221 nd T cells cultured in conditioned medium of HNSCC cells in which Sema4D was knocked down promoted an

222 hat drives invasive growth and metastasis of HNSCC.

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

224 In a mouse xenograft model of HNSCC, pharmacologic inhibition of Vps34, a key mediator

225 reduce tumor growth in a xenograft model of HNSCC.

226 al lymph node metastasis in a mouse model of HNSCC.

227 d the phosphotyrosine profiles of a panel of HNSCC cell lines to a normal oral keratinocyte cell line

228 homeobox gene, HOPX, in the pathogenesis of HNSCC.

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

230 geting can enhance the radiosensitization of HNSCC.

231 functionally important to the regulation of HNSCC progression.

232 ulation and the antitumor immune response of HNSCC.

233 PV types, but their association with risk of HNSCC is unknown.

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

235 IB suppresses EMT and stemness of HNSCC cells through inhibition of Twist1-mediated let-7i

236 and to improve the treatment and survival of HNSCC patients.

237 nsight into early diagnosis and treatment of HNSCC.

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

239 Np63 isoforms is observed in the majority of HNSCCs.

240 oter methylation was observed in a subset of HNSCCs and was associated with a worse overall survival

241 analysis of clinically-annotated multi-omics HNSCC data released by the Cancer Genome Atlas.

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

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

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

245 Over time, the proportion of non-OP HNSCCs that were p16+ (or ISH+) increased among whites (

246 ortion (26 of 62 [42%]) of these p16+ non-OP HNSCCs were found in sites adjacent to the oropharynx.

247 Few non-OP HNSCCs were HPV related.

248 The proportion of p16+ and ISH+ non-OP HNSCCs were similar by sex.

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

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

251 M16A expression is decreased in HPV-positive HNSCC at the DNA, RNA, and protein levels in patient sam

252 The HPV-positive HNSCC is characterized by genetic alterations, clinical

253 e down-regulation of TMEM16A in HPV-positive HNSCC makes TMEM16A a poor therapeutic target in HPV-pos

254 favorable clinical outcomes of HPV-positive HNSCC patients.

255 6A a poor therapeutic target in HPV-positive HNSCC, but a potentially useful target in HPV-negative H

256 f the mutations associated with HPV-positive HNSCC, which may be a useful resource for genomic-based

257 poor survival in patients with HPV-positive HNSCC.

258 HPV-positive HNSCCs, which frequently harbor wild-type p53, carry a m

259 activation are highly correlated in primary HNSCC and predict poor patient survival.

260 atients with histologically verified primary HNSCC were recruited from Odense University Hospital fro

261 s significantly more effective at protecting HNSCC cells from VSV oncolysis than was IFN-alpha2a.

262 of 2840 patients with pathologically proven HNSCC undergoing curative RT at a single academic cancer

263 ons in primary, metastatic, and/or recurrent HNSCC cancers, with potential implications for precision

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

265 Smoking-related HNSCC is associated with few targetable mutations but is

266 spatial stochastic model of tobacco-related HNSCC at the tissue level and calibrated the model using

267 re favorable prognostic factors for resected HNSCC.

268 ent for both primary and cisplatin-resistant HNSCC cells.

269 ncreased production of IFN-beta in resistant HNSCC cells.

270 ting the same epitope as cetuximab, restored HNSCC sensitivity in a manner associated with antibody-d

271 MUC4 knockdown (KD) in SCC1 and SCC10B HNSCC cell lines resulted in significant inhibition of g

272 st a biomarker-driven strategy for selecting HNSCC patients who may benefit the most from CHKi therap

273 st a biomarker-driven strategy for selecting HNSCC patients who may benefit the most from therapy wit

274 Inhibition of autophagy sensitizes HNSCC cells to EGFR blockade.

275 Similarly, HNSCC cell lines harboring endogenous and engineered DDR

276 tion was rare; (2) Regardless of HPV status, HNSCCs of wild-type TP53 implied a good survival chance

277 er, our data demonstrate that DEK stimulates HNSCC cellular growth and identify DeltaNp63 as a novel

278 We showed that HNSCC cells forced into tumor island-like 3D aggregates

279 complexes and signatures genome wide in the HNSCC model UM-SCC46 using chromatin immunoprecipitation

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

281 The addition of anti-Sema4D Ab to HNSCC conditioned medium significantly reduced the expan

282 oxygen species-dependent PBMC chemotaxis to HNSCC spheroids.

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

284 In the chemoradiotherapy-treated HNSCC cohort, mitochondrial-rich (COX5B) metabolism corr

285 Using two HNSCC datasets with differential expression of ANO1, we

286 Data using HNSCC PDX models showed significant reduction in tumor v

287 l, 307 patients with histologically verified HNSCC were included.

288 we report that autophagy was activated when HNSCC cells are treated with the proteasome inhibitor bo

289 in HNSCC and how autophagy is initiated when HNSCC cells undergo cytotoxic stress.

290 Notably, when HNSCC cells were cocultured with normal fibroblasts, the

291 pain in 1,368 patients newly diagnosed with HNSCC, we conducted a genome-wide association study base

292 vironment of cetuximab-treated patients with HNSCC enrolled in a novel neoadjuvant, single-agent cetu

293 ically meaningful outcomes for patients with HNSCC in conjunction with systematic verification of the

294 However, many patients with HNSCC respond poorly to the EGFR inhibitors (EGFRI) cetu

295 ients (14%) (13 of 53 [25%] of patients with HNSCC) by refining diagnoses and matching patients to sp

296 predict oncologic outcomes for patients with HNSCC, whereas weight loss after RT initiation does not

297 lso predicts poor prognosis in patients with HNSCC.

298 and non-coding RNA for pain in patients with HNSCC.

299 recise treatment selection for patients with HNSCC.

300 Patients with the KRAS-variant with HNSCC significantly benefit from the addition of cetuxim