ライフサイエンスコーパス: oral cancer

1 additional genetic damage, can develop into oral cancer.

2 m, HPV infection, and the risk of developing oral cancer.

3 n individual's susceptibility to the risk of oral cancer.

4 hat have a high likelihood of progression to oral cancer.

5 375 as a candidate tumor suppressor miRNA in oral cancer.

6 , but to date, only limited studies apply to oral cancer.

7 romotes gingival and periodontal disease and oral cancer.

8 st for diagnosis and personalized therapy of oral cancer.

9 e of the existence and signs and symptoms of oral cancer.

10 genes as contributors to human clefting and oral cancer.

11 l carcinoma (SCC) is the most common form of oral cancer.

12 es disturbances in intercellular adhesion in oral cancer.

13 nderlying causes for cellular discohesion in oral cancer.

14 dose 13cRA in reducing the long-term risk of oral cancer.

15 ge in buccal cells and increases the risk of oral cancer.

16 ntify molecular signatures or biomarkers for oral cancer.

17 to functionally link periodontal disease and oral cancer.

18 the risk-benefit ratio of agents to prevent oral cancer.

19 tions have been suggested in the etiology of oral cancer.

20 a common feature of human tumors, including oral cancer.

21 ce the devastating worldwide consequences of oral cancer.

22 the first reported inducible mouse model for oral cancer.

23 the oral epithelium are known precursors of oral cancer.

24 GF2R may influence significantly the risk of oral cancer.

25 tion and treatment improve the prognosis for oral cancer.

26 ion in both the incidence and mortality from oral cancer.

27 that have not been previously implicated in oral cancer.

28 , and genes that have not been implicated in oral cancer.

29 oxidative stress is tightly associated with oral cancer.

30 latest information on the genes involved in oral cancer.

31 characterize transformation-related genes in oral cancer.

32 ng to dental caries, periodontal disease, or oral cancer.

33 e effects on dental caries, and 1 considered oral cancer.

34 icacy of this three-drug regimen in advanced oral cancer.

35 with poor oral hygiene, tobacco smoking, and oral cancer.

36 e, nor microbial community associations with oral cancer.

37 t immunosensor for non-invasive detection of oral cancer.

38 an cancer but has not been fully assessed in oral cancers.

39 oral premalignant lesions (OPLs) and prevent oral cancers.

40 at may affect the etiology of colorectal and oral cancers.

41 r tumors of the anogenital tract, as well as oral cancers.

42 ety of cancer patients, including those with oral cancers.

43 emerging mechanisms of immunosuppression in oral cancers.

44 irus (HPV) has recently been associated with oral cancers.

45 evidence for an etiological role for HPV in oral cancers.

46 genes, which are present in more than 27% of oral cancers.

47 e etiologically linked to human cervical and oral cancers.

48 be an early indicator of increased risk for oral cancers.

49 ic genotype in HPV-associated anogenital and oral cancers.

50 corresponding to the gene doc-1 (deleted in oral cancer 1), is a tumor suppressor protein.

51 differential expression included deleted-in-oral-cancer-1 (DOC-1), a highly conserved growth suppres

52 ncident head and neck cancers (patients; 180 oral cancers, 135 oropharynx cancers, and 247 hypopharyn

53 outcomes were periodontal diseases (42%) and oral cancers (30%).

54 ide insight into potential stratification of oral cancer according to risk of occult metastasis, guid

55 In the United States, oral cancer accounts for more deaths annually than cervi

56 There are numerous risk factors for oral cancer, among which periodontal disease is gaining

57 proximately 90% of the attributable risk for oral cancer and 80% of the attributable risk for larynx

58 targeting the enzyme PARP1/2, can delineate oral cancer and accurately identify positive margins, bo

59 study was to identify deregulated miRNAs in oral cancer and further focus on specific miRNAs that we

60 been made in the molecular understanding of oral cancer and its application for diagnosis, prognosis

61 ide in mediating RNAi-based therapeutics for oral cancer and its prospective applicability in clinica

62 reported lack of knowledge and awareness of oral cancer and its signs and symptoms among the partici

63 e and from models of inflammation induced by oral cancer and Legionella pneumophila infection.

64 ode metastases in a segment of patients with oral cancer and N0 neck.

65 In a prospective study, 31 patients with oral cancer and no evidence of lymph node metastases by

66 c endothelial marker, is highly expressed in oral cancer and some oral premalignancies.

67 frequent events preceding the development of oral cancer and that p16(INK4a) inactivation occurs to a

68 uate the association between E. faecalis and oral cancer and to determine the underlying mechanisms t

69 m cells (CSCs) have been isolated from human oral cancers and been considered as the driving force of

70 We studied Lgmn activation in human oral cancers and oral cancer mouse models.

71 owledge regarding chromosomal instability in oral cancer, and discuss various mechanisms that enhance

72 s with malignant melanoma, multiple myeloma, oral cancer, and esophageal squamous cell carcinoma did

73 n the incidence, management, and survival of oral cancer, and then, to review possible explanations f

74 pression of CIP2A is clearly demonstrated in oral cancers, and inverse correlation between miR-375 an

75 nd dental caries; 16 (12 studies) considered oral cancer; and 2 studied periodontal disease.

76 iples of image-based approaches to detecting oral cancer are placed within the context of clinical ne

77 reatment options for recurrent or refractory oral cancers are limited.

78 g tooth loss, itself a major risk factor for oral cancer, are likely a result of severe ecological di

79 certain cancers such as cervical cancer and oral cancer as well, and the HPV oncoprotein E6 may indu

80 pairing segment of microRNAs associated with oral cancer, as well as serotype-specific detection of d

81 These oral cancer associated genes include oncogenes, tumor su

82 About 600 genes were found to be oral cancer associated.

83 tistry are growing rapidly: the treatment of oral cancer, bacterial and fungal infection therapies, a

84 research will result in earlier diagnosis of oral cancer, better knowledge of prognostic factors, and

85 sparities in both incidence and mortality of oral cancer between ethnic groups.

86 ent biosensing platform for detection of the oral cancer biomarker (CYFRA-21-1).

87 For example, the oral cancer burden in India has been identified as a pub

88 factor for cancers of the mouth and pharynx (oral cancer), but the differential risks by beverage typ

89 rovide a molecular basis for gene therapy of oral cancer by IkappaBalpha gene transfer in vivo.

90 udies with histologically confirmed incident oral cancer cases are necessary to confirm this relation

91 lications are advancing our understanding of oral cancer cell biology.

92 NSCC biomarkers from a single cell lysate of oral cancer cell cultures was demonstrated.

93 oral cancer cells and consequently inhibited oral cancer cell invasiveness and anchorage-independent

94 V-immortalized oral keratinocytes, and in an oral cancer cell line expressing mutant p53.

95 calize and form a complex with Rap-1A in the oral cancer cell line.

96 on the cell proliferation of the HSC-2 human oral cancer cell line.

97 er down-regulated or lost in the majority of oral cancer cell lines (8/8), prostate cancer cell lines

98 unknown transcript were up-regulated in the oral cancer cell lines analysed as well as in HOK-16B ce

99 ng, we examined premalignant oral lesion and oral cancer cell lines and found no intragenic mutations

100 ring IL-6 and IL-8 in conditioned media from oral cancer cell lines and showing good correlations wit

101 region (LCR) of HPV-16 or HPV-18 from three oral cancer cell lines and two lines of HPV-16-immortali

102 d from HOK-16B (HOK-16B-BaP-T) and the human oral cancer cell lines Hep-2, SCC-9 and Tu-177.

103 talized oral epithelial cell lines and three oral cancer cell lines were simultaneously monitored usi

104 tionally, overexpressed Rap-1A could promote oral cancer cell migration and invasion by Transwell cha

105 In this study, human oral cancer cells (OEC-M1) were encapsulated in 3D agaro

106 target the CIP2A oncoprotein (siCIP2A) into oral cancer cells and consequently inhibited oral cancer

107 tations were found in the LCRs isolated from oral cancer cells and HPV-immortalized oral epithelial c

108 gene is absent or down-regulated in hamster oral cancer cells and in many other cancer cell types.

109 ound that the N-glycans of B7-H3 from Ca9-22 oral cancer cells contain the terminal alpha-galactose a

110 ly expressing iCaspase-9 (HDMEC-iCasp9) with oral cancer cells expressing luciferase (OSCC3-luc or UM

111 In addition, oral cancer cells overexpressing cellular HuR increased

112 We determined that oral cancer cells overexpressing cyclooxygenase-2 (COX-2

113 Transient transfection of miR-375 in oral cancer cells reduces the expression of CIP2A, resul

114 han that of the equivalent wild-type LCRs in oral cancer cells that contained the same HPV type.

115 and sequencing (RIP-seq) analyses of HuR in oral cancer cells treated with ionizing radiation (IR),

116 cleavage associated with active caspase-3 in oral cancer cells treated with ionizing radiation and ch

117 y, untransduced HDMEC were co-implanted with oral cancer cells, and a transcriptionaly targeted adeno

118 and cleavage of HuR in paclitaxel-resistant oral cancer cells, both in vitro and in vivo.

119 inhibits MMP-9-dependent invasion of UMSCC-1 oral cancer cells, preosteoclast migration, and receptor

120 Using human oral cancer cells, we support the clinical findings and

121 tors induce nuclear translocation of rap1 in oral cancer cells.

122 which is both amplified and overexpressed in oral cancer cells.

123 tion into both normal oral keratinocytes and oral cancer cells.

124 ing genes were likely to be overexpressed in oral cancer cells.

125 e rate of cell death in paclitaxel resistant oral cancer cells.

126 , for the management of paclitaxel resistant oral cancer cells.

127 he glycoproteins differentially expressed on oral cancer cells.

128 One group of subjects (55 controls without oral cancer) collected oral rinse samples at home or wor

129 tion pathway genes are frequently mutated in oral cancers, comparatively little is known about the me

130 IGF2R genotype had a 2.7-fold higher risk of oral cancer compared with subjects with other genotypes

131 The incidence and mortality rate of oral cancer continue to rise, partly due to the lack of

132 s imply that mutations in the LCR of HPVs in oral cancer could lead to increased expression of HPV-tr

133 te the application of this model in lung and oral cancer datasets, and the results indicate that the

134 bined utility and implications for improving oral cancer detection and outcomes.

135 ensitivity of 89% and specificity of 98% for oral cancer detection, demonstrating high diagnostic uti

136 doplanin was the only independent factor for oral cancer development (hazard ratio = 3.087; 95% CI, 1

137 between 3-month OPL response and subsequent oral cancer development (P = .11).

138 s and clinicopathologic parameters including oral cancer development during the follow-up were analyz

139 determine a role of podoplanin in predicting oral cancer development in patients with OPL.

140 a powerful biomarker to predict the risk for oral cancer development in patients with OPL.

141 y based strategies to predict and/or prevent oral cancer development in patients with oral premaligna

142 Oral cancer development is a tobacco-related multistep a

143 may partly contribute to the pathogenesis of oral cancer development.

144 transformation and the early stages of human oral cancer development.

145 co use and mark individuals at high risk for oral cancer development.

146 Interestingly, of the oral cancers devoid of nuclear hCG2 (112 cases), 58 case

147 d we validate the protein panel for accurate oral cancer diagnostics.

148 This review focuses on oral cancer disease mechanisms and discusses ongoing res

149 al growth factor receptor (EGFR) therapy for oral cancer does not provide satisfactory efficacy due t

150 nique to complement the visual inspection of oral cancers during transoral robotic surgery (TORS) in

151 However, only 11.1% of oral cancer epithelia (14 of 126) showed mild hCG2 nucle

152 wn-regulated in laser capture microdissected oral cancer epithelia.

153 The Erlotinib Prevention of Oral Cancer (EPOC) study was a randomized, placebo-contr

154 the 18 participants who were offered a free oral cancer examination at a dental practice took up thi

155 Patient education and periodic oral cancer examinations by dental professionals are nec

156 Evaluation of oral cancers for such heterogeneity identified two compa

157 nal Cancer Institute USA, Eli Lilly, and The Oral Cancer Foundation.

158 Similar oral cancer-free survival rates were observed across all

159 rm OPL response as a surrogate end point for oral cancer-free survival.

160 Oral cancers frequently contain DNA of human papillomavi

161 The Oral Cancer Gene Database was developed to provide the b

162 he past years, progress has been made in the oral cancer genetic markers field, which includes altera

163 Platinum-resistant oral cancer has a dismal outcome with limited treatment

164 Oral cancer has a high annual incidence rate all over th

165 nk between E. faecalis and EGFR signaling in oral cancer has not been elucidated.

166 ve) patients based on their LOH profiles and oral cancer history.

167 In an attempt to model oral cancer in a human cell-based system, we analyzed no

168 lance of benefits and harms of screening for oral cancer in asymptomatic adults.

169 utive patients with histologically confirmed oral cancer in Greece.

170 although complete resection does not prevent oral cancer in high-risk patients.

171 ompared in a 1992-1995 case-control study of oral cancer in Puerto Rico.

172 studies examined this relationship in human oral cancer in vivo, and none addressed the issue of how

173 e the histopathology associated with painful oral cancers in a preclinical model.

174 s and for explaining increased incidences of oral cancers in users of snuff and chewing tobacco in wh

175 Human oral cancers in vivo did not exhibit immunostaining for

176 t alcohol concentration is a risk factor for oral cancer independent of the total quantity of alcohol

177 This report demonstrates that, even though oral cancers involving the periodontium are a relatively

178 ll remains unclear whether targeting CSCs in oral cancer is a clinically relevant strategy to combat

179 An alternate effective therapy for oral cancer is a light based spatially-targeted cytotoxi

180 Oral cancer is a major global threat to public health, c

181 Progression of oral cancer is associated with enhanced expression of al

182 Gene therapy for oral cancer is currently under investigation in clinical

183 The extent of ethnic differences in oral cancer is masked by the scarcity of information ava

184 The most common form of oral cancer is oral squamous cell carcinoma (OSCC).

185 tionale for molecular-targeted prevention of oral cancer is strong.

186 Oral cancer is the sixth most common cause of death from

187 Oral cancer is unique in that it causes intense pain at

188 al squamous-cell carcinoma, the main type of oral cancer, is among the ten most common cancers in the

189 Cells of two different human oral cancer lines, JMAR and MDA1986, were injected into

190 hem are being used in a clinical setting for oral cancer management.

191 nslation and could aid surgeons in assessing oral cancer margins in vivo.

192 Decorin expressed in oral cancer may have lost its ability to inhibit TGF-bet

193 there were significantly increased risks of oral cancer, melanoma, meningioma, and leukemia.

194 We have shown previously that oral cancer metastasis and pain are controlled by the en

195 an available drug to effectively treat both oral cancer metastasis and pain in a preclinical model.

196 d and neck cancer in the hamster cheek pouch oral cancer model is presented.

197 umor progression in this genetically defined oral cancer model system, thereby prolonging animal surv

198 ene isolated and identified from the hamster oral cancer model.

199 re synergistically pathogenic within in vivo oral cancer models.

200 uently impair tumor growth using a xenograft oral cancer mouse model.

201 ed Lgmn activation in human oral cancers and oral cancer mouse models.

202 ld be advised that delay in the diagnosis of oral cancer occurs frequently, even in individuals who d

203 ks per week) had strongly increased risks of oral cancer (odds ratio = 6.4, 95% confidence interval:

204 dividual/household income is associated with oral cancer (odds ratio, 2.41; 95% confidence interval [

205 e oral screening examination for identifying oral cancer or potentially malignant disorders that have

206 tificial intelligence approaches can improve oral cancer outcomes through improved detection and diag

207 with imaging can have considerable impact on oral cancer outcomes, with applications ranging from low

208 tigated for their applicability to improving oral cancer outcomes, yet none of them have found widesp

209 ORAOV1 (oral cancer overexpressed) is overexpressed in many soli

210 review is to explore the current studies on oral cancer pain and their implications in clinical mana

211 We propose that oral cancer pain has underlying biologic mechanisms that

212 Oral cancer pain is initiated and maintained in the canc

213 a unique opportunity to study mechanisms of oral cancer pain.

214 lized means of the four protein levels in 78 oral cancer patient serum samples and 49 controls gave c

215 ding domain (DBD) in a sample from an Indian oral cancer patient.

216 the reference peptide in hemoglobin from 18 oral cancer patients and 15 healthy control subjects.

217 ization is associated with poor prognosis of oral cancer patients and keratinization-associated miRNA

218 Metastasis reduces survival in oral cancer patients and pain is their greatest complain

219 -99 of globin were significantly elevated in oral cancer patients compared to healthy subjects, while

220 Oral cancer patients experience pain at the site of the

221 Oral cancer patients often have severe, chronic, and mec

222 d beta-His-2 is also significantly higher in oral cancer patients than in healthy subjects (p < 0.05)

223 and function of the oral microbiomes of 121 oral cancer patients to 242 age- and gender-matched cont

224 gh the alterations in the oral microbiome of oral cancer patients were significant, they were of subs

225 Finally, not only do oral cancer patients with p53 mutations exhibit higher l

226 Of 46 oral cancer patients with squamous cell carcinoma, appro

227 f oral cancer tissues, plasma, and saliva of oral cancer patients, have allowed the identification of

228 Among tumors from 188 oral cancer patients, upregulated ROS1 expression strong

229 argets a pathway shown to be dysregulated in oral cancer patients, using gene therapy and repurposing

230 tial biomarker to assess oxidative stress in oral cancer patients.

231 )Zr-nanocolloidal albumin was evaluated in 5 oral cancer patients.

232 ate tolerance and improve quality of life in oral cancer patients.

233 es (TILs) have been documented previously in oral cancer patients.

234 ciencies of tumor-associated immune cells in oral cancer patients.

235 better stratification and prognostication of oral cancer patients.

236 bles was also investigated in a cohort of 72 oral cancer patients.

237 ased glutamate metabolism metal transport in oral cancer patients.

238 the mouse model and more pain experienced by oral cancer patients.

239 nosorbent assay (ELISA) in saliva samples of oral cancer patients.

240 Oral cancer, predominantly oral squamous cell carcinoma

241 Oral cancer prevalence is increasing at an alarming rate

242 Oral cancers, primarily squamous cell carcinomas (SCCs),

243 These results indicate that human oral cancers produce 92K-GL, 72K-GL, and FIB-CL in vivo

244 ent effects of aberrant decorin expressed in oral cancer progression are warranted.

245 modifications that characterize each step of oral cancer progression can now be profiled by several h

246 in oral premalignant archival tissues and an oral cancer progression cellular model.

247 s as well as representative cell lines of an oral cancer progression model.

248 ion of immortality at the dysplasia stage of oral cancer progression was consistently associated with

249 mechanism that controls c-Myc expression in oral cancer progression.

250 a6 signaling activates Fyn and thus promotes oral cancer progression.

251 reness of the role of dentists in diagnosing oral cancer, promotion of oral cancer screening by healt

252 n of two biomarkers associated with salivary oral cancer, protein IL-8 and its messenger RNA (IL-8 mR

253 e for the DEJ instability observed following oral cancer radiotherapy.

254 viewed the evidence on whether screening for oral cancer reduces morbidity or mortality and on the ac

255 Patients with metastatic oral cancers report greater pain.

256 A retrospective analysis of samples from oral cancer revealed that p53 status was associated with

257 this trial, LOH was validated as a marker of oral cancer risk and found to be associated with increas

258 Importantly, oral cancer risk can be further stratified by considerin

259 xtensively characterized molecular marker of oral cancer risk described to date.

260 n this 1992-1995 study, the authors examined oral cancer risk in Puerto Rico, comparing alcohol intak

261 OF REVIEW: To discuss the recent advances in oral cancer risk prediction, as well as agents that have

262 Data on RDS and oral cancer risk were inconclusive.

263 sted no association between total starch and oral cancer risk, and low-quality evidence suggested tha

264 , nonspecialists such as dentists screen for oral cancer risk, and then they refer high-risk patients

265 heterogeneous oral lesion with an increased oral cancer risk.

266 ke growth factor II receptor gene (IGF2R) in oral cancer risk.

267 uality evidence suggested that SDS decreases oral cancer risk.

268 ists in diagnosing oral cancer, promotion of oral cancer screening by health professionals during rou

269 rs or cancers were identified during partner oral cancer screening examinations.

270 The uptake of oral cancer screening may be improved by increasing know

271 These individuals were enrolled in Taiwan's Oral Cancer Screening Program.

272 arly detection of OSCC during routine visual oral cancer screenings.

273 g with PARPi-FL can enhance the detection of oral cancer, serve as a screening tool and help to guide

274 Whether patients with early-stage oral cancers should be treated with elective neck dissec

275 Immunohistochemistry analysis done on oral cancers showed that normal oral mucosa (100%, 12 of

276 roups to identify knowledge and awareness of oral cancer signs and symptoms and the factors likely to

277 ion was confirmed by the evaluation of human oral cancer specimens by immunohistochemistry, which sho

278 One hundred forty patients with invasive oral cancers, stage T1 and T2, N0 including 95 cancers o

279 Certain risk factors for oral cancer, such as tobacco, age, and alcohol, are also

280 ive resection margins are a major problem in oral cancer surgery.

281 iation between p53 Arg72Pro polymorphism and oral cancer susceptibility in all genetic models.

282 sitive had significantly higher incidence of oral cancer than did those whose OPL was podoplanin nega

283 s treat conditions such as facial trauma and oral cancer that can result from alcohol misuse.

284 nd EGFR could potentially offer an effective oral cancer therapy.

285 /conditions such as rheumatoid arthritis and oral cancer, there are no reported studies on their util

286 immunocytochemistry (ICC) methods to examine oral cancer tissue specimens from 20 surgery patients.

287 Genomic and proteomic studies of oral cancer tissues, plasma, and saliva of oral cancer p

288 Oral cancer was associated with two new regions, 2p23.3

289 e biopsy (SLNB) for T1 or T2, clinically N0, oral cancer was tested by correlation of sentinel node p

290 h cleft lip/palate were also associated with oral cancer, we genotyped 188 individuals with OSCC and

291 ose of endogenous neurons in mouse models of oral cancer, we identified an adrenergic differentiation

292 To identify new markers for oral cancer, we used a sialylation probe to investigate

293 ine which MMPs are produced in vivo by human oral cancers, we used specific anti-human-MMP antibodies

294 ngue, 26 of the floor of mouth, and 19 other oral cancers were studied.

295 en p53 Arg72Pro polymorphism and the risk of oral cancer with HPV infection remains inconclusive.

296 en p53 Arg72Pro polymorphism and the risk of oral cancer with HPV infection was detected in the Arg/A

297 ppears to be associated with HNC, especially oral cancers, with snuff being more strongly associated

298 A role for HPV in the progression of oral cancer would be more plausible if the viral transfo

299 ith characteristics and molecular drivers of oral cancer would likely enhance understandings and func

300 Treatment of pre-established human oral cancer xenografts with a BMI1 inhibitor resulted in