ライフサイエンスコーパス: oral cancer

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

2 genes as contributors to human clefting and oral cancer.

3 e, nor microbial community associations with oral cancer.

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

5 es disturbances in intercellular adhesion in oral cancer.

6 nderlying causes for cellular discohesion in oral cancer.

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

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

9 ntify molecular signatures or biomarkers for oral cancer.

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

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

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

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

14 ce the devastating worldwide consequences of oral cancer.

15 the first reported inducible mouse model for oral cancer.

16 the oral epithelium are known precursors of oral cancer.

17 GF2R may influence significantly the risk of oral cancer.

18 tion and treatment improve the prognosis for oral cancer.

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

20 that have not been previously implicated in oral cancer.

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

22 latest information on the genes involved in oral cancer.

23 characterize transformation-related genes in oral cancer.

24 additional genetic damage, can develop into oral cancer.

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

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

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

28 375 as a candidate tumor suppressor miRNA in oral cancer.

29 romotes gingival and periodontal disease and oral cancer.

30 st for diagnosis and personalized therapy of oral cancer.

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

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

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

34 emerging mechanisms of immunosuppression in oral cancers.

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

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

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

38 e etiologically linked to human cervical and oral cancers.

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

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

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

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

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

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

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

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

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

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

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

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

51 differences in the smoking-related risks for oral cancer and in the risk for nonsmoking-related oral

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 ancer and in the risk for nonsmoking-related oral cancer as well.

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

68 These oral cancer associated genes include oncogenes, tumor su

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 In addition, oral cancer cells overexpressing cellular HuR increased

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 he glycoproteins differentially expressed on oral cancer cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

125 Oral cancer development is a tobacco-related multistep a

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

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

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

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

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

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

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

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

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

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

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

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

138 Evaluation of oral cancers for such heterogeneity identified two compa

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

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

141 Oral cancers frequently contain DNA of human papillomavi

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

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

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

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

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

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

148 utive patients with histologically confirmed oral cancer in Greece.

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

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

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

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

153 Human oral cancers in vivo did not exhibit immunostaining for

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 ased glutamate metabolism metal transport in oral cancer patients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 heterogeneous oral lesion with an increased oral cancer risk.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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