ライフサイエンスコーパス: cervical carcinoma

1 lomavirus (HPV), such as HPV 16, cause human cervical carcinoma.

2 V-16), which is prevalent in the etiology of cervical carcinoma.

3 rognostic sign in women with HPV 16 positive cervical carcinoma.

4 apillomavirus (HR-HPV) causes nearly 100% of cervical carcinoma.

5 atment approaches for patients with invasive cervical carcinoma.

6 0% of patients (eight of 16) with measurable cervical carcinoma.

7 ated in bladder carcinoma and only rarely in cervical carcinoma.

8 at has been implicated in the development of cervical carcinoma.

9 strongly associated with the development of cervical carcinoma.

10 alignant lesions and is a necessary cause of cervical carcinoma.

11 strongly associated with the development of cervical carcinoma.

12 omavirus (HPV) genotypes are associated with cervical carcinoma.

13 treatment of patients with locally advanced cervical carcinoma.

14 finding that p16 hypermethylation occurs in cervical carcinoma.

15 was found associated with the development of cervical carcinoma.

16 U6 gene might be useful for gene therapy of cervical carcinoma.

17 PT-11 has significant activity in refractory cervical carcinoma.

18 sition from severe dysplasia/CIS to invasive cervical carcinoma.

19 curcumin for the treatment of HPV18-infected cervical carcinoma.

20 r therapy for patients with early ovarian or cervical carcinoma.

21 rized site of HPV16 integration in a primary cervical carcinoma.

22 r suppressor and a possible tumor marker for cervical carcinoma.

23 their association with severe dysplasia and cervical carcinoma.

24 d viral load in early and advanced stages of cervical carcinoma.

25 causes a wide range of pathologies including cervical carcinoma.

26 oropharynx, anus, vulva, vagina or penis, or cervical carcinoma.

27 in select patients with low-risk early-stage cervical carcinoma.

28 into the host genome plays a crucial role in cervical carcinoma.

29 l) were calculated for incidence of invasive cervical carcinoma.

30 90/NF45 function could assist in controlling cervical carcinoma.

31 cal intraepithelial neoplasia, but not frank cervical carcinoma.

32 are considered the major causative agents of cervical carcinoma.

33 ublet combinations in advanced and recurrent cervical carcinoma.

34 or is a key promoter of tumor progression in cervical carcinoma.

35 owth of malignant tumors in a mouse model of cervical carcinoma.

36 es found in lung squamous cell carcinoma and cervical carcinoma.

37 andard for the treatment of locally advanced cervical carcinoma.

38 iated with different risks of progression to cervical carcinoma.

39 contribute to oncogenesis in endometrial and cervical carcinomas.

40 on of CD40, a TNF receptor family member, in cervical carcinomas.

41 the only FGFR3 mutation described to date in cervical carcinomas.

42 patients with multiple myeloma, bladder and cervical carcinomas.

43 rating cells of the infected epithelia or in cervical carcinomas.

44 ) are consistently expressed in HPV-positive cervical carcinomas.

45 pithelia, low and high grade dysplasias, and cervical carcinomas.

46 ss of Fhit protein in 25 of 33 (76%) primary cervical carcinomas.

47 (3p13-21.1) have been observed frequently in cervical carcinomas.

48 way plays a major role in the development of cervical carcinomas.

49 cinoma cell lines and 17 of 25 (68%) primary cervical carcinomas.

50 ich are responsible for anogenital warts and cervical carcinomas.

51 ted etiologically with the majority of human cervical carcinomas.

52 has been observed for invasive squamous cell cervical carcinomas.

53 be important in the origin or progression of cervical carcinomas.

54 considered at increased risk of adenomatous cervical carcinomas.

55 sease; HPV is now implicated in up to 90% of cervical carcinomas.

56 a minority of patients with early stages of cervical carcinomas.

57 py-number alterations in the pathogenesis of cervical carcinomas.

58 E6, E7, and L1 genes in flash-frozen HPV-16 cervical carcinomas.

59 and HPV18 are causative agents of most human cervical carcinomas.

60 aviruses (HPVs) are present in virtually all cervical carcinomas.

61 vulvar carcinoma and metastatic melanoma, 1 cervical carcinoma, 1 Bowen disease of the vulva, and 1

62 ; CIN 2, 28 cases; and CIN 3, 33 cases), and cervical carcinoma (29 cases).

63 In group 1, ADCs from cervical carcinoma (757 x 10(-6) mm(2)/sec +/- 110) and

64 men who were diagnosed with CIN3 or invasive cervical carcinoma after a short latency.

65 Our data imply that the presence of HPVs in cervical carcinomas alleviates the requirement for RASSF

66 Invasive cervical carcinomas almost invariably carry extra copies

67 The rate ratio for invasive cervical carcinoma among all women from recruitment to e

68 In the case of cervical carcinomas, an increasing body of evidence impl

69 25 married women with invasive squamous cell cervical carcinoma and 791 hospitalized controls, all of

70 sal human papilloma viruses, including human cervical carcinoma and a growing number of head-and-neck

71 man papillomaviruses (HPVs) cause almost all cervical carcinoma and a significant percentage of other

72 omavirus (HPV) infections cause nearly every cervical carcinoma and a subset of tumors in the orophar

73 of CD46 also blocked Ad37 infection of human cervical carcinoma and conjunctival cells, indicating a

74 bined chemotherapy and radiation therapy for cervical carcinoma and evaluate the risk of local recurr

75 squamous cell and 42 women with adenomatous cervical carcinoma and from 291 hospitalized controls di

76 metastasis in patients with locally advanced cervical carcinoma and no evidence of extrapelvic diseas

77 ADCs from invasive cervical carcinoma and nontumor regions were compared wi

78 The incidences of cervical carcinoma and of high-grade dysplasia (CIN 3) w

79 We find that specific OAT knockdown in human cervical carcinoma and osteosarcoma cells by RNA interfe

80 year-old woman with stage IIIB squamous cell cervical carcinoma and patient B is a 37-year-old woman

81 here to investigate the association between cervical carcinoma and pattern of oral contraceptive use

82 V-16 and HPV-18, are the causative agents of cervical carcinomas and are linked to several other tumo

83 e etiologically linked to the development of cervical carcinomas and contribute to a number of other

84 HPVs) are the causative agents of almost all cervical carcinomas and many other tumors, including man

85 ported to occur in three of 12 (25%) uterine cervical carcinomas and nine of 26 (35%) bladder carcino

86 d mutational analysis of FGFR3 in 51 primary cervical carcinomas and seven cervical carcinoma-derived

87 rst time the induction of CSF-1 and c-fms in cervical carcinomas and suggest that c-fms activation ma

88 FGFR3 are associated with multiple myeloma, cervical carcinoma, and bladder cancer.

89 al tumour types including bladder carcinoma, cervical carcinoma, and multiple myeloma.

90 ], anal/rectal SCC, vulvar SCC, vaginal SCC, cervical carcinoma, and penile SCC) cancers from the US

91 ssion in cervical cancer cell lines, primary cervical carcinomas, and normal tissues.

92 ing the induction of aromatase expression in cervical carcinomas, and opens the possibility that arom

93 18 are associated with the majority of human cervical carcinomas, and two viral genes, HPV E6 and E7,

94 derlying down-regulation of ESR1 in invasive cervical carcinomas appear to be complex and likely hete

95 penile carcinoma (42%) is lower than that in cervical carcinoma (approximately 100%) and similar to v

96 ADCs from invasive cervical carcinoma are significantly lower than those fr

97 Cervical carcinomas are almost universally associated wi

98 hromosome segments that are often altered in cervical carcinomas are also frequently altered in sever

99 Over 95% of cervical carcinomas are human papillomavirus (HPV) DNA p

100 Cervical carcinomas are initiated through a series of we

101 Greater than 90% of all cervical carcinomas are positive for HPV infection.

102 The higher overall incidence of LOH in cervical carcinomas as compared to other cancers, and th

103 geal, gastric, colorectal, renal, breast and cervical carcinomas, as well as non-Hodgkin, Hodgkin and

104 nner in carcinoma cell lines including HeLa (cervical carcinoma), BG-1 (ovarian carcinoma), and IGROV

105 anscription factor is overexpressed in human cervical carcinoma biopsies and is able to activate expr

106 Finally, human cervical carcinoma biopsies showed almost complete elimi

107 of high-risk human papillomavirus (HPV) in a cervical carcinoma biopsy].

108 are associated with autoimmune diseases and cervical carcinoma, but it is not known whether they act

109 quent alterations in FHIT expression in many cervical carcinomas, but not in normal tissues, suggest

110 atin reduces the relative risk of death from cervical carcinoma by approximately 50% by decreasing lo

111 15 person-years) and identified 107 invasive cervical carcinomas by linkage with screening, pathology

112 Transfection into human cervical carcinoma C33A cells and mouse melanoma BL6 cel

113 4HPR-induced apoptosis in human cervical carcinoma C33A cells involves enhanced generati

114 We evaluated tumor tissue from invasive cervical carcinomas, carefully microdissected to elimina

115 r loci on chromosome 3p is a common event in cervical carcinoma (CC), the frequency and affected regi

116 es involved in the multistage development of cervical carcinoma (CC), we investigated the presence of

117 he long arm of chromosome 2 (2q) in invasive cervical carcinoma (CC).

118 ic changes that occur in the pathogenesis of cervical carcinoma (CC).

119 moter-binding protein 1 (MBP-1) from a human cervical carcinoma cell expression library which negativ

120 ulates c-myc promoter activity, from a human cervical carcinoma cell expression library.

121 e have investigated the situation in a human cervical carcinoma cell line (HeLa cells) and found that

122 subsequent isolation of the metastatic human cervical carcinoma cell line (HeLa cells) from normal hu

123 CaT) or transformed (HOK-16B-Bap-T) nor in a cervical carcinoma cell line (HeLa).

124 In HPV type 16-containing cervical carcinoma cell line Caski, E7 localizes to both

125 equirements between two unrelated cells, the cervical carcinoma cell line HeLa and the renal carcinom

126 ells but not in the T-cell line Molt4 or the cervical carcinoma cell line HeLa.

127 ical cancer cells, we infected HeLa cells, a cervical carcinoma cell line that contains HPV18 DNA, wi

128 minal repeat/beta-galactosidase cells (human cervical carcinoma cell line) and CEMx174 cells (human T

129 chain reaction analysis we determined that a cervical carcinoma cell line, C33A, lacks CD44 expressio

130 characterized the response of RR in a human cervical carcinoma cell line, Caski, after damage by ion

131 aled that overexpression of SPF45 in HeLa, a cervical carcinoma cell line, resulted in drug resistanc

132 Treatment of two human cervical carcinoma cell lines (HeLa and SiHa) with gelda

133 nscripts were readily demonstrated in 6 of 7 cervical carcinoma cell lines and 17 of 25 (68%) primary

134 s and other small RNA segments for six human cervical carcinoma cell lines and five normal cervical s

135 anti-E7 scFvs into the HPV16-positive human cervical carcinoma cell lines CaSki and SiHa and tested

136 ot seen in C-4I, ectocervical cells or other cervical carcinoma cell lines examined.

137 Thus, CD40 stimulation in cervical carcinoma cell lines expressing a TAP-dependent

138 us type 1 (BPV1) E2 protein in HeLa and HT-3 cervical carcinoma cell lines greatly reduced cellular p

139 18 (HPV18) URR enhancer and promoter in the cervical carcinoma cell lines HeLa and C4-II.

140 Six of 10 cervical carcinoma cell lines overexpressed ets-2 RNA su

141 apillomavirus E2 regulatory protein in human cervical carcinoma cell lines repressed expression of th

142 Only three colorectal and one cervical carcinoma cell lines were methylated at LKB1, a

143 The stimulation of CD40-positive cervical carcinoma cell lines with soluble CD40L (CD154)

144 antitumour potential selective to colon and cervical carcinoma cell lines) to be explored in the pha

145 illomaviruses (HPVs), along with HPV-induced cervical carcinoma cell lines, are excellent models for

146 A clonally related pair of cervical carcinoma cell lines, C-4I and C-4II, showed di

147 Here, we show that pretreatment of two cervical carcinoma cell lines, HeLa and SiHa, with curcu

148 bition of the proliferation of several human cervical carcinoma cell lines, including HeLa cells whic

149 ted reduced or absent FHIT expression in the cervical carcinoma cell lines, particularly those with a

150 nital epithelial cells and in HPV-containing cervical carcinoma cell lines.

151 complex for viral E6 expression in infected cervical carcinoma cell lines.

152 s exhibited enhanced apoptosis, whereas HeLa cervical carcinoma cells activated autophagy, blocked ap

153 gions of AAG mRNA were transfected into HeLa cervical carcinoma cells and A2780-SCA ovarian carcinoma

154 estern blotting we showed that HeLa and SiHa cervical carcinoma cells and human cervical carcinomas e

155 ein is required for optimal proliferation of cervical carcinoma cells and that the two viral proteins

156 the anti-angiogenic mechanism of bergenin in cervical carcinoma cells by modulation of multiple angio

157 7 expression in HPV16- and HPV18-transformed cervical carcinoma cells by RNA interference increased e

158 papillomavirus (HPV) type 18 E7 gene in HeLa cervical carcinoma cells by the bovine papillomavirus E2

159 Cervical carcinoma cells display high telomerase activit

160 Human cervical carcinoma cells exhibited progressively increas

161 chanism of repression of cell cycle genes in cervical carcinoma cells following E6/E7 repression, we

162 he expression of the p53 and p21 proteins in cervical carcinoma cells infected with high-risk human p

163 Transfection of NOL7 into cervical carcinoma cells inhibited their growth in mouse

164 iability of mesenchymal stem cells and human cervical carcinoma cells labeled with a combination of T

165 e expressed wild-type and mutant Rb in human cervical carcinoma cells lacking functional Rb.

166 As a well characterized model we chose cervical carcinoma cells positive for human papillomavir

167 HeLa cervical carcinoma cells rapidly undergo senescence when

168 Specific disruption of circE7 in CaSki cervical carcinoma cells reduces E7 protein levels and i

169 n of the bovine papillomavirus E2 protein in cervical carcinoma cells represses expression of integra

170 an antisense rp L23a sequence in human HeLa cervical carcinoma cells results in a reduction in colon

171 APF also inhibits the proliferation of HeLa cervical carcinoma cells that are known to express CKAP4

172 dramatically increase the susceptibility of cervical carcinoma cells to CD40L-induced apoptosis.

173 we use human diploid fibroblasts (HDFs) and cervical carcinoma cells to study this regulatory paradi

174 d to target and destroy the E6 or E7 gene in cervical carcinoma cells transformed by HPV, resulting i

175 odendrocyte progenitor CG-4 cells, and human cervical carcinoma cells were incubated 2-48 hours with

176 otch1 gene is markedly reduced in a panel of cervical carcinoma cells whereas expression of Notch2 re

177 (monkey kidney fibroblasts), and HeLa (human cervical carcinoma cells), hPR-A functions as a transcri

178 Rb, but activated B-myb in HeLa cells (human cervical carcinoma cells), which express a lower amount

179 ncluding HT-1080 (fibrosarcoma cells); HeLa (cervical carcinoma cells); A549 (lung carcinoma cells);

180 n MCF-7 breast cancer cells, HeLa and ME-180 cervical carcinoma cells, and NIH 3T3 cells but was with

181 components controlling the proliferation of cervical carcinoma cells, and that autocrine IGF-2 produ

182 ctively prevent senescence from occurring in cervical carcinoma cells, and that once viral oncogene e

183 man hematopoietic progenitor cells and human cervical carcinoma cells, both of which also express FR.

184 ition of HPV-positive, but not HPV-negative, cervical carcinoma cells, but exerts no such effects on

185 sage primary human fibroblasts and senescent cervical carcinoma cells, suggesting that this Rb family

186 hen both HPV oncogenes are repressed in HeLa cervical carcinoma cells, the dormant p53 and retinoblas

187 After expression of BEF in HeLa cervical carcinoma cells, we detected cleavage at E2 bin

188 Using HeLa human cervical carcinoma cells, we find that transfection of s

189 Using human C33A cervical carcinoma cells, which lack BRG1 and also expre

190 merase reverse transcriptase (hTERT) in HeLa cervical carcinoma cells.

191 nance of the proliferative phenotype of HeLa cervical carcinoma cells.

192 Similar results were obtained in HT-3 cervical carcinoma cells.

193 is required to maintain the proliferation of cervical carcinoma cells.

194 ed the cytotoxic effect of cisplatin in HeLa cervical carcinoma cells.

195 tein encoded by integrated HPV18 DNA in HeLa cervical carcinoma cells.

196 e gene linked to the cdc25A promoter in HT-3 cervical carcinoma cells.

197 ignaling pathway was evaluated in human SiHa cervical carcinoma cells.

198 tion in both HL-60 cells and HeLa epithelial cervical carcinoma cells.

199 concentration at the translational level in cervical carcinoma cells.

200 in 3 and MMP-9 (Matrix Metalloprotease 9) in cervical carcinoma cells.

201 es leading to growth cessation in HeLa human cervical carcinoma cells.

202 for the anchorage-independent growth of HeLa cervical carcinoma cells.

203 ircRNAs interacting with AUF1 in HeLa (human cervical carcinoma) cells, we focused on hsa_circ_003243

204 s 60-70% greater protection against invasive cervical carcinomas compared with cytology.

205 s and its ligand are significantly higher in cervical carcinomas compared with normal samples.

206 ent or reduced in lung, stomach, kidney, and cervical carcinomas, consistent with function as a tumor

207 rvical intraepithelial neoplasias as well as cervical carcinomas, consistent with studies in HPV-posi

208 al load, RNA expression patterns typical for cervical carcinomas (CxCaRNA(+)), and the HPV-targeted t

209 uthern blot analysis of DNA from five of the cervical carcinomas demonstrated alterations in four of

210 apoptosis of Stat1 and Stat3, we studied the cervical carcinoma-derived cell line, Me180, which under

211 3000 genotypes from 89 primary tumors and 10 cervical carcinoma-derived cell lines and showed that fi

212 in 51 primary cervical carcinomas and seven cervical carcinoma-derived cell lines.

213 otein to the nucleus of breast, ovarian, and cervical carcinoma-derived cell lines.

214 stitutive expression of exogenous MT1-MMP in cervical carcinoma-derived cells and HPV-immortalized ke

215 d replication initiation protein E1, whereas cervical carcinoma-derived, HPV-18-positive HeLa cells o

216 and SiHa cervical carcinoma cells and human cervical carcinomas express EpoR, and that hypoxia enhan

217 Most cervical carcinomas express high-risk human papillomavir

218 itors may be potential therapeutic agents in cervical carcinomas expressing aromatase.

219 on observed in vitro paralleled that seen in cervical carcinomas expressing aromatase.

220 thought to be lost during the progression to cervical carcinoma following integration of HPV DNA into

221 Invasive cervical carcinomas frequently reveal additional copies

222 ts with metastatic, persistent, or recurrent cervical carcinoma from 81 centres in the USA, Canada, a

223 f the same 3p segments have been reported in cervical carcinomas from different parts of the world.

224 ggest the cell of origin of 279 HPV-positive cervical carcinomas from The Cancer Genome Atlas and to

225 of the mutant virus into p53-deficient human cervical carcinomas grown in nude mice caused a signific

226 umors, and, in the case of adolescent girls, cervical carcinomas, has been reported in HIV-infected c

227 of heterozygosity (LOH) analyses of invasive cervical carcinomas have identified several chromosomal

228 eral neuroepithelioma (PNET) cell line and a cervical carcinoma HeLa cell line which exhibits efficie

229 g easy-to-transfect cancer cells (e.g. human cervical carcinoma HeLa cell line) as well as hard-to-tr

230 encing of RNA prepared using RPAD from human cervical carcinoma HeLa cells and mouse C2C12 myoblasts

231 regulation of HIF-1alpha expression in human cervical carcinoma HeLa cells responding to the hypoxia

232 Continuous exposure of human cervical carcinoma HeLa cells to 50 ng/ml paclitaxel res

233 Here, exposure of breast carcinoma MCF-7 or cervical carcinoma HeLa cells to anticancer agents, incl

234 Here, we employed human cervical carcinoma HeLa cells to test the hypothesis tha

235 In human cervical carcinoma HeLa cells, analysis of a traceable N

236 HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its associatio

237 In human cervical carcinoma HeLa cells, the RNA-binding protein H

238 diating cisplatin-induced apoptosis of human cervical carcinoma HeLa cells.

239 of the enzyme, SHP-1-(Cys --> Ser), in human cervical carcinoma HeLa cells.

240 cloned from normal human kidney and from the cervical carcinoma HeLa S3 predict a bipartite structure

241 orm of Cdc42 (Cdc42 F28L), or from the human cervical carcinoma (HeLa) cell line, inhibits the abilit

242 vely) growth and regression of labeled human cervical carcinoma (HeLa) cells engrafted into immunodef

243 hepatocellular carcinoma (HepG2), and human cervical carcinoma (HeLa) cells.

244 The expression of folate receptors (FRs) in cervical carcinoma (HeLa-IU1) cells was modulated by sta

245 In most invasive cervical carcinomas, high-risk human papillomavirus (HPV

246 individuals are at high risk for developing cervical carcinoma; however, the molecular mechanisms th

247 hoblastic leukemia (i.e. CEM and MOLT-4) and cervical carcinoma (i.e. HeLa) cells was shown to be ass

248 rvical dysplasia and progression to invasive cervical carcinoma (ICC).

249 stases derived from human colon carcinoma or cervical carcinoma in a mouse model.

250 dent observers to identify possible invasive cervical carcinoma in group 2, patients with suspected d

251 iated with different risks of progression to cervical carcinoma in infected humans.

252 The risks of cervical carcinoma in monogamous women and of oncogenic

253 examine the physical status of HPV-16 in 126 cervical carcinoma in situ and 92 invasive cervical canc

254 Finally, immunohistochemical analyses of cervical carcinoma in situ and primary tumors have shown

255 The cumulative incidence of invasive cervical carcinoma in women with negative entry tests wa

256 ndocrine tumors (PNETs) in RIP-Tag2 mice and cervical carcinomas in HPV16/E2 mice.

257 Recent data in cervical carcinomas in patients suggest that fractionate

258 (HPV-16) genome is commonly present in human cervical carcinoma, in which a subset of the viral genes

259 en Jan 1, 2011 and Dec 31, 2021, the overall cervical carcinoma incidence was 30.4 cases per 100 000

260 ne is commonly associated with malignancy in cervical carcinoma, indicating that E2 has a role in reg

261 n cancer cells converts metastatic PNETs and cervical carcinomas into benign lesions.

262 Cervical carcinoma is an AIDS-defining illness.

263 the posttherapy evaluation of patients with cervical carcinoma is predictive of survival outcome.

264 Cervical carcinoma is the most prevalent malignancy seco

265 Progression to advanced-stage cervical carcinomas is characterized by a recurrent patt

266 high-risk human papilloma viruses (HPVs) in cervical carcinomas is well established.

267 In this in vitro experimental cervical carcinoma model, primary human keratinocytes im

268 eport whole-exome sequencing analysis of 115 cervical carcinoma-normal paired samples, transcriptome

269 th measurable stage IVB persistent/recurrent cervical carcinoma not amenable to curative therapy and

270 vity and specificity to help detect invasive cervical carcinoma on T2-weighted images were 55.6% and

271 90/NF45 function could assist in controlling cervical carcinoma.Oncogene advance online publication,

272 illomavirus, such as type 18 (HPV-18), cause cervical carcinoma, one of the most frequent causes of c

273 lar factors necessary for the progression to cervical carcinoma only occurs in a minority of those in

274 tients with newly diagnosed locally advanced cervical carcinomas or recurrences after surgery undergo

275 NA generated only pseudo-revertants in HeLa (cervical carcinoma) or SK-N-SH (neuroblastoma) cells.

276 HPV 18-related cervical carcinomas, particularly those diagnosed at an

277 he most common high-risk HPV associated with cervical carcinoma, preferentially integrates at loci co

278 in HPV16 L1 isolated from high-grade CIN or cervical carcinoma prevent self-assembly of L1 VLPs.

279 f LOH patterns found, suggest that different cervical carcinomas probably arise and/or progress, in p

280 virus in the cases of gastric non-cardia and cervical carcinomas, respectively.

281 nuclear staining of beta-catenin in invasive cervical carcinoma samples from 48 patients.

282 ponsible for the second peak in incidence of cervical carcinoma seen in older women.

283 In vulvar and cervical carcinomas, sentinel node identification may si

284 is message is especially abundant in HeLa S3 cervical carcinoma, SW480 adenocarcinoma, and A549 lung

285 rt a novel finding that approximately 35% of cervical carcinomas tested (n = 19) express aromatase, t

286 ate several recurrent genomic alterations in cervical carcinomas that suggest new strategies to comba

287 Cervical carcinoma, the second leading cause of cancer d

288 volvement and in showing the relationship of cervical carcinoma to the internal os and, hence, the pa

289 Thirty patients with early cervical carcinoma underwent MR imaging with use of a 1.

290 test-retest imaging study, 10 patients with cervical carcinoma underwent PET on separate days with (

291 ade 2 or 3, adenocarcinoma in situ, invasive cervical carcinoma), vulvar disease (vulvar intraepithel

292 Detection of invasive cervical carcinoma was similar between screening methods

293 d threshold ADC level indicative of invasive cervical carcinoma was used with T2-weighted imaging by

294 hypoxia has prognostic significance in human cervical carcinomas, we examined the relationship betwee

295 t the 3p region in ovarian, endometrial, and cervical carcinomas, we examined the status of the FHIT

296 e Gynecologie et d'Obstetrique (FIGO) IA-IIB cervical carcinoma were included between March 2016 and

297 12 serous ovarian carcinomas and 10 squamous cervical carcinomas were analyzed and were negative for

298 16 (HPV16) is the primary etiologic agent of cervical carcinoma, whereas bovine papillomavirus type 1

299 ation of Gynecology and Obstetrics stage IB1 cervical carcinoma who underwent attempted radical trach

300 eliminated detectable clonogens in some SiHa cervical carcinoma xenografts, and in combination with g