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1 apillomavirus (HR-HPV) causes nearly 100% of cervical carcinoma.
2 lomavirus (HPV), such as HPV 16, cause human cervical carcinoma.
3 V-16), which is prevalent in the etiology of cervical carcinoma.
4 rognostic sign in women with HPV 16 positive cervical carcinoma.
5 strongly associated with the development of cervical carcinoma.
6 strongly associated with the development of cervical carcinoma.
7 lomavirus (HPV), such as HPV 16, cause human cervical carcinoma.
8 atment approaches for patients with invasive cervical carcinoma.
9 0% of patients (eight of 16) with measurable cervical carcinoma.
10 ated in bladder carcinoma and only rarely in cervical carcinoma.
11 at has been implicated in the development of cervical carcinoma.
12 alignant lesions and is a necessary cause of cervical carcinoma.
13 omavirus (HPV) genotypes are associated with cervical carcinoma.
14 treatment of patients with locally advanced cervical carcinoma.
15 finding that p16 hypermethylation occurs in cervical carcinoma.
16 curcumin for the treatment of HPV18-infected cervical carcinoma.
17 was found associated with the development of cervical carcinoma.
18 U6 gene might be useful for gene therapy of cervical carcinoma.
19 their association with severe dysplasia and cervical carcinoma.
20 PT-11 has significant activity in refractory cervical carcinoma.
21 sition from severe dysplasia/CIS to invasive cervical carcinoma.
22 l) were calculated for incidence of invasive cervical carcinoma.
23 r therapy for patients with early ovarian or cervical carcinoma.
24 rized site of HPV16 integration in a primary cervical carcinoma.
25 90/NF45 function could assist in controlling cervical carcinoma.
26 cal intraepithelial neoplasia, but not frank cervical carcinoma.
27 are considered the major causative agents of cervical carcinoma.
28 ublet combinations in advanced and recurrent cervical carcinoma.
29 or is a key promoter of tumor progression in cervical carcinoma.
30 owth of malignant tumors in a mouse model of cervical carcinoma.
31 es found in lung squamous cell carcinoma and cervical carcinoma.
32 andard for the treatment of locally advanced cervical carcinoma.
33 iated with different risks of progression to cervical carcinoma.
34 on of CD40, a TNF receptor family member, in cervical carcinomas.
35 the only FGFR3 mutation described to date in cervical carcinomas.
36 patients with multiple myeloma, bladder and cervical carcinomas.
37 rating cells of the infected epithelia or in cervical carcinomas.
38 ) are consistently expressed in HPV-positive cervical carcinomas.
39 pithelia, low and high grade dysplasias, and cervical carcinomas.
40 ss of Fhit protein in 25 of 33 (76%) primary cervical carcinomas.
41 (3p13-21.1) have been observed frequently in cervical carcinomas.
42 way plays a major role in the development of cervical carcinomas.
43 cinoma cell lines and 17 of 25 (68%) primary cervical carcinomas.
44 ich are responsible for anogenital warts and cervical carcinomas.
45 ted etiologically with the majority of human cervical carcinomas.
46 has been observed for invasive squamous cell cervical carcinomas.
47 be important in the origin or progression of cervical carcinomas.
48 considered at increased risk of adenomatous cervical carcinomas.
49 py-number alterations in the pathogenesis of cervical carcinomas.
50 sease; HPV is now implicated in up to 90% of cervical carcinomas.
51 E6, E7, and L1 genes in flash-frozen HPV-16 cervical carcinomas.
52 and HPV18 are causative agents of most human cervical carcinomas.
53 contribute to oncogenesis in endometrial and cervical carcinomas.
54 aviruses (HPVs) are present in virtually all cervical carcinomas.
55 vulvar carcinoma and metastatic melanoma, 1 cervical carcinoma, 1 Bowen disease of the vulva, and 1
59 Our data imply that the presence of HPVs in cervical carcinomas alleviates the requirement for RASSF
63 25 married women with invasive squamous cell cervical carcinoma and 791 hospitalized controls, all of
64 sal human papilloma viruses, including human cervical carcinoma and a growing number of head-and-neck
65 man papillomaviruses (HPVs) cause almost all cervical carcinoma and a significant percentage of other
66 omavirus (HPV) infections cause nearly every cervical carcinoma and a subset of tumors in the orophar
67 of CD46 also blocked Ad37 infection of human cervical carcinoma and conjunctival cells, indicating a
68 bined chemotherapy and radiation therapy for cervical carcinoma and evaluate the risk of local recurr
69 squamous cell and 42 women with adenomatous cervical carcinoma and from 291 hospitalized controls di
70 metastasis in patients with locally advanced cervical carcinoma and no evidence of extrapelvic diseas
73 We find that specific OAT knockdown in human cervical carcinoma and osteosarcoma cells by RNA interfe
74 year-old woman with stage IIIB squamous cell cervical carcinoma and patient B is a 37-year-old woman
75 here to investigate the association between cervical carcinoma and pattern of oral contraceptive use
76 V-16 and HPV-18, are the causative agents of cervical carcinomas and are linked to several other tumo
77 e etiologically linked to the development of cervical carcinomas and contribute to a number of other
78 HPVs) are the causative agents of almost all cervical carcinomas and many other tumors, including man
79 ported to occur in three of 12 (25%) uterine cervical carcinomas and nine of 26 (35%) bladder carcino
80 d mutational analysis of FGFR3 in 51 primary cervical carcinomas and seven cervical carcinoma-derived
81 rst time the induction of CSF-1 and c-fms in cervical carcinomas and suggest that c-fms activation ma
85 ing the induction of aromatase expression in cervical carcinomas, and opens the possibility that arom
86 18 are associated with the majority of human cervical carcinomas, and two viral genes, HPV E6 and E7,
87 derlying down-regulation of ESR1 in invasive cervical carcinomas appear to be complex and likely hete
88 penile carcinoma (42%) is lower than that in cervical carcinoma (approximately 100%) and similar to v
91 hromosome segments that are often altered in cervical carcinomas are also frequently altered in sever
96 geal, gastric, colorectal, renal, breast and cervical carcinomas, as well as non-Hodgkin, Hodgkin and
97 nner in carcinoma cell lines including HeLa (cervical carcinoma), BG-1 (ovarian carcinoma), and IGROV
98 anscription factor is overexpressed in human cervical carcinoma biopsies and is able to activate expr
100 are associated with autoimmune diseases and cervical carcinoma, but it is not known whether they act
101 quent alterations in FHIT expression in many cervical carcinomas, but not in normal tissues, suggest
102 atin reduces the relative risk of death from cervical carcinoma by approximately 50% by decreasing lo
103 15 person-years) and identified 107 invasive cervical carcinomas by linkage with screening, pathology
106 We evaluated tumor tissue from invasive cervical carcinomas, carefully microdissected to elimina
107 r loci on chromosome 3p is a common event in cervical carcinoma (CC), the frequency and affected regi
108 es involved in the multistage development of cervical carcinoma (CC), we investigated the presence of
111 moter-binding protein 1 (MBP-1) from a human cervical carcinoma cell expression library which negativ
113 e have investigated the situation in a human cervical carcinoma cell line (HeLa cells) and found that
114 subsequent isolation of the metastatic human cervical carcinoma cell line (HeLa cells) from normal hu
117 equirements between two unrelated cells, the cervical carcinoma cell line HeLa and the renal carcinom
119 ical cancer cells, we infected HeLa cells, a cervical carcinoma cell line that contains HPV18 DNA, wi
120 minal repeat/beta-galactosidase cells (human cervical carcinoma cell line) and CEMx174 cells (human T
121 chain reaction analysis we determined that a cervical carcinoma cell line, C33A, lacks CD44 expressio
122 characterized the response of RR in a human cervical carcinoma cell line, Caski, after damage by ion
123 aled that overexpression of SPF45 in HeLa, a cervical carcinoma cell line, resulted in drug resistanc
125 nscripts were readily demonstrated in 6 of 7 cervical carcinoma cell lines and 17 of 25 (68%) primary
126 s and other small RNA segments for six human cervical carcinoma cell lines and five normal cervical s
127 anti-E7 scFvs into the HPV16-positive human cervical carcinoma cell lines CaSki and SiHa and tested
130 us type 1 (BPV1) E2 protein in HeLa and HT-3 cervical carcinoma cell lines greatly reduced cellular p
133 apillomavirus E2 regulatory protein in human cervical carcinoma cell lines repressed expression of th
136 antitumour potential selective to colon and cervical carcinoma cell lines) to be explored in the pha
137 illomaviruses (HPVs), along with HPV-induced cervical carcinoma cell lines, are excellent models for
140 bition of the proliferation of several human cervical carcinoma cell lines, including HeLa cells whic
141 ted reduced or absent FHIT expression in the cervical carcinoma cell lines, particularly those with a
144 s exhibited enhanced apoptosis, whereas HeLa cervical carcinoma cells activated autophagy, blocked ap
145 gions of AAG mRNA were transfected into HeLa cervical carcinoma cells and A2780-SCA ovarian carcinoma
146 estern blotting we showed that HeLa and SiHa cervical carcinoma cells and human cervical carcinomas e
147 ein is required for optimal proliferation of cervical carcinoma cells and that the two viral proteins
148 7 expression in HPV16- and HPV18-transformed cervical carcinoma cells by RNA interference increased e
149 papillomavirus (HPV) type 18 E7 gene in HeLa cervical carcinoma cells by the bovine papillomavirus E2
152 chanism of repression of cell cycle genes in cervical carcinoma cells following E6/E7 repression, we
153 he expression of the p53 and p21 proteins in cervical carcinoma cells infected with high-risk human p
155 iability of mesenchymal stem cells and human cervical carcinoma cells labeled with a combination of T
159 n of the bovine papillomavirus E2 protein in cervical carcinoma cells represses expression of integra
160 an antisense rp L23a sequence in human HeLa cervical carcinoma cells results in a reduction in colon
161 APF also inhibits the proliferation of HeLa cervical carcinoma cells that are known to express CKAP4
162 dramatically increase the susceptibility of cervical carcinoma cells to CD40L-induced apoptosis.
163 we use human diploid fibroblasts (HDFs) and cervical carcinoma cells to study this regulatory paradi
164 d to target and destroy the E6 or E7 gene in cervical carcinoma cells transformed by HPV, resulting i
165 odendrocyte progenitor CG-4 cells, and human cervical carcinoma cells were incubated 2-48 hours with
166 otch1 gene is markedly reduced in a panel of cervical carcinoma cells whereas expression of Notch2 re
167 (monkey kidney fibroblasts), and HeLa (human cervical carcinoma cells), hPR-A functions as a transcri
168 Rb, but activated B-myb in HeLa cells (human cervical carcinoma cells), which express a lower amount
169 ncluding HT-1080 (fibrosarcoma cells); HeLa (cervical carcinoma cells); A549 (lung carcinoma cells);
170 n MCF-7 breast cancer cells, HeLa and ME-180 cervical carcinoma cells, and NIH 3T3 cells but was with
171 components controlling the proliferation of cervical carcinoma cells, and that autocrine IGF-2 produ
172 ctively prevent senescence from occurring in cervical carcinoma cells, and that once viral oncogene e
173 man hematopoietic progenitor cells and human cervical carcinoma cells, both of which also express FR.
174 ition of HPV-positive, but not HPV-negative, cervical carcinoma cells, but exerts no such effects on
175 sage primary human fibroblasts and senescent cervical carcinoma cells, suggesting that this Rb family
176 hen both HPV oncogenes are repressed in HeLa cervical carcinoma cells, the dormant p53 and retinoblas
194 ent or reduced in lung, stomach, kidney, and cervical carcinomas, consistent with function as a tumor
195 al load, RNA expression patterns typical for cervical carcinomas (CxCaRNA(+)), and the HPV-targeted t
196 uthern blot analysis of DNA from five of the cervical carcinomas demonstrated alterations in four of
197 apoptosis of Stat1 and Stat3, we studied the cervical carcinoma-derived cell line, Me180, which under
198 3000 genotypes from 89 primary tumors and 10 cervical carcinoma-derived cell lines and showed that fi
201 stitutive expression of exogenous MT1-MMP in cervical carcinoma-derived cells and HPV-immortalized ke
202 d replication initiation protein E1, whereas cervical carcinoma-derived, HPV-18-positive HeLa cells o
203 and SiHa cervical carcinoma cells and human cervical carcinomas express EpoR, and that hypoxia enhan
207 thought to be lost during the progression to cervical carcinoma following integration of HPV DNA into
209 ts with metastatic, persistent, or recurrent cervical carcinoma from 81 centres in the USA, Canada, a
210 f the same 3p segments have been reported in cervical carcinomas from different parts of the world.
211 of the mutant virus into p53-deficient human cervical carcinomas grown in nude mice caused a signific
212 umors, and, in the case of adolescent girls, cervical carcinomas, has been reported in HIV-infected c
213 of heterozygosity (LOH) analyses of invasive cervical carcinomas have identified several chromosomal
214 eral neuroepithelioma (PNET) cell line and a cervical carcinoma HeLa cell line which exhibits efficie
215 encing of RNA prepared using RPAD from human cervical carcinoma HeLa cells and mouse C2C12 myoblasts
216 regulation of HIF-1alpha expression in human cervical carcinoma HeLa cells responding to the hypoxia
218 Here, exposure of breast carcinoma MCF-7 or cervical carcinoma HeLa cells to anticancer agents, incl
221 HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its associatio
225 cloned from normal human kidney and from the cervical carcinoma HeLa S3 predict a bipartite structure
226 orm of Cdc42 (Cdc42 F28L), or from the human cervical carcinoma (HeLa) cell line, inhibits the abilit
227 vely) growth and regression of labeled human cervical carcinoma (HeLa) cells engrafted into immunodef
229 The expression of folate receptors (FRs) in cervical carcinoma (HeLa-IU1) cells was modulated by sta
231 individuals are at high risk for developing cervical carcinoma; however, the molecular mechanisms th
232 hoblastic leukemia (i.e. CEM and MOLT-4) and cervical carcinoma (i.e. HeLa) cells was shown to be ass
234 dent observers to identify possible invasive cervical carcinoma in group 2, patients with suspected d
237 examine the physical status of HPV-16 in 126 cervical carcinoma in situ and 92 invasive cervical canc
238 Finally, immunohistochemical analyses of cervical carcinoma in situ and primary tumors have shown
242 (HPV-16) genome is commonly present in human cervical carcinoma, in which a subset of the viral genes
243 ne is commonly associated with malignancy in cervical carcinoma, indicating that E2 has a role in reg
246 the posttherapy evaluation of patients with cervical carcinoma is predictive of survival outcome.
251 eport whole-exome sequencing analysis of 115 cervical carcinoma-normal paired samples, transcriptome
252 th measurable stage IVB persistent/recurrent cervical carcinoma not amenable to curative therapy and
253 vity and specificity to help detect invasive cervical carcinoma on T2-weighted images were 55.6% and
254 90/NF45 function could assist in controlling cervical carcinoma.Oncogene advance online publication,
255 illomavirus, such as type 18 (HPV-18), cause cervical carcinoma, one of the most frequent causes of c
256 lar factors necessary for the progression to cervical carcinoma only occurs in a minority of those in
257 NA generated only pseudo-revertants in HeLa (cervical carcinoma) or SK-N-SH (neuroblastoma) cells.
259 he most common high-risk HPV associated with cervical carcinoma, preferentially integrates at loci co
260 in HPV16 L1 isolated from high-grade CIN or cervical carcinoma prevent self-assembly of L1 VLPs.
261 f LOH patterns found, suggest that different cervical carcinomas probably arise and/or progress, in p
265 is message is especially abundant in HeLa S3 cervical carcinoma, SW480 adenocarcinoma, and A549 lung
266 rt a novel finding that approximately 35% of cervical carcinomas tested (n = 19) express aromatase, t
267 ate several recurrent genomic alterations in cervical carcinomas that suggest new strategies to comba
269 volvement and in showing the relationship of cervical carcinoma to the internal os and, hence, the pa
271 test-retest imaging study, 10 patients with cervical carcinoma underwent PET on separate days with (
272 ade 2 or 3, adenocarcinoma in situ, invasive cervical carcinoma), vulvar disease (vulvar intraepithel
274 d threshold ADC level indicative of invasive cervical carcinoma was used with T2-weighted imaging by
275 hypoxia has prognostic significance in human cervical carcinomas, we examined the relationship betwee
276 t the 3p region in ovarian, endometrial, and cervical carcinomas, we examined the status of the FHIT
277 12 serous ovarian carcinomas and 10 squamous cervical carcinomas were analyzed and were negative for
278 16 (HPV16) is the primary etiologic agent of cervical carcinoma, whereas bovine papillomavirus type 1
279 ation of Gynecology and Obstetrics stage IB1 cervical carcinoma who underwent attempted radical trach
280 eliminated detectable clonogens in some SiHa cervical carcinoma xenografts, and in combination with g
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