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1 tant metastases compared with in the primary cervical tumor.
2   Seven patients had palliative debulking of cervical tumor.
3 tures extracted from (18)F-FDG PET images of cervical tumors.
4 CS-1, a cytosolic sorting protein in primary cervical tumors.
5 the sites of HPV16 integration in 26 primary cervical tumors.
6  have been disrupted by HPV18 integration in cervical tumors.
7  preferred sites of integration for HPV18 in cervical tumors.
8 play an important role in the development of cervical tumors.
9 y expressed in advanced stages of breast and cervical tumors.
10 g the sites of HPV16 integrations in primary cervical tumors.
11 luorodeoxyglucose was taken up by 91% of the cervical tumors.
12  regions of chromosome 4 commonly altered in cervical tumors.
13 and 19p are involved in LOH in 20-33% of the cervical tumors.
14 on through RNA-Seq analysis of human primary cervical tumors.
15              LOH of 17p was found in 5 (15%) cervical tumors; 2 of these were HPV negative and expres
16 onist, is downregulated in all human primary cervical tumors and cell lines analyzed.
17                                          For cervical tumors and cell lines combined, the Pearson's c
18                                 HPV-positive cervical tumors and human papillomavirus-positive cell l
19 erns in cervical cancer, a series of primary cervical tumors and normal control samples were studied
20 ate a consistent expression of L1 in primary cervical tumors and the possibility of inducing effectiv
21 ittle data, if any, are available on whether cervical tumors are responsive to stimulation by the mac
22  is required for expression of E6E7 mRNAs in cervical tumor but not nontumor cells and may act by inh
23 ion of the POU2F3 promoter in 18 of 46 (39%) cervical tumors but never in normal epithelium.
24 op-2 expression was evaluated in 147 primary cervical tumors by immunohistochemistry, real-time polym
25 l of the cervical cancer cell lines, primary cervical tumor cell cultures, and normal ectocervical cu
26 in human cervical cancer cell lines, primary cervical tumor cell cultures, and normal ectocervical ep
27 hylation occurs heterogeneously within early cervical tumor cell populations that are separate from t
28        Endothelial cells and 3D spheroids of cervical tumor cells were co-cultured in the networks.
29 viously showed that curcumin radiosensitizes cervical tumor cells without increasing the cytotoxic ef
30 iquitin-proteasome pathway in HPV-containing cervical tumor cells.
31                      Greater than 99% of all cervical tumors contain HPV DNA.
32 FRA3B gene expression analysis on a panel of cervical tumor-derived cell lines revealed that three of
33 ise appearance of kinase requirements during cervical tumor development.
34 y in human keratinocytes, a model system for cervical tumor formation.
35  data demonstrate that HPV16 integrations in cervical tumors frequently occur within CFSs at the mole
36                              Our analysis of cervical tumors from four separate data sets found a sig
37 A promoter methylation may lead to selective cervical tumor growth.
38                    In conclusion, Guatemalan cervical tumors have a high frequency of very high-risk
39                  Using highly adherent human cervical tumor (HeLa) cells as a model system, cell adhe
40                      Here, we report that in cervical tumors, HPV-18, -39, and -45 transcribe E6/E7 m
41 ; AC) for two HPV types commonly observed in cervical tumors, HPV16 and HPV18.
42 ivo and suppressed the growth of xenografted cervical tumor implanted in nude mouse.
43 igh-grade cervical dysplasia and established cervical tumors, indicating that they depend on the cont
44                            Recently an HPV16 cervical tumor integration, 2 Mb centromeric to the publ
45 egulator of HPV16 oncoprotein expression and cervical tumor maintenance.
46  identified in the expression profile of the cervical tumor microenvironment.
47 xamined the expression of c-fms and CSF-1 in cervical tumor (n = 17) and normal cervix (n = 8) sample
48 a (CIN) found on smear (n = 20) or stage Ib1 cervical tumors (n = 18).
49 demonstrate that 11/23 HPV16 integrations in cervical tumors occurred within CFSs (P&<0.001).
50 served in squamous cell carcinomas (SCC) and cervical tumors of glandular origin (e.g., adenocarcinom
51 e identified 27 unique HPV18 integrations in cervical tumors, of which 63% (P<0.001) occur in CFSs.
52 ificant difference in NADPH was seen between cervical tumor orthotopic implants in vivo, without a co
53 tly better than CT (AUC, 0.73) for detecting cervical tumors (P = .014).
54 d most prevalent high-risk HPV type found in cervical tumors, preferentially targets the CFSs.
55 found that MT1-MMP expression increases with cervical tumor progression (Spearman correlation coeffic
56 esting that SRSF2 has oncogenic functions in cervical tumor progression.
57 increased levels of SRSFs 1, 2, and 3 during cervical tumor progression.
58 hat appear to be required for HPV-associated cervical tumor progression.
59 important genetic alteration contributing to cervical tumor progression.
60 Multimers of the HPV genome are generated in cervical tumors replicating as extrachromosomal episomes
61   Genomic sequencing on 36 paired normal and cervical tumors revealed several somatic mutations and n
62       Here we show that approximately 95% of cervical tumor samples examined overexpress Cat-1, sugge
63 l-derived tumorigenic hybrids, and a primary cervical tumor, suggesting the presence of a tumor suppr
64 a 300-kb minimal area of deletion in primary cervical tumors that overlaps with deletions observed in
65  of human tumors and can in part explain why cervical tumors that possess low pO2 values are more agg
66 de resolution confirm that in HPV18-positive cervical tumors, the region surrounding c-myc is indeed
67 lation with aberrant CCND1 protein levels in cervical tumor tissue lysates.
68 xpression of the FHIT gene may be altered in cervical tumor tissue, potentially implicating this gene
69 s iners reprograms metabolic capabilities of cervical tumors to support chemoradiotherapy resistance.
70 uman integration events in 16 HPV16-positive cervical tumors using the Nanopore long-read sequencing
71 ine whether 11q13 deletions occur in primary cervical tumors, we analysed 36 tumors using 20 differen
72  total RNA samples from breast, ovarian, and cervical tumors were either undetectable (breast and cer
73 in a broad array of carcinomas, including in cervical tumors, where it has both diagnostic and progno