ライフサイエンスコーパス: cervical tumor

1 tant metastases compared with in the primary cervical tumor.

2 Seven patients had palliative debulking of cervical tumor.

3 y expressed in advanced stages of breast and cervical tumors.

4 the sites of HPV16 integration in 26 primary cervical tumors.

5 have been disrupted by HPV18 integration in cervical tumors.

6 preferred sites of integration for HPV18 in cervical tumors.

7 play an important role in the development of cervical tumors.

8 g the sites of HPV16 integrations in primary cervical tumors.

9 luorodeoxyglucose was taken up by 91% of the cervical tumors.

10 regions of chromosome 4 commonly altered in cervical tumors.

11 and 19p are involved in LOH in 20-33% of the cervical tumors.

12 LOH of 17p was found in 5 (15%) cervical tumors; 2 of these were HPV negative and expres

13 onist, is downregulated in all human primary cervical tumors and cell lines analyzed.

14 For cervical tumors and cell lines combined, the Pearson's c

15 HPV-positive cervical tumors and human papillomavirus-positive cell l

16 erns in cervical cancer, a series of primary cervical tumors and normal control samples were studied

17 ate a consistent expression of L1 in primary cervical tumors and the possibility of inducing effectiv

18 ittle data, if any, are available on whether cervical tumors are responsive to stimulation by the mac

19 is required for expression of E6E7 mRNAs in cervical tumor but not nontumor cells and may act by inh

20 ion of the POU2F3 promoter in 18 of 46 (39%) cervical tumors but never in normal epithelium.

21 l of the cervical cancer cell lines, primary cervical tumor cell cultures, and normal ectocervical cu

22 in human cervical cancer cell lines, primary cervical tumor cell cultures, and normal ectocervical ep

23 hylation occurs heterogeneously within early cervical tumor cell populations that are separate from t

24 Endothelial cells and 3D spheroids of cervical tumor cells were co-cultured in the networks.

25 viously showed that curcumin radiosensitizes cervical tumor cells without increasing the cytotoxic ef

26 iquitin-proteasome pathway in HPV-containing cervical tumor cells.

27 Greater than 99% of all cervical tumors contain HPV DNA.

28 FRA3B gene expression analysis on a panel of cervical tumor-derived cell lines revealed that three of

29 ise appearance of kinase requirements during cervical tumor development.

30 y in human keratinocytes, a model system for cervical tumor formation.

31 data demonstrate that HPV16 integrations in cervical tumors frequently occur within CFSs at the mole

32 Our analysis of cervical tumors from four separate data sets found a sig

33 A promoter methylation may lead to selective cervical tumor growth.

34 Using highly adherent human cervical tumor (HeLa) cells as a model system, cell adhe

35 ; AC) for two HPV types commonly observed in cervical tumors, HPV16 and HPV18.

36 ivo and suppressed the growth of xenografted cervical tumor implanted in nude mouse.

37 igh-grade cervical dysplasia and established cervical tumors, indicating that they depend on the cont

38 Recently an HPV16 cervical tumor integration, 2 Mb centromeric to the publ

39 egulator of HPV16 oncoprotein expression and cervical tumor maintenance.

40 identified in the expression profile of the cervical tumor microenvironment.

41 xamined the expression of c-fms and CSF-1 in cervical tumor (n = 17) and normal cervix (n = 8) sample

42 a (CIN) found on smear (n = 20) or stage Ib1 cervical tumors (n = 18).

43 demonstrate that 11/23 HPV16 integrations in cervical tumors occurred within CFSs (P&<0.001).

44 served in squamous cell carcinomas (SCC) and cervical tumors of glandular origin (e.g., adenocarcinom

45 e identified 27 unique HPV18 integrations in cervical tumors, of which 63% (P<0.001) occur in CFSs.

46 tly better than CT (AUC, 0.73) for detecting cervical tumors (P = .014).

47 d most prevalent high-risk HPV type found in cervical tumors, preferentially targets the CFSs.

48 found that MT1-MMP expression increases with cervical tumor progression (Spearman correlation coeffic

49 esting that SRSF2 has oncogenic functions in cervical tumor progression.

50 hat appear to be required for HPV-associated cervical tumor progression.

51 increased levels of SRSFs 1, 2, and 3 during cervical tumor progression.

52 important genetic alteration contributing to cervical tumor progression.

53 Genomic sequencing on 36 paired normal and cervical tumors revealed several somatic mutations and n

54 Here we show that approximately 95% of cervical tumor samples examined overexpress Cat-1, sugge

55 l-derived tumorigenic hybrids, and a primary cervical tumor, suggesting the presence of a tumor suppr

56 a 300-kb minimal area of deletion in primary cervical tumors that overlaps with deletions observed in

57 of human tumors and can in part explain why cervical tumors that possess low pO2 values are more agg

58 de resolution confirm that in HPV18-positive cervical tumors, the region surrounding c-myc is indeed

59 lation with aberrant CCND1 protein levels in cervical tumor tissue lysates.

60 xpression of the FHIT gene may be altered in cervical tumor tissue, potentially implicating this gene

61 ine whether 11q13 deletions occur in primary cervical tumors, we analysed 36 tumors using 20 differen

62 total RNA samples from breast, ovarian, and cervical tumors were either undetectable (breast and cer

63 in a broad array of carcinomas, including in cervical tumors, where it has both diagnostic and progno