ライフサイエンスコーパス: ovarian tumour

1 port of a TP53 mutation in a solitary benign ovarian tumour.

2 ication of microenvironmental composition of ovarian tumours.

3 The Cancer Genome Atlas datasets on primary ovarian tumours.

4 t, to differentiate borderline and malignant ovarian tumours.

5 es in management of epithelial and germ cell ovarian tumours.

6 that have the highest genetic similarity to ovarian tumours.

7 been mainly identified in young females with ovarian tumours.

8 ound in the coding region of RASSF2 in these ovarian tumours.

9 ovarian cancer and 88 had benign epithelial ovarian tumours.

10 d in 11% of breast cancer cases and in 5% of ovarian tumours.

11 11q and 17p in 31 solitary benign epithelial ovarian tumours.

12 mpared to patients with malignant and benign ovarian tumours.

13 a predictor of platinum sensitivity in human ovarian tumours.

14 cal cancers, ovarian cancers, and borderline ovarian tumours.

15 We also did not detect RASSF2 methylation in ovarian tumours (0/17).

16 ginal ultrasounds performed by International Ovarian Tumour Analysis consortium (IOTA)-certified sono

17 s at D6S193 (62%) on chromosomal arm 6q27 in ovarian tumours and mapped the minimal region of allele

18 o find that peritoneal LPMs infiltrate early ovarian tumours and that RXR deletion diminishes LPM acc

19 d in recurrent compared with matched-primary ovarian tumours and their expression is associated with

20 ic and gene expression level between primary ovarian tumours and their peritoneal metastases are hope

21 Ovarian tumours are the second most common cause of deat

22 Ovarian tumours are usually surgically removed because o

23 MLH1, NTS and PSMB9) acquired methylation in ovarian tumours at relapse following chemotherapy or che

24 was expressed in some but not all breast and ovarian tumour cell lines and also in a glioma cell line

25 Importantly, the 25 new ovarian tumour cell lines described here retain the geno

26 a high frequency event following exposure of ovarian tumour cells to cisplatin and may be critically

27 s is supported by the finding that, in human ovarian tumour cells, loss of hMLH1 correlated with acqu

28 confers cisplatin resistance in these human ovarian tumour cells.

29 In ovarian tumours classified as indeterminate at ultrasono

30 hology and transcriptome analysis on a large ovarian tumour cohort and develop a machine learning app

31 Ovarian tumour deubiquitinases are cysteine proteases th

32 Here we show that ovarian tumour deubiquitinases are susceptible to revers

33 Ovarian tumour deubiquitinases comprise a family of four

34 phenic acid intermediates, we show that many ovarian tumour deubiquitinases undergo reversible oxidat

35 Here we show that the ovarian tumour domain-containing Ub aldehyde-binding pro

36 a de-ubiquitinating (DUB) enzyme of the OTU (ovarian tumour) family, removes lysine-63 (K63)-linked u

37 We then genotyped 314 ovarian tumours for several tSNPs in CASP5 and RBBP8 to

38 ations were present in carboplatin-resistant ovarian tumours from c.6174delT mutation carriers.

39 itosan nanoparticles significantly decreases ovarian tumour growth and metastasis in vivo, suggesting

40 en observed in 30-40% of sporadic breast and ovarian tumours, implying that BRCA2 may act as a tumour

41 ully detect a point mutation typical of some ovarian tumours in clinical samples.

42 2% SCLC, 36% NSCLC, 80% of breast and 40% of ovarian tumour lines.

43 this data supports the theory that malignant ovarian tumours may arise from benign and borderline pre

44 ions which supports the idea that all benign ovarian tumours may carry a genetic predisposition to ma

45 An increase in the proportion of ovarian tumours negative for the hMLH1 subunit is observ

46 es (epithelial ovarian carcinoma, borderline ovarian tumours, normal ovarian stroma) were compared as

47 In 21 cases of borderline ovarian tumours, of which 11 were regarded as malignant

48 Deubiquitinating enzymes of the ovarian tumour (OTU) family regulate cellular signalling

49 engineered mice bearing mutations in the A20 ovarian tumour (OTU)-type deubiquitinase domain or in th

50 mutations for two P body components, Cup and Ovarian tumour (Otu).

51 Inhibiting USP13 remarkably suppresses ovarian tumour progression and sensitizes tumour cells t

52 accumulation in tumours and strongly reduces ovarian tumour progression in mice.

53 ovarian cancer using microdissected stromal ovarian tumour samples and find that stromal microfibril

54 Furthermore, 12.5% (3/ 24) of ovarian tumours show hypermethylation of the hMLH1 promo

55 ivalent gene sets to gene expression data of ovarian tumour 'stem cell-like' sustaining cells versus

56 ed dynamic contrast-enhanced MRI to study 68 ovarian tumours that were classified as indeterminate at

57 er with our previous investigation of benign ovarian tumours this data supports the theory that malig

58 One of the mechanisms of resistance of ovarian tumours to cisplatin is increased nucleotide exc

59 ffusion coefficient value to distinguish the ovarian tumour types, with various results.

60 eterozygosity (LOH) analysis of tSNPs in 314 ovarian tumours was used to identify associations betwee

61 y early stage malignant and seven borderline ovarian tumours were analysed for loss of heterozygosity

62 Angiogenesis, growth and metastasis in ovarian tumour xenografts were markedly inhibited by the