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 es in management of epithelial and germ cell ovarian tumours.

3 that have the highest genetic similarity to ovarian tumours.

4 been mainly identified in young females with ovarian tumours.

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

6 ovarian cancer and 88 had benign epithelial ovarian tumours.

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

8 11q and 17p in 31 solitary benign epithelial ovarian tumours.

9 ication of microenvironmental composition of ovarian tumours.

10 The Cancer Genome Atlas datasets on primary ovarian tumours.

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

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

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

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

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

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

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

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

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

20 confers cisplatin resistance in these human ovarian tumour cells.

21 Ovarian tumour deubiquitinases are cysteine proteases th

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

23 Ovarian tumour deubiquitinases comprise a family of four

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

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

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

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

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

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

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

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

32 2% SCLC, 36% NSCLC, 80% of breast and 40% of ovarian tumour lines.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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