ライフサイエンスコーパス: HGSOC

1 is associated with shorter survival in 1000 HGSOC patients.

2 s with time-to-disease progression (TTP) and HGSOC transcriptomic profiles (Classification of Ovarian

3 he accumulation of HBA metabolites caused by HGSOC was also associated with reduced expression of suc

4 , a chemokine receptor commonly expressed by HGSOC cells.

5 tly reported that Elafin is overexpressed by HGSOC and is associated with poor overall survival.

6 ients with high-grade serous ovarian cancer (HGSOC) and 100 control patients with benign or non-neopl

7 notypes of high-grade serous ovarian cancer (HGSOC) and to evaluate CT indicators of cytoreductive ou

8 eatment of high-grade serous ovarian cancer (HGSOC) is the development of progressive resistance to p

9 lopment of high-grade serous ovarian cancer (HGSOC) may define the molecular basis of the profound st

10 ely 30% of high-grade serous ovarian cancer (HGSOC) patients and is a recurrent lesion in uterine car

11 e of human high-grade serous ovarian cancer (HGSOC) should not only resemble its tumour of origin at

12 eatures of high-grade serous ovarian cancer (HGSOC), to assess their associations with time-to-diseas

13 changes in high-grade serous ovarian cancer (HGSOC), we performed whole genome sequencing on a rare c

14 laparib in high-grade serous ovarian cancer (HGSOC).

15 ients with high-grade serous ovarian cancer (HGSOC).

16 high-grade serous epithelial ovarian cancer (HGSOC).

17 High-grade serous ovarian carcinoma (HGSOC) and basal-like breast cancer (BLBC) share many fe

18 High-grade serous ovarian carcinoma (HGSOC) is a lethal disease for which improved screening

19 ture of high-grade serous ovarian carcinoma (HGSOC) is frequent amplification of the 3q26 locus harbo

20 High-grade serous ovarian carcinoma (HGSOC) is the most common and aggressive form of epithel

21 High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of ovarian cancer and h

22 High-grade serous ovarian carcinoma (HGSOC), the most lethal gynecological cancer, often lead

23 ture of high-grade serous ovarian carcinoma (HGSOC).

24 d from high-grade serous ovarian carcinomas (HGSOC), an aggressive cancer characterized by ubiquitous

25 he current gold-standard response marker for HGSOC in blood, as well as to disease volume on computed

26 of CXCR4 pathway in expression profiles from HGSOC correlated with enrichment of a mutated TP53 gene

27 vivo shRNA screen using an established human HGSOC cell line growing either subcutaneously or intrape

28 otypically, and genomically similar to human HGSOC.

29 first comprehensive metabolomics analysis in HGSOC and propose a new set of metabolites as biomarkers

30 ons are present in pre-treatment biopsies in HGSOC and can undergo expansion during chemotherapy, cau

31 on of p53 aggregation and chemoresistance in HGSOC cells, we further demonstrated that the overexpres

32 nce that structural variants (SV) cluster in HGSOC, but are absent in one ultramutated tumor, providi

33 ate by perturbing expression of each gene in HGSOC precursor cells.

34 specific early molecular response marker in HGSOC and warrants further investigation in larger cohor

35 emergence of subclonal tumour populations in HGSOC was associated with the development of resistant d

36 er to characterize their respective roles in HGSOC development.

37 cytogenetic changes typical of those seen in HGSOC ovarian cancer cell lines and biopsies.

38 for survival after chemotherapy treatment in HGSOC.

39 ersecting regulatory biofeatures at 17 known HGSOC susceptibility loci in FTSECs (P = 3.8 x 10(-30)),

40 Therefore, limiting HGSOC research to modeling based on ovarian surface epit

41 ic analysis of 26 ovarian cancer cell lines, HGSOC tumours, immortalized ovarian surface epithelial c

42 o a predominantly epithelial and mesenchymal HGSOC tumour cluster.

43 orter PFS for both patients with BRCA-mutant HGSOC (multiple regression: hazard ratio [HR] = 26.7 P <

44 s differed between patients with BRCA-mutant HGSOC and patients with BRCA wild-type HGSOC.

45 orter PFS for both patients with BRCA-mutant HGSOC and those with BRCA wild-type HGSOC.

46 me and survival in patients with BRCA-mutant HGSOC and those with BRCA wild-type HGSOC.

47 uctive outcome for patients with BRCA-mutant HGSOC, presence of PD in lesser sac (odds ratio [OR] = 2

48 laparib therapy, we performed an analysis of HGSOC tumors from three patients without germline BRCA1/

49 us may be early events in the development of HGSOC, and associated with chromosomal instability.

50 r HOXD9 overexpression reveals enrichment of HGSOC risk variants within HOXD9 target genes (P=6 x 10(

51 the need for a fallopian tube-based model of HGSOC, we have developed a system for studying human fal

52 human tumours indicates a possible origin of HGSOC either from the fallopian tube or from the ovarian

53 demonstrated that in a unique population of HGSOC cancer cells with cancer stem cell properties, p53

54 fallopian tube cancers may be precursors of HGSOC but evolutionary evidence for this hypothesis has

55 gesting both cell types may be precursors of HGSOC.

56 rstand the poor chemoresponse of a subset of HGSOC patients and suggest p53 aggregation as a new mark

57 reas is impeded by our poor understanding of HGSOC pathogenesis.

58 elapse from patients with platinum-sensitive HGSOC recurrence who were treated > 5 years with olapari

59 insights into the pathogenesis of low stage HGSOC.

60 cer research is based on the hypothesis that HGSOC arises from ovarian surface epithelial cells.

61 or this network in genetic susceptibility to HGSOC.

62 f incomplete cytoreduction in BRCA wild-type HGSOC (multiple regression: P < .001 each CT feature).

63 26.7 P < .001) and those with BRCA wild-type HGSOC (univariate analysis: reader 1, HR = 2.42, P < .00

64 with BRCA mutant and 75 with BRCA wild-type HGSOC) who underwent CT before primary debulking.

65 utant HGSOC and patients with BRCA wild-type HGSOC.

66 A-mutant HGSOC and those with BRCA wild-type HGSOC.

67 A-mutant HGSOC and those with BRCA wild-type HGSOC.

68 L associations at 47 regions associated with HGSOC risk (P</=10(-5)).

69 t retrospective analysis of 92 patients with HGSOC (median age, 61 years) with abdominopelvic CT befo

70 outine clinical visits from 40 patients with HGSOC undergoing heterogeneous standard of care treatmen

71 ally separated samples from 14 patients with HGSOC who received platinum-based chemotherapy.

72 LOVAR subtypes and survival in patients with HGSOC.

73 of peritoneal fluid samples from women with HGSOC (frequency as low as 1 mutant per 24,736 normal ge

74 17 peritoneal fluid samples from women with HGSOC and 20 from women without cancer.

75 ease at the start of treatment in women with HGSOC and that a decrease of </=60% in TP53MAF after one

76 efore cytoreductive surgery in 46 women with HGSOC, whose tumors were subjected to molecular analysis