ライフサイエンスコーパス: lung tumour

1 ethane, which induces Kras mutation-positive lung tumours.

2 8S) and Kras(C118S/C118S) mice develop fewer lung tumours.

3 hylation of this MGMT promoter CpG island in lung tumours.

4 e increased cell migration and metastasis in lung tumours.

5 tochondrial heterogeneity within subtypes of lung tumours.

6 from surgically resected tissues to classify lung tumours.

7 endothelium such as mouse thymomas and human lung tumours.

8 ics and cellular origins of lineage-specific lung tumours.

9 nduced regression of established murine LSCC lung tumours.

10 igate their impact on somatic environment of lung tumours.

11 erapies to address orthotopic and metastatic lung tumours.

12 phages that were enriched in human and mouse lung tumours.

13 identified in a subset of KRAS-driven human lung tumours.

14 ng clone-specific copy numbers in TRACERx421 lung tumours(5,6), we find evidence of increased chromos

15 present the complete sequences of a primary lung tumour (60x coverage) and adjacent normal tissue (4

16 From one such secondary lung tumour, a cell line was established designated Ca2-

17 of hTR expression could be demonstrated in a lung tumour and its metastasis with hTR amplification.

18 ted in the regression of NY-ESO-1-expressing lung tumour and subcutaneous tumour, respectively.

19 mour lines; (b) chromosome 3p allele loss in lung tumours and (c) RASSF1 mutation analysis in breast

20 ic spectra were obtained and aligned from 79 lung tumours and 14 normal lung tissues.

21 roteomic patterns in a training cohort of 42 lung tumours and eight normal lung samples, and assessed

22 (also known as HER2 or Neu) from 120 primary lung tumours and identified 4% that have mutations withi

23 lung microenvironment promotes both primary lung tumours and lung metastasis from extrapulmonary neo

24 ulate the tissue architecture of the primary lung tumours and maintain the genomic alterations of the

25 d to tobacco carcinogen, KACs emerged before lung tumours and persisted for months after cessation of

26 model to a blinded test cohort, including 37 lung tumours and six normal lung samples, to estimate th

27 However, extensive mutation analysis in lung tumours and tumour lines revealed only rare inactiv

28 soform A of RASSF1 (RASSF1A) was reported in lung tumours and tumour lines.

29 sive view of somatic alterations in a single lung tumour, and provide the first evidence, to our know

30 highly methylated in 24 of 60 (40%) primary lung tumours, and 4 of 41 tumours analysed carried misse

31 support our first finding that nonangiogenic lung tumours are fast-growing tumours filling the alveol

32 uppression of tumorigenesis, suggesting that lung tumours are highly sensitive to ferroptosis.

33 Our data demonstrate that mutant Kras lung tumours are not a single disease but rather a heter

34 Furthermore, Mad2+/- mice develop lung tumours at high rates after long latencies, implica

35 LA1) mice, CS exposure markedly enhances the lung tumour burden and genetic deletion of leukotriene B

36 transgenic overexpression of Trim7 increases lung tumour burden in a Ras-driven cancer model, and kno

37 enes (RASSF1A) was absent in the majority of lung tumour cell lines analysed.

38 ted in the majority of primary lung tumours, lung tumour cell lines and in a variable percentage of b

39 Conversely, in lung tumour cell lines expressing Kras(G12D) and lacking

40 expression was downregulated in a subset of lung tumour cell lines.

41 t and nasopharynx, as well as in a subset of lung tumour cell lines.

42 ) polymerase signalling to inhibit growth of lung tumour cells.

43 By applying the vision transformer to a lung-tumour dataset, we identified and validated a monoc

44 apid regression of incipient and established lung tumours, defining an unexpected role for endogenous

45 All 15 lung tumours demonstrate distinct genomic profiles, sugg

46 Bayesian inference methodologies to analyse lung tumour-derived methylation data from a CpG island i

47 nerve transection markedly inhibits primary lung tumour development and progression, highlighting a

48 ritical function for NF-kappaB signalling in lung tumour development and, further, that this requirem

49 and in the first exon of the promoter during lung tumour development.

50 vity that are sufficient for early stages of lung tumour development.

51 ttern for the TP53 tumour suppressor gene in lung tumours differs to other cancer types by having a h

52 Furthermore, human brain and lung tumours display robust glucose oxidation by mitocho

53 ssion of NFS1, whereas metastatic or primary lung tumours do not.

54 The growth and survival of lung tumours driven by KRAS(G12D) is diminished in the a

55 mutant Kras allele is sufficient to promote lung tumour formation in mice but malignant progression

56 We recently showed that advanced lung tumours from Kras(G12D/+);p53-null mice frequently

57 SMBA1 potently suppresses lung tumour growth via apoptosis by selectively activati

58 prognostic indicator in a further 1100 male lung tumours (HR 1.67, 95% CI 1.4-2.0, P = 1.2 x 10(-10)

59 ng in human lung cancer cell lines and mouse lung tumours identified a variety of metastasis-promotin

60 tochthonous KRAS(G12C)-driven pancreatic and lung tumours in mouse models to a comparable level as KR

61 Inhibition of the pathway in lung tumours in vivo, from the time of tumour initiation

62 ation rate, thereby significantly increasing lung tumour incidence in Gprc5a(-/-) mice.

63 offer crucial insights into the processes of lung tumour invasion and metastasis may therefore provid

64 hat restoration of p53 in established murine lung tumours leads to significant but incomplete tumour

65 inactivating somatic mutations were found in lung tumour lines; however, NORE1A promoter region CpG i

66 F1A is methylated in the majority of primary lung tumours, lung tumour cell lines and in a variable p

67 In an implantable lung tumour model, CS exposure results in rapid tumour g

68 tail vein injections in breast, myeloma and lung tumour mouse models.

69 ing the high oxygen environment of incipient lung tumours, NFS1 lies in a region of genomic amplifica

70 of pulmonary adenocarcinoma, a transmissible lung tumour of sheep.

71 edict that G:C>T:A mutations at codon 157 in lung tumours of smokers are predominantly caused by BPDE

72 Lung tumours of the same individuals are no more similar

73 We show that lung tumours prime accessibility for Nfe2l2 (NRF2) in bo

74 pGs near the 5' end of the CpG island in two lung tumour samples for both alleles of a nearby polymor

75 int, activity and safety profiles of primary lung tumour SBRT followed by concurrent mediastinal chem

76 Moreover, patients with RSK1-negative lung tumours showed increased number of metastases.

77 karyograms of a series of 89 non-small cell lung tumours specifically of the squamous cell subtype.

78 s indicate a potential role for RASSF1A as a lung tumour suppressor gene.

79 GPRC5A functions as a lung tumour suppressor to prevent spontaneous and enviro

80 adherin axis is also observed in Kras mutant lung tumours that are regressing due to blockade of RAS

81 We show, in a mouse model of lung tumours, that the lack of Par-4 dramatically enhanc

82 directly from small amounts of fresh frozen lung-tumour tissue could be used to accurately classify

83 ll lung cancer and large-cell neuroendocrine lung tumours, TP53 and RB1 mutations are rare events, su

84 in 39 resected primary human non-small cell lung tumours versus normal lung tissue.

85 e bearing A375Pbeta6 experimental metastatic lung tumours were treated with L-ALD or t-L-ALD as monot

86 oes not affect the regression of Kras-driven lung tumours when Kras is inhibited.

87 and in vivo, in spontaneous advanced murine lung tumours (which display a high frequency of Kras(G12

88 Adenosquamous lung tumours, which are extremely poor prognosis, may re

89 -tumour efficacy in mice with non-small cell lung tumour xenografts.