ライフサイエンスコーパス: BFB

1 BFB amplifications are prevalent in cervical, head and n

2 BFB can be observed in progress using cytogenetic techni

3 BFB is a common mechanism of chromosomal alterations in

4 ive cell lines have a chromosomal region 11q BFB event, with YAP1-BIRC3-BIRC2 amplification.

5 We identify 371 BFB events through whole genome sequencing of 2557 prima

6 as microarrays or sequencing collected after BFB has ceased.

7 Tumors with BFB amplifications (BFB(+)) show reduced structural heterogeneity in amplico

8 Remarkably, the 12p chromothripsis and BFB events were stabilized by independent fusions to chr

9 zed cytogenetically may be more complex, and BFB cycles may play an important role in generating term

10 These findings highlight ecDNA and BFB amplifications as distinct oncogene amplification me

11 en the complexity of some cancer genomes and BFB's ability to generate a wide range of rearrangement

12 for whole chromosome loss and the associated BFB-mediated instability in tumorigenesis and may shed l

13 Syncope in patients with bifascicular block (BFB) is a common event whose causes might be difficult t

14 Both breakage fusion bridge (BFB) cycles and extrachromosomal DNA (ecDNA) can lead to

15 The breakage-fusion-bridge (BFB) cycle has been proposed to be one of the main drive

16 The chromosome breakage-fusion-bridge (BFB) cycle is a mutational process that produces gene am

17 Breakage-fusion-bridge (BFB) cycle is a series of chromosome breaks and duplicat

18 notably seen in the breakage-fusion-bridge (BFB) cycle.

19 ication involves the breakage-fusion-bridge (BFB) cycle.

20 ering article on the breakage-fusion-bridge (BFB) cycle.

21 t of cancers display breakage-fusion-bridge (BFB) cycles and chromothripsis, hallmarks of experimenta

22 Chromosome breakage and break-fusion-bridge (BFB) cycles can also be observed during early embryo sac

23 that have undergone breakage-fusion-bridge (BFB) cycles leading to gene amplification.

24 (DM) chromosomes and breakage-fusion-bridge (BFB) cycles, have been repeatedly linked to genomic ampl

25 as micronucleation, breakage-fusion-bridge (BFB) cycles, or chain-like translocations.

26 ndergoes a series of breakage-fusion-bridge (BFB) cycles.

27 sions resulting from breakage-fusion-bridge (BFB) cycles.

28 Breakage-fusion-bridge (BFB) is a mechanism of genomic instability characterized

29 t to arise through a breakage-fusion-bridge (BFB) mechanism.

30 indicating a series of breaks and fusions by BFB cycles.

31 fy a chromosomal region likely rearranged by BFB cycles, demonstrating the practicality of our approa

32 In contrast, BFB cycles and chromothripsis occurred in MRC5 fibroblas

33 rsions are sufficient evidence for detecting BFB.

34 lts elucidate nucleotide-level events during BFB cycles and end processing for naturally occurring mi

35 ms to aid the interpretation of evidence for BFB.

36 th fold-back inversions to develop tests for BFB.

37 biosensors in slices of the basal forebrain (BFB) to study both depolarization-evoked adenosine relea

38 using cytogenetic techniques, but generally BFB must be inferred from data such as microarrays or se

39 ision (>93%) and recall (92%) in identifying BFB amplifications across cancer cell lines, patient-der

40 nd of a broken chromosome) further indicated BFB cycles as underlying processes.

41 Breakpoints initiating BFB cycles were determined from recent array data from 1

42 To elucidate the molecular basis of BFB-mediated DNA amplification, we cloned 1q31 fragile s

43 inverted repeat structure characteristic of BFB; instead PDE9A was fused to intergenic regions of ch

44 ghts into the mechanisms and consequences of BFB cycles in cervical cancer using long-read sequencing

45 tic tumors and confirm a previous finding of BFB as well as identify a chromosomal region likely rear

46 igh oncogene copy numbers, but the impact of BFB amplifications on intratumoral heterogeneity, treatm

47 wide spectrum of SVs implying that a lack of BFB patterns and chromothripsis in cancer genomes does n

48 is clones did not show prominent patterns of BFB cycles or chromothripsis.

49 Signatures of BFB cycles can be observed in cancer genomes alongside c

50 A critical step of BFB cycles leading to gene amplification is a palindromi

51 he germ line and passes through at least one BFB cycle to produce gametes with terminal deletions ass

52 olve the dicentric chromosomes, and only one BFB breakpoint showed chromothripsis.

53 , OM2BFB, designed to detect and reconstruct BFB amplifications using optical genome mapping (OGM).

54 Some BFB events are complex, involving inter- or intra-chromo

55 Comparisons using OGM reveal that BFB detection with our AmpliconSuite toolkit for short-r

56 Evoked and basal adenosine release in the BFB in vitro exhibited three key features: the magnitude

57 ristics of adenosine release recorded in the BFB in vitro reflect those that have been linked in vivo

58 -guide RNA (sgTelo) can be used to model the BFB cycle.

59 None of the BFB breakpoints had telomere sequences added to resolve

60 ed mechanism for the individual steps of the BFB cycle warrants further investigation.

61 Of the three steps of the BFB cycle, breakage remains the least understood despite

62 new light on the molecular mechanisms of the BFB cycle, which will advance our understanding of tumor

63 g, preceded or accompanied initiation of the BFB cycle.

64 We first pose the BFB count-vector problem: given a chromosome segmentatio

65 ted with mdr1 gene amplification through the BFB mechanism.

66 Genes amplified through BFB exhibit lower expression variance, with limited pote

67 ion and segment copy numbers, decide whether BFB can yield a chromosome with the given segment counts

68 Tumors with BFB amplifications (BFB(+)) show reduced structural hete