ライフサイエンスコーパス: molecular disease

1 red for response by QPCR studies for minimal molecular disease.

2 tinib daily have variable levels of residual molecular disease.

3 ant disorder but rather a family of distinct molecular diseases.

4 Pauling & Castle established the notion of a molecular disease (3).

5 led to a paradigm shift in the diagnosis of molecular diseases and disorders.

6 rk, which recognized sickle-cell anemia as a molecular disease, and with Ingram's demonstration of a

7 Pauling's concept of "molecular disease," based on this discovery, opened a ne

8 Thus, there is a high clinical need for molecular disease biomarkers to aid in differentiating t

9 Detection of molecular disease by immunoglobulin high-throughput sequ

10 Detectable molecular disease by PCR was highly predictive of diseas

11 overlap or distinguish the diseases in each molecular disease category.

12 h that considers patient characteristics and molecular disease characteristics.

13 riptomics is a valid strategy to establish a molecular disease classification and to identify pathoge

14 different infection states and allowing for molecular disease classification of this highly neglecte

15 overview of techniques used for noninvasive molecular disease detection in selected myeloid and lymp

16 herapies tailored to the underlying cell and molecular disease drivers.

17 3 AML/MDS-EB should be considered a distinct molecular disease entity.

18 Although the WARBM molecular disease etiology remains unclear, both the bs

19 ib prevents GFR loss, improves histologic or molecular disease features, or reduces DSA, despite sign

20 d on patient characteristics and cytogenetic/molecular disease features.

21 f accessible biofluids to identify and track molecular disease has revolutionized the fields of oncol

22 tion for Bcl-2 gene rearrangements to detect molecular disease, however, may identify patients with e

23 Detection of molecular disease in the plasma often preceded PET/CT de

24 We sought to establish a molecular disease map of chronic idiopathic erythroderma

25 decades that followed, other cytogenetic and molecular disease markers have been described and effect

26 ed by diagnostic algorithms that incorporate molecular disease markers, which complement histological

27 Molecular disease measured from plasma, compared with ci

28 To gain more insight into the molecular disease mechanism of this mutant, we used NMR

29 brain development is largely unknown and the molecular disease mechanism underlying cortical malforma

30 d treatment informed by the knowledge of the molecular disease mechanism.

31 Molecular disease mechanisms caused by mutations in prot

32 Different molecular disease mechanisms have been proposed, and pat

33 , and provide comprehensive insight into the molecular disease mechanisms of cystic fibrosis caused b

34 To understand the molecular disease mechanisms of this disease, we investi

35 hin the first three decades of life, but its molecular disease mechanisms remain unclear.

36 disease and remains important in delineating molecular disease mechanisms.

37 ational predictions through consideration of molecular disease mechanisms.

38 ough different and in some cases overlapping molecular disease mechanisms.

39 ht the role of ctDNA as a minimally invasive molecular disease monitoring strategy in MDS.

40 pilepsies aiming to improve understanding of molecular disease pathobiology, recognize affected biolo

41 lker Warburg Syndrome patients modeled their molecular disease pathologies and were responsive to sma

42 ator II, or iron supplementation rescued the molecular disease pathway and recovered contractility.

43 that estimates the fit between the specific molecular disease pathway(s) identified in an individual

44 ntal involvement may then implicate cellular/molecular disease pathways for treatment and targeted ph

45 vances in AMD research also highlight common molecular disease pathways with other neurodegenerative

46 is assumed to be a central component of the molecular disease pathways.

47 SSc dermal fibroblasts retained most of the molecular disease phenotype upon in vitro culture for at

48 tant DNA repair complex and suggest possible molecular disease principles.

49 calar data sets, captures each participant's molecular disease processes at the time of kidney biopsy

50 state cancer incidence, and understanding of molecular disease progression is advancing rapidly.

51 Epresentation Mapping Approach to Predicting molecular-disease relations (M2REMAP) by incorporating c

52 A molecular disease signature in the blood was studied at

53 Understanding the molecular disease signatures across inflammasomopathies

54 ve for FDG, reserving PET to be used for the molecular disease-specific amyloid and tau tracers.

55 ation, risk stratification and assignment of molecular, disease-specific therapies to improve the car

56 ession and use this ordering to estimate the molecular disease stage-or disease pseudotime-for each s

57 This review outlines the molecular disease states in kidney transplant biopsies a

58 now yields ever richer insights into diverse molecular disease subtypes and the patterns of cellular

59 nt and difficult problem is the discovery of molecular disease subtypes characterized by relevant cli

60 to have a heterogeneous pathophysiology, but molecular disease subtypes have not been identified.

61 ncer-type-specific genes and pathways define molecular disease subtypes.

62 le for COVID-19, exploring it as a transient molecular disease that causes negative regulation of ang

63 g, sickle-cell disease) were among the first molecular diseases to be identified, and have been inves

64 Before treatment, molecular disease was detected in the plasma of 82% of p

65 However, molecular disease was detected significantly more freque

66 a-GAL brings Fabry disease into the realm of molecular diseases, where insights into the structural b

67 o an understanding of the complexity of this molecular disease with protean manifestations.