ライフサイエンスコーパス: breast disease

1 nhibition in the management of proliferative breast disease.

2 y history of breast cancer, and prior benign breast disease.

3 r and do not generally occur in noncancerous breast disease.

4 ypical ductal hyperplasia, an early stage of breast disease.

5 s to the etiology and molecular pathology of breast disease.

6 xenograft model of progressive proliferative breast disease.

7 d prevent progestin-dependent progression of breast disease.

8 than 60% (high volume) of their practice to breast disease.

9 CK2, frequently found overexpressed in human breast disease.

10 s for lesion detection and identification in breast disease.

11 e II microcalcifications that correlate with breast disease.

12 st tissues that comprise a broad spectrum of breast disease.

13 agnostics and improving our understanding of breast disease.

14 with cancer as compared to women with benign breast disease.

15 amenable to therapies for treatment of human breast disease.

16 d 20 were subsequently diagnosed with benign breast disease.

17 use SCNB in the evaluation and treatment of breast disease.

18 o assess their usefulness as models of human breast disease.

19 e risk of breast cancer in women with benign breast disease.

20 he presence of a PTEN mutation and malignant breast disease.

21 n 52 women suspected of having or with known breast disease.

22 sors could distinguish benign from malignant breast disease.

23 ation noted in the group of CD families with breast disease.

24 risk lesions resembling human proliferative breast disease.

25 that ZAG plays a role in the development of breast diseases.

26 Here, we examined at what stage of breast disease 14-3-3 zeta overexpression occurs, and we

27 s than 30% (low volume) of their practice to breast disease, 32.5% by surgeons who devoted 30% to 60%

28 who had been initially diagnosed with benign breast disease according to the Nurses' Health Studies.

29 The novel findings for benign breast disease and asthma warrant further investigation.

30 Thyroid disease, breast disease and granulomatosis lung disease were the

31 reast cancer, endometriosis, and fibrocystic breast disease and has been hypothesized to exert its ef

32 BN uses probabilistic relationships between breast disease and mammography findings to estimate the

33 witch" to the angiogenic phenotype" in human breast disease and/or correlates with the thromboembolic

34 3-3zeta overexpression occurs in early stage breast diseases and contributes to transformation of hum

35 alization (percentage of practice devoted to breast disease) and hospital cancer program status, with

36 to 60% (medium volume) of their practice to breast disease, and 33.0% by surgeons who devoted more t

37 overexpression is a critical event in early breast disease, and down-regulation of p53 is one of the

38 ndetectable in normal breast tissues, benign breast diseases, and immortalized epithelial MCF-10A cel

39 hort of women who were diagnosed with benign breast disease at the Mayo Clinic and who were subsequen

40 all women who received a diagnosis of benign breast disease at the Mayo Clinic between 1967 and 1991.

41 res of biopsy tissues from women with benign breast disease (BBD) and compare its performance to the

42 mber of nevi with personal history of benign breast disease (BBD) and family history of breast cancer

43 atypia were identified from the Mayo Benign Breast Disease (BBD) cohort (1967 to 1991).

44 on and density association in a large benign breast disease (BBD) cohort.

45 We incorporated benign breast disease (BBD) diagnoses into the Breast Cancer Su

46 different pathogenetic pathways, and benign breast disease (BBD) predicts future non-TNBC.

47 history of breast or ovarian cancer, benign breast disease/biopsies, alcohol consumption, and body m

48 Women with benign proliferative breast disease (BPBD) are at increased risk for developi

49 not only in the detection and evaluation of breast disease, but also in the diagnosis and management

50 These stages are comparable to human breast diseases classified as benign or in situ prolifer

51 sibility of sampling error and the nature of breast disease, close mammographic and clinical follow-u

52 with atypical hyperplasia in the Mayo Benign Breast Disease Cohort were identified through pathology

53 42 age-matched controls from the Mayo Benign Breast Disease Cohort, by determining number of acini pe

54 luding 62 in situ carcinomas) and 186 benign breast disease controls were recruited into the study.

55 positively associated with history of benign breast disease, family history of breast cancer, hormone

56 ng led to small changes in effects of benign breast disease, family history, and hormone therapy.

57 of breast cancer, personal history of benign breast disease, height at age 25 years, age at menarche,

58 onfidence interval (CI): 1.73, 3.20), benign breast disease (HR = 1.56, 95% CI: 1.08, 2.26), asthma (

59 has progressed from the simple assessment of breast disease in a selected small number of symptomatic

60 breast cancer after the diagnosis of benign breast disease include the histologic classification of

61 Benign breast disease is an important risk factor for breast ca

62 History of benign breast disease is associated with a 57% increase (95% co

63 ocystic change and papillomas, in all benign breast disease lesions, and in 89% of in situ and in 83%

64 nt therapy use, somatotype at age 18, benign breast disease, mammographic density, polygenic risk sco

65 Further stratification by type of breast disease; menopausal, parity, and lactation status

66 inoma than those patients with either benign breast disease or carcinoma-in-situ (P =.0001).

67 2% (95% CI, 61%-80%) for those with residual breast disease (P < .001).

68 use was concentrated in women without benign breast disease (p=0.01) or a family history of breast ca

69 in breast cancer and seldom in proliferative breast disease (PBD).

70 regardless of the histologic type of benign breast disease (relative risk, 1.8; 95 percent confidenc

71 None of the control cases (women without any breast disease) revealed LOH either in the epithelial or

72 ween number of nevi and benign and malignant breast disease risk.

73 e frequency of nodules showing proliferative breast disease rose from 23% in the first transplant gen

74 F10AT xenograft model of human proliferative breast disease to examine the early effects of estradiol

75 e studied a large group of women with benign breast disease to obtain reliable estimates of this risk

76 Reproductive risk factors, benign breast disease, use of postmenopausal hormones, weight,

77 ds ratio for protection against non-invasive breast disease was 0.26 (95% confidence interval 0.12-0.

78 mplification and/or overexpression in benign breast disease was associated with an increased risk of

79 To produce models of breast disease with these etiologies, mice were generate

80 iparous v parous; P =.45), history of benign breast disease (yes v no; P =.99), or family history of