ライフサイエンスコーパス: ductal hyperplasia

1 age and HRL histologic results (eg, atypical ductal hyperplasia).

2 ds also display mammary trees with extensive ductal hyperplasia.

3 al scar, fibroadenoma, and areas of atypical ductal hyperplasia.

4 I, 0.4 to 5.6) for the diagnosis of atypical ductal hyperplasia.

5 , conditional PAF expression induces mammary ductal hyperplasia.

6 tively insufficient is described as atypical ductal hyperplasia.

7 Atypical ductal hyperplasia ([1.48 +/- 0.36] x 10(-3) mm(2)/sec;

8 +/- 0.38] x 10(-3) mm(2)/sec; n = 13), usual ductal hyperplasia ([1.83 +/- 0.49] x 10(-3) mm(2)/sec;

9 lts in patients with a diagnosis of atypical ductal hyperplasia (ADH) (75 of 6,081 [1.2%]) were revie

10 sess the rate of underestimation of atypical ductal hyperplasia (ADH) and ductal carcinoma in situ (D

11 ity (LOH) on 11q13 (PYGM, INT-2) in atypical ductal hyperplasia (ADH) and various histological types

12 east lesions diagnosed initially as atypical ductal hyperplasia (ADH) by core needle biopsy.

13 psy revealed carcinoma in 19 (61%), atypical ductal hyperplasia (ADH) in eight (26%), and benign find

14 wo, papilloma with adjacent foci of atypical ductal hyperplasia (ADH) in eight, and well-differentiat

15 Atypical ductal hyperplasia (ADH) is a known risk factor for brea

16 advised for the 143 carcinomas, 25 atypical ductal hyperplasia (ADH) lesions, and five radial scars.

17 Atypical ductal hyperplasia (ADH) underestimates were lesions tha

18 cinoma in situ (DCIS), one focus of atypical ductal hyperplasia (ADH), and one atypical lobular hyper

19 simple ductal hyperplasia (SH) and atypical ductal hyperplasia (ADH), are candidate precursors to du

20 Three yielded atypical ductal hyperplasia (ADH); one, residual LCIS; and one, A

21 Transplantation of Trp53+/- ductal hyperplasias also indicated an association betwee

22 expression of 14-3-3 zeta begins at atypical ductal hyperplasia, an early stage of breast disease.

23 cinoma in situ were reclassified as atypical ductal hyperplasia and considered false-positive results

24 ductal in morphology and progressed through ductal hyperplasia and ductal carcinoma in situ before i

25 lands from the virgin MTA1s-TG mice revealed ductal hyperplasia and ductal carcinoma in situ, and low

26 ninvasive breast lesions, including atypical ductal hyperplasia and ductal carcinoma in situ.

27 e mS100a7a15 was induced exhibited increased ductal hyperplasia and expression of molecules involved

28 Precursor lesions including ductal hyperplasia and hyperplastic alveolar nodules wer

29 High-risk lesions (atypical ductal hyperplasia and lobular neoplasia) showed signifi

30 pry1 and Spry2 in prostate epithelium causes ductal hyperplasia and low-grade prostatic intraepitheli

31 four histological types: normal cases, usual ductal hyperplasia and low/high grade ductal carcinoma i

32 tion in early tumorigenic lesions, including ductal hyperplasia and mammary intraepithelial neoplasia

33 lands via doxycycline, causing a decrease in ductal hyperplasia and ODD.

34 Defects are mainly ductal hyperplasias and dysplasias characterized by mult

35 l and lobular carcinoma in situ and atypical ductal hyperplasia), and 277 controls without these brea

36 east lesions, including focal solid nodules, ductal hyperplasia, and mini-intraductal neoplasm and ad

37 nitiating cells results in the production of ductal hyperplasia, and modulation of Bmi-1 expression i

38 Microdissected foci of ductal hyperplasia, apocrine metaplasia, sclerosing aden

39 though premalignant lesions such as atypical ductal hyperplasia are highly ER-alpha-positive.

40 ditional lesions, unfolded lobules and usual ductal hyperplasia, are sometimes considered to be very

41 ith atypia 9% (95% CI: 5%-14%), and atypical ductal hyperplasia associated with CCL 20% (95% CI: 13%-

42 without atypia, CCL with atypia and atypical ductal hyperplasia associated with CCL followed by surgi

43 NB diagnosis of CCL with atypia and atypical ductal hyperplasia associated with CCL, surgical excisio

44 racterized premalignant lesions are atypical ductal hyperplasia, atypical lobular hyperplasia, and lo

45 A high-risk lesion (ie, atypical ductal hyperplasia, atypical lobular hyperplasia, lobula

46 nduced cellular transformation and extensive ductal hyperplasia by 4 months of age.

47 ession in mammary epithelial cells developed ductal hyperplasia (DH), lobular hyperplasia, and ductal

48 Atypical ductal hyperplasia diagnosed via excisional biopsy was a

49 re crisis in normal ductal epithelium, usual ductal hyperplasia, ductal carcinoma in situ and invasiv

50 ry tumor virus LTR enhancer causes extensive ductal hyperplasia early in life and mammary adenocarcin

51 ded high-risk lesions, including 21 atypical ductal hyperplasia, eight atypical lobular hyperplasia,

52 ent of premalignant lesions such as atypical ductal hyperplasia, elevated growth factors, or increase

53 These lesions include lobular and ductal hyperplasia, fibroadenoma, cystic expansions, and

54 tological analysis revealed extensive breast ductal hyperplasia in females of all genotypes after rHR

55 e show that deleting the Tip30 gene leads to ductal hyperplasia in mouse mammary glands early in life

56 focal lobular carcinoma in situ in one, and ductal hyperplasia in one.

57 sults: fibrocystic changes in four, atypical ductal hyperplasia in two, atypical lobular hyperplasia

58 ogical alterations similar to micropapillary ductal hyperplasias in the human breast.

59 Atypical ductal hyperplasia is a lesion with significant malignan

60 Two (25%) of eight atypical ductal hyperplasia lesions were upgraded to DCIS at exci

61 her malignant or high-risk lesions (atypical ductal hyperplasia, lobular carcinoma in situ, atypical

62 evelopment, and glands were characterized by ductal hyperplasia, luminal filling, and highly disorgan

63 = 1), lobular neoplasia (n = 1), or atypical ductal hyperplasia (n = 1).

64 r periductal inflammatory cell accumulation, ductal hyperplasia, or dysplastic lesions/pancreatic int

65 se lesions such as papillomatosis, papillary ductal hyperplasia, papillary ductal carcinoma in situ (

66 eases QR levels and results in a decrease in ductal hyperplasia, proliferation, oxidative DNA damage

67 Proliferative breast lesions, such as simple ductal hyperplasia (SH) and atypical ductal hyperplasia

68 h atypical lobular hyperplasia plus atypical ductal hyperplasia, the ratio was 1/1.

69 sed progressively during the transition from ductal hyperplasia to ductal carcinoma in situ to adenoc

70 cancer occurs during progression from usual ductal hyperplasia to ductal carcinoma in situ.

71 Usual ductal hyperplasia (UDH) of the breast is generally rega

72 ion of breast lesions as either benign usual ductal hyperplasia (UDH) or malignant ductal carcinoma i

73 ransgenic (AEBP1(TG)) mice, and the onset of ductal hyperplasia was accelerated in AEBP1(TG) mice fed

74 Atypical ductal hyperplasia was found in 23 (4.5%) of 510 lesions

75 ased cell division and a distinctive form of ductal hyperplasia with 'squamoid' ghost cell nodules in

76 The glands of adult mice also exhibit ductal hyperplasia with a disorganized basement membrane

77 Ductal hyperplasia with and without atypia exhibited hig

78 The pancreas exhibited significant ductal hyperplasia, with an increase in the number of du