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1 res were age and HRL histologic results (eg, atypical ductal hyperplasia).
2 sis, radial scar, fibroadenoma, and areas of atypical ductal hyperplasia.
3 .5 (95% CI, 0.4 to 5.6) for the diagnosis of atypical ductal hyperplasia.
4 quantitatively insufficient is described as atypical ductal hyperplasia.
6 he TAM-01 population included 500 women (20% atypical ductal hyperplasia, 11% LCIS, and 69% DCIS).
7 CNB results in patients with a diagnosis of atypical ductal hyperplasia (ADH) (75 of 6,081 [1.2%]) w
8 ose To assess the rate of underestimation of atypical ductal hyperplasia (ADH) and ductal carcinoma i
9 terozygosity (LOH) on 11q13 (PYGM, INT-2) in atypical ductal hyperplasia (ADH) and various histologic
10 lpable breast lesions diagnosed initially as atypical ductal hyperplasia (ADH) by core needle biopsy.
11 core biopsy revealed carcinoma in 19 (61%), atypical ductal hyperplasia (ADH) in eight (26%), and be
12 osis in two, papilloma with adjacent foci of atypical ductal hyperplasia (ADH) in eight, and well-dif
14 Management of percutaneously diagnosed pure atypical ductal hyperplasia (ADH) is an unresolved clini
15 ision was advised for the 143 carcinomas, 25 atypical ductal hyperplasia (ADH) lesions, and five radi
17 uctal carcinoma in situ (DCIS), one focus of atypical ductal hyperplasia (ADH), and one atypical lobu
18 , such as simple ductal hyperplasia (SH) and atypical ductal hyperplasia (ADH), are candidate precurs
19 thylation landscape of normal breast tissue, atypical ductal hyperplasia (ADH), DCIS and invasive bre
20 (DCIS), as well as the co-occurrence rate of atypical ductal hyperplasia (ADH), with 95% CIs were cal
22 ncreased expression of 14-3-3 zeta begins at atypical ductal hyperplasia, an early stage of breast di
23 uctal carcinoma in situ were reclassified as atypical ductal hyperplasia and considered false-positiv
24 sed in noninvasive breast lesions, including atypical ductal hyperplasia and ductal carcinoma in situ
25 tem and luminal progenitor cells, and induce atypical ductal hyperplasia and intraepithelial neoplasi
27 ns (ductal and lobular carcinoma in situ and atypical ductal hyperplasia), and 277 controls without t
28 ative, although premalignant lesions such as atypical ductal hyperplasia are highly ER-alpha-positive
29 %), CCL with atypia 9% (95% CI: 5%-14%), and atypical ductal hyperplasia associated with CCL 20% (95%
30 s of CCL without atypia, CCL with atypia and atypical ductal hyperplasia associated with CCL followed
31 with a CNB diagnosis of CCL with atypia and atypical ductal hyperplasia associated with CCL, surgica
33 best-characterized premalignant lesions are atypical ductal hyperplasia, atypical lobular hyperplasi
35 ance, and apparent complete lesion removal), atypical ductal hyperplasia diagnosed with percutaneous
36 20%) yielded high-risk lesions, including 21 atypical ductal hyperplasia, eight atypical lobular hype
37 development of premalignant lesions such as atypical ductal hyperplasia, elevated growth factors, or
38 benign results: fibrocystic changes in four, atypical ductal hyperplasia in two, atypical lobular hyp
41 randomly assigned 500 women with breast IEN (atypical ductal hyperplasia, lobular carcinoma in situ [
42 were either malignant or high-risk lesions (atypical ductal hyperplasia, lobular carcinoma in situ,
43 ted from the metastatic pleural effusion and atypical ductal hyperplasia mammary tumor specimens (21M