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1 , since only 10% of all cancers are invasive lobular carcinoma).
2 at 30, 48, and 60 months-including two with lobular carcinoma.
3 The technique is not recommended for lobular carcinoma.
4 ctal carcinoma, and ER-positive infiltrating lobular carcinoma.
5 inoma, and one had mixed invasive ductal and lobular carcinoma.
6 om this cohort, we studied SLN from cases of lobular carcinoma.
7 es, using any technique, to evaluate SLN for lobular carcinoma.
8 several 2-5-mm foci of invasive tubular and lobular carcinoma.
9 the incidence of DCIS or invasive ductal or lobular carcinoma.
10 e in the progression to the invasive form of lobular carcinoma.
11 proportionately high percentage are invasive lobular carcinoma.
12 1 patients with invasive cancer had invasive lobular carcinoma.
13 vealed 35 ductal carcinomas and two invasive lobular carcinomas.
14 might also participate in the development of lobular carcinomas.
15 tal carcinoma (IDC) (0.2-8.9 cm), 3.5 cm for lobular carcinoma (1.6-8.0 cm), and 5.7 cm for phyllodes
16 carcinoma, 1 high-grade mammary carcinoma, 3 lobular carcinoma, 1 invasive papilloma, and 4 sentinel
18 invasive ductal carcinoma; and 12, invasive lobular carcinoma (a large percentage [33%], since only
19 (95% CI, 1.7-4.3) increased risk of invasive lobular carcinoma, a 1.5-fold (95% CI, 1.1-2.0) increase
20 tients yielded 3 carcinomas: an infiltrating lobular carcinoma, a ductal carcinoma in situ, and an in
21 Twist expression is correlated with invasive lobular carcinoma, a highly infiltrating tumor type asso
22 are the predominant appearances of invasive lobular carcinoma, and a computer-aided detection system
23 invasive ductal carcinoma, two had invasive lobular carcinoma, and one had mixed invasive ductal and
27 erative discovery of predefined factors (eg, lobular carcinoma) could trigger addition of external be
29 ases versus 10 of 29 (34%) cases of invasive lobular carcinoma (ILC) (P < .001) and 21 of 38 (55%) ca
31 Invasive ductal carcinoma (IDC) and invasive lobular carcinoma (ILC) are the two major histological t
37 e ductal carcinoma (IDC) or classic invasive lobular carcinoma (ILC) who were randomly assigned onto
40 biased by small sample size, by interpreting lobular carcinoma in situ (LCIS) as a positive result, b
41 east cancer risk conferred by a diagnosis of lobular carcinoma in situ (LCIS) is poorly understood.
42 tu (DCIS) and 282 women with a first primary lobular carcinoma in situ (LCIS) were followed for contr
43 red the association between risk factors and lobular carcinoma in situ (LCIS; n = 186) with that of r
44 in the atypical lobular hyperplasia (n = 2), lobular carcinoma in situ (n = 5), or radial scar (n = 3
46 ith proliferative breast lesions (ductal and lobular carcinoma in situ and atypical ductal hyperplasi
48 two, atypical lobular hyperplasia and focal lobular carcinoma in situ in one, and ductal hyperplasia
49 ical type (p=0.03), with a relative risk for lobular carcinoma in situ of 2.82 (1.72-4.63) and 1.56 (
50 ecent year of diagnosis, and the presence of lobular carcinoma in situ were significantly associated
51 nly rare cells of the noninvasive component (lobular carcinoma in situ) in the same tissue sections s
54 diotherapy, ductal carcinoma with concurrent lobular carcinoma in situ, and DCIS in elderly people an
55 h-risk lesions (atypical ductal hyperplasia, lobular carcinoma in situ, atypical lobular hyperplasia)
56 ++ were classified as being within ductal or lobular carcinoma in situ, invasive carcinoma, carcinoma
57 l hyperplasia, atypical lobular hyperplasia, lobular carcinoma in situ, or radial scar) was identifie
58 ost in the vast majority (13/17) of cases of lobular carcinoma in situ, which is defined by cellular
65 or atypical ductal or lobular hyperplasia or lobular carcinoma in situ; or ductal carcinoma in situ w
66 nfiltrating ductal carcinoma or infiltrating lobular carcinoma in the breast or axillary lymph nodes)
67 ive breast cancer (IBC) after a diagnosis of lobular carcinoma-in-situ (LCIS) by using Surveillance,
69 pical hyperplasia, Gail risk greater than 5, lobular carcinoma-in-situ, or two or more first-degree r
72 ase presents a clinical challenge given that lobular carcinoma is more difficult to detect than ducta
76 ion, we orthotopically transplanted invasive lobular carcinoma (mILC) fragments into mammary glands o
79 was more likely to show malignancy, invasive lobular carcinoma, or ductal carcinoma in situ alone (P
81 ations generally were similar for ductal and lobular carcinomas (P-heterogeneity=0.43) and by tumor s
84 conclude that the vast majority of invasive lobular carcinomas show overexpression of cyclin D1 prot
85 comprises 27 indisputable cases of invasive lobular carcinoma showing varying degrees of cytological
86 d in cell lines derived from mouse and human lobular carcinomas that possess high FGFR1 activity.
87 s a critical component of FGFR1 signaling in lobular carcinomas, thus implicating RSK as a candidate
88 cyclin D1 protein overexpression in invasive lobular carcinoma, to investigate the cause of the prote
91 was significantly increased in patients with lobular carcinoma vs those with ductal carcinoma (adjust
93 was excluded as a positive result, invasive lobular carcinoma was not significantly more bilateral t
94 oplasms may be broadly divided into invasive lobular carcinoma, well-differentiated subtypes of invas
97 mplete loss, as exemplified by E-cadherin in lobular carcinoma (where E-cadherin is frequently mutate
98 he high ER mRNA group, 5 (18%) were invasive lobular carcinomas whereas all 24 tumors with low ER mRN
99 ptions are becoming widely used for invasive lobular carcinoma, yielding outcomes equivalent to those
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