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1 spiration of a right axillary node confirmed metastatic carcinoma.
2 asive adenocarcinoma to castration-resistant metastatic carcinoma.
3 paradigm for clinical intervention of liver metastatic carcinoma.
4 of the three sentinel lymph nodes contained metastatic carcinoma.
5 differentiation from cholangiocarcinoma and metastatic carcinoma.
6 carcinoma, and in metastatic cell lines and metastatic carcinoma.
7 ary for active cell migration in invasive or metastatic carcinoma.
8 Two of the 11 axillary lymph nodes contained metastatic carcinoma.
9 ken for an intraparotid lymph node harboring metastatic carcinoma.
10 erts preneoplastic lesions into invasive and metastatic carcinomas.
11 plasms that progress to locally invasive and metastatic carcinomas.
12 r-reaching implications for the treatment of metastatic carcinomas.
13 or macrophage-activating factors secreted by metastatic carcinomas.
14 adhesion kinase (FAK) are expressed in colon metastatic carcinomas.
15 of non-invasive tumor cells into malignant, metastatic carcinomas.
16 protease associated with rapidly growing and metastatic carcinomas.
17 ents a testable therapeutic approach against metastatic carcinomas.
18 s but delayed their development to invasive, metastatic carcinomas.
19 mas, 18 of 28 primary carcinomas, and 5 of 5 metastatic carcinomas.
20 A1, a human gene with elevated expression in metastatic carcinomas.
21 derstood and unleveraged in the treatment of metastatic carcinomas.
22 n reaction in 30 of 33 EBVaGC cases, 8 of 10 metastatic carcinomas, 14 non-neoplastic tissues from 27
23 ary tumor growth and lung dissemination of a metastatic carcinoma (4T1), but not of a nonmetastatic c
24 nulosa cell (GC) tumors that can progress to metastatic carcinoma and thus provide a model system for
25 on of BKV large T antigen in the primary and metastatic carcinoma, but not in the nonneoplastic uroth
26 concurrently with the transition to invasive metastatic carcinoma, but they were expressed in differe
27 ntous G proteins, which are overexpressed in metastatic carcinomas, but their functions in epithelial
29 r actin polymerization in the invadopodia of metastatic carcinoma cells and define four distinct stag
31 In addition, silencing alphaB-crystallin in metastatic carcinoma cells reduced the number of viable
34 he splenic lesion was performed and revealed metastatic carcinoma, consistent with the lung primary.
35 epithelial neoplasia (HGPIN) to invasive and metastatic carcinoma could facilitate study of the regul
37 hyperplasias, papillomas, and dysplasias to metastatic carcinomas developed in squamous epithelia of
38 distinguish adenocarcinoma of the NPCE from metastatic carcinoma, especially metastatic clear cell r
39 6 per million in Asians) from hemangioma and metastatic carcinoma following the clinical practice.
40 patients in the radical group, only 10% had metastatic carcinoma in the resected retroperitoneal lym
41 ation, lymphoproliferative inflammation, and metastatic carcinomas in the lung after a period of late
42 e been linked to various diseases, including metastatic carcinomas in which the 9 carbon sialic acid
44 were maintained when stratifying tumor into metastatic carcinoma (N = 57) and meningioma (N = 17).
46 biopsy of the gastric antrum later showed a metastatic carcinoma of breast origin with typical tumor
48 18 years) diagnosed with locally advanced or metastatic carcinoma of the pancreas confirmed by cytolo
49 Identifying the primary site in cases of metastatic carcinoma of unknown origin has profound clin
51 d 18 years or older initially diagnosed with metastatic carcinoma or who subsequently developed metas
55 promotes cell migration and is a hallmark of metastatic carcinomas, we asked whether it increases FA
56 biopsies from patients with various advanced metastatic carcinomas, wherein these cells are transitio
57 hat develop extensive HGPIN and invasive and metastatic carcinoma with neuroendocrine (NE) differenti
58 t inhibitor, in 41 patients with progressive metastatic carcinoma with or without mismatch-repair def