Comedo-ductal carcinoma in situ: A paradoxical role for programmed cell death
about
Analysis of stromal signatures in the tumor microenvironment of ductal carcinoma in situ.Identification of PADI2 as a potential breast cancer biomarker and therapeutic target.Longitudinal study of mammary epithelial and fibroblast co-cultures using optical coherence tomography reveals morphological hallmarks of pre-malignancy.Rad6B acts downstream of Wnt signaling to stabilize β-catenin: Implications for a novel Wnt/β-catenin target.Regulation of DCIS to invasive breast cancer progression by Singleminded-2s (SIM2s).Cleavage of galectin-3 by matrix metalloproteases induces angiogenesis in breast cancerMyoepithelial cell differentiation markers in ductal carcinoma in situ progression.Silencing of HSulf-2 expression in MCF10DCIS.com cells attenuate ductal carcinoma in situ progression to invasive ductal carcinoma in vivo.Cullin-3 protein expression levels correlate with breast cancer progression.Phenotypic and Molecular Characterization of MCF10DCIS and SUM Breast Cancer Cell Lines.Gold nanoparticle conjugated Rad6 inhibitor induces cell death in triple negative breast cancer cells by inducing mitochondrial dysfunction and PARP-1 hyperactivation: Synthesis and characterization.Matrix detachment and proteasomal inhibitors diminish Sulf-2 expression in breast cancer cell lines and mouse xenograftsOcimum gratissimum retards breast cancer growth and progression and is a natural inhibitor of matrix metalloproteasesComedo-DCIS is a precursor lesion for basal-like breast carcinoma: identification of a novel p63/Her2/neu expressing subgroupNovel multicellular organotypic models of normal and malignant breast: tools for dissecting the role of the microenvironment in breast cancer progressionOver-expression of the BRMS1 family member SUDS3 does not suppress metastasis of human cancer cells.Genome based cell population heterogeneity promotes tumorigenicity: the evolutionary mechanism of cancerCancer stem cells and early stage basal-like breast cancer.Glucocorticoids promote transition of ductal carcinoma in situ to invasive ductal carcinoma by inducing myoepithelial cell apoptosis.
P2860
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P2860
Comedo-ductal carcinoma in situ: A paradoxical role for programmed cell death
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh
2008年學術文章
@zh-hant
name
Comedo-ductal carcinoma in situ: A paradoxical role for programmed cell death
@ast
Comedo-ductal carcinoma in situ: A paradoxical role for programmed cell death
@en
type
label
Comedo-ductal carcinoma in situ: A paradoxical role for programmed cell death
@ast
Comedo-ductal carcinoma in situ: A paradoxical role for programmed cell death
@en
prefLabel
Comedo-ductal carcinoma in situ: A paradoxical role for programmed cell death
@ast
Comedo-ductal carcinoma in situ: A paradoxical role for programmed cell death
@en
P2093
P2860
P356
P1476
Comedo-ductal carcinoma in situ: A paradoxical role for programmed cell death
@en
P2093
Daniel W Visscher
Fred R Miller
Gen Sheng Wu
Gloria H Heppner
Hind Nassar
Larry Tait
Malathy P V Shekhar
Robert J Pauley
Steven J Santner
Varun Shekhar
P2860
P304
P356
10.4161/CBT.7.11.6781
P577
2008-11-12T00:00:00Z