Stromal Effects on Mammary Gland Development and Breast Cancer

By B. Wiseman, Zena Werb. Science, 2002

868 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/9b3fe77e8ca15ea23db0a676dec17e8a14d59f87

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Citations in the corpus

GATA-3 maintains the differentiation of the luminal cell fate in the mammary gland. (2006, neutral): “In the mammary gland, differentiated luminal cells rely on survival signals from the basement membrane ( Wiseman and Werb, 2002 ).”
From signatures to models: understanding cancer using microarrays (2005, background): “…functional categories (cell cycle, DNA and RNA repair, and metabolism), we found multiple modules enriched for genes associated with extracellular inflammation, immunity and extracellular matrix, processes that are increasingly recognized to be important in tumor generation and progression 44,45 .”
In vitro propagation and transcriptional profiling of human mammary stem/progenitor cells. (2003, background): “Factors intrinsic to these putative stem cells as well as their interactions with stromal cells and extracellular matrix are important in the normal morphogenesis of the gland (Wiseman and Werb 2002).”
Tumors as organs: complex tissues that interface with the entire organism (2010, positive): “The stroma is essential for normal organ development (e.g., Cunha, 2008; Puri and Hebrok, 2010; Wiseman and Werb, 2002).”
Extracellular matrix: a dynamic niche component during cancer progression (2012, positive): “The concept that local microenvironments, or niches, play an impor tant role in regulating cell behavior, which is one of the central themes in classical embryology, has become increasingly ac cepted in cancer biology (Bissell and Radisky, 2001; Wiseman and Werb, 2002; Bissell and Labarge, 2005).”
Dynamic interplay between the collagen scaffold and tumor evolution (2010, background): “For example, the epithelial migration and invasion occurring in mammary carcinomas are morphologically and molecularly similar to epithelial branching morphogenesis in mammary gland development [2,3].”
Cancer-associated adipocytes exhibit an activated phenotype and contribute to breast cancer invasion. (2011, background): “In addition, because mature adipocytes are the most abundant cells in the breast tumor stroma (3), their cumulative secretion of IL-6 could therefore have profound impact on tumor progression.”
The tumour microenvironment as a target for chemoprevention (2007, background): “? There is no intrinsic reason to postulate that carcinogenesis necessarily begins with epithelial dysfunction, especially because underlying mesenchymal cells control epithelial differentiation during embryogenesi”
Molecular characterization of the tumor microenvironment in breast cancer. (2004, background): “, 2003 ; Tlsty , 2001 ; Tlsty and Hein , 2001 ; Wiseman and Werb , 2002 ) .”
Integrin signalling during tumour progression (2004, background): “But despite their relative anchorage independence, cancer cells still benefit from integrin signals, both during tumour initiation and tumour progressio”
Axis of evil: molecular mechanisms of cancer metastasis (2003, background): “We now view cancer as a complex tissue resulting from disrupted organ homeostasis, rather than focusing on the cancer cell, and the genes within it, alone (Hanahan and Weinberg, 2000; Bissell and Radisky, 2001; Bogenrieder and Herlyn, 2002; Wiseman and Werb, 2002).”
Fibroblasts in cancer (2006, positive): “In addition, fibroblasts are important in maintaining the homeostasis of adjacent epithelia through the secretion of growth factors and direct mesenchymal–epithelial cell interaction”
Diverse regulation of mammary epithelial growth and branching morphogenesis through noncanonical Wnt signaling (2017, background): “The morphogenetic changes of the breast epithelium are closely coordinated within the context of its microenvironment, which consists of a variety of stromal cells such as adipocytes, macrophages, and fibroblasts (6, 7).”
Extracellular matrix and cell signalling: the dynamic cooperation of integrin, proteoglycan and growth factor receptor. (2011, background): “Metastatic tumours arise when the cancer cells gain the capacity to degrade the normal tissue architecture and migrate out into interstitial spaces and eventually to different sites after breaking away from the surrounding ECM boundaries (Wiseman & Werb 2002).”