Mediators of vascular remodelling co-opted for sequential steps in lung metastasis

By G. Gupta, D. Nguyen, A. Chiang, Paula D. Bos, Juliet Y. Kim, C. Nadal, R. Gomis, K. Manova-Todorova, J. Massagué. Nature, 2007

736 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/c2c8c06cf5438a3e20c314192ae8faea9f75a720

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Citations in the corpus

A Distinct Macrophage Population Mediates Metastatic Breast Cancer Cell Extravasation, Establishment and Growth (2009, background): “Despite the considerable efforts that have been expended on studying the interaction between metastasizing tumor cells and blood vessel in target organs, no uniform conclusions have been reached [40,41].”
Protease-dependent versus -independent cancer cell invasion programs: three-dimensional amoeboid movement revisited (2009, background): “Although both MMP-1 and MMP-2 can modulate breast cancer behavior in vivo (Tester et al., 2004; Wyatt et al., 2005; Gupta et al., 2007), silencing both proteases in tandem does not affect MDA-MB-231 or SUM-159 invasion (Fig.”
Monoacylglycerol lipase regulates a fatty acid network that promotes cancer pathogenesis (2010, background): “Within the MAGL-fatty acid network are several protumorigenic lipid messengers, including LPA and PGE2, that have been shown to promote the aggressiveness of cancer cells (Gupta et al., 2007; Mills and Moolenaar, 2003).”
Structure and dynamics of molecular networks: A novel paradigm of drug discovery: A comprehensive review (2012, background): “s 138 (2013) 333–408 385 prevented the desired pharmacological goal. Combination therapies and multi-target drugs may both overcome system robustness and provide less side-effects (see Section 4.1.5; Gupta et al., 2007; Berger & Iyengar, 2009; Wilson et al., 2009; Azmi et al., 2010; Glaser, 2010”
Tumor self-seeding by circulating cancer cells (2009, methodology): “note, the intrinsic proliferation rate of MDA231-LM2 is similar to that of the parental MDA231 population (Gupta et al., 2007), and the same applies to the MDA231-S1a and S1b lines (data not shown).”
Polyclonal breast cancer metastases arise from collective dissemination of keratin 14-expressing tumor cell clusters (2016, neutral): “effectors involved in niche remodeling (29, 37).”
Cancer Cell Metabolism: One Hallmark, Many Faces (2012, background): “Lipidomics analysis further suggested that elevated MAGL activity was particularly responsible for the increased production of specific lipid messengers, such as lysophosphatidic acid (LPA) and prostaglandin E (PGE2) (79), which have been shown to promote tumor cell aggressiveness (80, 81).”