Parallel progression of primary tumours and metastases

By Christophe Klein. Nature Reviews. Cancer, 2009

1,145 citations recorded by the source corpus.

Subfields: Cancer Research, Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/b3881256ddfc4ac98fc058c5ea79d465ea8c037c

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Citations in the corpus

EMT and dissemination precede pancreatic tumor formation (2012, methodology): “This model has several conceptual problems (Gupta et al., 2005; Klein, 2009) and fails to account for two clinical observations: the appearance of metastatic lesions years after resection of small tumors with no clinically evident metastases at diagnosis (Pantel et al., 2008) and metastases of…”
Genomic Evolution of Breast Cancer Metastasis and Relapse (2017, background): “…relapsing ormetastatic clones disseminated early from the primary breast cancer with extensive parallel evolution, as has been suggested previously (Klein, 2009), then targeting somatic mutations found in the primary would not necessarily have much relevance to disseminated cells without those…”
Hallmarks of cancer: the next generation. (2011, positive): “On the other hand, evidence has recently emerged indicating that cells can disseminate remarkably early, dispersing from ostensibly noninvasive premalignant lesions in both mice and humans (Coghlin and Murray, 2010; Klein, 2009).”
The perivascular niche regulates breast tumor dormancy (2013, background): “(a) Heat map of ECM proteins (spectral counts) from (1) neovascular tiphigh cultures (LF+ctrl shRNA EC) normalized by lung stroma (LF), (2) neovascular tiplow cultures (LF+Notch1 shRNA EC) normalized by lung stroma (LF) and (3) tiphigh cultures normalized by tiplow cultures (sorted high to low with ”
Breast cancer development and progression: Risk factors, cancer stem cells, signaling pathways, genomics, and molecular pathogenesis (2018, background): “There are currently two prevailing and competitive models of metastasis, the early dissemination model, which hypothesizes that cancer cells with metastatic potential are seeded early in tumor formation and lay dormant for a period of time, and the late dissemination model, which suggests that metas”
Tumor Metastasis: Molecular Insights and Evolving Paradigms (2011, neutral): “…to undergo multiple rounds of genetic diversification followed by clonal selection within the distant organ sites in which overt metastases ultimately develop—specifically, microenvironments where mutations in metastasis virulence genes can now be selectively advantageous (Figure 6E) (Klein, 2009).”
Epithelial-Mesenchymal Plasticity: A central regulator of cancer progression (2015, background): “The known functions of the EMT would not seem to confer such adaptive powers, suggesting that disseminated cells must invent such adaptations on their own following their arrival at distant tissues (Klein 2009).”
EMERGING BIOLOGICAL PRINCIPLES OF METASTASIS (2017, positive): “These studies favor the linear progression model rather than the parallel progression model, which posits that metastasis occurs as an early event during tumorigenesis, after which the primary tumor and disseminated colonies evolve independently at sites far removed from one another (Klein, 2009).”
Early dissemination seeds metastasis in breast cancer (2016, neutral): “Therefore, parallel progression 7 seems to be typical rather than exceptional.”