The pathogenesis of cancer metastasis: the 'seed and soil' hypothesis revisited

By I. J. Fidler. Nature Reviews. Cancer, 2003

4,750 citations recorded by the source corpus.

Subfields: Biotechnology, Cancer Research, Oncology

View Paper: https://www.semanticscholar.org/paper/7e67c778de9aa3c15124b9948314b783e884e596

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Citations in the corpus

Hallmarks of cancer: the next generation. (2011, neutral): “The multistep process of invasion and metastasis has been schematized as a sequence of discrete steps, often termed the invasion-metastasis cascade (Talmadge and Fidler, 2010; Fidler, 2003).”
Therapeutic targeting of the tumor microenvironment. (2005, neutral): “Metastatic cells need an appropriate microenvi ronment in which they can survive and proliferate (Fidler, 2003).”
A microRNA DNA methylation signature for human cancer metastasis (2008, background): “Metastasis is responsible for 90% of deaths in patients with solid tumors (10, 11), so understanding its pathogenesis at the systemic, cellular, and molecular levels has become one of the most ambitious goals in cancer research (10, 11).”
Axis of evil: molecular mechanisms of cancer metastasis (2003, background): “It has been recognized for over a century (Stephen Paget, 1889 – please refer to reference by Fidler, 2003) that the organ preference for metastatic colonization is influenced by interactions between the circulating tumor cell (the ‘seed’) and the target host tissue (the ‘soil’).”
TGFβ in Cancer (2008, background): “new host microenvironment, and eventually grow into lethal tumor colonies in those distal organs (Fidler, 2003; Gupta and Massagué, 2006).”
The basics of epithelial–mesenchymal transition (EMT): A study from a structure, dynamics, and functional perspective (2019, background): “Cancer metastasis is a complex process where the variety of alternations occur termed as the invasion‐metastasis cascade (Croker & Allan, 2008; Fidler, 2003) followed by a variation of the gene expression signatures and cellular morphology (Fidler, 2003).”
AACR Centennial Series: The Biology of Cancer Metastasis: Historical Perspective (2010, neutral): “Although this hypothesis was challenged (2), it is now largely accepted that the anatomic architecture of the blood flow is not sufficient to fully describe the patterns of metastatic tumor spread.”
Circulating Tumor Cell Clusters are Oligoclonal Precursors of Breast Cancer Metastasis (2014, background): “…School, Boston, MA 02129, USA 7Department of Surgery, Harvard Medical School, Boston, MA 02129, USA 8Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA *Correspondence: dhaber@mgh.harvard.edu (D.A.H.), maheswaran@helix.mgh.harvard.edu (S.M.) http://dx.doi.org/10.1016/j.cell.2014.07.013”
Epithelial–mesenchymal plasticity in carcinoma metastasis (2013, background): “…stromal environment, an even smaller subset of tumor cells establish micrometastases with the potential to proliferate into fully malignant, secondary tumors that are clinically detectable and eventually life-threatening (step V: colonization) (Thiery 2002; Fidler 2003; Kalluri and Weinberg 2009).”
MicroRNA function in cancer: oncogene or a tumor suppressor? (2009, background): “The molecular requirements for some of these steps may be tissue-specific, as was noted more than a century ago in breast carcinomas that metastasized to bone and lung [78].”
A Unique Metastasis Gene Signature Enables Prediction of Tumor Relapse in Early Stage Hepatocellular Carcinoma Patients (2010, neutral): “The traditional tumor evolution model suggests that a primary tumor is initially benign and over time acquires mutations that give a few tumor cells the ability tometastasize (8, 33).”
Cancer as a metabolic disease (2010, background): “distant capillary bed, and invade and proliferate in distant organs [185-189].”