A molecular signature of metastasis in primary solid tumors

By Sridhar Ramaswamy, K. Ross, Eric S. Lander, Todd R. Golub. Nature Genetics, 2003

2,508 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/4f86c5a0349d335bcbbb193e5c76db455e17e683

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Citations in the corpus

Circulating tumor cells (CTC) detection: clinical impact and future directions. (2007, background): “In fact, it has been demonstrated that cancer cells in the primary tumor may harbor a gene-expression signature matching that observed in the metastatic colony and that this signature can be used to predict, with high accuracy, whether the tumor will remain localized or whether the patient will expe”
Beyond tumorigenesis: cancer stem cells in metastasis (2007, background): “This suggests that the metastasis gene program is shared by the majority of cancer cells found in primary tumors [ 113-116 ].”
Tumor cell traffic through the extracellular matrix is controlled by the membrane-anchored collagenase MT1-MMP (2004, background): “…content and structure can differ dramatically from tissue to tissue even during postnatal states (Hay, 1991), gene-expression profiles demonstrate that type I collagen is up-regulated consistently at both primary and metastatic sites in a wide variety of human carcinomas (Ramaswamy et al., 2003).”
Tumor morphology and phenotypic evolution driven by selective pressure from the microenvironment. (2006, background): “These results are consistent with recent clinical studies showing that metastases have the same genotype as primary tumors (Ramaswamy et al., 2003).”
Functional proteomic screens reveal an essential extracellular role for hsp90α in cancer cell invasiveness (2004, background): “For example, microarray analyses have identified differentially expressed genes from many classes that might contribute to invasivenes”
Axis of evil: molecular mechanisms of cancer metastasis (2003, background): “Data for this reasoning stem from cDNA-microarray analyses revealing that the gene-expression pattern of metastatic tumor cells is often strikingly similar to the cells of the primary tumor from which they were derived (Ramaswamy et al., 2003).”
Identification of diagnostic subnetwork markers for cancer in human protein-protein interaction network (2010, background): “Extensive work has been done to identify differentially expressed genes across different phenotypes [1-5], which can be used as diagnostic markers for classifying different disease states or predicting the clinical outcomes [6-11].”
Pericytes: developmental, physiological, and pathological perspectives, problems, and promises. (2011, background): “…events and reduced expression ofmural cell markers has been demonstrated across a wide range of 206 Developmental Cell 21, August 16, 2011 ª2011 Elsevier Inc. human solid tumors, suggesting that low pericyte coverage may trigger metastasis and correlate to poorer prognosis (Ramaswamy et al., 2003).”
Gene expression profiling spares early breast cancer patients from adjuvant therapy: derived and validated in two population-based cohorts (2005, background): “CDKN1C, a tumor suppressor gene that regulates cell proliferation, was recently found to be downregulated in metastatic tumors [28].”
Integrative analysis of the cancer transcriptome (2005, background): “In a demonstration of such an analysis, Ramaswamy and colleagues identified a gene-expression signature that was differentially expressed in metastatic tumors of diverse origins relative to primary cancer”