Tumor self-seeding by circulating cancer cells
By Mi-Young Kim, Thordur Oskarsson, Swarnali Acharyya, D. Nguyen, X. Zhang, Larry Norton, J. Massagué. Cell, 2009
1,320 citations recorded by the source corpus.
Summary The dissemination of cancer cells from a primary tumor is conventionally viewed as a unidirectional process that culminates with the metastatic colonization of distant organs. Here we show that circulating tumor cells (CTCs) can also colonize their tumors of origin, in a process that we call “tumor self-seeding”. Self-seeding of breast cancer, colon cancer, and melanoma tumors in mice is preferentially mediated by aggressive CTCs, including those with bone, lung or brain metastatic tropism. The tumor-derived cytokines IL-6 and IL-8 acted as CTC attractants and the poor-prognosis markers MMP1/collagenase-1 and the actin cytoskeleton component fascin-1 as mediators of CTC infiltration into mammary tumors. Self-seeding can accelerate tumor growth, angiogenesis, and stromal recruitment through seed-derived factors including, in a breast cancer model, the chemokine CXCL1. Tumor self-seeding could explain the relationships between anaplasia, tumor size, vascularity and prognosis, and local recurrence seeded by disseminated cells following ostensibly complete tumor excision.
Subfields: Cancer Research, Cell Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/89164c1fe12fb75883239dc64bea848d1fa4ab90
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Citations in the corpus
- Polyclonal breast cancer metastases arise from collective dissemination of keratin 14-expressing tumor cell clusters (2016, result): “These data are consistent with the reported ability of metastases to reseed primary tumors, termed “tumor self-seeding” (21).”
- Chemotaxis in cancer (2011, background): “However, invasion and dissemination can still be clinically relevant targets after resection of the primary tumour, because tumour cells can disseminate from metastatic sites and seed back to the primary tumour site or other metastatic site”
- Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling. (2011, background): “Metastatic lesions have been shown to cross seed via circulating tumor cells, which may in principle distribute small numbers of resistant cells across many metastatic foci.(72) In such a case, treatment-refractory clones could”
- Tumor microenvironment complexity and therapeutic implications at a glance (2020, background): “Finally, there is the prognosis for local recurrence by seeding of disseminated cells after apparently complete tumor ablation [147, 148] .”
- Hallmarks of cancer: the next generation. (2011, positive): “Accordingly, tissuespecific colonization programs that are evident among cells within a primary tumor may originate not from classical tumor progression occurring within the primary lesion but instead from emigrants that have returned home (Kim et al., 2009).”
- The Two Faces of IL-6 in the Tumor Microenvironment (2014, background): “IL-6 has also been reported to promote tumor self-seeding by attracting the most aggressive metastatic cells out of circulation to primary tumor sites [44].”