
NCBI . NLM . NIH . GOV {
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Title[redir]:
Non-cell autonomous tumor-growth driving supports sub-clonal heterogeneity - PMC
Description:
Cancers arise through a process of somatic evolution that can result in substantial sub-clonal heterogeneity within tumors. The mechanisms responsible for the coexistence of distinct sub-clones and the biological consequences of this coexistence ...
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Keywords {π}
tumor, tumors, cells, growth, doi, clonal, cell, data, fig, extended, google, scholar, pubmed, subclones, cancer, pmc, heterogeneity, polyclonal, article, proliferation, noncell, expansion, model, parental, free, nature, autonomous, open, tab, clones, subclone, rates, figure, metastasis, loxl, ilrΞ±, individual, mathematical, monoclonal, analysis, driving, evolution, lines, dynamics, initial, frequency, doxorubicin, performed, shrna, increase,
Topics {βοΈ}
dana-farber cancer institute stat1 mediate il-11-dependent hrp conjugated anti-mouse heat-induced antigen retrieval human-specific reference amplicon 3/v5-dest expressed anchor mda-mb-468 derivate lines wnt-driven mammary cancers dormant micro-metastatic lesions microenvironmentally-constrained progression bottleneck bi-lateral orthotopic injection pmc beta search cell-autonomously acting factors cell-autonomous fitness advantage il11-driven tumors displayed direct autocrine/paracrine stimulation mda-mb-468 cell line mcherry/luciferase lentiviral construct inducing tumor-promoting microenvironmental inter-clonal interactions suggest supplementary materials included sample kolmogorov-smirnov test enabling inter-clonal interactions single cell-derived clones human-il11 elisa single-cell based analyses figf/il11 tumors displayed tumor-growth promoting effects parental mda-mb-468 cells anti-cd31 immunohistochemical staining tumor volume-density relation il11-driven polyclonal tumors anti-brdu immunohistochemical staining il11-expressing clones derived [google scholar] 12 karmanos cancer institute rabbit monoclonal igg experiments il11-expressing cells volume-based cellularity inferences strong driver mutations cell death occurs abolishing apoptotic response peritoneal wall metastases obtain additional benefit higher proliferative output observe elevated rates exogenously expressed il11rΞ± exponential growth pattern abc peroxidase system license information pmcid
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- Challenging the axiom: does the occurrence of oncogenic mutations truly limit cancer development with age?
- Why donβt we get more cancer?
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