Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
2010-1-21
pubmed:abstractText
Tumors are heterogeneous collections of cells with highly variable abilities to survive, grow, and metastasize. This variability likely stems from epigenetic and genetic influences, either stochastic or hardwired by cell type-specific lineage programs. That differentiation underlies tumor cell heterogeneity was elegantly demonstrated in hematopoietic tumors, in which rare primitive cells (cancer stem cells (CSCs)) resembling normal hematopoietic stem cells are ultimately responsible for tumor growth and viability. Because of the compelling clinical implications CSCs pose--across the entire spectrum of cancers--investigators applied the CSC model to cancers arising in tissues with crudely understood differentiation programs. Instead of relying on differentiation, these studies used empirically selected markers and statistical arguments to identify CSCs. The empirical approach has stimulated important questions about "stemness" in cancer cells as well as the validity and stoichiometry of CSC assays. The recent identification of urothelial differentiation programs in urothelial carcinomas (UroCas) supports the idea that solid epithelial cancers (carcinomas) develop and differentiate analogously to normal epithelia and provides new insights about the spatial localization and molecular makeup of carcinoma CSCs. Importantly, CSCs from invasive UroCas (UroCSCs) appear well situated to exchange important signals with adjacent stroma, to escape immune surveillance, and to survive cytotoxic therapy. These signals have potential roles in treatment resistance and many participate in druggable cellular pathways. In this review, we discuss the implications of these findings in understanding CSCs and in better understanding how UroCas form, progress, and should be treated.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1573-7233
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
291-304
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed-meshheading:20012172-Animals, pubmed-meshheading:20012172-Carcinoma, Papillary, pubmed-meshheading:20012172-Carcinoma, Transitional Cell, pubmed-meshheading:20012172-Cell Differentiation, pubmed-meshheading:20012172-Cell Transformation, Neoplastic, pubmed-meshheading:20012172-Disease Progression, pubmed-meshheading:20012172-Drug Resistance, Neoplasm, pubmed-meshheading:20012172-Hematologic Neoplasms, pubmed-meshheading:20012172-Humans, pubmed-meshheading:20012172-Mice, pubmed-meshheading:20012172-Neoplasm Invasiveness, pubmed-meshheading:20012172-Neoplasm Recurrence, Local, pubmed-meshheading:20012172-Neoplastic Stem Cells, pubmed-meshheading:20012172-Stromal Cells, pubmed-meshheading:20012172-Tumor Escape, pubmed-meshheading:20012172-Urinary Bladder Neoplasms, pubmed-meshheading:20012172-Urologic Neoplasms, pubmed-meshheading:20012172-Urothelium, pubmed-meshheading:20012172-Wnt Proteins, pubmed-meshheading:20012172-Xenograft Model Antitumor Assays
pubmed:year
2009
pubmed:articleTitle
Urothelial carcinoma: stem cells on the edge.
pubmed:affiliation
Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural