rdf:type |
|
lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0017262,
umls-concept:C0032659,
umls-concept:C0086418,
umls-concept:C0185117,
umls-concept:C0205345,
umls-concept:C0281361,
umls-concept:C0441655,
umls-concept:C0684287,
umls-concept:C1418946,
umls-concept:C2349975,
umls-concept:C2911684
|
pubmed:issue |
6
|
pubmed:dateCreated |
2011-6-22
|
pubmed:abstractText |
Multiple studies in recent years have identified highly tumorigenic populations of cells that drive tumor formation. These cancer stem cells (CSCs), or tumor-initiating cells (TICs), exhibit properties of normal stem cells and are associated with resistance to current therapies. As pancreatic adenocarcinoma is among the most resistant human cancers to chemo-radiation therapy, we sought to evaluate the presence of cell populations with tumor-initiating capacities in human pancreatic tumors. Understanding which pancreatic cancer cell populations possess tumor-initiating capabilities is critical to characterizing and understanding the biology of pancreatic CSCs towards therapeutic ends.
|
pubmed:grant |
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-10430905,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-10935470,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-12629218,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-14522905,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-14645703,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-15051286,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-15549107,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-15790790,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-16269619,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-16293577,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-17051156,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-17122771,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-17122772,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-17283135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-18202660,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-18371365,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-18371377,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-18371393,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-18451159,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-18539958,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-18539962,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-19052619,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-19064739,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-19336570,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-19816957,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-19876027,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-20164446,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21695188-20804964
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/AC133 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD24,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD44,
http://linkedlifedata.com/resource/pubmed/chemical/Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Isoenzymes,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Retinal Dehydrogenase,
http://linkedlifedata.com/resource/pubmed/chemical/aldehyde dehydrogenase 1
|
pubmed:status |
MEDLINE
|
pubmed:issn |
1932-6203
|
pubmed:author |
|
pubmed:issnType |
Electronic
|
pubmed:volume |
6
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
e20636
|
pubmed:meshHeading |
pubmed-meshheading:21695188-Adenocarcinoma,
pubmed-meshheading:21695188-Animals,
pubmed-meshheading:21695188-Antigens, CD,
pubmed-meshheading:21695188-Antigens, CD24,
pubmed-meshheading:21695188-Antigens, CD44,
pubmed-meshheading:21695188-Cell Separation,
pubmed-meshheading:21695188-Flow Cytometry,
pubmed-meshheading:21695188-Glycoproteins,
pubmed-meshheading:21695188-Humans,
pubmed-meshheading:21695188-Isoenzymes,
pubmed-meshheading:21695188-Mice,
pubmed-meshheading:21695188-Mice, SCID,
pubmed-meshheading:21695188-Neoplastic Stem Cells,
pubmed-meshheading:21695188-Pancreatic Neoplasms,
pubmed-meshheading:21695188-Peptides,
pubmed-meshheading:21695188-Retinal Dehydrogenase,
pubmed-meshheading:21695188-Xenograft Model Antitumor Assays
|
pubmed:year |
2011
|
pubmed:articleTitle |
ALDH activity selectively defines an enhanced tumor-initiating cell population relative to CD133 expression in human pancreatic adenocarcinoma.
|
pubmed:affiliation |
Department of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|