scholarly journals Neoadjuvant chemotherapy with gemcitabine for pancreatic cancer increases in situ expression of the apoptosis marker M30 and stem cell marker CD44

2012 ◽  
Vol 3 (6) ◽  
pp. 1186-1190 ◽  
Author(s):  
HIDEHIRO TAJIMA ◽  
TETSUO OHTA ◽  
HIROHISA KITAGAWA ◽  
KOICHI OKAMOTO ◽  
SEISHO SAKAI ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Neoadjuvant Chemotherapy ◽  
Stem Cell Marker ◽  
Cell Marker ◽  
Apoptosis Marker

658 CD44, Pancreatic Cancer Stem Cell Marker, Positive Cells Are Responsible for the Acquiring Gemcitabine Induced Chemoresistance In Vitro

2008 ◽  
Vol 134 (4) ◽  
pp. A-96
Author(s):  
Sung Pil Hong ◽  
Jeong Youp Park ◽  
Jing Wen ◽  
Jin Wook Yoon ◽  
Kyung Hwa Park ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Stem Cell Marker ◽  
Cancer Stem Cell Marker ◽  
Cell Marker

Expression of Oct4, a Stem Cell Marker, in the Hamster Pancreatic Cancer Model

Pancreatology ◽  
2006 ◽  
Vol 6 (4) ◽  
pp. 406-413 ◽  
Author(s):  
Katsumichi Iki ◽  
Parviz M. Pour
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Stem Cell Marker ◽  
Cell Marker ◽  
Cancer Model

scholarly journals Cancer Stem Cell Marker Phenotypes Are Reversible and Functionally Homogeneous in a Preclinical Model of Pancreatic Cancer

2015 ◽  
Vol 75 (21) ◽  
pp. 4582-4592 ◽  
Author(s):  
Joseph S. Dosch ◽  
Elizabeth K. Ziemke ◽  
Amrith Shettigar ◽  
Alnawaz Rehemtulla ◽  
Judith S. Sebolt-Leopold
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Stem Cell Marker ◽  
Preclinical Model ◽  
Cancer Stem Cell Marker ◽  
Cell Marker

scholarly journals Identification of a novel putative pancreatic stem/progenitor cell marker DCAMKL-1 in normal mouse pancreas

2010 ◽  
Vol 299 (2) ◽  
pp. G303-G310 ◽  
Author(s):  
Randal May ◽  
Sripathi M. Sureban ◽  
Stan A. Lightfoot ◽  
Aimee B. Hoskins ◽  
Daniel J. Brackett ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Suspension Culture ◽  
Progenitor Cell ◽  
Expression Patterns ◽  
Stem Cell Marker ◽  
Nodule Formation ◽  
Cell Marker ◽  
Pancreatic Development ◽  
Cytokeratin 14

Stem cells are critical in maintaining adult homeostasis and have been proposed to be the origin of many solid tumors, including pancreatic cancer. Here we demonstrate the expression patterns of the putative intestinal stem cell marker DCAMKL-1 in the pancreas of uninjured C57BL/6 mice compared with other pancreatic stem/progenitor cell markers. We then determined the viability of isolated pancreatic stem/progenitor cells in isotransplantation assays following DCAMKL-1 antibody-based cell sorting. Sorted cells were grown in suspension culture and injected into the flanks of athymic nude mice. Here we report that DCAMKL-1 is expressed in the main pancreatic duct epithelia and islets, but not within acinar cells. Coexpression was observed with somatostatin, NGN3, and nestin, but not glucagon or insulin. Isolated DCAMKL-1+ cells formed spheroids in suspension culture and induced nodule formation in isotransplantation assays. Analysis of nodules demonstrated markers of early pancreatic development (PDX-1), glandular epithelium (cytokeratin-14 and Ep-CAM), and isletlike structures (somatostatin and secretin). These data taken together suggest that DCAMKL-1 is a novel putative stem/progenitor marker, can be used to isolate normal pancreatic stem/progenitors, and potentially regenerates pancreatic tissues. This may represent a novel tool for regenerative medicine and a target for anti-stem cell-based therapeutics in pancreatic cancer.

411 Role of Intestinal Stem Cell Marker DCAMKL-1 in Pancreatic Cancer

2010 ◽  
Vol 138 (5) ◽  
pp. S-61
Author(s):  
Sripathi M. Sureban ◽  
Randal May ◽  
James H. Wyche ◽  
Shrikant Anant ◽  
Courtney W. Houchen
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Stem Cell Marker ◽  
Intestinal Stem Cell ◽  
Cell Marker

Abstract 408: Stem cell marker Nestin regulated the migration and invasion of pancreatic cancer cells

2010 ◽  
Author(s):  
Yoko Matsuda ◽  
Toshiyuki Ishiwata ◽  
Masao Kawamoto ◽  
Tetsushi Yamomoto ◽  
Kiyoko Kawahara ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cell ◽  
Cancer Cells ◽  
Stem Cell Marker ◽  
Migration And Invasion ◽  
Cell Marker ◽  
Pancreatic Cancer Cells

Mutation in the Zebrafish Homolog of the RNA Helicase DHX8 Result in Hematopoietic Defects.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 126-126
Author(s):  
Milton A. English ◽  
Lin Lei ◽  
Trevor Blake ◽  
Raman Sood ◽  
Paul P. Liu
Keyword(s):  
Stem Cell ◽  
Positional Cloning ◽  
Rna Helicase ◽  
Stem Cell Marker ◽  
Chemical Mutagenesis ◽  
Specific Marker ◽  
Cell Marker ◽  
Wild Type ◽  
Hematopoietic Stem

Abstract Hematopoiesis is a tightly regulated process that requires the coordinated efforts of many tissue-specific transcription factors. Lateral mesoderm tissue undergoes a series of restricted proliferation and differentiation that result in the production of the hematopoietic stem cells. These cells then differentiate to populate the different cell lineages. While some factors essential for this process have been defined, many remain unknown. Zebrafish offer a powerful model system in which it is possible to conduct forward phenotype-driven screening. We have undertaken a chemical mutagenesis screen using N-nitroso-N-ethylurea (ENU) in the zebrafish to uncover mutants in myelopoiesis and early hematopoiesis. Adult male fish were exposed to ENU in a protocol designed to mutagenize spermatagonia with a mutation frequency of approximately 1:1000. Mutagenized males were crossed to wild-type females to generate F1 females. Haploid embryos from F1 females were screened at 27 hours of development by RNA in situ hybridization using the myeloid-specific marker, leukocyte-specific plastin (l-plastin), and the stem cell marker, core binding factor b (cbfb). One mutant line identified from this screen, mummy, showed reduced cbfb expression and lack of l-plastin expression. Additional in situ staining has confirmed that mummy has a myeloid defect as other myeloid markers such as Lys.C, Mpo, and C/ebp1 were also significantly reduced. Mummy mutant also have a degreased expression of gata1 and bE1 globin (RBC markers) as well as the stem cell marker scl. These results suggested that the defect in mummy is at or up-stream of the HSC level. The mummy mutant embryos also suffer from widespread cell death and die around 36 hours post fertilization. Genetic mapping and positional cloning has identified the mutated gene as the zebrafish homolog of DHX8, which encodes an RNA helicase. The yeast homolog of dhx8, prp22, functions during mRNA splicing and RNA processing. Morpholino injection into wild-type embryos has confirmed that reduced expression of dhx8 can produce a similar phenotype. The wild-type zebrafish dhx8 cDNA but not the mutated dhx8 cDNA identified in mummy was able to partially rescue the mummy phenotype. Preliminary data from RT-PCR and microarray analysis suggest that mummy mutants have defects in the production of spliced transcripts of some genes but not others. Genes with decreased spliced transcripts in the mummy mutant include scl, cbfb, and gata1, which may explain the hematpoietic defects observed. Our results demonstrate that mutations in an RNA helicase involved in splicing could result in specific blockage of hematopoiesis.

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