LaTeX Forum

\begin{filecontents}{\jobname.bib}
@article{mycitation,
   author   = {John Doe and Jane Doe}, 
   title    = {The Title of the Thing}, 
   journal  = {Some Imprtant Journal},
   volume   = {1}, 
   number   = {2}, 
   pages    = {4-4}, 
   abstract = {Some text with % in it},  
   year     = {2012} 
}
\end{filecontents}
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\usepackage[T1]{fontenc} 
\usepackage[babel]{csquotes}
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{% \catcode`\%=12 nützt hier nix
\addbibresource{\jobname.bib}}

\begin{document} 

\parencite{mycitation}

% \catcode`\%=12 nützt hier auch nix
\printbibliography
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@article{Li2007,
   author = {Li, Chenwei and Heidt, David G and Dalerba, Piero and Burant, Charles F and Zhang, Lanjing and Adsay, Volkan and Wicha, Max and Clarke, Michael F and Simeone, Diane M},
   title = {Identification of pancreatic cancer stem cells},
   journal = {Cancer Res},
   volume = {67},
   number = {3},
   pages = {1030-7},
   abstract = {Emerging evidence has suggested that the capability of a tumor to grow and propagate is dependent on a small subset of cells within a tumor, termed cancer stem cells. Although data have been provided to support this theory in human blood, brain, and breast cancers, the identity of pancreatic cancer stem cells has not been determined. Using a xenograft model in which primary human pancreatic adenocarcinomas were grown in immunocompromised mice, we identified a highly tumorigenic subpopulation of pancreatic cancer cells expressing the cell surface markers CD44, CD24, and epithelial-specific an Pancreatic cancer cells with the CD44(+)CD24(+)ESA(+) phenotype (0.2-0.8% of pancreatic cancer cells) had a 100-fold increased tumorigenic potential compared with nontumorigenic cancer cells, with 50% of animals injected with as few as 100 CD44(+)CD24(+)ESA(+) cells forming tumors that were histologically indistinguishable from the human tumors from which they originated. The enhanced ability of CD44(+)CD24(+)ESA(+) pancreatic cancer cells to form tumors was confirmed in an orthotopic pancreatic tail injection model. The CD44(+)CD24(+)ESA(+) pancreatic cancer cells showed the stem cell properties of self-renewal, the ability to produce differentiated progeny, and increased expression of the developmental signaling molecule sonic hedgehog. Identification of pancreatic cancer stem cells and further elucidation of the signaling pathways that regulate their growth and survival may provide novel therapeutic approaches to treat pancreatic cancer, which is notoriously resistant to standard chemotherapy and radiation.tigen (ESA).},
   keywords = {Adenocarcinoma/immunology/*pathology
Animals
Antigens, CD24/biosynthesis
Antigens, CD44/biosynthesis
Antigens, Neoplasm/biosynthesis
Disease Models, Animal
Humans
Male
Mice
Mice, Inbred NOD
Mice, SCID
Neoplastic Stem Cells/immunology/*parasitology
Pancreatic Neoplasms/immunology/*pathology
Signal Transduction
Transplantation, Heterologous
Up-Regulation},
   year = {2007}
}