A bright future for protein kinase D1 as a drug target to prevent or treat pancreatic cancer

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A bright future for protein kinase D1 as a drug target to prevent or treat pancreatic cancer

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2015 nî lūn-bûn

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

@zh-hk

2015年論文

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2015年論文

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2015年论文

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2015年论文

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2015年论文

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A bright future for protein ki ...... ent or treat pancreatic cancer

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A bright future for protein ki ...... ent or treat pancreatic cancer

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A bright future for protein ki ...... ent or treat pancreatic cancer

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P1476

A bright future for protein ki ...... ent or treat pancreatic cancer

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P2093

Geou-Yarh Liou

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Michael Leitges

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Peter Storz

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P2860

Protein kinase D2 induces invasion of pancreatic cancer cells by regulating matrix metalloproteinases.

Pancreatic cancer stem cells and EMT in drug resistance and metastasis.

Notch2 is required for progression of pancreatic intraepithelial neoplasia and development of pancreatic ductal adenocarcinoma

Notch-1 induces epithelial-mesenchymal transition consistent with cancer stem cell phenotype in pancreatic cancer cells

Protein kinase D1 drives pancreatic acinar cell reprogramming and progression to intraepithelial neoplasia

Crosstalk between the canonical NF-κB and Notch signaling pathways inhibits Pparγ expression and promotes pancreatic cancer progression in mice.

Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia

Delta like ligand 4 induces impaired chemo-drug delivery and enhanced chemoresistance in pancreatic cancer.

Protein kinase D1 promotes anchorage-independent growth, invasion, and angiogenesis by human pancreatic cancer cells.

Oncogenic Kras is required for both the initiation and maintenance of pancreatic cancer in mice.

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e1035477

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scholarly article

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10.1080/23723556.2015.1035477

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P433

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P478

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P577

2015-12-10T00:00:00Z

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27308552

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P932

4845192

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