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Emerging Kinase Therapeutic Targets in Pancreatic Ductal Adenocarcinoma and Pancreatic Cancer Desmoplasia.
Creeden, Justin F; Alganem, Khaled; Imami, Ali S; Henkel, Nicholas D; Brunicardi, F Charles; Liu, Shi-He; Shukla, Rammohan; Tomar, Tushar; Naji, Faris; McCullumsmith, Robert E.
Afiliación
  • Creeden JF; Department of Neurosciences, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 43614, USA.
  • Alganem K; Department of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 43614, USA.
  • Imami AS; Department of Surgery, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 6038, USA.
  • Henkel ND; Department of Neurosciences, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 43614, USA.
  • Brunicardi FC; Department of Neurosciences, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 43614, USA.
  • Liu SH; Department of Neurosciences, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 43614, USA.
  • Shukla R; Department of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 43614, USA.
  • Tomar T; Department of Surgery, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 6038, USA.
  • Naji F; Department of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 43614, USA.
  • McCullumsmith RE; Department of Surgery, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 6038, USA.
Int J Mol Sci ; 21(22)2020 Nov 21.
Article en En | MEDLINE | ID: mdl-33233470
Kinase drug discovery represents an active area of therapeutic research, with previous pharmaceutical success improving patient outcomes across a wide variety of human diseases. In pancreatic ductal adenocarcinoma (PDAC), innovative pharmaceutical strategies such as kinase targeting have been unable to appreciably increase patient survival. This may be due, in part, to unchecked desmoplastic reactions to pancreatic tumors. Desmoplastic stroma enhances tumor development and progression while simultaneously restricting drug delivery to the tumor cells it protects. Emerging evidence indicates that many of the pathologic fibrotic processes directly or indirectly supporting desmoplasia may be driven by targetable protein tyrosine kinases such as Fyn-related kinase (FRK); B lymphoid kinase (BLK); hemopoietic cell kinase (HCK); ABL proto-oncogene 2 kinase (ABL2); discoidin domain receptor 1 kinase (DDR1); Lck/Yes-related novel kinase (LYN); ephrin receptor A8 kinase (EPHA8); FYN proto-oncogene kinase (FYN); lymphocyte cell-specific kinase (LCK); tec protein kinase (TEC). Herein, we review literature related to these kinases and posit signaling networks, mechanisms, and biochemical relationships by which this group may contribute to PDAC tumor growth and desmoplasia.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Pancreáticas / Adenocarcinoma / Tumor Desmoplásico de Células Pequeñas Redondas / Proteínas de Neoplasias Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Pancreáticas / Adenocarcinoma / Tumor Desmoplásico de Células Pequeñas Redondas / Proteínas de Neoplasias Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza