Analysis of circulating blood and tissue biopsy PDX1 and MSX2 gene expression in patients with pancreatic cancer

Duarte-Medrano, Gilberto; López-Méndez, Iván; Ramírez-Luna, Miguel Ángel; Valdovinos-Andraca, Francisco; Cruz-Martínez, Rodrigo; Medina‐Vera, Isabel; Pérez‐Monter, Carlos; Téllez-Ávila, Félix Ignacio

doi:10.1097/md.0000000000015954

Cited by 4 publications

(1 citation statement)

References 29 publications

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“…While PDX1 demonstrates protective effects during certain stages of gastric [ 53 ] and pancreatic cancer [ 54 ], it frequently switches from tumor-suppressor to oncogene after neoplastic transformation is complete [ 55 ]. We have previously proposed and investigated PDX1 as a potential target for pancreatic cancer therapy [ 56 , 57 , 58 ]; our group and others provide support for the oncogenic properties of PDX1 in pancreatic cancer and suggest additional clinical significance for PDX1 as a biomarker in other solid human malignancies such as colon, prostate, kidney, and breast cancer [ 59 , 60 , 61 , 62 , 63 ].…”

Section: B Lymphoid Kinase (Blk)mentioning

confidence: 93%

Emerging Kinase Therapeutic Targets in Pancreatic Ductal Adenocarcinoma and Pancreatic Cancer Desmoplasia

Creeden

Alganem

Imami

et al. 2020

IJMS

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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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