Pancreatic Islet and Stellate Cells Are the Main Sources of Endocrine Gland-Derived Vascular Endothelial Growth Factor/Prokineticin-1 in Pancreatic Cancer
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Cited by (39)
Pancreatic Cancer UK Grand Challenge: Developments and challenges for effective CAR T cell therapy for pancreatic ductal adenocarcinoma
2020, PancreatologyCitation Excerpt :Platelet-derived growth factor (PDGF) from the stellate cells induces cancer cell proliferation and aids migration of more stellate cells to the tumor in a feed-forward loop [27]. They stimulate angiogenesis via VEGF release, aiding the growth of the tumor [28] and potentially increasing CAR T cell perfusion into the TME. However, contrastingly, VEGF can play an immunosuppressive role in the TME by inducing inhibitory checkpoints such as PD-1 in CD8+ T cells and can thus render CAR T cells ineffective [29,30].
EG-VEGF silencing inhibits cell proliferation and promotes cell apoptosis in pancreatic carcinoma via PI3K/AKT/mTOR signaling pathway
2019, Biomedicine and PharmacotherapyCitation Excerpt :Most of EG-VEGF exists in endocrine steroid organs, including ovaries, testes, adrenal glands, and placenta, and is closely related to the occurrence and development of various specific tissue tumors [4–6]. Much evidence suggests that EG-VEGF is distributed diffusely in PC tissues and its positive expression rate is up to 95% [7,8], suggesting a correlation between EG-VEGF and PC progression. EG-VEGF has two receptors, PKR1 (prokineticin receptor 1) and PKR2 (prokineticin receptor 2), which can be coupled with Gq, Gs or Gi protein.
Galectin-1-driven upregulation of SDF-1 in pancreatic stellate cells promotes pancreatic cancer metastasis
2017, Cancer LettersCitation Excerpt :Galectin-1 is involved in a wide range of biological activities including apoptosis, migration, adhesion, malignant transformation, carcinogenesis, tumor angiogenesis, and immunosuppression [23,31–37]. Pancreatic tumor cells have been found to stimulate PSCs to express enhanced levels of Galectin-1 by secreting cytokine transforming growth factor TGF-β1 [20,38]; this in turn induced activation and proliferation of PSCs resulting in a cycle that sustained the stromal reaction and promoted the malignant behavior of PDAC [21,39,40]. We previously demonstrated that Galectin-1 was overexpressed in PSCs leading to the formation of fibroblasts surrounding the tumor cells and was associated with perineural invasion, advanced tumor stage, lower differentiation and poor prognosis in patients with pancreatic cancer [16,20,41].
Pregnancy induces pancreatic insulin secretion in women with long-standing type 1 diabetes
2022, BMJ Open Diabetes Research and Care
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Jörg Kleeff, MD Department of Surgery, Technische Universität München Ismaningerstrasse 22, DE-81675 Munich (Germany) Tel. +49 89 4140 5098, Fax +49 89 4140 4870