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Tyrosine Kinases in Helicobacter pylori Infections and Gastric Cancer

1
Department of Biosciences, Paris-Lodron University of Salzburg, 5020 Salzburg, Austria
2
Cancer Cluster Salzburg, Department of Biosciences, Paris-Lodron University of Salzburg, 5020 Salzburg, Austria
*
Author to whom correspondence should be addressed.
Toxins 2019, 11(10), 591; https://doi.org/10.3390/toxins11100591
Received: 30 August 2019 / Revised: 2 October 2019 / Accepted: 9 October 2019 / Published: 11 October 2019
(This article belongs to the Special Issue Helicobacter pylori Infection–Inducement of Gastroenteric Diseases)
Helicobacter pylori (H. pylori) has been identified as a leading cause of gastric cancer, which is one of the most frequent and malignant types of tumor. It is characterized by its rapid progression, distant metastases, and resistance to conventional chemotherapy. A number of receptor tyrosine kinases and non-receptor tyrosine kinases have been implicated in H. pylori-mediated pathogenesis and tumorigenesis. In this review, recent findings of deregulated EGFR, c-Met, JAK, FAK, Src, and c-Abl and their functions in H. pylori pathogenesis are summarized. View Full-Text
Keywords: Helicobacter pylori; tyrosine kinases; c-Abl; CagA; Src family kinases; EGFR; c-Met Helicobacter pylori; tyrosine kinases; c-Abl; CagA; Src family kinases; EGFR; c-Met
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Chichirau, B.E.; Diechler, S.; Posselt, G.; Wessler, S. Tyrosine Kinases in Helicobacter pylori Infections and Gastric Cancer. Toxins 2019, 11, 591.

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