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Article summary:

1. Loss of regulation of glucose uptake is a recognized feature of cancer metabolism and can be used to assess response to treatment in esophageal cancer patients.

2. Phosphohistidine signaling contributes to glucose uptake and metabolism in tumor cells, leading to metabolic reprogramming and tumor progression.

3. Glucose-induced phosphorylation of FAK-His58 enables CDK4/6-independent CDK2 activation and cell cycle transit, promoting growth factor-independent proliferation in esophageal squamous cell carcinoma cells.

Article analysis:

The article provides an interesting insight into the role of glucose as a mitogenic factor in esophageal squamous cell carcinoma (ESCC). The authors provide evidence that glucose can promote G1 to S/G2 transition and DNA replication in the absence of growth factors, through its ability to induce phosphorylation of FAK-His58 which then enables CDK4/6-independent CDK2 activation and cell cycle transit. The article is well written and provides a comprehensive overview of the relevant literature on this topic.

However, there are some potential biases that should be noted. Firstly, the article does not explore any counterarguments or alternative explanations for the observed effects. Secondly, it does not discuss any possible risks associated with targeting these pathways as a novel therapeutic option for ESCC patients. Thirdly, it does not present both sides equally; instead it focuses solely on the positive aspects of targeting these pathways without considering any potential drawbacks or limitations. Finally, there is some promotional content included in the article which could be seen as biased towards this approach as a potential therapeutic option for ESCC patients.

In conclusion, while this article provides an interesting insight into the role of glucose as a mitogenic factor in ESCC, it should be read with caution due to its potential biases and lack of exploration into counterarguments or alternative explanations for the observed effects.