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Item specifics

Condition:
New
Country/Region of Manufacture:
Brazil
Pulley Type:
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Other Part Number:
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Type:
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5511
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a leading international journal from BMJ and BSG, publishes cutting-edge gastroenterology and hepatology research and reviews

Impact Factor: 23.059
Citescore: 35.6
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Gut is a Plan S compliant Transformative Journal.

Gut is a leading international journal in gastroenterology and hepatology and has an established reputation for publishing first class clinical research of the alimentary tract, the liver, biliary tree and pancreas. Gut delivers up-to-date, authoritative, clinically oriented coverage in all areas of gastroenterology and hepatology. Regular features include articles by leading authorities describing novel mechanisms of disease and new management strategies, both diagnostic and therapeutic, likely to impact on clinical practice within the foreseeable future.

Gut is an official journal of the British Society of Gastroenterology and has two companion titles: Frontline Gastroenterology for education and practice and BMJ Open Gastroenterology for sound science clinical research.

Editor-in-Chief: Professor Emad El-Omar, University of New South Wales, Sydney, Australia
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COVID-19 Gastroenterology Collection

 

Our new online collection highlights all research relating to the COVID-19 pandemic published by Gut, Frontline Gastroenterology and BMJ Open Gastroenterology. It is updated regularly as new articles are published.

 

The COVID-19 collection includes original research, commentaries, letters and editorials from all three journals published with the British Society of Gastroenterology (BSG)

 

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Synergistic targeting and resistance to PARP inhibition in pancreatic cancer

To cite: Gout J, Perkhofer L, Morawe M, et al. Gut 2021;70:743-760.

Read the full article here: link
Objective: ATM serine/threonine kinase (ATM) is the most frequently mutated DNA damage response gene, involved in homologous recombination (HR), in pancreatic ductal adenocarcinoma (PDAC).

Conclusion: Analysis of the molecular susceptibilities triggered by ATM deficiency in PDAC allow elaboration of an efficient mutation-specific combinational therapeutic approach that can be also implemented in a genotype-independent manner by ATM inhibition.

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