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Editorial
. 2024 Aug 31;15(4):1996-2001.
doi: 10.21037/jgo-24-326. Epub 2024 Aug 1.

Mutant KRAS inhibitors enter the scene of precision therapeutics for pancreatic cancer

Affiliations
Editorial

Mutant KRAS inhibitors enter the scene of precision therapeutics for pancreatic cancer

Gareth Pollin et al. J Gastrointest Oncol. .
No abstract available

Keywords: MRTX1133; Pancreatic ductal adenocarcinoma (PDAC); RASopathy; inhibitors; mutant KRAS.

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Conflict of interest statement

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jgo.amegroups.com/article/view/10.21037/jgo-24-326/coif). The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Prevalence and heterogeneity of mutant KRAS in pancreatic cancer. (A) Bar chart illustrating the prevalence of mutant KRAS in pancreatic cancer patients in GENIE (n=6,410) and GDC (n=281) as of April 2024. (B) Pie chart showing distribution of mutant KRAS heterogeneity among pancreatic cancer patients, based on data from the GENIE patient samples. WT, wild-type; GENIE, Genomics Evidence Neoplasia Information Exchange; GDC, Genomic Data Commons.
Figure 2
Figure 2
Structural comparison of KRAS drug binding conformations. All models are Human variations of substrate-bound KRAS. KRAS colored by secondary structure features, helices in blue and strands in yellow; p-loop and hotspots in red; switch-I in pink, switch-II in violet, and ligands in CPK colors for non-carbon atoms and tan for carbon atoms. (A) Non-hydrolysable ATP bound WT KRAS (PDB: 4OBE). (B) GDP bound KRASG12D in complex with YK-8S (8JHL). (C) WT KRAS in complex with BI-2865 (8AZV). CPK, Corey-Pauling-Koltun; ATP, adenosine triphosphate; GDP, guanosine diphosphate; WT, wild-type.

Comment on

References

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