Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma

The relevance of KRAS mutation alleles to clinical outcome remains inconclusive in pancreatic adenocarcinoma (PDAC). We conducted a retrospective study of 803 patients with PDAC (42% with metastatic disease) at MD Anderson Cancer Center. Overall survival (OS) analysis demonstrated that KRAS mutation...

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Published inNPJ precision oncology Vol. 8; no. 1; pp. 27 - 13
Main Authors Yousef, Abdelrahman, Yousef, Mahmoud, Chowdhury, Saikat, Abdilleh, Kawther, Knafl, Mark, Edelkamp, Paul, Alfaro-Munoz, Kristin, Chacko, Ray, Peterson, Jennifer, Smaglo, Brandon G., Wolff, Robert A., Pant, Shubham, Lee, Michael S., Willis, Jason, Overman, Michael, Doss, Sudheer, Matrisian, Lynn, Hurd, Mark W., Snyder, Rebecca, Katz, Matthew H. G., Wang, Huamin, Maitra, Anirban, Shen, John Paul, Zhao, Dan
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 03.02.2024
Nature Publishing Group
Nature Portfolio
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692/308/409
692/4028/67/1504/1713
Cancer Research
Clinical outcomes
Gene Therapy
Human Genetics
Internal Medicine
Medical prognosis
Medicine
Medicine & Public Health
Metastasis
Mutation
Oncology
Pancreatic cancer
Tumors
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Abstract The relevance of KRAS mutation alleles to clinical outcome remains inconclusive in pancreatic adenocarcinoma (PDAC). We conducted a retrospective study of 803 patients with PDAC (42% with metastatic disease) at MD Anderson Cancer Center. Overall survival (OS) analysis demonstrated that KRAS mutation status and subtypes were prognostic ( p  < 0.001). Relative to patients with KRAS wildtype tumors (median OS 38 months), patients with KRAS G12R had a similar OS (median 34 months), while patients with KRAS Q61 and KRAS G12D mutated tumors had shorter OS (median 20 months [HR: 1.9, 95% CI 1.2–3.0, p  = 0.006] and 22 months [HR: 1.7, 95% CI 1.3–2.3, p  < 0.001], respectively). There was enrichment of KRAS G12D mutation in metastatic tumors (34% vs 24%, OR: 1.7, 95% CI 1.2–2.4, p  = 0.001) and enrichment of KRAS G12R in well and moderately differentiated tumors (14% vs 9%, OR: 1.7, 95% CI 1.05–2.99, p  = 0.04). Similar findings were observed in the external validation cohort (PanCAN’s Know Your Tumor® dataset, n  = 408).
AbstractList The relevance of KRAS mutation alleles to clinical outcome remains inconclusive in pancreatic adenocarcinoma (PDAC). We conducted a retrospective study of 803 patients with PDAC (42% with metastatic disease) at MD Anderson Cancer Center. Overall survival (OS) analysis demonstrated that KRAS mutation status and subtypes were prognostic (p < 0.001). Relative to patients with KRAS wildtype tumors (median OS 38 months), patients with KRASG12R had a similar OS (median 34 months), while patients with KRASQ61 and KRASG12D mutated tumors had shorter OS (median 20 months [HR: 1.9, 95% CI 1.2–3.0, p = 0.006] and 22 months [HR: 1.7, 95% CI 1.3–2.3, p < 0.001], respectively). There was enrichment of KRASG12D mutation in metastatic tumors (34% vs 24%, OR: 1.7, 95% CI 1.2–2.4, p = 0.001) and enrichment of KRASG12R in well and moderately differentiated tumors (14% vs 9%, OR: 1.7, 95% CI 1.05–2.99, p = 0.04). Similar findings were observed in the external validation cohort (PanCAN’s Know Your Tumor® dataset, n = 408).
The relevance of KRAS mutation alleles to clinical outcome remains inconclusive in pancreatic adenocarcinoma (PDAC). We conducted a retrospective study of 803 patients with PDAC (42% with metastatic disease) at MD Anderson Cancer Center. Overall survival (OS) analysis demonstrated that KRAS mutation status and subtypes were prognostic (p < 0.001). Relative to patients with KRAS wildtype tumors (median OS 38 months), patients with KRAS had a similar OS (median 34 months), while patients with KRAS and KRAS mutated tumors had shorter OS (median 20 months [HR: 1.9, 95% CI 1.2-3.0, p = 0.006] and 22 months [HR: 1.7, 95% CI 1.3-2.3, p < 0.001], respectively). There was enrichment of KRAS mutation in metastatic tumors (34% vs 24%, OR: 1.7, 95% CI 1.2-2.4, p = 0.001) and enrichment of KRAS in well and moderately differentiated tumors (14% vs 9%, OR: 1.7, 95% CI 1.05-2.99, p = 0.04). Similar findings were observed in the external validation cohort (PanCAN's Know Your Tumor® dataset, n = 408).
The relevance of KRAS mutation alleles to clinical outcome remains inconclusive in pancreatic adenocarcinoma (PDAC). We conducted a retrospective study of 803 patients with PDAC (42% with metastatic disease) at MD Anderson Cancer Center. Overall survival (OS) analysis demonstrated that KRAS mutation status and subtypes were prognostic ( p  < 0.001). Relative to patients with KRAS wildtype tumors (median OS 38 months), patients with KRAS G12R had a similar OS (median 34 months), while patients with KRAS Q61 and KRAS G12D mutated tumors had shorter OS (median 20 months [HR: 1.9, 95% CI 1.2–3.0, p  = 0.006] and 22 months [HR: 1.7, 95% CI 1.3–2.3, p  < 0.001], respectively). There was enrichment of KRAS G12D mutation in metastatic tumors (34% vs 24%, OR: 1.7, 95% CI 1.2–2.4, p  = 0.001) and enrichment of KRAS G12R in well and moderately differentiated tumors (14% vs 9%, OR: 1.7, 95% CI 1.05–2.99, p  = 0.04). Similar findings were observed in the external validation cohort (PanCAN’s Know Your Tumor® dataset, n  = 408).
The relevance of KRAS mutation alleles to clinical outcome remains inconclusive in pancreatic adenocarcinoma (PDAC). We conducted a retrospective study of 803 patients with PDAC (42% with metastatic disease) at MD Anderson Cancer Center. Overall survival (OS) analysis demonstrated that KRAS mutation status and subtypes were prognostic (p < 0.001). Relative to patients with KRAS wildtype tumors (median OS 38 months), patients with KRASG12R had a similar OS (median 34 months), while patients with KRASQ61 and KRASG12D mutated tumors had shorter OS (median 20 months [HR: 1.9, 95% CI 1.2-3.0, p = 0.006] and 22 months [HR: 1.7, 95% CI 1.3-2.3, p < 0.001], respectively). There was enrichment of KRASG12D mutation in metastatic tumors (34% vs 24%, OR: 1.7, 95% CI 1.2-2.4, p = 0.001) and enrichment of KRASG12R in well and moderately differentiated tumors (14% vs 9%, OR: 1.7, 95% CI 1.05-2.99, p = 0.04). Similar findings were observed in the external validation cohort (PanCAN's Know Your Tumor® dataset, n = 408).The relevance of KRAS mutation alleles to clinical outcome remains inconclusive in pancreatic adenocarcinoma (PDAC). We conducted a retrospective study of 803 patients with PDAC (42% with metastatic disease) at MD Anderson Cancer Center. Overall survival (OS) analysis demonstrated that KRAS mutation status and subtypes were prognostic (p < 0.001). Relative to patients with KRAS wildtype tumors (median OS 38 months), patients with KRASG12R had a similar OS (median 34 months), while patients with KRASQ61 and KRASG12D mutated tumors had shorter OS (median 20 months [HR: 1.9, 95% CI 1.2-3.0, p = 0.006] and 22 months [HR: 1.7, 95% CI 1.3-2.3, p < 0.001], respectively). There was enrichment of KRASG12D mutation in metastatic tumors (34% vs 24%, OR: 1.7, 95% CI 1.2-2.4, p = 0.001) and enrichment of KRASG12R in well and moderately differentiated tumors (14% vs 9%, OR: 1.7, 95% CI 1.05-2.99, p = 0.04). Similar findings were observed in the external validation cohort (PanCAN's Know Your Tumor® dataset, n = 408).
Abstract The relevance of KRAS mutation alleles to clinical outcome remains inconclusive in pancreatic adenocarcinoma (PDAC). We conducted a retrospective study of 803 patients with PDAC (42% with metastatic disease) at MD Anderson Cancer Center. Overall survival (OS) analysis demonstrated that KRAS mutation status and subtypes were prognostic (p < 0.001). Relative to patients with KRAS wildtype tumors (median OS 38 months), patients with KRAS G12R had a similar OS (median 34 months), while patients with KRAS Q61 and KRAS G12D mutated tumors had shorter OS (median 20 months [HR: 1.9, 95% CI 1.2–3.0, p = 0.006] and 22 months [HR: 1.7, 95% CI 1.3–2.3, p < 0.001], respectively). There was enrichment of KRAS G12D mutation in metastatic tumors (34% vs 24%, OR: 1.7, 95% CI 1.2–2.4, p = 0.001) and enrichment of KRAS G12R in well and moderately differentiated tumors (14% vs 9%, OR: 1.7, 95% CI 1.05–2.99, p = 0.04). Similar findings were observed in the external validation cohort (PanCAN’s Know Your Tumor® dataset, n = 408).
ArticleNumber 27
Author Matrisian, Lynn
Peterson, Jennifer
Wang, Huamin
Yousef, Abdelrahman
Snyder, Rebecca
Edelkamp, Paul
Yousef, Mahmoud
Chowdhury, Saikat
Wolff, Robert A.
Willis, Jason
Zhao, Dan
Hurd, Mark W.
Lee, Michael S.
Pant, Shubham
Abdilleh, Kawther
Knafl, Mark
Maitra, Anirban
Chacko, Ray
Doss, Sudheer
Alfaro-Munoz, Kristin
Katz, Matthew H. G.
Shen, John Paul
Smaglo, Brandon G.
Overman, Michael
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/38310130$$D View this record in MEDLINE/PubMed
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– reference: 37609177 - Res Sq. 2023 Aug 10:rs.3.rs-3195257. doi: 10.21203/rs.3.rs-3195257/v1
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Snippet The relevance of KRAS mutation alleles to clinical outcome remains inconclusive in pancreatic adenocarcinoma (PDAC). We conducted a retrospective study of 803...
The relevance of KRAS mutation alleles to clinical outcome remains inconclusive in pancreatic adenocarcinoma (PDAC). We conducted a retrospective study of 803...
Abstract The relevance of KRAS mutation alleles to clinical outcome remains inconclusive in pancreatic adenocarcinoma (PDAC). We conducted a retrospective...
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692/4028/67/1504/1713
Cancer Research
Clinical outcomes
Gene Therapy
Human Genetics
Internal Medicine
Medical prognosis
Medicine
Medicine & Public Health
Metastasis
Mutation
Oncology
Pancreatic cancer
Tumors
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Title Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma
URI https://link.springer.com/article/10.1038/s41698-024-00505-0
https://www.ncbi.nlm.nih.gov/pubmed/38310130
https://www.proquest.com/docview/2921586213
https://www.proquest.com/docview/2922448480
https://pubmed.ncbi.nlm.nih.gov/PMC10838312
https://doaj.org/article/07e4c9e5f98d41abaef00dd9155ae1ad
Volume 8
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