Evidence map›Paper›PMID 41701177›Full record

Observational studyThe oncologist2026

MEK inhibitor-based genomically matched combinatorial targeted therapies in metastatic pancreatic adenocarcinoma with KRAS alterations.

Elizabeth D Auckley, Stephanie Yohay, Grace Ying, Aniko Szabo, Jacquelyn Wittmann, Justin Grahl, Mohammed Aldakkak, Samih Z Thalji, Thomas McFall, Razelle Kurzrock and 2 more

Abstract readObservational Study
In one paragraph

Observational study in The oncologist, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Elizabeth D AuckleyDepartment of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, United States.ORCID 0000-0003-3267-0247
Stephanie YohayDepartment of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, United States.
Grace YingDepartment of Medicine, Division of Hematology and Oncology, Medical College of Wisconsin, Milwaukee, WI 53226, United States.
Aniko SzaboData Science Institute, Division of Biostatistics, Medical College of Wisconsin, Milwaukee, WI 53226, United States.ORCID 0000-0002-8129-0614
Jacquelyn WittmannDepartment of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, United States.
Justin GrahlDepartment of Pharmacy, Froedtert Health, Milwaukee, WI 53226, United States.
Mohammed AldakkakDepartment of Surgery, Medical College of Wisconsin and the LaBahn Pancreatic Cancer Program, Milwaukee, WI 53226, United States.ORCID 0009-0001-2855-3278
Samih Z ThaljiDepartment of Surgery, Medical College of Wisconsin and the LaBahn Pancreatic Cancer Program, Milwaukee, WI 53226, United States.ORCID 0000-0002-2681-2109
Thomas McFallDepartment of Biochemistry, Medical College of Wisconsin and the LaBahn Pancreatic Cancer Program, Milwaukee, WI 53226, United States.ORCID 0000-0002-5284-6994
Razelle KurzrockDepartment of Medicine, Division of Hematology and Oncology, Medical College of Wisconsin and the LaBahn Pancreatic Cancer Program, Milwaukee, WI 53226, United States.ORCID 0000-0003-4110-1214
Ben GeorgeDepartment of Medicine, Division of Hematology and Oncology, Medical College of Wisconsin and the LaBahn Pancreatic Cancer Program, Milwaukee, WI 53226, United States.
Mandana KamgarDepartment of Medicine, Division of Hematology and Oncology, Medical College of Wisconsin and the LaBahn Pancreatic Cancer Program, Milwaukee, WI 53226, United States.

Funding

Clinical and Translational Science AwardUL1TR001436 · NCATS · MEDICAL COLLEGE OF WISCONSIN · PI FREED, JULIE K · 2015 to 2025
$47.5M
NCATS NIH HHS UL1 TR001436
6 · The paper itself

Abstract

introductionPancreatic ductal adenocarcinoma (PDAC) is often caused by mutations in multiple genes, including KRAS (activating the Ras-Raf-MEK-ERK pathway). This study evaluated the role of MEK inhibitor (MEKi)-based combinatorial targeted therapies in patients with PDAC.

methodsThis is a retrospective/prospective observational, single-institution study, including 29 patients with metastatic PDAC with KRAS alterations, treated with MEKi therapies between 2022 and 2024.

resultsTen patients had KRAS G12R (34.5%), ten G12D (34.5%), and nine G12V (31%). The majority of patients received MEKi therapy as third-line and beyond (KRAS G12R/G12D/G12V: 60%/50%/78%, respectively). Median overall survival from MEKi initiation for KRAS G12R/G12D/G12V was 8.2/5.1/4.7 months (P = .5), respectively, and median progression-free survival was 4.4/2.3/1.4 months (P = .11). Six (21%) patients discontinued at least one drug in the treatment combination due to toxicity.

conclusionsMEKi-based combinatorial therapies had modest disease control in patients with KRAS G12R, and minimal disease control in patients with KRAS G12D/V in the late-line setting.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsCarcinoma, Pancreatic DuctalPancreatic NeoplasmsProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)AgedFemaleHumansMaleMiddle AgedMolecular Targeted TherapyMutationNeoplasm MetastasisPancreasProspective StudiesRetrospective StudiesKRAS protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)KRASMEK inhibitorspancreatic ductal adenocarcinomatargeted therapy

Identifiers

PMID41701177
PMCPMC13592677

What OpenQuestion holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.