In one paragraphArticle in Journal of the National Cancer Institute, 2025. 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 itWhat 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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
14 authors.
Yijian FanDepartment of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, GA, United States.
Rui JinDepartment of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, GA, United States.ORCID 0000-0003-3946-1181 Lenore MonterrozaDepartment of Pediatrics, Emory University School of Medicine, Atlanta, GA, United States.ORCID 0000-0002-2956-215X Xiuju LiuDepartment of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, GA, United States.
Chunzi HuangCancer Animal Models Shared Resource of Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA, United States.
Angelo MarraDepartment of Biostatistics and Bioinformatics, Emory University Rollins School of Public Health, Atlanta, GA, United States.ORCID 0009-0004-0004-4027 Xiulei MoDepartment of Pharmacology and Chemical Biology, Emory University School of Medicine, Atlanta, GA, United States.ORCID 0000-0002-7558-3453 Haian FuDepartment of Pharmacology and Chemical Biology, Emory University School of Medicine, Atlanta, GA, United States.ORCID 0000-0002-2362-7979 Melissa Gilbert-RossDepartment of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, GA, United States.ORCID 0000-0002-1960-8302 Adam I MarcusDepartment of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, GA, United States.ORCID 0000-0003-0484-3569 Rabindra TirouvanziamDepartment of Pediatrics, Emory University School of Medicine, Atlanta, GA, United States.ORCID 0000-0003-3526-9985 Yuan LiuDepartment of Biostatistics and Bioinformatics, Emory University Rollins School of Public Health, Atlanta, GA, United States.ORCID 0000-0001-8926-3058 Frank SchneiderDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, United States.
Wei ZhouDepartment of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, GA, United States.ORCID 0000-0002-6783-9957 Funding
Winship Cancer Institute Cancer Center Support GrantP30CA138292 · NCI · EMORY UNIVERSITY · PI Suresh S Ramalingam · 2009 to 2026
$47.5MNeuro HPA Project 1U54AG062334 · NIA · EMORY UNIVERSITY · PI Ighovwerha Ofotokun · 2018 to 2026
$12.2MProject 3: Inhibiting FAK to enhance immune checkpoint inhibitor therapy in LKB1-mutant lung adenocarcinomaP01CA257906 · NCI · EMORY UNIVERSITY · PI Sumin Kang · 2022 to 2026
$10.7MProject 3: Targeting Bax signaling to overcome treatment resistance in NSCLCP50CA217691 · NCI · EMORY UNIVERSITY · PI SICA, GABRIEL LARKIN · 2019 to 2024
$10.1MDeveloping a pharmacologic approach to treat LKB1 mutant NSCLC patientsR01CA194027 · NCI · EMORY UNIVERSITY · PI GILBERT-ROSS, MELISSA, MARCUS, ADAM I. · 2016 to 2020
$2.5MTargeted inhibition of ribosomal RNA synthesis in LKB1-deficient cancersR01CA203928 · NCI · EMORY UNIVERSITY · PI ZHOU, WEI · 2017 to 2021
$1.8MTargeting LKB1-null lung adenocarcinoma with innate immune systemR01CA284648 · NCI · EMORY UNIVERSITY · PI Wei Zhou · 2023 to 2026
$1.7MPro-Oncogenic Role of LKB1 in NSCLCR01CA140571 · NCI · EMORY UNIVERSITY · PI ZHOU, WEI · 2011 to 2015
$1.6MCareer Enhancement CoreCareer Enhancement Program U54AG062334NCI Lung Cancer Spore P50CA217691NCI NIH HHS P01 CA257906NCI NIH HHS P01-CA257906NCI NIH HHS P30 CA138292NCI NIH HHS P50 CA217691NCI NIH HHS R01 CA140571NCI NIH HHS R01-CA140571NCI NIH HHS R01 CA194027NCI NIH HHS R01-CA194027NCI NIH HHS R01 CA203928NCI NIH HHS R01CA203928NCI NIH HHS R01 CA284648NCI NIH HHS R01-CA284648NIA NIH HHS U54 AG062334NIHWinship Invest$Team ScienceWinship shared resources P30CA138292
6 · The paper itselfAbstract
backgroundThis study addressed the enigma of sex differences in smoking-related lung cancer, particularly focusing on the low LKB1 mutation frequency in female patients with lung adenocarcinoma.
methodsSex bias was studied with a genetically engineered mouse model and various tail-vein injection models. Immune cells were analyzed by antibody-depletion study, flow cytometry, and immunofluorescence. The relevance of our findings to human disease was validated by evaluating various lung adenocarcinoma datasets. All statistical tests are 2-sided.
resultsA statistically significant percentage of females are resistant to LKB1-mutant tumor formation in our models, reflecting this sex difference in humans. Natural killer (NK) cells were identified as a critical factor in this sex-biased response. This sex difference was observed primarily in LKB1-mutant lung adenocarcinoma, probably due to their low major histocompatibility complex class I level, making them the ideal target for NK cells through the missing-self recognition. Although females resistant to LKB1-mutant lung adenocarcinoma formation did not have enhancement of any specific NK subpopulation, our immunofluorescence analysis revealed high numbers of NKs in female lungs even with the presence of LKB1-mutant lung adenocarcinoma. Our gene set enrichment analysis of The Cancer Genome Atlas-lung adenocarcinoma dataset also showed that female LKB1-mutant lung adenocarcinoma patients have a stronger NK-mediated response after adjusting for other male-female differences using the LKB1 wild-type lung adenocarcinoma dataset.
conclusionFemales have a stronger NK-mediated response against LKB1-mutant lung adenocarcinoma, which was present in our mouse model and the human lung adenocarcinoma dataset. This study revealed a novel role of NK cells in suppressing LKB1-mutant lung adenocarcinoma in females, which should be assessed in the clinical setting in the future.
Indexed as
Adenocarcinoma of LungKiller Cells, NaturalLung NeoplasmsProtein Serine-Threonine KinasesAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAnimalsDisease Models, AnimalFemaleHumansMaleMiceMutationSex FactorsAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesProtein Serine-Threonine KinasesSTK11 protein, humanStk11 protein, mouse
Identifiers
PMID40511603
PMCPMC12415955
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