Evidence map›Paper›PMID 26477306›Full record

ArticleOncogene2016

Differential association of STK11 and TP53 with KRAS mutation-associated gene expression, proliferation and immune surveillance in lung adenocarcinoma.

M B Schabath, E A Welsh, W J Fulp, L Chen, J K Teer, Z J Thompson, B E Engel, M Xie, A E Berglund, B C Creelan and 7 more

Abstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 272 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
272citing papers in PubMed, 2 pooled it
6.2field-weighted citation impact, top 2% of its field
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

272 citing papers in PubMed, 2 syntheses or guidelines pooled it, 439 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Cancers · 2026
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  19. Diagnostics (Basel, Switzerland) · 2026
    Article
  20. Article

212 more citing papers are in PubMed but not listed here.

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

17 authors at 2 institutions in 1 country.

M B SchabathDepartment of Cancer Epidemiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
E A WelshDepartment of Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
W J FulpDepartment of Biostatisics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
L ChenDepartment of Biostatisics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
J K TeerDepartment of Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Z J ThompsonDepartment of Biostatisics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
B E EngelCancer Biology Graduate Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
M XieCancer Biology Graduate Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
A E BerglundDepartment of Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
B C CreelanDepartment of Thoracic Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
S J AntoniaDepartment of Thoracic Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
J E GrayDepartment of Thoracic Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
S A EschrichDepartment of Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
D-T ChenDepartment of Biostatisics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
W D CressDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
E B HauraDepartment of Thoracic Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
A A BegDepartment of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Moffitt Cancer Center · USMolecular Oncology (United States) · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI John L. Cleveland · 1998 to 2026
$93.5M
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI HEYMACH, JOHN V. · 1996 to 2024
$57.4M
SPORE in Lung CancerP50CA119997 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI HAURA, ERIC B. · 2008 to 2012
$11.0M
Integrative Molecular Epidemiology WorkshopR25CA174664 · NCI · AMERICAN ASSOCIATION FOR CANCER RESEARCH · PI Shelley S Tworoger · 2013 to 2026
$2.8M
NCI NIH HHS P30 CA076292NCI NIH HHS P50 CA070907NCI NIH HHS P50 CA119997NCI NIH HHS R25 CA174664
6 · The paper itself

Abstract

While mutations in the KRAS oncogene are among the most prevalent in human cancer, there are few successful treatments to target these tumors. It is also likely that heterogeneity in KRAS-mutant tumor biology significantly contributes to the response to therapy. We hypothesized that the presence of commonly co-occurring mutations in STK11 and TP53 tumor suppressors may represent a significant source of heterogeneity in KRAS-mutant tumors. To address this, we utilized a large cohort of resected tumors from 442 lung adenocarcinoma patients with data including annotation of prevalent driver mutations (KRAS and EGFR) and tumor suppressor mutations (STK11 and TP53), microarray-based gene expression and clinical covariates, including overall survival (OS). Specifically, we determined impact of STK11 and TP53 mutations on a new KRAS mutation-associated gene expression signature as well as previously defined signatures of tumor cell proliferation and immune surveillance responses. Interestingly, STK11, but not TP53 mutations, were associated with highly elevated expression of KRAS mutation-associated genes. Mutations in TP53 and STK11 also impacted tumor biology regardless of KRAS status, with TP53 strongly associated with enhanced proliferation and STK11 with suppression of immune surveillance. These findings illustrate the remarkably distinct ways through which tumor suppressor mutations may contribute to heterogeneity in KRAS-mutant tumor biology. In addition, these studies point to novel associations between gene mutations and immune surveillance that could impact the response to immunotherapy.

Indexed as

Genes, rasMutationAdenocarcinomaAdenocarcinoma of LungAMP-Activated Protein Kinase KinasesCell ProliferationFemaleGene ExpressionHumansImmunologic SurveillanceLung NeoplasmsMaleProtein Serine-Threonine KinasesProto-Oncogene Proteins p21(ras)Signal TransductionTumor Suppressor Protein p53AMP-Activated Protein Kinase KinasesKRAS protein, humanProtein Serine-Threonine KinasesProto-Oncogene Proteins p21(ras)STK11 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID26477306
PMCPMC4837098
OpenAlexW2342639474

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.