Evidence map›Paper›PMID 28202526›Full record

ArticleCancer research2017

Radiation Resistance in KRAS-Mutated Lung Cancer Is Enabled by Stem-like Properties Mediated by an Osteopontin-EGFR Pathway.

Meng Wang, Jing Han, Lynnette Marcar, Josh Black, Qi Liu, Xiangyong Li, Kshithija Nagulapalli, Lecia V Sequist, Raymond H Mak, Cyril H Benes and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

68 citing papers in PubMed, 106 citations in OpenAlex.

  1. Trial
  2. Review
  3. Radiosensitization of Glioblastoma by the K-ras Inhibitor RMC-6236.bioRxiv : the preprint server for biology · 2026
    Article
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  5. Article
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  8. Article
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  10. Review
  11. Article
  12. Article
  13. Targeting oncogenicMolecular therapy. Nucleic acids · 2023
    Article
  14. CT-based radiomics prediction of complete response after stereotactic body radiation therapy for patients with lung metastases.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023
    Article
  15. Article
  16. Review
  17. Review
  18. The Mutational Landscape of Cancer's Vulnerability to Ionizing Radiation.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
  19. Review
  20. Article

8 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 2 countries.

Meng WangDepartment of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Jing HanDepartment of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Lynnette MarcarDepartment of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Josh BlackUniversity of Colorado School of Medicine, Aurora, Colorado.
Qi LiuDepartment of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Xiangyong LiLaboratory for Lipid Medicine and Technology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts.
Kshithija NagulapalliCenter for Computational Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Lecia V SequistDepartment of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Raymond H MakDepartment of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts.
Cyril H BenesCenter for Cancer Research, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts.
Theodore S HongDepartment of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Kristin GurtnerDepartment of Radiation Oncology, Medical Faculty and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Mechthild KrauseDepartment of Radiation Oncology, Medical Faculty and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Michael BaumannDepartment of Radiation Oncology, Medical Faculty and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Jing X KangLaboratory for Lipid Medicine and Technology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts.
Johnathan R WhetstineCenter for Cancer Research, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts.
Henning WillersDepartment of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. hwillers@partners.org.
Helmholtz-Zentrum Dresden-Rossendorf · DEUniversity of Colorado Denver · US

Funding

VectorP30CA006516 · NCI · DANA-FARBER CANCER INSTITUTE · PI A. Heather Eliassen · 1985 to 2026
$330.6M
Translational studies of Hsp90 inhibitors in NSCLCP50CA090578 · NCI · DANA-FARBER CANCER INST · PI JOHNSON, BRUCE D · 2008 to 2012
$11.4M
Understanding the Role of Histone Demethylases and Heterochromatin in Cell CycleR01GM097360 · NIGMS · RESEARCH INST OF FOX CHASE CAN CTR · PI WHETSTINE, JOHNATHAN R. · 2012 to 2020
$3.4M
PROTON THERAPY RESEARCH AND TREATMENT CENTERC06CA059267 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI GOITEIN, MICHAEL · 1992 to 1995
–
NCI NIH HHS C06 CA059267NCI NIH HHS P30 CA006516NCI NIH HHS P50 CA090578NIGMS NIH HHS R01 GM097360Wellcome Trust
6 · The paper itself

Abstract

Lung cancers with activating KRAS mutations are characterized by treatment resistance and poor prognosis. In particular, the basis for their resistance to radiation therapy is poorly understood. Here, we describe a radiation resistance phenotype conferred by a stem-like subpopulation characterized by mitosis-like condensed chromatin (MLCC), high CD133 expression, invasive potential, and tumor-initiating properties. Mechanistic investigations defined a pathway involving osteopontin and the EGFR in promoting this phenotype. Osteopontin/EGFR-dependent MLCC protected cells against radiation-induced DNA double-strand breaks and repressed putative negative regulators of stem-like properties, such as CRMP1 and BIM. The MLCC-positive phenotype defined a subset of KRAS-mutated lung cancers that were enriched for co-occurring genomic alterations in TP53 and CDKN2A. Our results illuminate the basis for the radiation resistance of KRAS-mutated lung cancers, with possible implications for prognostic and therapeutic strategies.

Indexed as

A549 CellsAnimalsCarcinoma, Non-Small-Cell LungErbB ReceptorsFemaleHeterograftsHumansLung NeoplasmsMaleMiceMice, NudeMutationNeoplastic Stem CellsOsteopontinProto-Oncogene Proteins p21(ras)Radiation ToleranceEGFR protein, humanErbB ReceptorsKRAS protein, humanOsteopontinProto-Oncogene Proteins p21(ras)SPP1 protein, human

Identifiers

PMID28202526
PMCPMC5445902
OpenAlexW2588094244

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.