Evidence map›Paper›PMID 28280984›Full record

ReviewSurgery today2018

Treatment of lung adenocarcinoma by molecular-targeted therapy and immunotherapy.

Motonobu Saito, Hiroyuki Suzuki, Koji Kono, Seiichi Takenoshita, Takashi Kohno

Abstract readReview
PubMed Publisher
In one paragraph

Review in Surgery today, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
9.6field-weighted citation impact, top 1% 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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

  1. Ethnic disparities in survival and progression among EGFR-mutated adenocarcinoma of lung cancer patients treated with tyrosine kinase inhibitors: a systematic review and meta-analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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  15. The progress of tumor vaccines clinical trials in non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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  18. Disulfidptosis-related geneTranslational cancer research · 2024
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18 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

5 authors at 2 institutions in 1 country.

Motonobu SaitoDivision of Genome Biology, National Cancer Center Research Institute, 5-1-1, Tsukiji, Chuo-ku, Tokyo, 1040045, Japan. mosaitoh@ncc.go.jp.
Hiroyuki SuzukiDepartment of Chest Surgery, Fukushima Medical University School of Medicine, Fukushima, Japan.
Koji KonoDepartment of Gastrointestinal Tract Surgery, Fukushima Medical University School of Medicine, Fukushima, Japan.
Seiichi TakenoshitaAdvanced Clinical Research Center, Fukushima Global Medical Science Center, Fukushima Medical University, Fukushima, Japan.
Takashi KohnoDivision of Genome Biology, National Cancer Center Research Institute, 5-1-1, Tsukiji, Chuo-ku, Tokyo, 1040045, Japan.
Fukushima Medical University · JPNational Cancer Centre Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung adenocarcinoma (LADC) is a cancer treatable using targeted therapies against driver gene aberrations. EGFR mutations and ALK fusions are frequent gene aberrations in LADC, and personalized therapies against those aberrations have become a standard therapy. These targeted therapies have shown significant positive efficacy and tolerable toxicity compared to conventional chemotherapy, so it is necessary to identify additional druggable genetic aberrations. Other than EGFR mutations and ALK fusions, mutations in KRAS, HER2, and BRAF, and driver fusions involving RET and ROS1, have also been identified in LADC. Interestingly, the frequency of driver gene aberrations differs according to ethnicity, sex, and smoking, which leads to differences in treatment efficacy. To date, several molecular-targeted drugs against driver genes have been developed, and several clinical trials have been conducted to evaluate the efficacy. However, targeted therapies against driver-gene-negative cases have not yet been well developed. Efforts to identify a new druggable target for such cases are currently underway. Furthermore, immune checkpoint blockade therapy might be effective for driver-negative cases, especially those with accumulated mutations.

Indexed as

Molecular Targeted TherapyAdenocarcinomaAnaplastic Lymphoma KinaseChromosome AberrationsErb-b2 Receptor Tyrosine KinasesErbB ReceptorsFemaleGene Drive TechnologyGene FusionGenetic TestingHumansImmunotherapyLung NeoplasmsMaleMutationPrecision MedicineALK protein, humanAnaplastic Lymphoma KinaseBRAF protein, humanEGFR protein, humanERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesErbB ReceptorsKRAS protein, humanProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-retProto-Oncogene Proteins p21(ras)Receptor Protein-Tyrosine KinasesRET protein, humanROS1 protein, humanDriver gene aberrationsImmunotherapyLung adenocarcinomaTargeted therapy

Identifiers

PMID28280984
OpenAlexW2594607611

What OpenQuestion holds

Textmetadata
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.