Evidence map›Paper›PMID 25122428›Full record

ArticleJournal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer2014

Therapeutic priority of the PI3K/AKT/mTOR pathway in small cell lung cancers as revealed by a comprehensive genomic analysis.

Shigeki Umemura, Sachiyo Mimaki, Hideki Makinoshima, Satoshi Tada, Genichiro Ishii, Hironobu Ohmatsu, Seiji Niho, Kiyotaka Yoh, Shingo Matsumoto, Akiko Takahashi and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 1 pooled it
7.3field-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

108 citing papers in PubMed, 1 synthesis or guideline pooled it, 218 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  5. Article
  6. Article
  7. Article
  8. Article
  9. Current and future therapies for small cell lung carcinoma.Journal of hematology & oncology · 2025
    Review
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  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Mechanisms of immunotherapy resistance in small cell lung cancer.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  18. mTOR hyperactivity andPathology oncology research : POR · 2024
    Review
  19. Actionable Driver Events in Small Cell Lung Cancer.International journal of molecular sciences · 2023
    Review
  20. Article

48 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

21 authors at 1 institution in 1 country.

Shigeki Umemura*Division of Thoracic Oncology, National Cancer Center Hospital East; †Exploratory Oncology Research and Clinical Trial Center, National Cancer Center; ‡Pathology Division, Research Center for Innovative Oncology, National Cancer Center Hospital East; §Division of Thoracic Surgery, National Cancer Center Hospital East, Kashiwa, Japan; and ‖Division of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
Sachiyo Mimaki
Hideki Makinoshima
Satoshi Tada
Genichiro Ishii
Hironobu Ohmatsu
Seiji Niho
Kiyotaka Yoh
Shingo Matsumoto
Akiko Takahashi
Masahiro Morise
Yuka Nakamura
Atsushi Ochiai
Kanji Nagai
Reika Iwakawa
Takashi Kohno
Jun Yokota
Yuichiro Ohe
Hiroyasu Esumi
Katsuya Tsuchihara
Koichi Goto
National Cancer Center Hospital East · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe information regarding therapeutically relevant genomic alterations in small cell lung cancer (SCLC) is not well developed. We analyzed the SCLC genome using an integrative approach to stratify the targetable alterations.

methodsWe performed whole exon sequencing (n = 51) and copy number analysis (n =47) on surgically resected tumors and matched normal tissue samples from treatment-naive Japanese SCLC patients.

resultsThe demographics of the 51 patients included in this study were as follows: median age, 67 years (range, 42-86 years); female, 9 (18%); history of smoking, 50 (98%); and pathological stage I/II/III/IV, 28/13/9/1, respectively. The average number of nonsynonymous mutations was 209 (range, 41-639; standard deviation, 130). We repeatedly confirmed the high prevalence of inactivating mutations in TP53 and RB1, and the amplification of MYC family members. In addition, genetic alterations in the PI3K/AKT/mTOR pathway were detected in 36% of the tumors: PIK3CA, 6%; PTEN, 4%; AKT2, 9%; AKT3, 4%; RICTOR, 9%; and mTOR, 4%. Furthermore, the individual changes in this pathway were mutually exclusive. Importantly, the SCLC cells harboring active PIK3CA mutations were potentially targetable with currently available PI3K inhibitors.

conclusionsThe PI3K/AKT/mTOR pathway is distinguishable in SCLC genomic alterations. Therefore, a sequencing-based comprehensive analysis could stratify SCLC patients by potential therapeutic targets.

Indexed as

MutationAdultAgedAged, 80 and overCell Line, TumorClass I Phosphatidylinositol 3-KinasesCombined Modality TherapyDNA Mutational AnalysisDNA, NeoplasmFemaleFollow-Up StudiesGenomicsHumansLung NeoplasmsMaleMiddle AgedClass I Phosphatidylinositol 3-KinasesDNA, NeoplasmMTOR protein, humanPhosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID25122428
PMCPMC4154841
OpenAlexW1997232290

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.