Evidence map›Paper›PMID 26823891›Full record

ArticleInternational journal of clinical and experimental pathology2015

KRAS mutation-positive bronchial surface epithelium (BSE)-type lung adenocarcinoma with strong expression of TTF-1: a case providing a further insight as for the role of TTF-1 in the oncogenesis.

Yusuke Takanashi, Shogo Tajima, Takamitsu Hayakawa, Hiroshi Neyatani, Kazuhito Funai

Open access · greenAbstract readCase Reports
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
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.

Yusuke TakanashiDepartment of Thoracic Surgery, Fujieda Municipal General Hospital Fujieda, Japan.
Shogo TajimaDepartment of Pathology, University of Tokyo, Graduate School of Medicine Tokyo, Japan.
Takamitsu HayakawaDepartment of Thoracic Surgery, Fujieda Municipal General Hospital Fujieda, Japan.
Hiroshi NeyataniDepartment of Thoracic Surgery, Fujieda Municipal General Hospital Fujieda, Japan.
Kazuhito FunaiDepartment of Surgery 1, Hamamatsu University School of Medicine Hamamatsu, Japan.
Hamamatsu University School of Medicine · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bronchial surface epithelium (BSE)-type lung adenocarcinoma is a subtype of non-terminal respiratory unit (TRU)-type lung adenocarcinoma originating in the bronchial surface epithelium. However, there are few known cases of BSE-type adenocarcinoma with marked expression of thyroid transcription factor-1 (TTF-1). This paper describes a very rare case of KRAS mutation-positive BSE-type adenocarcinoma that exhibited strong expression of TTF-1 that was putatively involved in oncogenesis. An 84-year-old woman, a never smoker, was referred to our hospital because of an abnormal chest radiograph. Chest computed tomography (CT) showed a solid mass lesion, 15 mm × 10 mm, with a relatively smooth margin in the left upper lobe. The patient underwent partial resection of the left upper lobe for strongly suspected lung cancer with a clinical stage of cT1aN0M0. Histopathological findings showed continuous migration of papillary, hyperplastic, atypical columnar tumor cells originating from normal bronchial surface epithelium, leading to a diagnosis of BSE-type adenocarcinoma. TTF-1 was strongly expressed in almost 100% of the tumor cells, which tested positive for the KRAS mutation. TTF-1 has recently attracted attention as an oncogene, and it is purportedly involved in the carcinogenesis and survival of lung adenocarcinoma cells. There is typically an inverse correlation between the respective expressions of KRAS and TTF-1, but in the present study, they appeared simultaneously and were both putatively involved as oncogenic driver alterations. This case is important in that it sheds some light on the largely unknown pathogenic mechanism of BSE-type adenocarcinoma.

Indexed as

MutationAdenocarcinomaAdenocarcinoma of LungAged, 80 and overBiomarkers, TumorBiopsyCarcinogenesisDNA Mutational AnalysisEpithelial CellsFemaleHumansImmunohistochemistryLung NeoplasmsNeoplasm StagingNuclear ProteinsPneumonectomyBiomarkers, TumorKRAS protein, humanNKX2-1 protein, humanNuclear ProteinsProto-Oncogene Proteins p21(ras)Thyroid Nuclear Factor 1Transcription FactorsBSE-type adenocarcinomaKRASTTF-1

Identifiers

PMID26823891
PMCPMC4713677
OpenAlexW2402216178

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.