Evidence map›Paper›PMID 31870097›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2019

Role of BIM Deletion Polymorphism and BIM Expression as Predictive Biomarkers to Maximize the Benefit of EGFR-TKI Treatment in EGFR-Positive NSCLC.

Pimpin Incharoen, Chanchai Charonpongsuntorn, Sakditat Saowapa, Ekaphop Sirachainan, Thitiya Dejthevaporn, Kaettipong Kampreasart, Narumol Trachu, Dittapol Muntham, Thanyanan Reungwetwattana

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 20% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
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  3. Article
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  5. 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

9 authors at 2 institutions in 1 country.

Pimpin IncharoenDepartment of Pathology, Faculty of Medine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Chanchai CharonpongsuntornDivision of Medical Oncology, Department of Internal Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Sakditat SaowapaDivision of Medical Oncology, Department of Internal Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Ekaphop SirachainanDivision of Medical Oncology, Department of Internal Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Thitiya DejthevapornDivision of Medical Oncology, Department of Internal Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Kaettipong KampreasartDepartment of Pathology, Faculty of Medine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Narumol TrachuReasearch Center, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Dittapol MunthamDepartment of Mathematics, Faculty of Science and Technology, Rajamangala University of Technology Suvarnabhumi, Thailand.
Thanyanan ReungwetwattanaDivision of Medical Oncology, Department of Internal Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.ORCID 0000-0003-2537-2903
Mahidol University · THRamathibodi Hospital · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveBIM is a modulator of apoptosis that is triggered by EGFR-TKIs. This study evaluated the role of BIM deletion and its expression as predictor of EGFR-TKI treatment outcome.

methodsThe medical record of 185 EGFR-positive advanced non-small cell lung cancer (NSCLC) patients with/ without EGFR-TKI treatment between 9/2012 and 12/2014 were retrospectively reviewed. BIM deletion polymorphism and expression were tested by RT-PCR and immunohistochemistry, respectively. Survival outcomes in EGFR-TKI-treated patients were analyzed according to treatment sequence and EGFR mutation. The correlation between BIM deletion polymorphism, expression, response rate (as a function of EGFR-TKI treatment) and schedule was also explored.

resultEGFR-TKIs were administered to 139 (75.1%) of the 185 patients: as the first-line in 52 (37.4%) patients and as later-line treatment in 87 (62.6%) patients. Median overall survival (mOS) was significantly longer in EGFR-TKIs treated patients (28.9 vs. 7.4 months, P<0.001). Among L858R-mutated patients, median progression-free survival (mPFS) was significantly longer in first-line EGFR TKI treatment than a later-line (12.6 vs. 6.3 months, P=0.03). BIM deletion polymorphism and expression was detected in 20.2% and 52.7%, respectively. Patients without BIM deletion polymorphism had a significantly longer mOS when treated with a first-line than with a later-line EGFR-TKI (28.9 vs. 20.7 months, P= 0.04). Patients without BIM expression had a significantly longer mPFS (9.6 vs. 7.3 months, P=0.01) better mOS and response rate (RR).

conclusionBIM deletion polymorphism and expression may predict an EGFR-TKI response in patients with EGFR-positive during therapy.

Indexed as

AgedApoptosisBcl-2-Like Protein 11Biomarkers, TumorCarcinoma, Non-Small-Cell LungErbB ReceptorsFemaleHumansLung NeoplasmsMaleMiddle AgedPolymorphism, Single NucleotideProgression-Free SurvivalProtein Kinase InhibitorsRetrospective StudiesBCL2L11 protein, humanBcl-2-Like Protein 11Biomarkers, TumorEGFR protein, humanErbB ReceptorsProtein Kinase Inhibitorsanti-apoptoticBCL2L11BH3 proteinpro-apoptotic

Identifiers

PMID31870097
PMCPMC7173394
OpenAlexW2997292489

What OpenQuestion holds

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LicenceCC BY
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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.