Evidence map›Paper›PMID 27998968›Full record

ArticleAnnals of oncology : official journal of the European Society for Medical Oncology2017

Drug-sensitive FGFR3 mutations in lung adenocarcinoma.

P Chandrani, K Prabhash, R Prasad, V Sethunath, M Ranjan, P Iyer, J Aich, H Dhamne, D N Iyer, P Upadhyay and 13 more

Open access · hybridAbstract read
In one paragraph

Article in Annals of oncology : official journal of the European Society for Medical Oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Uniqueness of lung cancer in Southeast Asia.The Lancet regional health. Southeast Asia · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020
    Review
  18. Article
  19. Review
  20. 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

23 authors at 3 institutions in 1 country.

P ChandraniIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
K PrabhashHomi Bhabha National Institute, Training School Complex, Anushakti Nagar, Mumbai, India.
R PrasadIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
V SethunathIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
M RanjanIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
P IyerIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
J AichIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
H DhamneIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
D N IyerIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
P UpadhyayIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
B MohantySmall Animal Imaging Facility, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
P ChandnaAceProbe Technologies Pvt. Ltd, New Delhi, India.
R KumarDepartment of Pathology, Tata Memorial Hospital, Navi Mumbai, India.
A JoshiDepartment of Medical Oncology, Tata Memorial Hospital, Navi Mumbai, India.
V NoronhaDepartment of Medical Oncology, Tata Memorial Hospital, Navi Mumbai, India.
V PatilDepartment of Medical Oncology, Tata Memorial Hospital, Navi Mumbai, India.
A RamaswamyDepartment of Medical Oncology, Tata Memorial Hospital, Navi Mumbai, India.
A KarpeDepartment of Medical Oncology, Tata Memorial Hospital, Navi Mumbai, India.
R ThoratDepartment of Pathology, Tata Memorial Hospital, Navi Mumbai, India.
P ChaudhariSmall Animal Imaging Facility, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
A IngleLaboratory Animal Facility, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
A ChoughuleDepartment of Medical Oncology, Tata Memorial Hospital, Navi Mumbai, India.
A DuttIntegrated Genomics Laboratory, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, India.
Tata Memorial Hospital · INAdvanced Centre for Treatment, Research and Education in Cancer · INHomi Bhabha National Institute · IN

Funding

DBT-Wellcome Trust India Alliance IA/I/11/2500278Wellcome Trust
6 · The paper itself

Abstract

Background: Lung cancer is the leading cause of cancer-related deaths across the world. In this study, we present therapeutically relevant genetic alterations in lung adenocarcinoma of Indian origin. Materials and methods: Forty-five primary lung adenocarcinoma tumors were sequenced for 676 amplicons using RainDance cancer panel at an average coverage of 1500 × (reads per million mapped reads). To validate the findings, 49 mutations across 23 genes were genotyped in an additional set of 363 primary lung adenocarcinoma tumors using mass spectrometry. NIH/3T3 cells over expressing mutant and wild-type FGFR3 constructs were characterized for anchorage independent growth, constitutive activation, tumor formation and sensitivity to FGFR inhibitors using in vitro and xenograft mouse models. Results: We present the first spectrum of actionable alterations in lung adenocarcinoma tumors of Indian origin, and shows that mutations of FGFR3 are present in 20 of 363 (5.5%) patients. These FGFR3 mutations are constitutively active and oncogenic when ectopically expressed in NIH/3T3 cells and using a xenograft model in NOD/SCID mice. Inhibition of FGFR3 kinase activity inhibits transformation of NIH/3T3 overexpressing FGFR3 constructs and growth of tumors driven by FGFR3 in the xenograft models. The reduction in tumor size in the mouse is paralleled by a reduction in the amounts of phospho-ERK, validating the in vitro findings. Interestingly, the FGFR3 mutations are significantly higher in a proportion of younger patients and show a trend toward better overall survival, compared with patients lacking actionable alterations or those harboring KRAS mutations. Conclusion: We present the first actionable mutation spectrum in Indian lung cancer genome. These findings implicate FGFR3 as a novel therapeutic in lung adenocarcinoma.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAdultAgedAnimalsCell ProliferationDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMiceMiddle AgedMutationNIH 3T3 CellsFGFR3 protein, humanKRAS protein, humanPD 173074Proto-Oncogene Proteins p21(ras)PyrimidinesReceptor, Fibroblast Growth Factor, Type 3actionable mutationsFGFR inhibitorsfibroblast growth factor receptor 3lung adenocarcinomamass spectrometryoncogene

Identifiers

PMID27998968
PMCPMC5391708
OpenAlexW2566209015

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.