Evidence map›Paper›PMID 35581383›Full record

ArticleJournal of cancer research and clinical oncology2023

All EGFR mutations are (not) created equal: focus on uncommon EGFR mutations.

Batra Ullas, Nathany Shrinidhi, Sharma Mansi, Satya Narayan, Jain Parveen, Dhanda Surender, Jose T Joslia, Mehta Anurag

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 6 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Batra UllasDepartment of Medical Oncology, Rajiv Gandhi Cancer Institute and Research Centre, Sector 5 Rohini, Sir Chhotu Ram Marg, New Delhi, Delhi, 110085, India. ullasbatra@gmail.com.ORCID http://orcid.org/0000-0003-3306-9824
Nathany ShrinidhiMolecular Diagnostics, Rajiv Gandhi Cancer Institute and Research Centre, New Delhi, Delhi, 110085, India.
Sharma MansiDepartment of Medical Oncology, Rajiv Gandhi Cancer Institute and Research Centre, Sector 5 Rohini, Sir Chhotu Ram Marg, New Delhi, Delhi, 110085, India.
Satya NarayanDepartment of Medical Oncology, Rajiv Gandhi Cancer Institute and Research Centre, Sector 5 Rohini, Sir Chhotu Ram Marg, New Delhi, Delhi, 110085, India.
Jain ParveenDepartment of Medical Oncology, Rajiv Gandhi Cancer Institute and Research Centre, Sector 5 Rohini, Sir Chhotu Ram Marg, New Delhi, Delhi, 110085, India.
Dhanda SurenderMolecular Diagnostics, Rajiv Gandhi Cancer Institute and Research Centre, New Delhi, Delhi, 110085, India.
Jose T JosliaDepartment of Medical Oncology, Rajiv Gandhi Cancer Institute and Research Centre, Sector 5 Rohini, Sir Chhotu Ram Marg, New Delhi, Delhi, 110085, India.
Mehta AnuragLaboratory Services, Molecular Diagnostics and Transfusion Services, Rajiv Gandhi Cancer Institute and Research Centre, New Delhi, Delhi, 110085, India.
Rajiv Gandhi Cancer Institute and Research Centre · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeMost common EGFR mutations in NSCLC include del19 and exon 21 L858R. Approximately 10% of patients have uncommon EGFR mutations (indels, missense mutations involving G719, L861 and S768 codons, and exon 20 insertions) that do not respond to TKIs.

methodsOf 490 EGFR mutated NSCLC samples, 60 cases harboring uncommon/compound EGFR mutations were reviewed retrospectively, and 44 were included for survival analysis.

resultsSixty (12.2%) patients with a median age of 63 years (25-84 years) had uncommon/compound EGFR mutations. Majority had no history of smoking (52; 86.7%). Most common major uncommon mutations (G719X in exon 18, L861Q in exon 21 and S768I in exon 20) were identified in 19 (31.7%) patients. 17 (28.3%) cases demonstrated exon 20 insertions. De novo T790M was observed in 7 (11.7%) cases and 9 cases exhibited compound/dual mutations. Among the 12 patients who received first-line EGFR TKI, 7 received afatinib. Median progression-free survival of patients following first-line afatinib was 8.13 months, irrespective of mutation type exhibited. Overall response rate to first-line afatinib therapy was 57.1%.

conclusionThe current study highlighted that rare/dual EGFR mutations are heterogeneous with distinct clinical features in a large Indian cohort of EGFR mutated patients with NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAfatinibErbB ReceptorsHumansMiddle AgedMutationProtein Kinase InhibitorsRetrospective StudiesAfatinibEGFR protein, humanErbB ReceptorsProtein Kinase InhibitorsAfatinibIndiaResponseUncommon EGFR

Identifiers

PMID35581383
PMCPMC11796488
OpenAlexW4280590926

What OpenQuestion holds

Textmetadata
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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.