Evidence map›Paper›PMID 37376053›Full record

ReviewPharmaceutics2023

The Resistance to EGFR-TKIs in Non-Small Cell Lung Cancer: From Molecular Mechanisms to Clinical Application of New Therapeutic Strategies.

Carmelo Laface, Felicia Maria Maselli, Anna Natalizia Santoro, Maria Laura Iaia, Francesca Ambrogio, Marigia Laterza, Chiara Guarini, Pierluigi De Santis, Martina Perrone, Palma Fedele

Open access · goldAbstract readReview
In one paragraph

Review in Pharmaceutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
11.4field-weighted citation impact, top 1% 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

44 citing papers in PubMed, 44 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

10 authors at 1 institution in 1 country.

Carmelo LafaceMedical Oncology, Dario Camberlingo Hospital, 72021 Francavilla Fontana, Italy.ORCID 0000-0002-5074-4951
Felicia Maria MaselliMedical Oncology, Dario Camberlingo Hospital, 72021 Francavilla Fontana, Italy.
Anna Natalizia SantoroMedical Oncology, Dario Camberlingo Hospital, 72021 Francavilla Fontana, Italy.
Maria Laura IaiaMedical Oncology, Dario Camberlingo Hospital, 72021 Francavilla Fontana, Italy.
Francesca AmbrogioSection of Dermatology, Department of Biomedical Science and Human Oncology, University of Bari, 70124 Bari, Italy.
Marigia LaterzaDivision of Cardiac Surgery, University of Bari, 70124 Bari, Italy.
Chiara GuariniMedical Oncology, Dario Camberlingo Hospital, 72021 Francavilla Fontana, Italy.ORCID 0000-0003-2225-6093
Pierluigi De SantisMedical Oncology, Dario Camberlingo Hospital, 72021 Francavilla Fontana, Italy.
Martina PerroneMedical Oncology, Dario Camberlingo Hospital, 72021 Francavilla Fontana, Italy.
Palma FedeleMedical Oncology, Dario Camberlingo Hospital, 72021 Francavilla Fontana, Italy.
University of Bari Aldo Moro · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Almost 17% of Western patients affected by non-small cell lung cancer (NSCLC) have an activating epidermal growth factor receptor (EGFR) gene mutation. Del19 and L858R are the most-common ones; they are positive predictive factors for EGFR tyrosine kinase inhibitors (TKIs). Currently, osimertinib, a third-generation TKI, is the standard first-line therapy for advanced NSCLC patients with common EGFR mutations. This drug is also administered as a second-line treatment for those patients with the T790M EGFR mutation and previously treated with first- (erlotinib, gefitinib) or second- (afatinib) generation TKIs. However, despite the high clinical efficacy, the prognosis remains severe due to intrinsic or acquired resistance to EGRF-TKIs. Various mechanisms of resistance have been reported including the activation of other signalling pathways, the development of secondary mutations, the alteration of the downstream pathways, and phenotypic transformation. However, further data are needed to achieve the goal of overcoming resistance to EGFR-TKIs, hence the necessity of discovering novel genetic targets and developing new-generation drugs. This review aimed to deepen the knowledge of intrinsic and acquired molecular mechanisms of resistance to EGFR-TKIs and the development of new therapeutic strategies to overcome TKIs' resistance.

Indexed as

EGFR mutationsnon-small cell lung cancerresistance mechanismstyrosine kinase inhibitors

Identifiers

PMID37376053
PMCPMC10302309
OpenAlexW4378529111

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.