Evidence map›Paper›PMID 36923435›Full record

ArticleFrontiers in oncology2023

Overcoming CEP85L-ROS1, MKRN1-BRAF and MET amplification as rare, acquired resistance mutations to Osimertinib.

Waleed Kian, Bilal Krayim, Hadel Alsana, Betsy Giles, Ofer Purim, Wafeek Alguayn, Farouq Alguayn, Nir Peled, Laila C Roisman

Open access · goldFull text read
In one paragraph

Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.6field-weighted citation impact, top 10% 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, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. [Research Progress of BRAF Fusion in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023
    Review
  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 5 institutions in 1 country.

Waleed KianThe Oncology Institute, Shaare Zedek Medical Center, Jerusalem, Israel.
Bilal KrayimThe Oncology Institute, Shaare Zedek Medical Center, Jerusalem, Israel.
Hadel AlsanaPulmonology Department, Soroka Medical Center & Ben-Gurion University, Beer-Sheva, Israel.
Betsy GilesMedical School of International Health, Faculty of Health Sciences at Ben-Gurion University, Beer-Sheva, Israel.
Ofer PurimThe Oncology Institute, Shaare Zedek Medical Center, Jerusalem, Israel.
Wafeek AlguaynDivision of Pediatric and Congenital Cardiac Surgery, Schneider Children's Medical Center of Israel, Petah Tikva, Israel.
Farouq AlguaynBarzilai Medical Center, Department of Intensive Care, Ashkelon, Israel and Soroka Medical Center, Department of Neurosurgery, Ben-Gurion University, Beer-Sheva, Israel.
Nir PeledThe Oncology Institute, Shaare Zedek Medical Center, Jerusalem, Israel.
Laila C RoismanThe Oncology Institute, Shaare Zedek Medical Center, Jerusalem, Israel.
Shaare Zedek Medical Center · ILBarzilai Medical Center · ILBen-Gurion University of the Negev · ILSchneider Children's Medical Center · ILSoroka Medical Center · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the most common cancer-related cause of death worldwide, most of which are non-small cell lung cancers (NSCLC). Epidermal growth factor receptor (EGFR) mutations are common drivers of NSCLC. Treatment plans for NSCLC, specifically adenocarcinomas, rely heavily on the presence or absence of specific actionable driver mutations. Liquid biopsy can guide the treatment protocol to detect the presence of various mechanisms of resistance to treatment. We report three NSCLC EGFR mutated cases, each treated with Osimertinib in a combination therapy regimen to combat resistance mechanisms. The first patient presented with EGFR L858R/L833V compound mutation with MET amplification alongside CEP85L-ROS1 fusion gene, the second with EGFR exon 19del and MKRN1-BRAF fusion, and the last EGFR L858R/V834L compound mutation with MET amplification. Each regimen utilized a tyrosine kinase inhibitor or monoclonal antibody in addition to osimertinib and allowed for a prompt and relatively durable treatment response.

Indexed as

CEP85L-ROS1 fusioncompound mutationsEGFRL833Vlung cancerMET amplificationMKRN1-BRAFV834L

Identifiers

PMID36923435
PMCPMC10009227
OpenAlexW4322502543

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read57
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.