# Oligoprogression in NSCLC with Other Actionable Oncogenic Drivers Beyond EGFR and ALK: An Emerging Entity

**Authors:** Ilaria Mariangela Scaglione, Adele Bonato, Alessandra Dodi, Marco Sposito, Serena Eccher, Alice Avancini, Daniela Tregnago, Jessica Insolda, Michele Milella, Sara Pilotto, Lorenzo Belluomini

PMC · DOI: 10.3390/ijms27062643 · 2026-03-13

## TL;DR

This paper explores oligoprogressive disease in non-small-cell lung cancer with oncogenic drivers beyond EGFR and ALK, emphasizing the potential role of local treatment.

## Contribution

The paper identifies a gap in evidence for local ablative treatment in oligoprogression beyond EGFR and ALK-driven NSCLC.

## Key findings

- Oligoprogressive NSCLC with drivers beyond EGFR and ALK is under-researched in terms of local ablative treatment benefits.
- Current evidence is limited to case reports and retrospective studies, highlighting a need for systematic research.
- The paper calls for multicenter studies to better understand treatment outcomes in this patient group.

## Abstract

Oligoprogressive disease (OPD) in non-small-cell lung cancer (NSCLC) is a clinical entity with peculiar behavior and treatment. OPD patients, during systemic therapy, may receive local ablative treatment (LAT) with survival benefit. The importance of OPD and the role of LAT has been comprehensively assessed in the setting of EGFR mutant and ALK-rearranged NSCLC during tyrosine kinase inhibitor (TKI) treatment, but it is still almost unexplored in the context of NSCLC harboring actionable oncogenic drivers other than EGFR and ALK. The aim of our review is to collect and discuss the available data about standard treatment in this latter setting, with special consideration given to the role of LAT in case of OPD in systemic treatment. Through a comprehensive PubMed and ClinicalTrials.gov search, we identified the available data and ongoing clinical trials addressing these aims. To date, only limited evidence supports the use of LAT in OPD involving NSCLC driven by these molecular alterations, mainly deriving from case reports and retrospective series. This highlights an unmet clinical need that warrants systematic and multicentric data collection to generate more robust evidence.

## Linked entities

- **Genes:** EGFR (epidermal growth factor receptor) [NCBI Gene 1956], ALK (ALK receptor tyrosine kinase) [NCBI Gene 238]
- **Diseases:** non-small-cell lung cancer (MONDO:0005233), NSCLC (MONDO:0005233)

## Full-text entities

- **Genes:** EGFR (epidermal growth factor receptor) [NCBI Gene 1956] {aka ERBB, ERBB1, ERRP, HER1, NISBD2, NNCIS}, ALK (ALK receptor tyrosine kinase) [NCBI Gene 238] {aka ALK1, CD246, NBLST3}
- **Diseases:** OPD (MESH:D004194), NSCLC (MESH:D002289)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13027157/full.md

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Source: https://tomesphere.com/paper/PMC13027157