Evidence map›Paper›PMID 40873540›Full record

ReviewCancer drug resistance (Alhambra, Calif.)2025

New advances in understanding the mechanisms and treatment challenges of ALK-targeted therapy resistance in lung cancer.

Mengle Long, Shixuan Peng, Qingyang Wen, Zhijian Yin, Xinwen Zhang, Haoyu Tan, Yun Xu, Yongjun Wu

Abstract readReview
In one paragraph

Review in Cancer drug resistance (Alhambra, Calif.), 2025. 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
–field-weighted citation impact
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.

  1. Review
  2. ALK-tyrosine kinase inhibitor resistance due to acquiredTranslational lung cancer research · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. 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

8 authors.

Mengle LongDepartment of Oncology, Graduate Collaborative Training Base of The First People's Hospital of Xiangtan City, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Shixuan PengDepartment of Oncology, Graduate Collaborative Training Base of The First People's Hospital of Xiangtan City, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Qingyang WenDepartment of Oncology, Graduate Collaborative Training Base of The First People's Hospital of Xiangtan City, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Zhijian YinDepartment of Oncology, Graduate Collaborative Training Base of Xiangtan Center Hospital, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Xinwen ZhangDepartment of Oncology, Graduate Collaborative Training Base of The First People's Hospital of Xiangtan City, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Haoyu TanDepartment of Oncology, Graduate Collaborative Training Base of Xiangtan Center Hospital, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Yun XuDepartment of Rehabilitation Medicine, The First People's Hospital of Xiangtan City, Xiangtan 411101, Hunan, China.
Yongjun WuDepartment of Pathology, Xiangtan Central Hospital, Xiangtan 411100, Hunan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the development of various effective anaplastic lymphoma kinase tyrosine kinase inhibitors (ALK-TKIs), therapeutic resistance remains a major challenge. Both on-target and off-target mechanisms have been identified as key contributors to resistance. With the popularization of genetic testing and the development of precision therapies, the prognosis and survival of patients with ALK-positive non-small cell lung cancer (NSCLC) have improved. However, even with second- and third-generation ALK-TKIs, overcoming resistance remains difficult. Resistance frequently arises during approved treatments, underscoring the need for further research to elucidate the molecular events and resistance mechanisms associated with ALK-positive lung cancer. The discovery of anaplastic lymphoma kinase (ALK) rearrangement as an actionable oncogenic driver in NSCLC has established a biomarker-driven treatment paradigm for advanced disease. This article summarizes current knowledge of the mechanisms of resistance to ALK-targeted therapy in lung cancer, including both primary and acquired mechanisms, treatment strategies following resistance, recent therapeutic advances, and the impact of the immune system and tumor microenvironment. A deeper understanding of ALK-targeted therapy resistance is critical for developing new treatment strategies and may provide important insights to guide the diagnosis, treatment, and management of patients with resistant ALK

Indexed as

Anaplastic lymphoma kinase (ALK)drug resistance mechanismsimmune microenvironmentmutationssmall cell transformationtargeted therapy

Identifiers

PMID40873540
PMCPMC12378566

What OpenQuestion holds

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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.