Evidence map›Paper›PMID 41181401›Full record

ReviewAnnals of medicine and surgery (2012)2025

Integration of ALK gene mutations and targeted therapies in pediatric high-risk neuroblastoma: advancements in precision oncology.

Bhumika Bheemavarapu, Mohammad Khalil, Aseef Rehman, Saman Javid, Fnu Cyrus, Sardar Noman Qayyum, Aasvi Gohil, Siraj Ul Muneer, Samim Noori

Abstract readReview
In one paragraph

Review in Annals of medicine and surgery (2012), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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.

Bhumika BheemavarapuPediatrics Department, PGY-1, Akron Children's Hospital, Akron, Ohio.
Mohammad KhalilMedicine Department, University of Science and Technology, Omdurman, Sudan.
Aseef RehmanMedicine Department, University College of Medicine and Dentistry, Lahore, Pakistan.
Saman JavidMedicine Department, CMH Kharian Medical College, Kharian Cantt, Pakistan.
Fnu CyrusMedicine Department, Sri Guru Ram Das University of Health Sciences and Research, Amritsar, India.
Sardar Noman QayyumMedicine Department, Bacha Khan Medical College, Mardan, Pakistan.
Aasvi GohilMedicine Department, GMERS Medical College and Hospital, Gotri, Vadodara, India.
Siraj Ul MuneerMedicine Department, Shaikh Khalifa Bin Zayed Al Nahyan Medical and Dental College, Lahore, Pakistan.
Samim NooriMedicine Department, Nangarhar University, Nangarhar, Afghanistan.ORCID https://orcid.org/0009-0009-7195-2010

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Neuroblastoma (NB) is the most common extracranial solid tumor in children. High-risk neuroblastoma remains a therapeutic challenge, with a 5-year survival rate of 60%. The anaplastic lymphoma kinase (ALK) oncogene plays a critical role in the pathogenesis of neuroblastoma, with mutations frequently observed in high-risk cases. In this review we explored the genomic landscape of high-risk neuroblastoma, focusing on ALK mutations and their role in disease progression. We have also discussed the efficacy of ALK-targeted therapies and potential combination strategies to overcome resistance. Methods: A comprehensive literature search was conducted to collect peer-reviewed publications related to neuroblastoma's biology, classification, and treatment. Articles published between 1980 and 2025 were identified using databases such as PubMed, Scopus, Web of Science, and ClinicalTrials.gov. Results: Neuroblastoma tumorigenesis implicates ALK mutations, particularly at ALK p.R1275Q, ALK p.F1174L, and ALK p.F1245C, with an enrichment in stage 4 tumors and younger patients. Several ALK inhibitors, like crizotinib, ceritinib, lorlatinib, repotrectinib, and alectinib, have shown different levels of success, but resistance to these treatments is still a big challenge. New treatment methods that combine farnesyltransferase inhibitors (FTIs) with ALK tyrosine kinase inhibitors (TKIs) are showing potential in improving how well the treatment works and in stopping the cancer from coming back. Conclusion: Precision oncology offers a novel and potentially more effective approach for treating high-risk neuroblastoma. While ALK inhibitors have shown promise, resistance mechanisms necessitate the development of combination therapies and next-generation inhibitors. Future research should focus on optimizing targeted treatment strategies to improve survival outcomes in pediatric patients with ALK-positive neuroblastoma.

Indexed as

ALK inhibitorsALK mutationsneuroblastomapediatric cancerprecision oncologyresistance mechanismstargeted therapy

Identifiers

PMID41181401
PMCPMC12577807

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