Evidence map›Paper›PMID 42045515›Full record

ReviewJournal of cancer research and clinical oncology2026

Knowledge mapping and bibliometric insights of scientific research on targeted protein degradation in oncology.

Moutaz W Sweileh

Abstract readReview
In one paragraph

Review in Journal of cancer research and clinical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

1 author.

Moutaz W SweilehFaculty of Medicine and Allied Medical Sciences, An-Najah National University, Nablus, Palestine. moutazsweileh@najah.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDisruption of cellular proteostasis leads to the accumulation and persistence of pathogenic proteins that drive oncogenesis. Key oncogenic and tumor suppressor proteins are frequently dysregulated in cancer, yet remain challenging to target by conventional small-molecule inhibitors. Targeted protein degradation (TPD), particularly through Proteolysis Targeting Chimeras (PROTACs) and molecular glues, has emerged as a transformative strategy that enables catalytic and selective elimination of disease-driving proteins. This study aimed to systematically map the global scientific landscape of TPD research in oncology using bibliometric methods.

methodsA comprehensive bibliometric analysis was conducted using the Scopus database covering articles published between January 2000 and December 2025. Bibliometric indicators including publication trends, compound annual growth rate (CAGR), citations, H-index, authorship pattern, and institutional contributions were analyzed. Network visualization of keyword co-occurrence, chronological evolution, and international collaboration were performed using VOSviewer.

resultsA total of 1334 publications were identified, demonstrating exponential growth, particularly after 2018, with a CAGR of 51.9% (2016–2025). The field is highly interdisciplinary, dominated by biochemistry, pharmacology, and chemistry. The dataset exhibited a high H-index (111), reflecting rapid intellectual maturation. Authorship analysis revealed a median of 10 authors per article, underscoring extensive collaboration. China and the United States emerged as dominant contributors, forming central hubs in the global research network. PROTAC technology represented the primary research focus, with strong association to ubiquitin–proteasome mechanisms and oncogenic targets such as BRD4, MYC, androgen receptor, and estrogen receptor. Highly cited articles were predominantly methodological, highlighting foundational advances in degrader design and mechanism. TPD research is rapidly evolving toward clinically driven innovations with emerging focus on advanced delivery systems, lysosome-targeting strategies, next-generation degrader design strategies, and combination therapies to overcome pharmacokinetic and therapeutic limitations.

conclusionTPD research in oncology is undergoing rapid expansion and transitioning from conceptual innovation to translational application. PROTACs dominate the field due to their modularity and catalytic efficiency, although challenges remain, including pharmacokinetic limitations, restricted E3 ligase diversity, and potential resistance mechanisms. Overall, TPD represents a paradigm shift toward event-driven pharmacology with significant potential to transform precision oncology by enabling the therapeutic elimination of previously intractable targets.

Indexed as

BibliometricsBiomedical ResearchMedical OncologyNeoplasmsProteolysisHumansMolecular Targeted TherapyProteolysis Targeting ChimeraProteolysis Targeting ChimeraBibliometric analysisOncologyPROTACTargeting protein degradationTranslational medicine

Identifiers

PMID42045515
PMCPMC13121638

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.