Evidence map›Paper›PMID 39456995›Full record

ReviewInternational journal of molecular sciences2024

Proteolysis Targeting Chimera Agents (PROTACs): New Hope for Overcoming the Resistance Mechanisms in Oncogene-Addicted Non-Small Cell Lung Cancer.

Nicoletta Cordani, Daniele Nova, Luca Sala, Maria Ida Abbate, Francesca Colonese, Diego Luigi Cortinovis, Stefania Canova

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. 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. Article
  3. Light-controlled disruption of cancer cell dormancy via photoswitchable stress hormone receptor degraders.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Review
  5. Review
  6. Review
  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

7 authors.

Nicoletta CordaniSchool of Medicine and Surgery, University of Milano-Bicocca, 20900 Monza, Italy.ORCID 0000-0002-3227-8280
Daniele NovaMedical Oncology Unit, Fondazione Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS) San Gerardo dei Tintori, 20900 Monza, Italy.
Luca SalaMedical Oncology Unit, Fondazione Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS) San Gerardo dei Tintori, 20900 Monza, Italy.ORCID 0000-0003-4568-5739
Maria Ida AbbateMedical Oncology Unit, Fondazione Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS) San Gerardo dei Tintori, 20900 Monza, Italy.
Francesca ColoneseMedical Oncology Unit, Fondazione Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS) San Gerardo dei Tintori, 20900 Monza, Italy.
Diego Luigi CortinovisSchool of Medicine and Surgery, University of Milano-Bicocca, 20900 Monza, Italy.ORCID 0000-0001-7611-7369
Stefania CanovaMedical Oncology Unit, Fondazione Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS) San Gerardo dei Tintori, 20900 Monza, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) remains a disease with a poor prognosis despite the advances in therapies. NSCLC with actionable oncogenic alterations represent a subgroup of diseases for which tyrosine kinase inhibitors (TKIs) have shown relevant and robust impact on prognosis, both in early and advanced stages. While the introduction of powerful TKIs increases the ratio of potentially curable patients, the disease does develop resistance over time through either secondary mutations or bypass activating tracks. Therefore, new treatment strategies are being developed to either overcome this inevitable resistance or to prevent it, and proteolysis targeting chimera agents (PROTACs) are among them. They consist of two linked molecules that bind to a target protein and an E3 ubiquitin ligase that causes ubiquitination and degradation of proteins of interest. In this paper, we review the rationale for PROTAC therapy and the current development of PROTACs for oncogene-addicted lung cancer. Moreover, we critically analyze the strengths and limitations of this promising technique that may help pave the way for future perspectives.

Indexed as

Carcinoma, Non-Small-Cell LungDrug Resistance, NeoplasmLung NeoplasmsProteolysisAnimalsAntineoplastic AgentsHumansMolecular Targeted TherapyOncogenesProtein Kinase InhibitorsProteolysis Targeting ChimeraUbiquitinationUbiquitin-Protein LigasesAntineoplastic AgentsProtein Kinase InhibitorsProteolysis Targeting ChimeraUbiquitin-Protein Ligasesoncogene-addicted NSCLCPROTACTKI resistance

Identifiers

PMID39456995
PMCPMC11508910

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.