Evidence map›Paper›PMID 35547806›Full record

ReviewFrontiers in cell and developmental biology2022

Overcoming Cancer Drug Resistance Utilizing PROTAC Technology.

Matthew R Burke, Alexis R Smith, Guangrong Zheng

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 1% of its field
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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. PROTACs in cancer therapy: targeted degradation of GPX4, PARP and epigenetic regulators.Journal of enzyme inhibition and medicinal chemistry · 2026
    Review
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  12. A Scalable Design for Proximity-Inducing Molecules.bioRxiv : the preprint server for biology · 2026
    Article
  13. Review
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  17. Elucidating biased signaling in class A GPCRs.Trends in pharmacological sciences · 2025
    Review
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  20. Article

6 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Matthew R BurkeDepartment of Medicinal Chemistry, College of Pharmacy, University of Florida, Gainesville, FL, United States.
Alexis R SmithDepartment of Medicinal Chemistry, College of Pharmacy, University of Florida, Gainesville, FL, United States.
Guangrong ZhengDepartment of Medicinal Chemistry, College of Pharmacy, University of Florida, Gainesville, FL, United States.
University of Florida · US

Funding

Inhibition of Bcl-xL by Targeted DegradationR01CA241191 · NCI · UNIVERSITY OF FLORIDA · PI KONOPLEVA, MARINA Y, ZHENG, GUANGRONG · 2020 to 2024
$2.6M
Use of BCL-xL Proteolysis targeting chimeras to treat pancreatic cancerR01CA242003 · NCI · UNIVERSITY OF FLORIDA · PI TREVINO, JOSE G., ZHENG, GUANGRONG · 2019 to 2023
$2.6M
NCI NIH HHS R01 CA241191
6 · The paper itself

Abstract

Cancer drug resistance presents a major barrier to continued successful treatment of malignancies. Current therapies inhibiting proteins indicated in cancer progression are consistently found to lose efficacy as a result of acquired drug resistance, often caused by mutated or overexpressed protein targets. By hijacking the cellular ubiquitin-proteasome protein degradation machinery, proteolysis-targeting chimeras (PROTACs) offer an alternative therapeutic modality to cancer treatments with various potential advantages. PROTACs specific for a number of known cancer targets have been developed in the last 5 years, which present new options for remission in patients with previously untreatable malignancies and provide a foundation for future-generation compounds. One notable advantage of PROTACs, supported by evidence from a number of recent studies, is that they can overcome some of the resistance mechanisms to traditional targeted therapies. More recently, some groups have begun researching the use of PROTACs to successfully degrade mutated targets conferring cancer resistance against first-line treatments. In this review, we focus on analyzing the developments in PROTACs geared towards cancer resistance and targets that confer it in the search for new and successful therapies.

Indexed as

acquired resistancecancer drug resistancedrug discoveryE3 ubiquitin ligaseproteolysis targeting chimeratargeted protein degradationtargeted therapy

Identifiers

PMID35547806
PMCPMC9083012
OpenAlexW4224815538

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.