Evidence map›Paper›PMID 35800362›Full record

ReviewCancer drug resistance (Alhambra, Calif.)2022

DNA damage and metabolic mechanisms of cancer drug resistance.

Deanna Tiek, Shi-Yuan Cheng

Open access · diamondAbstract readReview
In one paragraph

Review in Cancer drug resistance (Alhambra, Calif.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.9field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  5. Cognitive dysfunction in chemobrain: Molecular mechanisms and therapeutic implications.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
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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

2 authors at 2 institutions in 1 country.

Deanna TiekThe Ken & Ruth Davee Department of Neurology, Lou and Jean Malnati Brain Tumor Institute at Northwestern Medicine, Robert H. Lurie Comprehensive Cancer Center, and Simpson Querry Institute for Epigenetics, Northwestern University, Feinberg School of Medicine, 303 E Superior St, Chicago, IL 60611, USA.
Shi-Yuan ChengThe Ken & Ruth Davee Department of Neurology, Lou and Jean Malnati Brain Tumor Institute at Northwestern Medicine, Robert H. Lurie Comprehensive Cancer Center, and Simpson Querry Institute for Epigenetics, Northwestern University, Feinberg School of Medicine, 303 E Superior St, Chicago, IL 60611, USA.
Northwestern Medicine · USRobert H. Lurie Comprehensive Cancer Center of Northwestern University

Funding

Targeting RNA Splicing in GliomaR01NS125318 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Shi-Yuan Cheng · 2022 to 2026
$2.4M
Role of Protein Methylation in Cell Mitosis and GlioblastomaR01NS115403 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHENG, SHI-YUAN · 2020 to 2024
$2.1M
Cysteine Depletion-induced Ferroptosis as a Therapeutic Vulnerability iR21NS126810 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHENG, SHI-YUAN · 2022 to 2023
$440k
Novel relationships of splicing factors in temozolomide-resistant glioblastomaK00CA234799 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI TIEK, DEANNA MARIE · 2020 to 2023
$369k
NCI NIH HHS K00 CA234799NINDS NIH HHS R01 NS115403NINDS NIH HHS R01 NS125318NINDS NIH HHS R21 NS126810
6 · The paper itself

Abstract

Cancer drug resistance is one of the main barriers to overcome to ensure durable treatment responses. While many pivotal advances have been made in first combination therapies, then targeted therapies, and now broadening out to immunomodulatory drugs or metabolic targeting compounds, drug resistance is still ultimately universally fatal. In this brief review, we will discuss different strategies that have been used to fight drug resistance from synthetic lethality to tumor microenvironment modulation, focusing on the DNA damage response and tumor metabolism both within tumor cells and their surrounding microenvironment. In this way, with a better understanding of both targetable mutations in combination with the metabolism, smarter drugs may be designed to combat cancer drug resistance.

Indexed as

Cancer drug resistanceDNA damageDNA repairdrug resistancehypoxiametabolismovercoming resistancesynthetic lethality

Identifiers

PMID35800362
PMCPMC9255237
OpenAlexW4285268574

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.