Evidence map›Paper›PMID 35365706›Full record

ArticleScientific reports2022

Bladder cancer cells shift rapidly and spontaneously to cisplatin-resistant oxidative phosphorylation that is trackable in real time.

Tong Xu, Jason A Junge, Alireza Delfarah, Yi-Tsung Lu, Cosimo Arnesano, Maheen Iqbal, Kevin Delijani, Tien-Chan Hsieh, Emmanuelle Hodara, Hemal H Mehta and 4 more

Abstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
  2. Review
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  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. mNAR cancer · 2023
    Article
  10. Article
  11. Review
  12. Review
  13. 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

14 authors.

Tong Xu *Division of Medical Oncology, Department of Internal Medicine, University of Southern California Keck School of Medicine and Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, Suite 3440, Los Angeles, CA, 90033, USA.
Jason A Junge *Translational Imaging Center, University of Southern California, Los Angeles, CA, 90089, USA.
Alireza DelfarahMork Family Department of Chemical Engineering and Materials Science, University of Southern California, Los Angeles, CA, 90089, USA.
Yi-Tsung LuDivision of Medical Oncology, Department of Internal Medicine, University of Southern California Keck School of Medicine and Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, Suite 3440, Los Angeles, CA, 90033, USA.
Cosimo ArnesanoTranslational Imaging Center, University of Southern California, Los Angeles, CA, 90089, USA.
Maheen IqbalDivision of Medical Oncology, Department of Internal Medicine, University of Southern California Keck School of Medicine and Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, Suite 3440, Los Angeles, CA, 90033, USA.
Kevin DelijaniDivision of Medical Oncology, Department of Internal Medicine, University of Southern California Keck School of Medicine and Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, Suite 3440, Los Angeles, CA, 90033, USA.
Tien-Chan HsiehDivision of Medical Oncology, Department of Internal Medicine, University of Southern California Keck School of Medicine and Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, Suite 3440, Los Angeles, CA, 90033, USA.
Emmanuelle HodaraDivision of Medical Oncology, Department of Internal Medicine, University of Southern California Keck School of Medicine and Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, Suite 3440, Los Angeles, CA, 90033, USA.
Hemal H MehtaThe Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA, 90089, USA.
Pinchas CohenThe Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA, 90089, USA.
Nicholas A GrahamMork Family Department of Chemical Engineering and Materials Science, University of Southern California, Los Angeles, CA, 90089, USA.
Scott E FraserTranslational Imaging Center, University of Southern California, Los Angeles, CA, 90089, USA.
Amir GoldkornDivision of Medical Oncology, Department of Internal Medicine, University of Southern California Keck School of Medicine and Norris Comprehensive Cancer Center, 1441 Eastlake Avenue, Suite 3440, Los Angeles, CA, 90033, USA. agoldkor@med.usc.edu.

Funding

USC/NORRIS COMPREHENSIVE CANCER CENTER (CORE) SUPPORTP30CA014089 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Fumito Ito · 1985 to 2026
$181.4M
Integrated radiomic and liquid biopsy monitoring in SWOG S1802: A phase 3 therapeutic trial for metastatic prostate cancerR01CA257610 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DUDDALWAR, VINAY, GOLDKORN, AMIR · 2021 to 2025
$3.4M
Biomarkers of Hormone Therapy Response in a Multicenter Prostate Cancer TrialR01CA172436 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GOLDKORN, AMIR, INGLES, SUE ANN · 2014 to 2018
$3.3M
NCI NIH HHS P30 CA014089NCI NIH HHS R01 CA172436NCI NIH HHS R01 CA172436, 1 R01 CA257610, and P30 CA014089NCI NIH HHS R01 CA257610
6 · The paper itself

Abstract

Genetic mutations have long been recognized as drivers of cancer drug resistance, but recent work has defined additional non-genetic mechanisms of plasticity, wherein cancer cells assume a drug resistant phenotype marked by altered epigenetic and transcriptional states. Currently, little is known about the real-time, dynamic nature of this phenotypic shift. Using a bladder cancer model of nongenetic plasticity, we discovered that rapid transition to drug resistance entails upregulation of mitochondrial gene expression and a corresponding metabolic shift towards the tricarboxylic acid cycle and oxidative phosphorylation. Based on this distinction, we were able to track cancer cell metabolic profiles in real time using fluorescence lifetime microscopy (FLIM). We observed single cells transitioning spontaneously to an oxidative phosphorylation state over hours to days, a trend that intensified with exposure to cisplatin chemotherapy. Conversely, pharmacological inhibition of oxidative phosphorylation significantly reversed the FLIM metabolic signature and reduced cisplatin resistance. These rapid, spontaneous metabolic shifts offer a new means of tracking nongenetic cancer plasticity and forestalling the emergence of drug resistance.

Indexed as

CisplatinUrinary Bladder NeoplasmsDrug Resistance, NeoplasmEpithelial CellsHumansOxidative PhosphorylationCisplatin

Identifiers

PMID35365706
PMCPMC8976067

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.