Evidence map›Paper›PMID 39933186›Full record

ArticleCancer research2025

Interactions between Ploidy and Resource Availability Shape Clonal Evolution in Glioblastoma.

Zuzanna Nowicka, Frederika Rentzeperis, Vural Tagal, Jamie K Teer, Didem Ilter, Richard J Beck, Jackson P Cole, Ana Forero Pinto, Joanne D Tejero, Elisa Scanu and 18 more

Abstract read
In one paragraph

Article in Cancer research, 2025. 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. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

28 authors.

Zuzanna Nowicka *Department of Biostatistics and Translational Medicine, Medical University of Łódź, Łódź, Poland.ORCID 0000-0001-7814-5830
Frederika Rentzeperis *Icahn School of Medicine at Mount Sinai, New York City, New York.ORCID 0000-0001-9797-1134
Vural TagalDepartment of Integrated Mathematical Oncology, Moffitt Cancer Center, Tampa, Florida.ORCID 0000-0002-0489-9725
Jamie K TeerDepartment of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.ORCID 0000-0003-4513-0282
Didem IlterDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.ORCID 0000-0001-7506-8198
Richard J BeckDepartment of Integrated Mathematical Oncology, Moffitt Cancer Center, Tampa, Florida.ORCID 0000-0002-6983-8835
Jackson P ColeDepartment of Integrated Mathematical Oncology, Moffitt Cancer Center, Tampa, Florida.ORCID 0009-0006-3416-6641
Ana Forero PintoDepartment of Integrated Mathematical Oncology, Moffitt Cancer Center, Tampa, Florida.ORCID 0000-0002-1694-5557
Joanne D TejeroDepartment of Molecular Medicine, University of South Florida Morsani College of Medicine, Tampa, Florida.ORCID 0009-0008-8084-4540
Elisa ScanuQueen Mary University of London, School of Mathematical Sciences, London, United Kingdom.ORCID 0009-0001-9989-5822
Thomas VeithDepartment of Integrated Mathematical Oncology, Moffitt Cancer Center, Tampa, Florida.ORCID 0000-0001-8411-9911
William Dominguez-ViqueiraDepartment of Cancer Imaging and Metabolism, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.ORCID 0009-0009-8707-7628
Konstantin MaksinThe University of Commerce and Services, Medical Department (WSHIU), Poznan, Poland.ORCID 0000-0001-6190-217X
Francisco Carrillo-PerezStanford Center for Biomedical Informatics Research (BMIR), Stanford University, School of Medicine, Stanford, California.ORCID 0000-0003-0974-4092
Olivier GevaertStanford Center for Biomedical Informatics Research (BMIR), Stanford University, School of Medicine, Stanford, California.ORCID 0000-0002-9965-5466
Xiaonan XuDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.ORCID 0000-0002-7366-580X
Florian A KarrethDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.ORCID 0000-0002-2350-9809
Mahmoud A AbdalahQuantitative Imaging Core, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.ORCID 0000-0002-0573-4121
Giada FiandacaUniversité Côte d'Azur, Inria, INRAE, CNRS, Sorbonne Université, Macbes Team, Sophia Antipolis, Valbonne, France.ORCID 0000-0002-7923-5878
Stefano PasettoDepartment of Integrated Mathematical Oncology, Moffitt Cancer Center, Tampa, Florida.ORCID 0000-0002-4926-3704
Sandhya PrabhakaranDepartment of Integrated Mathematical Oncology, Moffitt Cancer Center, Tampa, Florida.ORCID 0000-0002-9537-507X
Andrew SchultzDepartment of Integrated Mathematical Oncology, Moffitt Cancer Center, Tampa, Florida.ORCID 0009-0002-1783-6931
Awino Maureiq E Ojwang'Department of Integrated Mathematical Oncology, Moffitt Cancer Center, Tampa, Florida.ORCID 0009-0000-3275-1974
Jill S Barnholtz-SloanCenter for Biomedical Informatics and Information Technology and Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.ORCID 0000-0001-6190-9304
Joaquim M FarinhasDepartment of Radiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.ORCID 0000-0003-1040-7894
Ana P GomesDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.ORCID 0000-0003-0881-727X
Parag KatiraDepartment of Mechanical Engineering and the Computational Sciences Research Center, San Diego State University, San Diego, California.ORCID 0000-0001-9873-5117
Noemi AndorDepartment of Integrated Mathematical Oncology, Moffitt Cancer Center, Tampa, Florida.ORCID 0000-0002-2469-5180

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI John L. Cleveland · 1998 to 2026
$93.5M
Characterizing cytotoxic therapy induced shifts in the cost-to-benefit ratio of high ploidyR37CA266727 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI Noemi Andor · 2022 to 2026
$2.6M
A clone's genomic stability as biomarker of its DNA-damage resilienceR00CA215256 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI ANDOR, NOEMI · 2019 to 2021
$747k
IMAT-ITCR Collaboration: Engineering model-based systems to monitor and steer subclonal dynamicsR21CA269415 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI ANDOR, NOEMI · 2023 to 2024
$499k
A framework to integrate live-cell imaging with single-cell sequencing and learn how cells adapt to new environmentsR03CA259873 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI ANDOR, NOEMI, HEISER, LAURA MADELINE · 2022 to 2023
$179k
Moffitt Cancer Center (MCC) Moffitt Cancer Center Evolutionary Therapy Center of Excellence (IMO workshop Pilot Award)National Institutes of Health (NIH) 1R37CA266727-01A1NCI NIH HHS P30 CA076292NCI NIH HHS R00 CA215256NCI NIH HHS R03 CA259873NCI NIH HHS R21 CA269415NCI NIH HHS R37 CA266727
6 · The paper itself

Abstract

Glioblastoma (GBM) is the most aggressive form of primary brain tumor. The infiltrative nature of GBM makes complete surgical resection impossible. The selective forces that govern gliomagenesis are strong, shaping the composition of tumor cells during the initial progression to malignancy with late consequences for invasiveness and therapy response. Here, we developed a mathematical model that incorporates ploidy level and the nature of the brain tissue microenvironment to simulate the growth and invasion of GBM and used the model to make inferences about GBM initiation and response to the standard-of-care treatment. The spatial distribution of resource access in the brain was approximated through integration of in silico modeling, multiomics data, and image analysis of primary and recurrent GBM. The in silico results suggested that high-ploidy cells transition faster from oxidative phosphorylation to glycolysis than low-ploidy cells because they are more sensitive to hypoxia. Between surgeries, simulated tumors with different ploidy compositions progressed at different rates; however, whether higher ploidy predicted fast recurrence was a function of the brain microenvironment. Historical data supported the dependence on available resources in the brain, as shown by a significant correlation between the median oxygen levels in human tissues and the median ploidy of cancers that arise in the respective tissues. Taken together, these findings suggest that the availability of metabolic substrates in the brain drives different cell fate decisions for cells with different ploidy, thereby modulating both gliomagenesis and GBM recurrence. Significance: Ploidy viewed in the context of the resources in the microenvironment has the potential to inform whether modulation of energetic availability can delay tumor progression and could help guide clinical decision making.

Indexed as

Brain NeoplasmsClonal EvolutionGlioblastomaPloidiesComputer SimulationHumansNeoplasm Recurrence, LocalTumor Microenvironment

Identifiers

PMID39933186
PMCPMC12261341

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.