Evidence map›Paper›PMID 42553785›Full record

ArticleNeuro-oncology advances

Intercellular adhesion molecule 1 links glioblastoma biology to a scalable prognostic model integrating clinical, imaging, and molecular features.

Shreya Gandhi, Beatriz Ocaña-Tienda, Manuel M Bettencourt, Olivia S Singh, Kaviya Devaraja, Emily R Irish, David Molina-García, Shirin Karimi, Yasin Mamatjan, Julio Sosa and 17 more

Abstract read
In one paragraph

Article in Neuro-oncology advances. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

27 authors.

Shreya GandhiMayo Clinic Alix School of Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Beatriz Ocaña-TiendaBioinformatics Unit, Spanish National Cancer Research Center, Madrid, Spain.
Manuel M BettencourtDepartment of Neurologic Surgery, Mayo Clinic, Rochester, Minnesota, USA.
Olivia S SinghDepartment of Neurologic Surgery, Mayo Clinic, Rochester, Minnesota, USA.
Kaviya DevarajaInstitute of Medical Sciences, University of Toronto, Toronto, Ontario, Canada.ORCID https://orcid.org/0000-0002-3433-5242
Emily R IrishDepartment of Neurologic Surgery, Mayo Clinic, Rochester, Minnesota, USA.
David Molina-GarcíaMathematical Oncology Laboratory, University of Castilla-La Mancha, Ciudad Real, Spain.ORCID https://orcid.org/0000-0002-6104-3894
Shirin KarimiDepartment of Neurosurgery, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada.
Yasin MamatjanDepartment of Engineering, Thompson Rivers University, Kamloops, British Columbia, Canada.
Julio SosaDepartment of Neurosurgery, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada.
Ian McIntyreDepartment of Neurosurgery, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada.
Andrew F GaoDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Julián Pérez-BetetaMathematical Oncology Laboratory, University of Castilla-La Mancha, Ciudad Real, Spain.ORCID https://orcid.org/0000-0003-0317-6215
Ana Ramos-GonzálezHospital Universitario, Madrid, Spain.
Aurelio Hernández-LaínHospital Universitario, Madrid, Spain.
Beatriz AsenjoHospital Regional Universitario de Málaga, Málaga, Spain.ORCID https://orcid.org/0000-0003-1299-5079
María Pino Flores-RialHospital Regional Universitario de Málaga, Málaga, Spain.
Pilar Sánchez-GómezNeuro-Oncology Unit, Instituto de Salud Carlos III, Madrid, Spain.ORCID https://orcid.org/0000-0002-0709-4973
Kenneth D AldapeDepartment of Laboratory Medicine and Pathobiology, Mayo Clinic, Rochester, Minnesota, USA.
Carlos SantosInstituto De Investigación Marqués De Valdecilla, Santander, Spain.ORCID https://orcid.org/0000-0002-6874-6736
Katharine J DrummondDepartment of Neurosurgery, The University of Melbourne, Melbourne, Victoria, Australia.
Ian F ParneyDepartment of Neurologic Surgery, Mayo Clinic, Rochester, Minnesota, USA.
Carlos VelasquezInstituto De Investigación Marqués De Valdecilla, Santander, Spain.
Alireza MansouriDepartment of Neurosurgery, Penn State Hershey Medical Center, Hershey, Pennsylvania, USA.ORCID https://orcid.org/0000-0002-7442-7539
Victor M Pérez-GarcíaMathematical Oncology Laboratory, University of Castilla-La Mancha, Ciudad Real, Spain.
Gelareh ZadehDepartment of Neurologic Surgery, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0009-0009-2002-5313
Sheila MansouriDepartment of Neurologic Surgery, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0009-0002-9785-2463

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Glioblastoma (GB) exhibits marked tumor microenvironmental heterogeneity, contributing to both therapy resistance and poor survival outcomes. Intercellular adhesion molecule 1 (ICAM1) is an inflammation-associated adhesion molecule implicated in immune-stromal interactions, but its clinical and biological significance in GB remains incompletely defined. Methods: We performed ICAM1 immunohistochemistry, bulk RNA sequencing, DNA methylation analysis, single-nucleus RNA sequencing, and preoperative MRI-derived morphologic feature analysis across multi-institutional cohorts of treatment-naïve IDH-wildtype GB. Results: High ICAM1 expression at both transcript and protein levels is associated with shorter overall survival, particularly within the mesenchymal transcriptional subtype. ICAM1 expression is inversely associated with promoter methylation. Single-nucleus RNA-sequencing analysis shows that ICAM1-high tumors are enriched for mesenchymal, hypoxia, stress-associated, and immunosuppressive myeloid programs, suggesting that ICAM1 reflects a multicompartment inflammatory tumor ecosystem. ICAM1 expression, tumor surface irregularity, and patient age are independently prognostic and minimally correlated, capturing complementary clinical, imaging, and molecular features of GB biology. When combined, our Clinical-Imaging-Molecular (CIM) framework refines outcome prediction across independent GB cohorts using routinely available clinical data, conventional imaging, and standard immunohistochemistry. Conclusions: ICAM1 characterizes an immune-remodeled, stress-adapted GB ecosystem associated with poor clinical outcomes. Integrating patient age, surface irregularity, and ICAM1 expression yields a scalable and clinically accessible prognostic framework for GB, supporting tailored outcome prediction, particularly in low- and middle-resource settings without routine access to advanced molecular profiling.

Indexed as

glioblastomaICAM1multi-omicsprognostictumor microenvironment

Identifiers

PMID42553785
PMCPMC13436593

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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.