Evidence map›Paper›PMID 40575293›Full record

ArticleJACS Au2025

LA-ICP-TOFMS Imaging Reveals Significant Influence of Cancer Cell Resistance on Oxaliplatin Compartmentalization in the Tumor Microenvironment.

Martin Schaier, Dina Baier, Sarah Theiner, Walter Berger, Gunda Koellensperger

Abstract read
In one paragraph

Article in JACS Au, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

5 authors.

Martin SchaierInstitute of Analytical Chemistry, Faculty of Chemistry, University of Vienna, Vienna 1090, Austria.ORCID https://orcid.org/0000-0003-4907-218X
Dina BaierInstitute of Inorganic Chemistry, Faculty of Chemistry, University of Vienna, Vienna 1090, Austria.
Sarah TheinerInstitute of Analytical Chemistry, Faculty of Chemistry, University of Vienna, Vienna 1090, Austria.ORCID https://orcid.org/0000-0001-5301-0139
Walter BergerCenter for Cancer Research and Comprehensive Cancer Center, Medical University of Vienna, Vienna 1090, Austria.ORCID https://orcid.org/0000-0003-0014-1658
Gunda KoellenspergerInstitute of Analytical Chemistry, Faculty of Chemistry, University of Vienna, Vienna 1090, Austria.ORCID https://orcid.org/0000-0002-1460-4919

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemoresistance in cancer cells, particularly in refractory types, such as colorectal cancer, poses a major challenge to effective treatment. In particular, the interaction between cancer cells and the tumor microenvironment (TME) has been shown to exert substantial influence on the efficacy of therapeutic agents. This study investigated whether an intrinsic resistance phenotype alters drug distribution in the TME using xenograft models derived from HCT116 colorectal cancer cells, including oxaliplatin (OxPt)-sensitive and OxPt-resistant (OxR) variants. Tumors were prepared as formalin-fixed paraffin-embedded (FFPE) sections, followed by single-cell analysis with laser ablation inductively coupled plasma time-of-flight mass spectrometry (LA-ICP-TOFMS). Based on histological evaluations, a panel of metal-conjugated antibodies was designed to target tissue architecture and distinct cell states within the TME. A dedicated calibration strategy was applied to accurately measure platinum (Pt) uptake in phenotypically defined single cells across both the tumor and its microenvironment. The results revealed substantial structural differences: HCT116/OxR tumors exhibited robust growth following drug administration, while parental tumors displayed extensive degradation. Notably, OxPt accumulated significantly in necrotic regions specific to HCT116/OxR, indicating resistance-dependent changes in drug compartmentalization. These findings suggest that an intrinsically resistant cancer cell phenotype is capable of markedly altering metal distributions within the TME.

Indexed as

antitumor agentsbioimagingchemoresistancelaser ablationmass spectrometrysingle-cell analysis

Identifiers

PMID40575293
PMCPMC12188412

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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.