Evidence map›Paper›PMID 41992363›Full record

ReviewBiomarker research2026

Cancer in transition: discovery of tumor-intrinsic transcriptional programs shaping the immune and microenvironmental landscape.

Alf Spitschak, Rosaely Casalegno Garduño, Brigitte M Pützer

Abstract readReview
In one paragraph

Review in Biomarker research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

3 authors.

Alf Spitschak *Institute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, 18057, Rostock, Germany.
Rosaely Casalegno Garduño *Institute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, 18057, Rostock, Germany.
Brigitte M PützerInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, 18057, Rostock, Germany. brigitte.puetzer@med.uni-rostock.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer biomarker discovery has traditionally focused on individual molecular features; however, tumor behavior and therapeutic response are governed by integrated transcriptional and epigenetic programs that shape immune and microenvironmental states. Deciphering the determinants of metastatic evolution and the complexity of cancer ecosystems is imperative for designing novel preventive and targeted therapies. Tumor complexity, driven by intrinsic cellular heterogeneity and the dynamic plasticity of cancer cells in response to microenvironmental cues, complicates therapeutic strategies based solely on defined molecular or genetic traits. Consequently, there is an urgent need for reliable predictive biomarkers that reflect cancer vulnerabilities, indicate disease progression, or predict patient-specific therapeutic responses to enable truly individualized treatment strategies. Current biomarkers encompass genetic and epigenetic alterations, non-coding RNAs, epithelial-mesenchymal transition-, stemness-, and metastasis-associated transcription factors, as well as cellular components of the tumor microenvironment, including immune cell subsets and cancer-associated fibroblasts. In immuno-oncology, additional biomarkers such as tumor mutational burden, mismatch repair deficiency/microsatellite instability-high status, and PD-L1 expression are widely used for patient stratification. Importantly, the reversible nature of epigenetic modifications, aberrant transcription factor activity, and cell-intrinsic signaling alterations, together with dynamic interactions within the tumor microenvironment, profoundly influence cancer behavior and treatment outcomes. This review summarizes recent advances in cancer and immune-related biomarker research. It outlines a regulatory, systems-level framework that integrates tumor-intrinsic gene control programs with multi-omic, cellular, spatial, and AI-enabled biomarkers. This framework aims to capture tumor plasticity more effectively and advance precision oncology.

Indexed as

Artificial intelligence in oncologyCancer biomarkersE2F1Epigenetic reprogrammingImmunotherapy biomarkersMulti-omics integrationNoncoding RNATranscriptional regulationTumor microenvironmentTumor plasticity

Identifiers

PMID41992363
PMCPMC13094380

What Socratic 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 Socratic graph.