ReviewBlood science (Baltimore, Md.)2026
The tumor microenvironment in hematologic malignancies: immune evasion, metabolic reprogramming, and therapeutic resistance.
Review in Blood science (Baltimore, Md.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Malaria and cancer: common features and interactions.Trends in parasitology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hematological malignancies, including leukemia, lymphoma, and multiple myeloma, develop within and remain dependent on a complex and dynamic tumor microenvironment (TME). Malignant cells interact continuously with the cellular and molecular components of the TME, which play a critical role in shaping disease progression, therapeutic response, and immune evasion. The TME comprises mesenchymal stromal cells, immune cells, fibroblasts, endothelial cells, and a range of signaling molecules such as chemokines, cytokines, and extracellular vesicles, embedded within a heterogeneous extracellular matrix (ECM). This integrated network, along with recently established mechanisms, establishes a supportive niche that promotes malignant cell survival, clonal evolution, immune modulation, and therapy resistance. This review examines the cellular and molecular architecture of the hematologic TME and its influence on chemoresistance and immune suppression. It further discusses therapeutic interventions that aim to disrupt or reprogram the TME, thereby restoring therapeutic sensitivity and enhancing immune-mediated clearance.
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Registered trials
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.