Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (535 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The milieu surrounding neoplasms consisting of cells, vessels, soluble factors, and molecules, that can influence and be influenced by, the neoplasm's growth.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Microenvironments, Tumor; Microenvironment, Tumor; Tumor Microenvironments; Cancer Microenvironment; Cancer Microenvironments; Microenvironment, Cancer; Microenvironments, Cancer.
Where it fits in the MeSH classification
- Broader topics
- Cellular Microenvironment
Research landscape
PubMed indexes 72,936 records tagged with the MeSH heading “Tumor Microenvironment” (counts retrieved 2026-10-29). 58,169 of them (79.8%) were published from 2020 onward, and the busiest period so far is 2020 onward with 58,169 records.
Reviews account for 24,007 records (32.9%) and meta-analyses for 147. Randomized controlled trials number 143 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 12 |
| 2010-2019 | 15,307 |
| 2020 onward | 58,169 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 24,007 | 32.9% |
| Meta-analyses | 147 | 0.2% |
| Randomized controlled trials | 143 | 0.2% |
Method: PubMed query "Tumor Microenvironment"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Myeloperoxidase promotes a tumorigenic microenvironment in non-small cell lung cancer | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 42753317 · DOI · PMC13602051 |
| Systemic and local chronic inflammation and hormone disposition promote a tumor-permissive environment for breast cancer in older women | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42509302 · DOI · PMC13472878 |
| CDK8 remodels the tumor microenvironment and promotes resistance to KRASG12D inhibitors and daraxonrasib in PDAC | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42436354 · DOI · PMC13483915 |
Myeloperoxidase promotes a tumorigenic microenvironment in non-small cell lung cancer [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Myeloperoxidase (MPO) is a heme peroxidase that is mainly expressed and secreted by neutrophils.
- Closing excerpt
- Our findings suggest that MPO plays an immunosuppressive role in NSCLC.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (201 words)
Myeloperoxidase (MPO) is a heme peroxidase that is mainly expressed and secreted by neutrophils. MPO's role in inflammatory diseases has been highlighted in recent years, but its role in tumor development remains unclear. Therefore, we investigated the role of MPO in non-small cell lung cancer (NSCLC). In silico analysis revealed a survival benefit in patients with NSCLC and low MPO expression. Furthermore, a syngeneic tumor model using MPO knockout (KO) mice revealed that mice lacking MPO had lower tumor growth than controls. The reduction in tumor size was accompanied by an increase in lymphoid populations, including natural killer cells and CD8+ T cells, suggesting a shift to a more anti-tumorigenic immune environment in MPO-KO mouse tumors. The T cell induced interferon-gamma (IFN-γ) expression was increased in MPO-KO tumors, indicating increased tumoricidal activity. CD8 depletion abolished the previously observed reduction in tumor size in MPO-KO mice, indicating that CD8+ T cells play an important role. In vitro, T cells treated with MPO showed reduced proliferation and IFN-γ expression. Furthermore, MPO associated directly with T cells. Interestingly, MPO+ lymphocytes, including CD8+ T cells, were found in tumor samples from patients with NSCLC. Our findings suggest that MPO plays an immunosuppressive role in NSCLC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42753317 · DOI · PMC13602051
Systemic and local chronic inflammation and hormone disposition promote a tumor-permissive environment for breast cancer in older women [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Estrogen receptor-positive (ER+) breast cancer is the most common subtype of breast cancer and is an age-related disease.
- Closing excerpt
- These findings support a model linking age-associated hormonal and inflammatory changes to features of a tumor-permissive microenvironment in ER+ breast cancer.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (156 words)
Estrogen receptor-positive (ER+) breast cancer is the most common subtype of breast cancer and is an age-related disease. How systemic and tumor microenvironment hormone signaling intersects with chronic inflammation and how this shapes aging-associated tumor biology remain incompletely understood. Here, using an aged rat model of ER+ tumors, we identify age-associated differences in tumor development and immune features. In parallel, analysis of samples from patients with ER+/HER2- breast cancer and age-matched controls demonstrated estrone-predominant systemic estrogen patterns and increased tumor HSD17B7 expression in older patients, consistent with enhanced local estrone-to-estradiol conversion. In patient-derived organoids from older women, pharmacologic inhibition of HSD17B7 reduced estrogen conversion and proliferation-associated transcriptional programs. Tumors from older patients also exhibited chemokine enrichment, including CCL2, associated with immunosuppressive macrophage features. Targeting both estrogen signaling and chemokine pathways attenuated macrophage polarization ex vivo. These findings support a model linking age-associated hormonal and inflammatory changes to features of a tumor-permissive microenvironment in ER+ breast cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42509302 · DOI · PMC13472878
CDK8 remodels the tumor microenvironment and promotes resistance to KRASG12D inhibitors and daraxonrasib in PDAC [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Mutations in KRAS are a dominant driver of pancreatic ductal adenocarcinoma (PDAC), with about 50% of patients presenting with KRASG12D mutations.
- Closing excerpt
- We also provide evidence of CDK8 upregulation in PDX tumors resistant to inhibitors selective for RAS(ON) and RASG12D(ON): daraxonrasib and zoldonrasib, respectively, highlighting a common KRAS vulnerability node for TME resistance.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (178 words)
Mutations in KRAS are a dominant driver of pancreatic ductal adenocarcinoma (PDAC), with about 50% of patients presenting with KRASG12D mutations. Small molecule inhibitors targeting KRASG12D suppress PDAC; however, the contribution of the tumor microenvironment (TME) to the sustained efficacy of KRASG12D inhibition and mechanisms of resistance to KRASG12D suppression remain to be elucidated. Here, integrated spatial transcriptomics, single-cell RNA sequencing, and CODEX-based spatial proteomics analyses of PDAC mouse models uncover that while KRASG12D inhibition by MRTX1133 initially increases CD11c+ cells and T cell infiltration proximal to cancer cells, long-term treatment results in reversal of the immune responses leading to resistance promoted by multiprotein mediator complex associated kinase CDK8. CDK8 imparts this resistance via induction of CXCL2 chemokine secretion, inhibition of FAS expression, and remodeling of the TME to promote immune evasion. Targeting CDK8 by itself or in combination with αCTLA-4 immunotherapy overcomes resistance to KRASG12D inhibition. We also provide evidence of CDK8 upregulation in PDX tumors resistant to inhibitors selective for RAS(ON) and RASG12D(ON): daraxonrasib and zoldonrasib, respectively, highlighting a common KRAS vulnerability node for TME resistance.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42436354 · DOI · PMC13483915
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Prognostic impact of tumor-associated macrophage infiltration in non-small cell lung cancer: A systemic review and meta-analysis [4]
- Research article Peri-prostatic adipose tissue: the metabolic microenvironment of prostate cancer [5]
- Research article The local inflammatory response in colorectal cancer - Type, location or density? A systematic review and meta-analysis [6]
- Research article Viral status, immune microenvironment and immunological response to checkpoint inhibitors in hepatocellular carcinoma [7]
- Research article Tumor-associated tissue eosinophilia predicts favorable clinical outcome in solid tumors: a meta-analysis [8]
- Research article Targeting PI3K-gamma in myeloid driven tumour immune suppression: a systematic review and meta-analysis of the preclinical literature [9]
References
- Valadez-Cosmes P, Maitz K, Lagler A, Kindler O, Mujkanovic NC, Raftopoulou S, et al.. Myeloperoxidase promotes a tumorigenic microenvironment in non-small cell lung cancer. . 2026. PMID 42753317 · DOI · PMC13602051
- Carleton N, Chang AC, Lee S, Li R, Zou J, Brown DD, et al.. Systemic and local chronic inflammation and hormone disposition promote a tumor-permissive environment for breast cancer in older women. . 2026. PMID 42509302 · DOI · PMC13472878
- McAndrews KM, Mahadevan KK, Li B, Comptdaer AM, Sockwell AM, Morse SJ, et al.. CDK8 remodels the tumor microenvironment and promotes resistance to KRASG12D inhibitors and daraxonrasib in PDAC. . 2026. PMID 42436354 · DOI · PMC13483915
- Mei J, Xiao Z, Guo C, Pu Q, Ma L, Liu C, et al.. Prognostic impact of tumor-associated macrophage infiltration in non-small cell lung cancer: A systemic review and meta-analysis. Oncotarget. 2016. PMID 27144518 · DOI · PMC5085150
- Nassar ZD, Aref AT, Miladinovic D, Mah CY, Raj GV, Hoy AJ, et al.. Peri-prostatic adipose tissue: the metabolic microenvironment of prostate cancer. BJU Int. 2018. PMID 29460324 · DOI
- Alexander PG, McMillan DC, Park JH. The local inflammatory response in colorectal cancer - Type, location or density? A systematic review and meta-analysis. Cancer Treat Rev. 2020. PMID 31869737 · DOI
- Ho WJ, Danilova L, Lim SJ, Verma R, Xavier S, Leatherman JM, et al.. Viral status, immune microenvironment and immunological response to checkpoint inhibitors in hepatocellular carcinoma. J Immunother Cancer. 2020. PMID 32303615 · DOI · PMC7204805
- Hu G, Wang S, Zhong K, Xu F, Huang L, Chen W, et al.. Tumor-associated tissue eosinophilia predicts favorable clinical outcome in solid tumors: a meta-analysis. BMC Cancer. 2020. PMID 32434481 · DOI · PMC7240929
- Xu H, Russell SN, Steiner K, O'Neill E, Jones KI. Targeting PI3K-gamma in myeloid driven tumour immune suppression: a systematic review and meta-analysis of the preclinical literature. Cancer Immunol Immunother. 2024. PMID 39105848 · DOI · PMC11303654
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.