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 (576 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
A carcinoma that originates usually from cells on the surface of the middle and lower third of the esophagus. Tumor cells exhibit typical squamous morphology and form large polypoid lesions. Mutations in RNF6, lzts1, tgfbr2, DEC1, and wwox1 genes are associated with this cancer.
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: Oesophageal Squamous Cell Carcinoma.
Where it fits in the MeSH classification
- Broader topics
- Carcinoma, Squamous Cell; Esophageal Neoplasms
Related concepts
- Esophagus
- Lzts1
- Tgfbr2
- Wwox1
Research landscape
PubMed indexes 8,985 records tagged with the MeSH heading “Esophageal Squamous Cell Carcinoma” (counts retrieved 2026-10-29). 5,715 of them (63.6%) were published from 2020 onward, and the busiest period so far is 2020 onward with 5,715 records.
Reviews account for 614 records (6.8%) and meta-analyses for 222. Randomized controlled trials number 210 (2.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 1 |
| 2010-2019 | 3,403 |
| 2020 onward | 5,715 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 614 | 6.8% |
| Meta-analyses | 222 | 2.5% |
| Randomized controlled trials | 210 | 2.3% |
Method: PubMed query "Esophageal Squamous Cell Carcinoma"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cancer and oncology
Cancer research spans very different kinds of evidence. Laboratory studies in cell lines and animal models reveal mechanisms but often do not translate to patients. Early-phase trials mainly test safety and dosing, while phase 3 randomized trials and their meta-analyses are the usual basis for treatment conclusions. Outcomes also differ in meaning: tumour shrinkage, progression-free survival and overall survival are not interchangeable, and screening studies can be distorted by lead-time and overdiagnosis. When reading a result, check the cancer type and stage studied, the comparison treatment, and which outcome was measured.
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 |
|---|---|---|---|---|
| Advancing immunotherapy for esophageal cancer: decoding the roles of PD-L1, TME, and tumor-intrinsic biomarkers | 2025 | Review article Design not recorded in structured metadata | 10 | cc by PMID 41341591 · DOI · PMC12669114 |
| MIF-expressing tumor cells mediate immunotherapeutic resistance in esophageal squamous cell carcinoma | 2026 | Research article Design not recorded in structured metadata | 9 | cc by PMID 41355948 · DOI · PMC12679699 |
| ARL5B Drives Esophageal Squamous Cell Carcinoma Progression via ROCK1-SREBP1-Mediated Lipid Metabolic Reprogramming | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41144804 · DOI · PMC12767069 |
Advancing immunotherapy for esophageal cancer: decoding the roles of PD-L1, TME, and tumor-intrinsic biomarkers [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Esophageal squamous cell carcinoma (ESCC) remains a global health challenge, with immune checkpoint inhibitors (ICIs) reshaping therapeutic strategies.
- Closing excerpt
- This review comprehensively examines evolving biomarkers and therapeutic trials, emphasizing the need for integrative precision strategies to optimize immunotherapy efficacy in ESCC.
- 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 (144 words)
Esophageal squamous cell carcinoma (ESCC) remains a global health challenge, with immune checkpoint inhibitors (ICIs) reshaping therapeutic strategies. However, heterogeneous responses underscore the urgent need for robust predictive biomarkers. While PD-L1 expression remains the most widely used marker, its limitations, including spatial heterogeneity and inducible expression, have prompted exploration of alternative and composite indicators. Recent advances highlight the predictive potential of tumor immune microenvironment (TME) features such as tumor-infiltrating lymphocytes (TILs), tertiary lymphoid structures (TLSs), stromal maturity, and T cell-inflamed gene expression profiles. Concurrently, tumor-intrinsic biomarkers, including microsatellite instability, tumor mutational burden, neoantigen load, and chromosomal alterations-have shown promise in stratifying immunotherapy responders. Multi-omics approaches, liquid biopsies, and integration of host factors such as gut microbiota are emerging to refine patient selection. This review comprehensively examines evolving biomarkers and therapeutic trials, emphasizing the need for integrative precision strategies to optimize immunotherapy efficacy in ESCC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41341591 · DOI · PMC12669114
MIF-expressing tumor cells mediate immunotherapeutic resistance in esophageal squamous cell carcinoma [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Background: Despite the use of immunotherapy in esophageal squamous cell carcinoma (ESCC), treatment failure occurs occasionally in patients, yet the underlying mechanisms remain poorly understood.
- Closing excerpt
- Conclusions: MIF+ tumor cells in GCs may be a biomarker for predicting immunotherapy resistance in ESCC.
- 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 (258 words)
Background: Despite the use of immunotherapy in esophageal squamous cell carcinoma (ESCC), treatment failure occurs occasionally in patients, yet the underlying mechanisms remain poorly understood. Methods: We conducted large-scale single-cell RNA sequencing (scRNA-seq) data analysis, which integrated seven independent datasets from 192 ESCC patients to yield over 440,000 high-quality single cells, to systematically characterize the tumor microenvironment (TME) landscape during ESCC progression and immunotherapy response. Additionally, we performed high-resolution spatial transcriptomics (stRNA-seq) using the 10x Visium HD platform on paired pre- and post-treatment tissues from two patients (one immunotherapy responder and one non-responder), which enhanced the findings from the scRNA-seq data and mapped therapy-induced TME at the spatial level. Multiplex immunohistochemistry was employed based on seven patients to confirm distinct patterns of intercellular crosstalk underlying differential therapeutic outcomes. Results: In scRNA-seq data, we found that B lineage cells were reduced during ESCC progression but were enriched in immunotherapy-resistant patients. Further analysis of malignant ESCC cells suggested that immunotherapy resistance might be associated with a subpopulation of tumor cells exhibiting aberrantly elevated cholesterol biosynthesis. Cell communication analysis of scRNA-seq and stRNA-seq data collectively revealed that immunotherapy resistance was linked to cellular crosstalk between cholesterol-biosynthetic tumor cells and germinal center (GC) B cells within tertiary lymphoid structures. Notably, single-cell, spatial data, and multiplex immunohistochemistry demonstrated that cholesterol biosynthesis-associated ESCC cells express elevated levels of MIF. This disrupts GC reactions by competing with the CXCL12-CXCR4 signaling axis via MIF-CXCR4 interactions, thereby impairing B cell-mediated immunity. Conclusions: MIF+ tumor cells in GCs may be a biomarker for predicting immunotherapy resistance in ESCC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41355948 · DOI · PMC12679699
ARL5B Drives Esophageal Squamous Cell Carcinoma Progression via ROCK1-SREBP1-Mediated Lipid Metabolic Reprogramming [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Esophageal squamous cell carcinoma (ESCC) remains a highly aggressive malignancy with a 5 year survival rate below 30%, underscoring the urgent need for targeted therapeutic approaches.
- Closing excerpt
- These results establish ARL5B as a central regulator of lipid metabolism in ESCC and highlight its potential as a therapeutic target for precision oncology.
- 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 (174 words)
Esophageal squamous cell carcinoma (ESCC) remains a highly aggressive malignancy with a 5 year survival rate below 30%, underscoring the urgent need for targeted therapeutic approaches. Here adenosine diphosphate (ADP)-ribosylation factor-like protein 5B (ARL5B) is identified as a key candidate oncogene that drives ESCC progression by modulating lipid metabolism via the ras homologous-associated coiled-coil containing protein kinase 1(ROCK1)-sterol regulatory element-binding protein 1 (SREBP1) signaling axis. Through the Cancer Genome Atlas (TCGA) pan-cancer analysis, ARL5B is initially identified as a promising candidate gene, correlating with advanced tumor, node, metastasis (TNM) stages and poor survival. Functional assays demonstrate that ARL5B knockdown significantly suppresses cell proliferation, invasion, and growth in vivo, while promoting apoptosis. Mechanistically, ARL5B facilitates the activation and nuclear translocation of SREBP1 through ROCK1, thereby enhancing lipogenic programming. Finally, pharmacological inhibition of either ROCK1 or SREBP1 abrogates the oncogenic effects induced by ARL5B overexpression, confirming the functional dependency on this pathway. These results establish ARL5B as a central regulator of lipid metabolism in ESCC and highlight its potential as a therapeutic target for precision oncology.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41144804 · DOI · PMC12767069
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 The Global Landscape of Esophageal Squamous Cell Carcinoma and Esophageal Adenocarcinoma Incidence and Mortality in 2020 and Projections to 2040: New Estimates From GLOBOCAN 2020 [4]
- Research article Epidemiology of esophageal cancer: update in global trends, etiology and risk factors [5]
- Research article Endoscopic submucosal dissection for superficial gastrointestinal lesions: European Society of Gastrointestinal Endoscopy (ESGE) Guideline - Update 2022 [6]
- Research article Tumor immune microenvironment and immune checkpoint inhibitors in esophageal squamous cell carcinoma [7]
- Research article Deciphering the cells of origin of squamous cell carcinomas [8]
- Research article Screening for esophageal squamous cell carcinoma: recent advances [9]
References
- Ma J, Wu D, Liu Y, Zhang G. Advancing immunotherapy for esophageal cancer: decoding the roles of PD-L1, TME, and tumor-intrinsic biomarkers. . 2025. PMID 41341591 · DOI · PMC12669114
- Song J, Song X, Xie Y, Guo H, Cun Y. MIF-expressing tumor cells mediate immunotherapeutic resistance in esophageal squamous cell carcinoma. . 2026. PMID 41355948 · DOI · PMC12679699
- Ma X, Sun Y, Mao H, Huang C, Li Z, Wang T, et al.. ARL5B Drives Esophageal Squamous Cell Carcinoma Progression via ROCK1-SREBP1-Mediated Lipid Metabolic Reprogramming. . 2026. PMID 41144804 · DOI · PMC12767069
- Morgan E, Soerjomataram I, Rumgay H, Coleman HG, Thrift AP, Vignat J, et al.. The Global Landscape of Esophageal Squamous Cell Carcinoma and Esophageal Adenocarcinoma Incidence and Mortality in 2020 and Projections to 2040: New Estimates From GLOBOCAN 2020. Gastroenterology. 2022. PMID 35671803 · DOI
- Uhlenhopp DJ, Then EO, Sunkara T, Gaduputi V. Epidemiology of esophageal cancer: update in global trends, etiology and risk factors. Clin J Gastroenterol. 2020. PMID 32965635 · DOI
- Pimentel-Nunes P, Libânio D, Bastiaansen BAJ, Bhandari P, Bisschops R, Bourke MJ, et al.. Endoscopic submucosal dissection for superficial gastrointestinal lesions: European Society of Gastrointestinal Endoscopy (ESGE) Guideline - Update 2022. Endoscopy. 2022. PMID 35523224 · DOI
- Baba Y, Nomoto D, Okadome K, Ishimoto T, Iwatsuki M, Miyamoto Y, et al.. Tumor immune microenvironment and immune checkpoint inhibitors in esophageal squamous cell carcinoma. Cancer Sci. 2020. PMID 32579769 · DOI · PMC7469863
- Sánchez-Danés A, Blanpain C. Deciphering the cells of origin of squamous cell carcinomas. Nat Rev Cancer. 2018. PMID 29849070 · DOI · PMC7170720
- Codipilly DC, Qin Y, Dawsey SM, Kisiel J, Topazian M, Ahlquist D, et al.. Screening for esophageal squamous cell carcinoma: recent advances. Gastrointest Endosc. 2018. PMID 29709526 · DOI · PMC7493990
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.