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 (560 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 malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm and not a synonym for 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: Carcinomas; Epithelioma; Epitheliomas; Malignant Epithelial Neoplasms; Epithelial Neoplasm, Malignant; Malignant Epithelial Neoplasm; Neoplasm, Malignant Epithelial; Neoplasms, Malignant Epithelial.
Where it fits in the MeSH classification
- Broader topics
- Neoplasms, Glandular and Epithelial
- Narrower topics
- Adenocarcinoma; Carcinoma in Situ; Carcinoma, Adenosquamous; Carcinoma, Basosquamous; Carcinoma, Ehrlich Tumor; Carcinoma, Giant Cell; Carcinoma, Krebs 2; Carcinoma, Large Cell; Carcinoma, Lewis Lung; Carcinoma, Ovarian Epithelial; Carcinoma, Papillary; Carcinoma, Small Cell; Carcinoma, Squamous Cell; Carcinoma, Transitional Cell
Research landscape
PubMed indexes 805,413 records tagged with the MeSH heading “Carcinoma” (counts retrieved 2026-10-29). 169,229 of them (21.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 251,125 records.
Reviews account for 79,607 records (9.9%) and meta-analyses for 7,124. Randomized controlled trials number 10,873 (1.3%) 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 | 251,125 |
| 2000-2009 | 154,274 |
| 2010-2019 | 230,785 |
| 2020 onward | 169,229 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 79,607 | 9.9% |
| Meta-analyses | 7,124 | 0.9% |
| Randomized controlled trials | 10,873 | 1.3% |
Method: PubMed query "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 |
|---|---|---|---|---|
| Fusion-driven oncogenic programs shape the immune landscape in translocation renal cell carcinoma | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42786155 · DOI · PMC13612822 |
| No phenotypes in Ttc22 knockout mice | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42912804 · DOI · PMC13693868 |
| Tumor cell-intrinsic stress states drive sensitivity to CAR T cell therapy in pancreatic cancer | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42826199 · DOI · PMC13641470 |
Fusion-driven oncogenic programs shape the immune landscape in translocation renal cell carcinoma [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Renal cell carcinomas (RCC) comprise multiple molecularly distinct cancers but most are treated empirically with therapies designed for clear cell RCC (ccRCC), the most common subtype, due to incomplete understanding of subtype-specific biology.
- Closing excerpt
- Our findings highlight unique TFE3 fusion-driven biology in tRCC, explaining its reduced immunotherapy responsiveness relative to ccRCC, and suggesting strategies for targeting fusion-driven oncogenic programs and TME reprogramming.
- 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 (154 words)
Renal cell carcinomas (RCC) comprise multiple molecularly distinct cancers but most are treated empirically with therapies designed for clear cell RCC (ccRCC), the most common subtype, due to incomplete understanding of subtype-specific biology. We analyzed single-cell transcriptomes and chromatin accessibility profiles from translocation renal cell carcinoma (tRCC), an aggressive RCC defined by oncogenic TFE3 gene fusions. We show that, despite arising from a proximal tubule cell of origin similar to ccRCC, tRCCs display distinct oncogenic programs and an immunosuppressive tumor microenvironment (TME). tRCCs exhibit six conserved tumor meta-programs, including epithelial-mesenchymal transition (EMT) and proximal tubule identity programs whose balance is regulated by TFE3 fusion activity. The fusion-driven EMT program drives a suppressive TME marked by progenitor-exhausted CD8 + T cells, anti-inflammatory SPP1+ macrophages, and matrix-associated fibroblasts. Our findings highlight unique TFE3 fusion-driven biology in tRCC, explaining its reduced immunotherapy responsiveness relative to ccRCC, and suggesting strategies for targeting fusion-driven oncogenic programs and TME reprogramming.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42786155 · DOI · PMC13612822
No phenotypes in Ttc22 knockout mice [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The TTC22 gene encodes a protein containing seven tetratricopeptide repeats (TPRs), which mediate protein‒protein interactions as chaperones.
- Closing excerpt
- In conclusion, no phenotypes were induced by Ttc22 inactivation in C57BL/6N mice.
- 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 (244 words)
The TTC22 gene encodes a protein containing seven tetratricopeptide repeats (TPRs), which mediate protein‒protein interactions as chaperones. We previously reported that the level of TTC22 transcript variant 1 (TTC22v1) was downregulated in human colon adenocarcinoma (COAD) and that TTC22 upregulated m6A-mediated WTAP and SNAI1 expression via the TTC22‒RPL4 interaction and subsequently promoted COAD metastasis. Thus, a commercially available C57BL/6N mouse model in which the Ttc22 exon 2&3 encoding the TPR4 (equal to the human TTC22 TPR3) domain was knocked out via CRISPR-Cas9 was used to evaluate the contribution of Ttc22 to the development of mice and COAD. To determine the status of Ttc22 expression in Ttc22 knockout mice, we prepared a rabbit polyclonal antibody against the mouse Ttc22 protein, which could bind both wild-type Ttc22 and TPR4-deleted Ttc22 proteins overexpressed in HEK293T cells, as determined by Western blot analysis. Ttc22 proteins were detected in colon tissue samples from wild-type mice and Ttc22 hemi-knockout (Ttc22+/-) mice but not in those from fully Ttc22 knockout (Ttc22-/-) mice. Unfortunately, the long-term observation results demonstrated that Ttc22 knockout (KO, including Ttc22+/- or Ttc22-/-) did not affect the body weight, development, fertility, or spontaneous tumor incidence of male or female mice. No differences in the incidence of AOM/DSS-induced COAD were observed between these mouse groups, although Ttc22 deletion partially resulted in the upregulation of genes related to the host adaptive response to inflammation in the colon mucosa. In conclusion, no phenotypes were induced by Ttc22 inactivation in C57BL/6N mice.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42912804 · DOI · PMC13693868
Tumor cell-intrinsic stress states drive sensitivity to CAR T cell therapy in pancreatic cancer [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Chimeric antigen receptor (CAR) T cell therapy has transformed the treatment of hematologic cancers but has shown limited efficacy in solid tumors, including pancreatic ductal adenocarcinoma (PDAC).
- Closing excerpt
- These findings provide a foundation to improve efficacy of CAR T cell therapy in solid malignancies and to better stratify patients with cancer by tumor genotype.
- 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 (162 words)
Chimeric antigen receptor (CAR) T cell therapy has transformed the treatment of hematologic cancers but has shown limited efficacy in solid tumors, including pancreatic ductal adenocarcinoma (PDAC). The cellular and molecular factors that influence CAR T cell therapy response remain largely unknown. By integrating modular in vivo CRISPR screens with single-cell genomics and immunocompetent orthotopic models of PDAC, we uncover oxidative and proteotoxic stress pathways as previously unknown modulators of CAR T cell therapy response. Disruption of stress regulatory genes, particularly Keap1 and Slc33a1, sensitizes PDAC tumors to CAR T cell killing in vivo. Hyperactivation of the Nrf2 pathway by genetic ablation of Keap1 or endogenous engineering of clinically observed Keap1 or Nfe2l2 mutations enhances tumor susceptibility to CAR T cell therapy. Thus, tumor-intrinsic molecular stress phenotypes can induce unexpected cell state-specific vulnerabilities to cell-based immunotherapies. These findings provide a foundation to improve efficacy of CAR T cell therapy in solid malignancies and to better stratify patients with cancer by tumor genotype.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42826199 · DOI · PMC13641470
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 PARP Inhibitor Maintenance After First-Line Chemotherapy in Advanced-Stage Epithelial Ovarian Cancer: A Systematic Review and Meta-Analysis [4]
- Research article Meta-Analysis: Utilisation of Hepatocellular Carcinoma Surveillance [5]
- Research article Pathologic Response and Survival After Neoadjuvant Immunotherapy for Resectable Mucosal HNSCC: A Systematic Review and Meta-Analysis [6]
- Research article Histopathology and outcomes of non-metastatic renal cell carcinoma with inferior vena cava tumor thrombus: systematic review and meta-analysis [7]
- Research article Minimally invasive liver surgery for perihilar and intrahepatic cholangiocarcinoma: systematic review and meta-analysis of comparative studies [8]
- Research article Prognostic significance of prognostic nutritional index in patients with head and neck squamous cell carcinoma [9]
References
- Konda P, Wakolbinger AJ, Cui Y, Roberti de Oliveira G, Nabil YL, Weiss CN, et al.. Fusion-driven oncogenic programs shape the immune landscape in translocation renal cell carcinoma. . 2026. PMID 42786155 · DOI · PMC13612822
- Liu J, Gu L, You A, Yuan H, Zhou J, Tian W, et al.. No phenotypes in Ttc22 knockout mice. . 2026. PMID 42912804 · DOI · PMC13693868
- Fröse J, Chen E, Whittaker CA, Leclerc P, Doherty S, Langenbucher A, et al.. Tumor cell-intrinsic stress states drive sensitivity to CAR T cell therapy in pancreatic cancer. . 2026. PMID 42826199 · DOI · PMC13641470
- Petousis S, Kahramanoglu I, Appenzeller-Herzog C, Angeles MA, Margioula-Siarkou C, Kacperczyk-Bartnik J, et al.. PARP Inhibitor Maintenance After First-Line Chemotherapy in Advanced-Stage Epithelial Ovarian Cancer: A Systematic Review and Meta-Analysis. JAMA Netw Open. 2025. PMID 41191357 · DOI · PMC12590296
- Tang NSY, Gunalan S, Ong CEY, Koh B, Tham EKJ, Lim RY, et al.. Meta-Analysis: Utilisation of Hepatocellular Carcinoma Surveillance. Aliment Pharmacol Ther. 2026. PMID 41077883 · DOI
- Mastrolonardo EV, De Ravin E, Kaki PC, Estephan LE, Nunes K, Kenny H, et al.. Pathologic Response and Survival After Neoadjuvant Immunotherapy for Resectable Mucosal HNSCC: A Systematic Review and Meta-Analysis. JAMA Otolaryngol Head Neck Surg. 2026. PMID 41410931 · DOI
- Lasorsa F, Pandolfo SD, Bignante G, Lambertini L, Orsini A, Rutigliano M, et al.. Histopathology and outcomes of non-metastatic renal cell carcinoma with inferior vena cava tumor thrombus: systematic review and meta-analysis. Eur J Surg Oncol. 2025. PMID 41046750 · DOI
- de Hondt J, Zwart MJW, Uijterwijk BA, Burchell GL, Görgeç B, Zonderhuis B, et al.. Minimally invasive liver surgery for perihilar and intrahepatic cholangiocarcinoma: systematic review and meta-analysis of comparative studies. Surg Endosc. 2025. PMID 40931102 · DOI · PMC12618328
- Wang Y, Wang J, Xiao B, Wang Y, Huang F, Jiang Y, et al.. Prognostic significance of prognostic nutritional index in patients with head and neck squamous cell carcinoma. Front Immunol. 2025. PMID 40936893 · DOI · PMC12421403
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.