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 (807 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
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
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: Tumors; Neoplasia; Neoplasias; Neoplasm; Tumor; Cancer; Cancers; Malignant Neoplasm.
Where it fits in the MeSH classification
- Narrower topics
- Cysts; Hamartoma; Neoplasms by Histologic Type; Neoplasms by Site; Neoplasms, Experimental; Neoplasms, Hormone-Dependent; Neoplasms, Multiple Primary; Neoplasms, Post-Traumatic; Neoplasms, Radiation-Induced; Neoplasms, Second Primary; Neoplastic Processes; Neoplastic Syndromes, Hereditary; Paraneoplastic Syndromes; Precancerous Conditions
Research landscape
PubMed indexes 4,309,314 records tagged with the MeSH heading “Neoplasms” (counts retrieved 2026-10-29). 964,940 of them (22.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,391,011 records.
Reviews account for 612,279 records (14.2%) and meta-analyses for 45,934. Randomized controlled trials number 68,865 (1.6%) 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 | 1,391,011 |
| 2000-2009 | 763,895 |
| 2010-2019 | 1,189,468 |
| 2020 onward | 964,940 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 612,279 | 14.2% |
| Meta-analyses | 45,934 | 1.1% |
| Randomized controlled trials | 68,865 | 1.6% |
Method: PubMed query "Neoplasms"[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 |
|---|---|---|---|---|
| No phenotypes in Ttc22 knockout mice | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42912804 · DOI · PMC13693868 |
| The PD-L1-mTOR intersection in tumor migration and invasion | 2026 | Review article Design not recorded in structured metadata | 0 | cc by PMID 42909562 · DOI · PMC13694484 |
| Microbeam radiotherapy - clinical and dosimetric investigation of a first clinical application | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42920150 · DOI · PMC13695295 |
No phenotypes in Ttc22 knockout mice [1]
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
The PD-L1-mTOR intersection in tumor migration and invasion [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Programmed death-ligand 1 (PD-L1) has emerged as an important player in intrinsic tumor cell biology besides its canonical immune checkpoint function.
- Closing excerpt
- We also summarize the main clinical trials combining mTOR pathway inhibitors with anti-PD-L1 antibodies in different cancer types.
- 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 (191 words)
Programmed death-ligand 1 (PD-L1) has emerged as an important player in intrinsic tumor cell biology besides its canonical immune checkpoint function. Cumulative experimental data points to a role for PD-L1 in promoting and maintaining an invasive cell phenotype within different cancer cells through its interaction with mechanistic target of rapamycin (mTOR) signaling. In this review, we summarize the main experimental data pointing to the PD-L1/mTOR interaction in tumor cell invasion capacity both in vitro and in vivo. In this crosstalk, PD-L1 expression is induced by IFN-γ/STAT1 and IL-6/STAT3 pathways, as well as mTOR activity by its upstream effectors like EGFR and other tyrosine kinase receptor ligands. Interestingly, PD-L1 itself seems to play a role in mTOR activation. In many of these models, the PD-L1 importance in cell migration capacity is evidenced by two major observations: (1) its knockout impairs cell invasion capacity and, (2) its upregulation is associated with increased cell migration and both the induction and maintenance of epithelial-mesenchymal transition (EMT) phenotype markers, such as increased N-cadherin and ZEB1 and decreased E-cadherin. We also summarize the main clinical trials combining mTOR pathway inhibitors with anti-PD-L1 antibodies in different cancer types.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42909562 · DOI · PMC13694484
Microbeam radiotherapy - clinical and dosimetric investigation of a first clinical application [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundMicrobeam Radiotherapy (MRT) is an emerging radiotherapy technique which delivers spatially fractionated beams on a micrometre scale.
- Closing excerpt
- Careful, safety-driven dose escalation studies will be required to establish a foundation for responsible and effective clinical application of MRT in early-phase clinical trials.
- 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 (372 words)
BackgroundMicrobeam Radiotherapy (MRT) is an emerging radiotherapy technique which delivers spatially fractionated beams on a micrometre scale. In preclinical studies MRT has demonstrated superior normal tissue sparing compared to conventional radiotherapy while maintaining tumour control. However, MRT has traditionally been achievable only at large synchrotron facilities which has impeded clinical translation. The development of a compact line-focus X-ray tube (LFXT) provides a pathway for clinical MRT, but identification of clinically and dosimetrically suitable patient scenarios is required for first-in-human trials.Materials and methodsPotentially eligible patients were selected from our patient cohort based on clinical criteria including palliative treatment indication, superficial tumour location, reproducible and safe positioning, minimal interference from other therapies, and expected benefit from MRT. Three-dimensional forward treatment planning was performed in Eclipse using gantry rotations, collimator positioning, and conformal masks to treat the clinical target volume (CTV). Dose was calculated in Eclipse using a custom Monte Carlo-based hybrid algorithm adapted for the compact LFXT system with a 300 kVp beam and an eccentric focal spot. A single-fraction equivalent uniform doses (EUD) of 3 Gy was prescribed to the target volume. Dose distributions were analysed using dose-volume histograms (DVHs), peak and valley depth dose profiles, and peak-to-valley dose ratios (PVDRs).ResultsSelected cases included primary lymphoma, squamous cell carcinoma, and superficial soft tissue metastases. Dosimetric analysis under exploratory assumptions demonstrated dosimetrically feasible treatment plans with optimal target coverage and organ-at-risk (OAR) sparing for gluteal, nuchal, and inguinal tumours. Maximum OAR doses remained below 8.5 Gy, except in bone or overlapping high-density regions. The mean peak and valley dose across all plans was 57.2 Gy and 3.9 Gy, respectively, with a mean PVDR of 15.4. Dose inhomogeneities were observed due to tissue heterogeneity, kilovoltage beam interactions, and a limited range of suitable gantry angles. Tumours in anatomically complex regions, including those in proximity to OARs or tissue inhomogeneities, showed less favourable trade-offs between target coverage and OAR sparing.ConclusionThis study identifies clinically and dosimetrically suitable scenarios for first-in-human MRT trials, highlighting superficial tumours as optimal initial indications. While peak, valley, and PVDR values align with preclinical evidence, their clinical significance remains uncertain. Careful, safety-driven dose escalation studies will be required to establish a foundation for responsible and effective clinical application of MRT in early-phase clinical trials.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42920150 · DOI · PMC13695295
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 Radiomics-Based AI for Predicting Neoadjuvant Immunochemotherapy Pathological Response in Non-Small Cell Lung Cancer: Systematic Review and Meta-Analysis [4]
- Research article Advancing precision immunotherapy in advanced pancreatic cancer: a systematic review and meta-analysis of first-line ICI-based combinations [5]
- Research article A systematic review and meta-analysis of radiation-induced oral complications in head and neck cancer: Prevalence and clinical outcomes [6]
- Research article Neoadjuvant Chemoradiotherapy Versus Chemotherapy in Patients with Pancreatic Ductal Adenocarcinoma: A Systematic Review and Meta-analysis of Randomised Controlled Trials [7]
- Research article Survival Benefit of ARSI Therapy in Japanese mCSPC: A Systematic Review and Meta-Analysis [8]
- Research article Circulating KIM-1 and survival outcomes in renal cell carcinoma: A systematic review and meta-analysis [9]
References
- 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
- Palavro R, Previato TTR, Pazzin DB, Gonçalves JB, Boff MO, Marinowic D, et al.. The PD-L1-mTOR intersection in tumor migration and invasion. . 2026. PMID 42909562 · DOI · PMC13694484
- Kraus KM, Day LR, Wilkens JJ, Combs SE, Bartzsch S. Microbeam radiotherapy - clinical and dosimetric investigation of a first clinical application. . 2026. PMID 42920150 · DOI · PMC13695295
- Jiang Z, Xu Y, Jia S, Liu H. Radiomics-Based AI for Predicting Neoadjuvant Immunochemotherapy Pathological Response in Non-Small Cell Lung Cancer: Systematic Review and Meta-Analysis. J Med Internet Res. 2026. PMID 42596052 · DOI · PMC13472773
- Qi X, Yang H, Zhang L, Yu P, Cheng C. Advancing precision immunotherapy in advanced pancreatic cancer: a systematic review and meta-analysis of first-line ICI-based combinations. Front Immunol. 2026. PMID 42500667 · DOI · PMC13396027
- Alnaeem MM, Darwish SK, Abu Sabra MA. A systematic review and meta-analysis of radiation-induced oral complications in head and neck cancer: Prevalence and clinical outcomes. J Craniomaxillofac Surg. 2026. PMID 42546465 · DOI
- Hajibandeh S, Hajibandeh S, Alfarah J, Psica A, Raza SS, Bartlett DC, et al.. Neoadjuvant Chemoradiotherapy Versus Chemotherapy in Patients with Pancreatic Ductal Adenocarcinoma: A Systematic Review and Meta-analysis of Randomised Controlled Trials. Ann Surg Oncol. 2026. PMID 42545416 · DOI
- Iwamoto H, Izumi K, Hori T, Inaba T, Nakagawa R, Kamijima T, et al.. Survival Benefit of ARSI Therapy in Japanese mCSPC: A Systematic Review and Meta-Analysis. Int J Urol. 2026. PMID 42603083 · DOI · PMC13476790
- Lu J, Luo B, Xue C, Shen J. Circulating KIM-1 and survival outcomes in renal cell carcinoma: A systematic review and meta-analysis. Urol Oncol. 2026. PMID 42493401 · DOI
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.