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: 4 complete abstracts (643 words), 10 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 developmental history of specific differentiated cell types as traced back to the original stem cells in the embryo.
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: Cell Lineages; Lineage, Cell; Lineages, Cell.
Where it fits in the MeSH classification
- Broader topics
- Cell Physiological Phenomena; Embryonic Development; Reproductive Physiological Phenomena
- See also
- Cell Differentiation
Related concepts
- Stem Cells
Research landscape
PubMed indexes 28,396 records tagged with the MeSH heading “Cell Lineage” (counts retrieved 2026-10-29). 4,638 of them (16.3%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 13,089 records.
Reviews account for 5,564 records (19.6%) and meta-analyses for 15. Randomized controlled trials number 23 (0.1%) 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 | 1,261 |
| 2000-2009 | 9,408 |
| 2010-2019 | 13,089 |
| 2020 onward | 4,638 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 5,564 | 19.6% |
| Meta-analyses | 15 | 0.1% |
| Randomized controlled trials | 23 | 0.1% |
Method: PubMed query "Cell Lineage"[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 |
|---|---|---|---|---|
| Non-stem cell lineages as an alternative origin of intestinal tumorigenesis in the context of inflammation | 2024 | Research article Design not recorded in structured metadata | 43 | cc by PMID 38902475 · DOI · PMC11250264 |
| Mesenchymal stem cells lineage and their role in disease development | 2024 | Review article Design not recorded in structured metadata | 43 | cc by PMID 39523306 · DOI · PMC11552129 |
| High-resolution spatial mapping of cell state and lineage dynamics in vivo with PEtracer | 2025 | Research article Design not recorded in structured metadata | 42 | cc by PMID 40705858 · DOI · PMC12766569 |
| Dissecting gene regulatory networks governing human cortical cell fate | 2026 | Research article Design not recorded in structured metadata | 17 | cc by PMID 41565813 · DOI · PMC12999477 |
Non-stem cell lineages as an alternative origin of intestinal tumorigenesis in the context of inflammation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- According to conventional views, colon cancer originates from stem cells.
- Closing excerpt
- Machine learning methods designed to predict the cell-of-origin of cancer from patient-derived tumor samples confirmed that, in a substantial fraction of sporadic cases, the origins of colon cancer reside in secretory lineages and not in stem cells.
- 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 (140 words)
According to conventional views, colon cancer originates from stem cells. However, inflammation, a key risk factor for colon cancer, has been shown to suppress intestinal stemness. Here, we used Paneth cells as a model to assess the capacity of differentiated lineages to trigger tumorigenesis in the context of inflammation in mice. Upon inflammation, Paneth cell-specific Apc mutations led to intestinal tumors reminiscent not only of those arising in patients with inflammatory bowel disease, but also of a larger fraction of human sporadic colon cancers. The latter is possibly because of the inflammatory consequences of western-style dietary habits, a major colon cancer risk factor. Machine learning methods designed to predict the cell-of-origin of cancer from patient-derived tumor samples confirmed that, in a substantial fraction of sporadic cases, the origins of colon cancer reside in secretory lineages and not in stem cells.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38902475 · DOI · PMC11250264
Mesenchymal stem cells lineage and their role in disease development [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundMesenchymal stem cells (MSCs) are widely dispersed in vivo and are isolated from several tissues, including bone marrow, heart, body fluids, skin, and perinatal tissues.
- Closing excerpt
- In this study, we describe various lineage analysis methods to explore lineage ontology in vitro and in vivo, elucidate the impact of MSC lineage differentiation on diseases, advance our understanding of the role of MSC differentiation in physiological and pathological states, and explore new targets and ideas associated with disease diagnosis and treatment.
- 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 (143 words)
BackgroundMesenchymal stem cells (MSCs) are widely dispersed in vivo and are isolated from several tissues, including bone marrow, heart, body fluids, skin, and perinatal tissues. Bone marrow MSCs have a multidirectional differentiation potential, which can be induced to differentiate the medium in a specific direction or by adding specific regulatory factors. MSCs repair damaged tissues through lineage differentiation, and the ex vivo transplantation of bone marrow MSCs can heal injured sites. MSCs have different propensities for lineage differentiation and pathological evolution for different diseases, which are crucial in disease progression. In this study, we describe various lineage analysis methods to explore lineage ontology in vitro and in vivo, elucidate the impact of MSC lineage differentiation on diseases, advance our understanding of the role of MSC differentiation in physiological and pathological states, and explore new targets and ideas associated with disease diagnosis and treatment.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39523306 · DOI · PMC11552129
High-resolution spatial mapping of cell state and lineage dynamics in vivo with PEtracer [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Charting the spatiotemporal dynamics of cell fate determination in development and disease is a long-standing objective in biology.
- Closing excerpt
- More generally, PEtracer enables systematic characterization of cell state and lineage relationships in intact tissues over biologically relevant temporal and spatial scales.
- 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 (129 words)
Charting the spatiotemporal dynamics of cell fate determination in development and disease is a long-standing objective in biology. Here, we present the design, development, and extensive validation of PEtracer, a prime editing (PE)-based, evolving lineage tracing technology compatible with both single-cell sequencing and multimodal imaging methodologies, created to jointly profile cell state and lineage in dissociated cells or while preserving cellular context in tissues with high spatial resolution. Using PEtracer coupled with MERFISH spatial transcriptomic profiling in a syngeneic mouse model of tumor metastasis, we reconstructed the growth of individually seeded tumors in vivo and uncovered distinct modules of cell-intrinsic and -extrinsic factors that coordinate tumor growth. More generally, PEtracer enables systematic characterization of cell state and lineage relationships in intact tissues over biologically relevant temporal and spatial scales.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40705858 · DOI · PMC12766569
Dissecting gene regulatory networks governing human cortical cell fate [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Human cortical neurogenesis involves conserved and specialized developmental processes during a restricted window of prenatal development.
- Closing excerpt
- Our study provides a framework for dissecting regulatory networks driving cell fate consequences during human neurogenesis.
- 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 (231 words)
Human cortical neurogenesis involves conserved and specialized developmental processes during a restricted window of prenatal development. Radial glia (RG) neural stem cells shape cortical cell diversity by giving rise to excitatory neurons, oligodendrocytes and astrocytes, as well as olfactory bulb interneurons (INs) and a recently characterized population of cortical INs1,2. Complex genetic programs orchestrated by transcription factor (TF) circuits govern the balance between self-renewal and differentiation, and between different cell fates3-8. Despite progress in measuring gene regulatory network activity during human cortical development9-12, functional studies are required to evaluate the roles of TFs and effector genes in human RG lineage progression. Here we establish a human primary culture system that allows sensitive discrimination of cell fate dynamics and apply single-cell CRISPR interference (CRISPRi) screening13,14 to examine the transcriptional and cell fate consequences of 44 TFs active during cortical neurogenesis. We identified several TFs with new roles in cortical neurogenesis, including ZNF219-previously uncharacterized-that represses neural differentiation and NR2E1 and ARX that have opposing roles in regulating RG lineage plasticity and progression across developmental stages. We also detected convergent effector genes downstream of multiple TFs enriched in neurodevelopmental and neuropsychiatric disorders and observed conserved mechanisms of RG lineage plasticity across primates. We further uncovered a post-mitotic role for ARX in safeguarding IN subtype specification through repressing LMO1. Our study provides a framework for dissecting regulatory networks driving cell fate consequences during human neurogenesis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41565813 · DOI · PMC12999477
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 Unfolded Protein Response and Cell Fate Control [5]
- Research article Challenges in unsupervised clustering of single-cell RNA-seq data [6]
- Research article The origin and evolution of cell types [7]
- Research article Cell fate specification and differentiation in the adult mammalian intestine [8]
- Research article Lineage tracing meets single-cell omics: opportunities and challenges [9]
- Research article The myogenic regulatory factors, determinants of muscle development, cell identity and regeneration [10]
References
- Verhagen MP, Joosten R, Schmitt M, Välimäki N, Sacchetti A, Rajamäki K, et al.. Non-stem cell lineages as an alternative origin of intestinal tumorigenesis in the context of inflammation. . 2024. PMID 38902475 · DOI · PMC11250264
- Xu Q, Hou W, Zhao B, Fan P, Wang S, Wang L, et al.. Mesenchymal stem cells lineage and their role in disease development. . 2024. PMID 39523306 · DOI · PMC11552129
- Koblan LW, Yost KE, Zheng P, Colgan WN, Jones MG, Yang D, et al.. High-resolution spatial mapping of cell state and lineage dynamics in vivo with PEtracer. . 2025. PMID 40705858 · DOI · PMC12766569
- Ding JW, Kim CN, Ostrowski MS, Abeykoon Y, Pavlovic BJ, Wallace JL, et al.. Dissecting gene regulatory networks governing human cortical cell fate. . 2026. PMID 41565813 · DOI · PMC12999477
- Hetz C, Papa FR. The Unfolded Protein Response and Cell Fate Control. Mol Cell. 2018. PMID 29107536 · DOI
- Kiselev VY, Andrews TS, Hemberg M. Challenges in unsupervised clustering of single-cell RNA-seq data. Nat Rev Genet. 2019. PMID 30617341 · DOI
- Arendt D, Musser JM, Baker CVH, Bergman A, Cepko C, Erwin DH, et al.. The origin and evolution of cell types. Nat Rev Genet. 2016. PMID 27818507 · DOI
- Beumer J, Clevers H. Cell fate specification and differentiation in the adult mammalian intestine. Nat Rev Mol Cell Biol. 2021. PMID 32958874 · DOI
- Wagner DE, Klein AM. Lineage tracing meets single-cell omics: opportunities and challenges. Nat Rev Genet. 2020. PMID 32235876 · DOI · PMC7307462
- Hernández-Hernández JM, García-González EG, Brun CE, Rudnicki MA. The myogenic regulatory factors, determinants of muscle development, cell identity and regeneration. Semin Cell Dev Biol. 2017. PMID 29127045 · DOI · PMC5723221
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.