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 (665 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 phase of cell nucleus division following metaphase, in which the chromatids separate and migrate to opposite poles of the spindle.
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: Anaphases.
Where it fits in the MeSH classification
Related concepts
Research landscape
PubMed indexes 2,446 records tagged with the MeSH heading “Anaphase” (counts retrieved 2026-10-29). 222 of them (9.1%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 820 records.
Reviews account for 205 records (8.4%) and meta-analyses for 0. Randomized controlled trials number 0 (0.0%) 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 | 747 |
| 2000-2009 | 820 |
| 2010-2019 | 657 |
| 2020 onward | 222 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 205 | 8.4% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 0 | 0.0% |
Method: PubMed query "Anaphase"[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 |
|---|---|---|---|---|
| Progression through mitosis promotes PARP inhibitor-induced cytotoxicity in homologous recombination-deficient cancer cells | 2017 | Research article Design not recorded in structured metadata | 100 | cc by PMID 28714471 · DOI · PMC5520019 |
| APC/C: current understanding and future perspectives | 2019 | Review article Design not recorded in structured metadata | 82 | cc by PMID 31164978 · DOI · PMC6534075 |
| The human SKA complex drives the metaphase-anaphase cell cycle transition by recruiting protein phosphatase 1 to kinetochores | 2016 | Research article Design not recorded in structured metadata | 71 | cc by PMID 26981768 · DOI · PMC4821802 |
| Targeting KIFC1 to disrupt centrosome clustering and trigger anaphase catastrophe in small-cell lung cancer | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 41948931 · DOI · PMC13134724 |
Progression through mitosis promotes PARP inhibitor-induced cytotoxicity in homologous recombination-deficient cancer cells [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Mutations in homologous recombination (HR) genes BRCA1 and BRCA2 predispose to tumorigenesis.
- Closing excerpt
- These findings provide insight into the cytotoxic effects of PARP inhibition, and point at combination therapies to potentiate PARP inhibitor treatment of HR-deficient tumours.
- 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 (147 words)
Mutations in homologous recombination (HR) genes BRCA1 and BRCA2 predispose to tumorigenesis. HR-deficient cancers are hypersensitive to Poly (ADP ribose)-polymerase (PARP) inhibitors, but can acquire resistance and relapse. Mechanistic understanding how PARP inhibition induces cytotoxicity in HR-deficient cancer cells is incomplete. Here we find PARP inhibition to compromise replication fork stability in HR-deficient cancer cells, leading to mitotic DNA damage and consequent chromatin bridges and lagging chromosomes in anaphase, frequently leading to cytokinesis failure, multinucleation and cell death. PARP-inhibitor-induced multinucleated cells fail clonogenic outgrowth, and high percentages of multinucleated cells are found in vivo in remnants of PARP inhibitor-treated Brca2-/-;p53-/- and Brca1-/-;p53-/- mammary mouse tumours, suggesting that mitotic progression promotes PARP-inhibitor-induced cell death. Indeed, enforced mitotic bypass through EMI1 depletion abrogates PARP-inhibitor-induced cytotoxicity. These findings provide insight into the cytotoxic effects of PARP inhibition, and point at combination therapies to potentiate PARP inhibitor treatment of HR-deficient tumours.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28714471 · DOI · PMC5520019
APC/C: current understanding and future perspectives [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The separation of sister chromatids at anaphase, which is regulated by an E3 ubiquitin ligase called the anaphase-promoting complex/cyclosome (APC/C), is arguably the most important irrevocable event during the cell cycle.
- Closing excerpt
- In this review, we will examine the historical background and current understanding of APC/C regulation.
- 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 (166 words)
The separation of sister chromatids at anaphase, which is regulated by an E3 ubiquitin ligase called the anaphase-promoting complex/cyclosome (APC/C), is arguably the most important irrevocable event during the cell cycle. The APC/C and cyclin-dependent kinase 1 (Cdk1) are just two of the many significant cell cycle regulators and exert control through ubiquitylation and phosphorylation, respectively. The temporal and spatial regulation of the APC/C is achieved by multiple mechanisms, including phosphorylation, interaction with the structurally related co-activators Cdc20 and Cdh1, loading of distinct E2 ubiquitin-conjugating enzymes, binding with inhibitors and differential affinities for various substrates. Since the discovery of APC/C 25 years ago, intensive studies have uncovered many aspects of APC/C regulation, but we are still far from a full understanding of this important cellular machinery. Recent high-resolution cryogenic electron microscopy analysis and reconstitution of the APC/C have greatly advanced our understanding of molecular mechanisms underpinning the enzymatic properties of APC/C. In this review, we will examine the historical background and current understanding of APC/C regulation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31164978 · DOI · PMC6534075
The human SKA complex drives the metaphase-anaphase cell cycle transition by recruiting protein phosphatase 1 to kinetochores [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The spindle- and kinetochore-associated (Ska) complex is essential for normal anaphase onset in mitosis.
- Closing excerpt
- Microtubule binding by Ska, rather than acting in force production for chromosome movement, may instead serve to promote PP1 recruitment to kinetochores fully attached to spindle microtubules at metaphase.
- 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 (149 words)
The spindle- and kinetochore-associated (Ska) complex is essential for normal anaphase onset in mitosis. The C-terminal domain (CTD) of Ska1 binds microtubules and was proposed to facilitate kinetochore movement on depolymerizing spindle microtubules. Here, we show that Ska complex recruits protein phosphatase 1 (PP1) to kinetochores. This recruitment requires the Ska1 CTD, which binds PP1 in vitro and in human HeLa cells. Ska1 lacking its CTD fused to a PP1-binding peptide or fused directly to PP1 rescues mitotic defects caused by Ska1 depletion. Ska1 fusion to catalytically dead PP1 mutant does not rescue and shows dominant negative effects. Thus, the Ska complex, specifically the Ska1 CTD, recruits PP1 to kinetochores to oppose spindle checkpoint signaling kinases and promote anaphase onset. Microtubule binding by Ska, rather than acting in force production for chromosome movement, may instead serve to promote PP1 recruitment to kinetochores fully attached to spindle microtubules at metaphase.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26981768 · DOI · PMC4821802
Targeting KIFC1 to disrupt centrosome clustering and trigger anaphase catastrophe in small-cell lung cancer [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Supernumerary centrosomes are a hallmark of cancer.
- Closing excerpt
- Together, these results suggest that disrupting centrosome clustering and triggering anaphase catastrophe via KIFC1 inhibition may represent a promising therapeutic strategy for SCLC.
- 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 (203 words)
Supernumerary centrosomes are a hallmark of cancer. To maintain viability, cancer cells cluster these centrosomes during mitosis, enabling bipolar division similar to that of normal cells. Disruption of this centrosome clustering leads to multipolar anaphase and apoptosis (anaphase catastrophe), which selectively eliminates cancer cells harboring supernumerary centrosomes. In this context, because the motor protein KIFC1 contributes to centrosome clustering, we investigated whether targeting of this mechanism through KIFC1 inhibition could be exploited in small-cell lung cancer (SCLC), an aggressive malignancy with limited treatment options and poor prognosis. Through in silico and in vitro analyses, as well as IHC of clinical samples, we found that KIFC1 is overexpressed and that centrosome amplification occurs more frequently in SCLC compared with normal tissues and other cancer types. Pharmacological and genetic inhibition of KIFC1 disrupted the clustering of supernumerary centrosomes, triggered multipolar mitosis, and exerted antineoplastic effects in SCLC cells, with minimal effects on noncancerous cells. These findings were validated and extended in vivo using SCLC xenograft models. Finally, cotargeting KIFC1 and the centrosome duplication regulator PLK4 further enhanced growth suppression in SCLC cells. Together, these results suggest that disrupting centrosome clustering and triggering anaphase catastrophe via KIFC1 inhibition may represent a promising therapeutic strategy for SCLC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41948931 · DOI · PMC13134724
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 Splitting the chromosome: cutting the ties that bind sister chromatids [5]
- Research article Waiting for anaphase: Mad2 and the spindle assembly checkpoint [6]
- Research article The anaphase-promoting complex: a key factor in the regulation of cell cycle [7]
- Research article Building a Regulatory Network with Short Linear Sequence Motifs: Lessons from the Degrons of the Anaphase-Promoting Complex [8]
- Research article Welcome to a new kind of tension: translating kinetochore mechanics into a wait-anaphase signal [9]
- Research article Fission yeast cut mutations revisited: control of anaphase [10]
References
- Schoonen PM, Talens F, Stok C, Gogola E, Heijink AM, Bouwman P, et al.. Progression through mitosis promotes PARP inhibitor-induced cytotoxicity in homologous recombination-deficient cancer cells. . 2017. PMID 28714471 · DOI · PMC5520019
- Yamano H. APC/C: current understanding and future perspectives. . 2019. PMID 31164978 · DOI · PMC6534075
- Sivakumar S, Janczyk PŁ, Qu Q, Brautigam CA, Stukenberg PT, Yu H, et al.. The human SKA complex drives the metaphase-anaphase cell cycle transition by recruiting protein phosphatase 1 to kinetochores. . 2016. PMID 26981768 · DOI · PMC4821802
- Nakagawa N, Toda M, Kunita A, Horie M, Tokunaga M, Ikushima H, et al.. Targeting KIFC1 to disrupt centrosome clustering and trigger anaphase catastrophe in small-cell lung cancer. . 2026. PMID 41948931 · DOI · PMC13134724
- Nasmyth K, Peters JM, Uhlmann F. Splitting the chromosome: cutting the ties that bind sister chromatids. Science. 2000. PMID 10827941 · DOI
- Shah JV, Cleveland DW. Waiting for anaphase: Mad2 and the spindle assembly checkpoint. Cell. 2000. PMID 11163175 · DOI
- Castro A, Bernis C, Vigneron S, Labbé JC, Lorca T. The anaphase-promoting complex: a key factor in the regulation of cell cycle. Oncogene. 2005. PMID 15678131 · DOI
- Davey NE, Morgan DO. Building a Regulatory Network with Short Linear Sequence Motifs: Lessons from the Degrons of the Anaphase-Promoting Complex. Mol Cell. 2016. PMID 27716480 · DOI · PMC5098475
- Maresca TJ, Salmon ED. Welcome to a new kind of tension: translating kinetochore mechanics into a wait-anaphase signal. J Cell Sci. 2010. PMID 20200228 · DOI · PMC2831757
- Yanagida M. Fission yeast cut mutations revisited: control of anaphase. Trends Cell Biol. 1998. PMID 9695827 · 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.