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POLE

DNA polymerase epsilon catalytic subunit A · UniProt Q07864

Length
2286 aa
Mass
261.5 kDa
Annotated
2026-06-10
100 papers in source corpus 12 papers cited in narrative 13 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

POLE encodes the catalytic and proofreading subunit of DNA polymerase epsilon, whose exonuclease (proofreading) domain corrects mispaired bases inserted during DNA replication; germline and somatic missense mutations in this domain impair proofreading and produce base-substitution hypermutation in tumors (PMID:23263490, PMID:25878334). Yeast functional assays directly confirm that such exonuclease-domain variants (e.g., p.Leu424Val, p.Trp347Cys, p.Tyr458Phe) raise mutation rates to levels comparable with complete loss of exonuclease activity, while non-exonuclease and loss-of-function variants do not cause the proofreading-associated cancer phenotype (PMID:23263490, PMID:25860647, PMID:26251183, PMID:32792570). The resulting genomic signature is highly characteristic — enrichment of C>A transversions and T>G substitutions with very high tumor mutational burden — and this proofreading defect dominates the mutational phenotype even when mismatch repair is concurrently defective (PMID:25878334, PMID:32497495, PMID:31829442). Different POLE mutant alleles drive distinct mutation spectra according to their degree of fidelity impairment, and cancer-associated mutants generate signature mutagenesis even in the presence of functional mismatch repair (PMID:32497495). The hypermutator phenotype generates an enriched repertoire of antigenic neoepitopes that elicits a robust intratumoral cytotoxic CD8+ T-cell response and confers sensitivity to immune checkpoint blockade (PMID:25878334, PMID:35817971). Complete loss of POLE catalytic function causes a distinct chromosome-instability syndrome with growth retardation, microcephaly, immune deficiency, and myelodysplasia (PMID:25948378).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2012 High

    Established that germline mutations in the POLE proofreading domain are causal for base-substitution hypermutation, linking a specific molecular defect to a cancer-predisposition phenotype.

    Evidence Whole-genome sequencing with linkage/association analysis and yeast functional assays of p.Leu424Val

    PMID:23263490

    Open questions at the time
    • Did not resolve the quantitative mutation rate of individual alleles
    • Did not address somatic versus germline contribution to tumor burden
  2. 2014 Low

    Predicted that distinct exonuclease-domain residues contribute to DNA/substrate binding and that different variants impair catalysis to differing degrees.

    Evidence Germline sequencing with in silico structural modeling of p.Asn363Lys

    PMID:24788313

    Open questions at the time
    • No direct biochemical assay performed; computational prediction only
    • Predicted differential severity not experimentally validated
  3. 2015 Medium

    Defined the somatic ultramutated genomic phenotype of POLE-mutant endometrial cancer and connected it to enhanced immunogenicity and favorable prognosis via neoepitope-driven cytotoxic T-cell responses.

    Evidence Whole-exome and mutational signature analysis, IHC for CD8+ TILs, and RNAseq in a TCGA cohort with in silico neoepitope prediction

    PMID:25878334

    Open questions at the time
    • Neoepitope immunogenicity inferred in silico, not functionally validated
    • Causal link between T-cell response and outcome correlative
  4. 2015 Medium

    Directly measured that specific exonuclease-domain germline variants (p.Tyr458Phe, p.Trp347Cys) raise mutation rates to levels comparable to complete exonuclease loss, validating their pathogenicity functionally.

    Evidence S. pombe functional mutation-rate assays of individual variants

    PMID:25860647 PMID:26251183

    Open questions at the time
    • Single-variant, single-lab assays
    • Yeast mutation rate may not fully reproduce human tumor spectrum
  5. 2015 Medium

    Demonstrated that POLE-mutant tumor cells are resistant to platinum chemotherapy, establishing that favorable prognosis derives from immunogenicity rather than chemosensitivity.

    Evidence Primary tumor cell line establishment with in vitro platinum sensitivity assays

    PMID:27894751

    Open questions at the time
    • Single-lab in vitro assay
    • Did not test in vivo chemotherapy response
  6. 2015 Medium

    Showed that complete loss of POLE catalytic function in humans causes a chromosome-instability/immunodeficiency syndrome distinct from the proofreading-associated cancer phenotype.

    Evidence Exome sequencing and clinical phenotyping of a homozygous splice-variant patient

    PMID:25948378

    Open questions at the time
    • Single case report
    • Mechanistic basis of multisystem phenotype not dissected
  7. 2017 Medium

    Extended the pathogenic variant spectrum by showing a variant outside the canonical exonuclease domain can also impair proofreading.

    Evidence S. pombe functional mutation-rate assays of p.Val474Ile

    PMID:28423643

    Open questions at the time
    • Single variant, single lab
    • Structural basis of proofreading impairment outside the domain unresolved
  8. 2020 High

    Resolved allele-specific behavior, showing that cancer POLE mutants drive signature mutagenesis even with functional mismatch repair, and that allele identity, abundance, and MMR status shape the final spectrum.

    Evidence CRISPR-Cas9 engineering of human cell lines expressing POLE tumor variants with whole-exome sequencing after defined population doublings

    PMID:32497495

    Open questions at the time
    • Limited set of alleles tested
    • Quantitative contribution of each factor to clinical spectrum not modeled
  9. 2020 Medium

    Clarified which variant classes are pathogenic, establishing that exonuclease-domain missense variants impairing proofreading—not loss-of-function or out-of-domain variants—drive the cancer syndrome.

    Evidence Multigene panel sequencing with yeast functional assays, cosegregation and case-control studies

    PMID:32792570

    Open questions at the time
    • Some intermediate variants of uncertain significance remain unclassified
  10. 2020 Medium

    Quantified a robust diagnostic genomic signature and showed the POLE proofreading defect dominates even when co-occurring with MSI-H.

    Evidence Whole-exome and genomic signature/TMB analysis of endometrial cancer cohorts

    PMID:31829442

    Open questions at the time
    • Thresholds derived from limited cohort
    • Generalizability across tumor types not fully tested
  11. 2022 High

    Provided in vivo causal evidence that POLE-driven mutagenesis enhances antitumor immunity and ICB sensitivity, and linked neoantigen biochemical features (hydrophobicity at TCR-contact residues) and signature spectrum to immune response.

    Evidence Murine syngeneic tumor models with Pole mutations, neoantigen biochemical feature analysis, and clinical ICB outcome correlation

    PMID:35817971

    Open questions at the time
    • Causal contribution of specific neoantigens to ICB response not isolated
    • Predictive value of signature spectrum requires prospective validation

Open questions

Synthesis pass · forward-looking unresolved questions
  • How POLE assembles into and functions within the holoenzyme replication complex, and the structural basis by which individual exonuclease-domain residues control proofreading fidelity, remain uncharacterized in this corpus.
  • No structural model of mutant proofreading defects
  • Holoenzyme partner interactions not addressed in the timeline

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140097 catalytic activity, acting on DNA 5 GO:0016787 hydrolase activity 3 GO:0003677 DNA binding 1
Pathway
R-HSA-1643685 Disease 3 R-HSA-69306 DNA Replication 2 R-HSA-73894 DNA Repair 2
Complex memberships
DNA polymerase epsilon

Evidence

Reading pass · 13 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 Germline heterozygous mutations in the proofreading (exonuclease) domain of POLE (p.Leu424Val) cause defective correction of mispaired bases inserted during DNA replication, leading to base substitution hypermutation in tumors. Yeast functional assays confirmed that these mutations impair exonuclease proofreading activity. Whole-genome sequencing, linkage/association analysis, yeast functional assays Nature genetics High 23263490
2015 Somatic POLE exonuclease domain mutations cause an ultramutated phenotype in endometrial cancer characterized by C>A transversions and T>G substitutions, with microsatellite-stable tumors, resulting from defective proofreading of mispaired bases during DNA replication. Whole-exome sequencing, mutational signature analysis, genomic characterization of TCGA cohort Clinical cancer research Medium 25878334
2014 POLE exonuclease domain mutations at position p.Asn363Lys (located in the proofreading exonuclease domain) are directly involved in DNA binding; theoretical modeling predicted a profound effect on substrate binding capability and more severe impairment of catalytic activity compared to the p.Leu424Val mutation. Germline sequencing, in silico structural prediction, clinical phenotyping International journal of oncology Low 24788313
2015 POLE exonuclease domain mutations generate an enriched repertoire of antigenic neoepitopes, which drives a robust intratumoral cytotoxic T-cell response (increased CD8+ TILs, upregulation of T-bet, Eomes, IFNG, PRF, granzyme B), explaining the favorable prognosis of POLE-ultramutated endometrial cancers. Immunohistochemistry for CD8+ TIL quantification, RNAseq analysis (TCGA), in silico neoepitope prediction Clinical cancer research Medium 25878334
2020 Different POLE cancer mutant alleles drive distinct mutation spectra through differing degrees of replication fidelity impairment; unlike an exonuclease active-site mutant, POLE cancer mutants readily drive signature mutagenesis even in the presence of functional mismatch repair (MMR). The identity, abundance, and MMR status of the mutant allele shape the final mutation spectrum. CRISPR-Cas9 engineering of human cell lines expressing POLE tumor variants, whole-exome sequencing after defined population doublings Molecular cell High 32497495
2015 A POLE germline mutation p.Tyr458Phe, located in the active site of the exonuclease domain, affects a residue important for exonuclease activity. Functional assays in S. pombe demonstrated increased DNA mutation rate comparable to a Pol ε mutant lacking exonuclease activity entirely. Exome sequencing, S. pombe functional mutation rate assays Familial cancer Medium 25860647
2015 A POLE germline mutation p.Trp347Cys in the exonuclease domain leads to an increased DNA mutation rate in S. pombe functional assays, comparable to that seen with a Pol ε mutant with no exonuclease activity. S. pombe functional assays measuring mutation rate Familial cancer Medium 26251183
2017 A POLE variant c.1420G>A (p.Val474Ile) outside the canonical exonuclease domain was shown by functional assays in Schizosaccharomyces pombe to impair proofreading activity, broadening the spectrum of POLE changes that can lead to mutator phenotype. S. pombe functional mutation rate assays, bioinformatics prediction Oncotarget Medium 28423643
2022 Murine syngeneic tumors harboring functional Pole mutations displayed enhanced antitumor immunity and sensitivity to immune checkpoint blockade. Pathogenic POLE/POLD1 mutations generate neoantigens with increased hydrophobicity at TCR-contact residues, potentially facilitating T-cell recognition. The spectrum of mutational signatures (not merely mutation presence) correlates with the biochemical features of neoantigens and predicts ICB response. Murine syngeneic tumor models with Pole mutations, mutational signature analysis, neoantigen biochemical feature analysis, clinical ICB outcome correlation Nature genetics High 35817971
2015 POLE exonuclease domain mutation (ultramutated EC) primary cell lines are significantly more resistant to platinum-based chemotherapy in vitro compared to POLE wild-type EC cell lines, suggesting that favorable prognosis of POLE-mutated tumors is not secondary to chemosensitivity but to enhanced immunogenicity. Primary tumor cell line establishment, in vitro platinum drug sensitivity assays Gynecologic oncology Medium 27894751
2015 A patient with POLE1 deficiency (homozygous splice variant c.4444+3A>G in the POLE1 gene encoding the catalytic subunit of DNA polymerase epsilon) manifested a severe chromosome instability syndrome with growth retardation, microcephaly, developmental delay, immune deficiency, and myelodysplasia, demonstrating that loss of POLE1 catalytic function causes a DNA instability phenotype in humans. Exome sequencing, clinical phenotyping of POLE1-deficient patient BMC medical genetics Medium 25948378
2020 Loss-of-function and outside-exonuclease-domain variants in POLE are likely not pathogenic for polymerase proofreading-associated cancer syndrome, whereas missense variants within the exonuclease domain that impair proofreading are the relevant pathogenic class. This was supported by cosegregation, case-control studies, and yeast-based functional assays. Multigene panel sequencing, yeast functional assays, cosegregation and case-control studies Genetics in medicine Medium 32792570
2020 Pathogenic POLE exonuclease domain mutations (EDMs) produce a characteristic genomic signature: C>A substitutions >20%, T>G substitutions >4%, C>G substitutions <0.6%, indels <5%, and TMB >100 mut/Mb. Co-existence of pathogenic POLE EDM with MSI-H still produces POLE-characteristic genomic alterations, demonstrating that the POLE proofreading defect dominates the mutational phenotype. Whole-exome sequencing, genomic signature analysis, mutational burden analysis (TCGA cohort and independent cohort) The Journal of pathology Medium 31829442

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Germline mutations affecting the proofreading domains of POLE and POLD1 predispose to colorectal adenomas and carcinomas. Nature genetics 777 23263490
2019 Marine DNA Viral Macro- and Microdiversity from Pole to Pole. Cell 549 31031001
2020 Interpretation of somatic POLE mutations in endometrial carcinoma. The Journal of pathology 340 31829442
2016 Immune activation and response to pembrolizumab in POLE-mutant endometrial cancer. The Journal of clinical investigation 317 27159395
1994 Localization of vasa protein to the Drosophila pole plasm is independent of its RNA-binding and helicase activities. Development (Cambridge, England) 295 8026330
2012 Chromosome- and spindle-pole-derived signals generate an intrinsic code for spindle position and orientation. Nature cell biology 277 22327364
2015 POLE Proofreading Mutations Elicit an Antitumor Immune Response in Endometrial Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 262 25878334
2008 A polymeric protein anchors the chromosomal origin/ParB complex at a bacterial cell pole. Cell 256 18805088
2012 Pole-to-pole biogeography of surface and deep marine bacterial communities. Proceedings of the National Academy of Sciences of the United States of America 193 23045668
2002 The anterior heart-forming field: voyage to the arterial pole of the heart. Trends in genetics : TIG 193 11932022
2013 Cytoarchitecture, probability maps and functions of the human frontal pole. NeuroImage 184 23702412
2014 Clinicopathological analysis of endometrial carcinomas harboring somatic POLE exonuclease domain mutations. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 167 25394778
1999 Sid2p, a spindle pole body kinase that regulates the onset of cytokinesis. The Journal of cell biology 159 10459013
1989 Centrosomes, and not nuclei, initiate pole cell formation in Drosophila embryos. Cell 155 2497990
2003 RHAMM is a centrosomal protein that interacts with dynein and maintains spindle pole stability. Molecular biology of the cell 150 12808028
2013 How do bacteria localize proteins to the cell pole? Journal of cell science 144 24345373
2000 Bacterial activity in South Pole snow. Applied and environmental microbiology 144 11010907
1995 Yeast spindle pole body duplication gene MPS1 encodes an essential dual specificity protein kinase. The EMBO journal 139 7737118
2012 A multidomain hub anchors the chromosome segregation and chemotactic machinery to the bacterial pole. Genes & development 138 23070816
2014 New insights into POLE and POLD1 germline mutations in familial colorectal cancer and polyposis. Human molecular genetics 123 24501277
2022 Mechanism of spindle pole organization and instability in human oocytes. Science (New York, N.Y.) 120 35143306
2004 Cytokinesis monitoring during development; rapid pole-to-pole shuttling of a signaling protein by localized kinase and phosphatase in Caulobacter. Cell 114 15339663
2015 Combined mismatch repair and POLE/POLD1 defects explain unresolved suspected Lynch syndrome cancers. European journal of human genetics : EJHG 107 26648449
2020 Role of POLE and POLD1 in familial cancer. Genetics in medicine : official journal of the American College of Medical Genetics 103 32792570
2013 Aurora at the pole and equator: overlapping functions of Aurora kinases in the mitotic spindle. Open biology 101 23516109
2018 Peptidoglycan precursor synthesis along the sidewall of pole-growing mycobacteria. eLife 100 30198841
2015 Aurora A Kinase Contributes to a Pole-Based Error Correction Pathway. Current biology : CB 99 26166783
2022 POLE/POLD1 mutation and tumor immunotherapy. Journal of experimental & clinical cancer research : CR 97 35780178
2005 Regulated pole-to-pole oscillations of a bacterial gliding motility protein. Science (New York, N.Y.) 97 16272122
1995 Cell adhesion to the apical pole of epithelium: a function of cell polarity. European journal of cell biology 90 7774604
2014 Bacterial scaffold directs pole-specific centromere segregation. Proceedings of the National Academy of Sciences of the United States of America 85 24778223
2006 Inhibitors of Polo-like kinase reveal roles in spindle-pole maintenance. Nature chemical biology 85 17028581
2018 Macropinosome formation by tent pole ruffling in macrophages. The Journal of cell biology 83 30150290
2001 Asymmetric spindle pole localization of yeast Cdc15 kinase links mitotic exit and cytokinesis. Current biology : CB 79 11267871
2011 Biogenesis of the posterior pole is mediated by the exosome/microvesicle protein-sorting pathway. The Journal of biological chemistry 77 21865156
2000 Phosphorylation and spindle pole body localization of the Cdc15p mitotic regulatory protein kinase in budding yeast. Current biology : CB 76 10744974
2002 The distal pole complex: a novel membrane domain distal to the immunological synapse. Immunological reviews 74 12445269
2015 From equator to pole: splitting chromosomes in mitosis and meiosis. Genes & development 71 25593304
2014 zic-1 Expression in Planarian neoblasts after injury controls anterior pole regeneration. PLoS genetics 70 24992682
2010 Arterial pole progenitors interpret opposing FGF/BMP signals to proliferate or differentiate. Development (Cambridge, England) 70 20702561
2019 Phenotype of POLE-mutated endometrial cancer. PloS one 68 30917185
2015 A novel POLE mutation associated with cancers of colon, pancreas, ovaries and small intestine. Familial cancer 66 25860647
2024 Immune checkpoint inhibitors for POLE or POLD1 proofreading-deficient metastatic colorectal cancer. Annals of oncology : official journal of the European Society for Medical Oncology 65 38777726
2005 Caulobacter crescentus requires RodA and MreB for stalk synthesis and prevention of ectopic pole formation. Journal of bacteriology 65 15629926
2011 Identification of a Tbx1/Tbx2/Tbx3 genetic pathway governing pharyngeal and arterial pole morphogenesis. Human molecular genetics 62 22116936
2022 Functional landscapes of POLE and POLD1 mutations in checkpoint blockade-dependent antitumor immunity. Nature genetics 61 35817971
2020 POLE Mutation Spectra Are Shaped by the Mutant Allele Identity, Its Abundance, and Mismatch Repair Status. Molecular cell 59 32497495
2016 Polymerase ε (POLE) ultra-mutation in uterine tumors correlates with T lymphocyte infiltration and increased resistance to platinum-based chemotherapy in vitro. Gynecologic oncology 59 27894751
2014 A mutation in POLE predisposing to a multi-tumour phenotype. International journal of oncology 59 24788313
2021 POLE, POLD1, and NTHL1: the last but not the least hereditary cancer-predisposing genes. Oncogene 58 34363023
2019 Clinical outcomes of patients with POLE mutated endometrioid endometrial cancer. Gynecologic oncology 58 31757464
2008 Aurora-A and ch-TOG act in a common pathway in control of spindle pole integrity. Oncogene 52 18663358
2019 POLE proofreading defects: Contributions to mutagenesis and cancer. DNA repair 51 30818169
2010 Cell pole-specific activation of a critical bacterial cell cycle kinase. Proceedings of the National Academy of Sciences of the United States of America 50 20351295
2003 A lytic transglycosylase homologue, PleA, is required for the assembly of pili and the flagellum at the Caulobacter crescentus cell pole. Molecular microbiology 50 12828633
2016 Increased incidence of FBXW7 and POLE proofreading domain mutations in young adult colorectal cancers. Cancer 48 27244218
2012 The cell pole: the site of cross talk between the DNA uptake and genetic recombination machinery. Critical reviews in biochemistry and molecular biology 48 23046409
2022 A root phloem pole cell atlas reveals common transcriptional states in protophloem-adjacent cells. Nature plants 47 35927456
2014 Lessons from yeast: the spindle pole body and the centrosome. Philosophical transactions of the Royal Society of London. Series B, Biological sciences 47 25047610
2019 Comprehensive analysis of POLE and POLD1 Gene Variations identifies cancer patients potentially benefit from immunotherapy in Chinese population. Scientific reports 46 31673068
2013 pbx is required for pole and eye regeneration in planarians. Development (Cambridge, England) 45 23318641
2017 Risk of colorectal cancer for carriers of a germ-line mutation in POLE or POLD1. Genetics in medicine : official journal of the American College of Medical Genetics 44 29120461
2017 POLE and POLD1 screening in 155 patients with multiple polyps and early-onset colorectal cancer. Oncotarget 43 28423643
2017 POLE somatic mutations in advanced colorectal cancer. Cancer medicine 43 29072370
2015 POLE mutations in families predisposed to cutaneous melanoma. Familial cancer 42 26251183
2007 Mechanisms of spindle-pole organization are influenced by kinetochore activity in mammalian cells. Current biology : CB 42 17276919
2022 Yeast osmoregulation - glycerol still in pole position. FEMS yeast research 41 35927716
2021 Distinct mutational profile and immune microenvironment in microsatellite-unstable and POLE-mutated tumors. Journal for immunotherapy of cancer 40 34607897
2005 Characterization and spontaneous mutation of a novel gene, polE, involved in pellicle formation in Acetobacter tropicalis SKU1100. Microbiology (Reading, England) 40 16339956
2018 Clinicopathological characteristics of POLE mutation in patients with non-small-cell lung cancer. Lung cancer (Amsterdam, Netherlands) 39 29572003
2015 GREM1 and POLE variants in hereditary colorectal cancer syndromes. Genes, chromosomes & cancer 38 26493165
2022 Pole position: How plant cells polarize along the axes. The Plant cell 37 34338785
2021 Tumor-infiltrating lymphocytes and POLE mutation in endometrial carcinoma. Gynecologic oncology 36 33715893
2015 PopZ identifies the new pole, and PodJ identifies the old pole during polar growth in Agrobacterium tumefaciens. Proceedings of the National Academy of Sciences of the United States of America 36 26324921
2000 A spindle pole body-associated protein, SNAD, affects septation and conidiation in Aspergillus nidulans. Molecular & general genetics : MGG 36 10821171
2020 A biphasic growth model for cell pole elongation in mycobacteria. Nature communications 35 31974342
2021 The biogeographic differentiation of algal microbiomes in the upper ocean from pole to pole. Nature communications 34 34531387
2018 Clinical impact of endometrial cancer stratified by genetic mutational profiles, POLE mutation, and microsatellite instability. PloS one 33 29659608
2014 The KASH protein Kms2 coordinates mitotic remodeling of the spindle pole body. Journal of cell science 32 24963130
2004 nanos expression at the embryonic posterior pole and the medusa phase in the hydrozoan Podocoryne carnea. Evolution & development 32 15330869
2016 Duplication of the Yeast Spindle Pole Body Once per Cell Cycle. Molecular and cellular biology 30 26951196
2007 Dialogue between LKB1 and AMPK: a hot topic at the cellular pole. Science's STKE : signal transduction knowledge environment 30 17878409
2019 Clinicopathological and mutational analyses of colorectal cancer with mutations in the POLE gene. Cancer medicine 29 31240875
2014 Frequent POLE1 p.S297F mutation in Chinese patients with ovarian endometrioid carcinoma. Mutation research 29 24472300
2017 Human microcephaly ASPM protein is a spindle pole-focusing factor that functions redundantly with CDK5RAP2. Journal of cell science 28 28883092
2019 Germline POLE mutation in a child with hypermutated medulloblastoma and features of constitutional mismatch repair deficiency. Cold Spring Harbor molecular case studies 27 31624068
2015 A patient with polymerase E1 deficiency (POLE1): clinical features and overlap with DNA breakage/instability syndromes. BMC medical genetics 27 25948378
2024 Mechanisms of minor pole-mediated spindle bipolarization in human oocytes. Science (New York, N.Y.) 26 39172836
2018 Molecular profiling and sequential somatic mutation shift in hypermutator tumours harbouring POLE mutations. Scientific reports 25 29880869
2010 Targeting and anchoring Tudor in the pole plasm of the Drosophila oocyte. PloS one 25 21179512
2019 Morphological, immunophenotypical and molecular features of hypermutation in colorectal carcinomas with mutations in DNA polymerase ε (POLE). Histopathology 24 31479159
2020 Genomic Alterations of NTRK, POLE, ERBB2, and Microsatellite Instability Status in Chinese Patients with Colorectal Cancer. The oncologist 23 32627883
2019 Centromere Dysfunction Compromises Mitotic Spindle Pole Integrity. Current biology : CB 22 31495582
2019 Detection of POLE Subtypes in High-Grade Endometrioid Carcinoma by BaseScope-ISH Assay. Frontiers in oncology 22 31552169
1992 From egg to pole cells: ultrastructural aspects of early cleavage and germ cell determination in insects. Microscopy research and technique 21 1617208
2023 Recommendations for the classification of germline variants in the exonuclease domain of POLE and POLD1. Genome medicine 20 37848928
2020 CEP215 and AURKA regulate spindle pole focusing and aMTOC organization in mouse oocytes. Reproduction (Cambridge, England) 18 31895686
2018 POLE gene hotspot mutations in advanced pancreatic cancer. Journal of cancer research and clinical oncology 18 30194485
2024 The Clinical and Pathological Characteristics of POLE-Mutated Endometrial Cancer: A Comprehensive Review. Cancer management and research 17 38463556
2022 Analysis of HubP-dependent cell pole protein targeting in Vibrio cholerae uncovers novel motility regulators. PLoS genetics 17 35020734

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