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Validated All-in-One™ qPCR Primer for RUNX1(NM_001001890.2) Search again
Product ID:
HQP114776
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AML1, AML1-EVI-1, AMLCR1, CBF2alpha, CBFA2, EVI-1, PEBP2aB, PEBP2alpha
Gene Description:
RUNX family transcription factor 1
Target Gene Accession:
NM_001001890.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
Core binding factor (CBF) is a heterodimeric transcription factor that binds to the core element of many enhancers and promoters. The protein encoded by this gene represents the alpha subunit of CBF and is thought to be involved in the development of normal hematopoiesis. Chromosomal translocations involving this gene are well-documented and have been associated with several types of leukemia. Three transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq].
Gene References into function
- Runx1/AML1, a chromosome 21q22 hematopoietic regulator, is frequently translocated in leukemia
- mutant RUNX1 proteins (missense and nonsense) may also inhibit wild-type RUNX1, possibly creating a higher propensity to develop leukemia.
- Mutations have been found in exons 3, 4, and 5 and in intron 4 of the AML1 gene in acute myeloid leukemia of FAB types M0 and M7.
- aml 1 gene chromosome translocation involves leukemia etiology
- Potential involvement of the AML1-MTG8 fusion protein in the granulocytic maturation characteristic of the t(8;21) acute myelogenous leukemia cell
- REVIEW: In hematologic malignancies, point mutations of the AML1 gene present in the region encoding the Runt domain cause loss of the DNA-binding ability.
- A new translocation, t(4;21)(q21;q22) disrupting the AML1 gene was found in a case of childhood T-ALL.
- AML1 activates transcription genes critical for the G1 to S transition via its C-terminal transactivation domain. Inactivation of AML in acute leukemia is expected to slow proliferation unless additional alterations co-exist which accelerate G1.
- the chromosomal translocation leads to formation of tel/aml1 fusion oncogene and is most common genetic aberration in childhood B-cell precursor ALL.
- AML1 amplification in a case of childhood acute lymphoblastic leukemia
- data demonstrate the capacity of AML1-ETO to promote the self-renewal of human hematopoietic cells and therefore support a causal role for t(8;21) translocations in leukemogenesis
- AML1 point mutations are related to low-dose radiation or alkylating agents and play a role distinct from that of leukemogenic chimeras; DNA binding ability and down-regulation of trans-activation of mutations
- review: genetics of CBFB and RUNX1 and roles in hematopoiesis and leukemogenesis, with emphasis on human and knockout mice studies
- 30% of acute myeloid leukemia cases express a Core Binding Factor oncoprotein or harbor point mutations in one or both AML1 (RUNX1) genes.
- Breakpoints in TEL intron 5 and AML1 intron 1 leading to TEL-AML1 fusion is shown to be the initiating step, preceding differentiation to pre-B cells, in childhood acute lymphoblastic leukemia.
- AML-1 plays a role in driving Mona protein expression in T and myelomonocytic cells.
- identification as tumor suppressor gene
- AML1 rearrangements leading to the AML1-ETO fusion gene are frequently the result of small hidden interstitial insertions.
- role in regulation of MIP-1 alpha expression in multiple myeloma
- how RUNX1 might program divergence from the erythroid pathway to the megakaryocytic lineage commitment through functional and physical interactions with GATA-1
- role in leukemogenesis
- Review. AML1 plays a vital role in the regulation of expression of many genes involved in hematopoietic cell development, and the impairment of AML1 function disregulates the pathways leading to cellular proliferation and differentiation.
- Double trisomy 8 and 21, one with rearrangement of the RUNX1 gene, in acute myelocytic leukemias
- Oncogene AML-1 protein is detected frequently in acute myelogenous leukemia and it is a favorable prognostic factor in disease survival.
- In t(8;21) leukaemic cells expressing the aberrant fusion protein AML1-ETO, we demonstrate that this protein is part of a transcription factor complex binding to extended sequences of the c-FMS intronic regulatory region rather than the promoter.
- In 241 patients with pediatric hematologic malignancies, AML1 mutations have been detected in seven patients (2.9%).
- Strong overexpression of NCAM(CD56) and RUNX1(AML1) is a constant and characteristic feature of cardiomyocytes within or adjacent to scars in ICM.
- Amplification of this gene in childhood acute lymphoblsatic leukemia is associatd with poor outcome.
- heterozygous mutation (G>T) in intron 3 at the splice acceptor site for exon 4; this mutation is associated with not only thrombocytopenia, but also impaired platelet protein phosphorylation and GPIIb-IIIa activation
- RUNX1 binds to protein kinase C beta and is linked to a myeloid apoptotic pathway
- reduced AML1 activities predispose cells to the acquisition of the activating FLT3 mutation as a secondary event leading to full transformation in acute myeloblastic leukemia M0.
- AML1 point mutation is one of the major driving forces of myelodysplastic syndrome and acute myeloid leukemia, and these mutations may represent a distinct clinicopathologic-genetic entity.
- In conclusion, we provide evidence for AML-1, PU.1, and Sp3 cooperatively and directly mediating BPI-expression during myeloid differentiation.
- AML1/RUNX1 increases during G1 to S cell cycle progression independent of cytokine-dependent phosphorylation and induces cyclin D3 gene expression
- acetylation of AML1 through p300 is a critical manner of posttranslational modification and identify a novel mechanism for regulating the function of AML1
- NERF/ELF-2 physically interacts with AML1 and mediates opposing effects on AML1-mediated transcription of the B cell-specific blk gene
- RUNX1 and RUNX2 regulate TIMP1 gene expression
- REVIEW: Familial mutations predispose to acute myeloid leukemia
- chromosome 21 tandem repetition resulted in amplification of the AML1 gene in one case but in another case the AML1 gene was not included in the tandem repeat, showing that apparently similar cytogenetic aberrations may be different at the molecular leve
- we found an incidence of 8.6% of TEL/AML1 translocation in ALL patients (12% of B-lineage ALL)
- AML1 mutations and deletion of genes on chromosome arm 7q cooperate in leukemogenesis and predispose to leukemic transformation.
- TEL-AML1 ALL has significantly lower de novo purine synthesis and differential expression of genes involved in purine metabolism.
- Data show that the repressor activity of TEL/RUNX1 differs from that of TEL, even though both TEL and TEL/RUNX1 interact with the nuclear hormone co-repressor (N-CoR) and histone deacetylase (mSin3A) in vivo.
- Review. A SNP in RUNX1 is significantly associated with with rheumatoid arthritis. It affects binding to the promoter of SLC22A4. It is possible that RUNX1 is a key molecule in autoimmunity.
- Present in acute myeloid leukemia of M2 subtype.
- study identifes E proteins as AML1-ETO targets whose dysregulation may be important for t(8;21) leukemogenesis
- Molecular diversity of the RUNX1 gene in phenotypically and cytogenetically similar cases ofmolecular diversity of the RUNX1 gene in phenotypically and cytogenetically similar cases of chronic myeloid leukemia.
- Expression of RUNX1 is down regulated in a significant portion of gastric cancer cases; may be involved in gastric carcinogenesis
- the ERK family of protein kinases is activated by phorbol esters to phosphorylate the (S/T)P sites within the AML1c molecule and markedly enhance the transcriptional activity of AML1c
- AML1/ETO fusion protein exerts its function in transcriptional dysregulation in AML
- Somatic point mutations in high-risk myelodysplastic syndrome, but not in myelofibrosis with myeloid metaplasia
- No point mutations of the AML1 gene were observed om acute myelocytic leukemia or myodisplastic syndromes.
- RUNX3 regulates RUNX1 expression in human B lymphoid cell lines.
- Fusion witw ETV6 may provide circumstantial evidence of an increased risk of relapse in leukemia.
- AML1-FOG2 and FOG2-AML1 are expressed in myelodysplastic syndrome; results suggest a central role for CtBP in AML1-FOG2 transcriptional repression and implicate coordinated disruption of AML1 and GATA developmental programs in the disease pathogenesis
- Alternative splicing in the AML1-MTG8 fusion gene occurs in leukemia cell lines as well as in cells of leukemia paatients with a(8;21) translocation
- Transfected human Runx1 coordinates the proliferation and neuronal differentiation of selected populations of murine neural progenitors.
- Results suggest a novel mechanism for gene silencing mediated by RUNX1/MTG8 and support the combination of HDAC and DNMT inhibitors as a novel therapeutic approach for t(8;21) AML.
- a C-terminal AML1 mutation leads to a decrease in Mpl receptor expression in familial thrombocytopenia
- AML1 and ETO are fused together at the t8;21 translocation breakpoint, resulting in the expression of a chimeric protein called AML1-ETO, which acts as a constitutive transcriptional repressor.
- increased Runx1 dosage is leukemogenic in myeloid lineage
- human AML1/EVI1/+ knock-in mouse embryos showed defective hematopoiesis in the fetal liver; fetal liver contained multilineage progenitors capable of differentiating into dysplastic myelocyte and megakaryocyte
- the mechanisms of drug sensitivity and resistance differs between TELAML1-positive ALL and other precursor B-lineage ALL patients.
- Increased expression of AML1-a is associated with chromosomal abnormalities in childhood acute lymphoblastic leukemia
- the uPA gene contains a novel 13-bp palindrome that contains the DNA consensus-binding hexamer for RUNX1
- Our results indicate that the NMTS region of Runx1 is required for functional interactions with PU.1.
- Runx1 functions to suppress the apoptotic sensitivity of transgenic double-positive thymocytes in the context of TCR signaling.
- TEL/AML1 rearrangement is not unique in childhood ALL, and cryptic TEL deletion without TEL/AML1 rearrangement was more frequent than the TEL/AML1 rearrangement in adult ALL.
- RUNX factors participate in prostate epithelial cell function and cooperate with an Ets transcription factor to regulate PSA gene expression
- TEL-AML1 may have a role in T-cell receptor gene rearrangements in pediatric acute lymphoblastic leukemia
- direct association of cyclin D3 with AML1 functions as a putative feedback mechanism to regulate cell cycle progression and differentiation
- AML1 positive patients characterized by significantly higher frequency of abnormalities involving long arm of chromosome 6 comparing with AML1 negative.
- Runx1 blocks the elongation by RNAPII, which may contribute to CD4 silencing during T-cell development.
- The TCR gene rearrangements in childhood B-lineage acute lymphoblastic leukemia was associated with expression of AML1 chimeric oncogene.
- KAP5 gene expression in human hair follicles is regulated by Runx1
- fusion of AML1 with ETO or MTG16 exhibits reduced intranuclear mobility compared with wild-type AML1 or either fusion partner
- A 3' RACE experiments followed by sequence-specific RT-PCR resulted in the identification of the PRDM16 gene as a novel fusion partner of the RUNX1 gene in a patient with rare t(1;21)(p36;q22).
- Oligomerization is also required for AML1/ETO's interactions with ETO, MTGR1, and MTG16, but not with other corepressor molecules.
- 8 mutations are in the runt domain; 1 in intron 3, & 2 in intron 5. Insertions of 3 AAs at c.416_417 & c.422_423 interfere with protein folding. The TTTAG duplication in intron 3 replaces the splice acceptor site with a premature stop codon.
- The physical interaction and synergy between GATA1 and RUNX1 are retained in DS-AMKL, although it is still possible that increased RUNX1 activity plays a role in the development of leukemia in DS.
- Suppression of AML1/MTG8 results in the increased expression of genes associated with myeloid differentiation, such as AZU1, BPI, CTSG, LYZ and RNASE2 as well as of antiproliferative genes such as IGFBP7, MS4A3 and SLA both in blasts and in cell lines
- The association between RUNX1, histone deacetylases and SUV39H1 provides a molecular mechanism for repression and possibly gene silencing mediated by RUNX1.
- the SLC22A4 and RUNX1 polymorphisms did not show a significant role in rheumatoid arthritis susceptibility in a Spanish population
- novel TEL-AML1 fusion in precursor B acute lymphoblastic leukemia
- These results suggest that RUNX1 down-regulates terminal differentiation of megakaryocytes and promotes proliferation of megakaryocytic progenitors.
- Our results suggest that mammalian RUNX family transcription factors are novel binding partners and substrates for the Pim-1 kinase, which may be able to regulate their activities during normal hematopoiesis as well as in leukemogenesis.
- Conditional expression of AML1-ETO by the ecdysone-inducible system dramatically increases the expression of connexin 43 together with growth arrest at G1 phase in leukemic U937 cells.
- an N-terminal transactivation domain of Runx1 separates molecular function from global differentiation function
- Notch signaling may modulate both expression and transcriptional activity of Runx1
- Isolation of 3 novel isoforms of AML 1 (RUNX1) with different transactivating function, that might be a regulatory element of the NCAM (CD56) overexpression in chronic myocardial ischemia.
- These results suggest that methylation profile may be a potential new biomarker of risk prediction in ETV6/RUNX1-positive acute lymphoblastic leukemias.
- RUNX1 is not involved in most cases of gastric cancers.
- TEL-AML1 fusion in transgenic zebrafish induces a B cell differentiation arrest and demonstrates leukemia development associated with loss of TEL expression and elevated Bcl2/Bax ratio.
- This review reports the high incidence of somatic mutations in the AML1/RUNX1 gene, which is a critical regulator of definitive hematopoiesis and the most frequent target for translocation of AML in myelodysplastic syndrome.
- Combined overexpression of RUNX1 and NCAM during stress hematopoiesis in Down syndrome might be a key factor in the development of overt leukemia.
- a marked accumulation of AML1 transcripts including a high frequency of a novel alternatively spliced AML1b transcript lacking exon 6 (AML1b(Del179-242)) in ovarian cancer
- Polymorphisms in RUNX1 might be one of the genetic factors for the regulation of IgE production.
- functional relationship between TEL/AML1, HSP90, and survivin provides the rational for targeted therapy.
- integrate three key determinants of hematopoietic stem cell development; the Scl transcriptional network, Runx1 activity, and the Bmp4/Smad signaling pathway
- RUNX1 DNA-binding mutants antagonize Runx1 function in early progenitors by disrupting a critical balance between DNA-binding-independent and DNA-binding-dependent signaling.
- One of the chromosome bands most often involved in structural rearrangements in B-cell precursor acute lymphoblastic leukemia.
- In natural T(R) cells, Foxp3 interacts physically with AML1
- haploinsufficiency of RUNX1 is possible mechanism underlying disease progression in the 8p11 myeloproliferative syndrome
- Trisomy 13 is strongly associated with AML1/RUNX1 mutations and increased FLT3 expression in acute myeloid leukemia
- identified a novel RUNX1 fusion partner, LRP16 on 11q13 involving t(11;21)(q13;q22)
- transcription mediated by AML1 is impaired by mutations of the HIPK2 gene in acute myeloid leukemia and myelodysplastic syndrome
- AML1 mutations were identified in 6.3% of acute myeloid leukemia patients with chromosomal translocations involving CBF, PML-RARalpha, HOX, or ETS transcription factor (TF) gene families
- Presence of AML1-ETO fusion protein increases the susceptibility of cells to chemical carcinogens, which favors the development of additional genetic alterations.
- Monocytopoiesis is controlled by a circuitry involving sequentially miRNA 17-5p-20a-106a, AML1 and M-CSFR, whereby miRNA 17-5p-20a-106a function as a master gene complex interlinked with AML1 in a mutual negative feedback loop.
- AML1-ETO and JAK2 may have a role in leukemogenesis, as shown by a myeloproliferative syndrome progressing to acute myeloid leukemia [case report]
- Trisomy 13 patients with a RUNX1 mutation showed a 4-fold higher expression of FLT3 mRNA compared to controls.
- c-MET is associated with FAS and when activated enhances drug-induced apoptosis in pediatric B acute lymphoblastic leukemia with TEL-AML1 translocation
- Runx1 overexpression inhibited DNA-binding and transcriptional activity of HIF-1alpha.
- ETV6/RUNX1-positive acute lymphoblastic leukemias have a high incidence of cryptic Xq duplications
- Disruption in the RUNX1 gene is associated with acute myeloid leukemia
- analysis of the prevalence of the ETV6-RUNX1 fusion gene in children with acute lymphoblastic leukemia in China
- RUNX1 may have a role in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia [case report]
- Inhibition of C/EBPalpha function may be causatively related to the leukemogenic potential of RUNX1/EVI1 chimeric transcription factor.
- RUNX1 mutation is associated with poor prognosis in patients with primary myelodysplastic syndrome. It may play a role in the development and progression of a subset of primary myelodysplastic syndrome
- Mutation of AML1 gene is associated with pediatric primary myelodysplastic syndrome and juvenile myelomonocytic leukemia
- Gene expression analyses of leukemia cells from children with TEL/AML1-positive and -negative B-lineage ALL led to the identification of five biological processes.
- AML1-ETO may facilitate accumulation of genetic alterations by suppressing endogenous DNA repair in acutet myeloid leukemia.
- constitutively and overexpressed AML1-ETO protein was cleaved to four fragments of 70, 49, 40 and 25 kDa by activated caspase-3 during apoptosis induction by extrinsic mitochondrial and death receptor signaling pathways.
- miR-223 is a direct transcriptional target of AML1/ETO
- cdk phosphorylation of RUNX1 potentially couples stem/progenitor proliferation and lineage progression
- RUNX1 gene single nucleotide polymorphism was associated with rheumatoid arthritis
- a heterozygous single nucleotide deletion in exon 8 of the RUNX1 gene may play a role in development of myeloid malignancies
- VP-16 causes the ETO gene repositioning which allows AML1 and ETO genes to be localized in the same nuclear layer; data corroborate the so called "breakage first" model of the origins of recurrent reciprocal translocation
- C-terminal truncated AML1 mutant (S291fsX300) induced pancytopenia with erythroid dysplasia in transplanted mice, followed by progression to Myelodysplastic syndrome or acute myelogenous leukemia
- RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance
- analysis of TEL-AML1-transduced cord blood cells suggests that TEL-AML1 functions as a first-hit mutation by endowing this preleukemic cell with altered self-renewal and survival properties
- RUNX1 over-representation is associated to a poor outcome of acute lymphoblastic leukemia.
- RUNX1 rearrangements in acute myeloblastic leukemia relapsing after hematopoietic stem cell transplantation.
- p19(INK4D) knockdown led to a moderate increase (31.7% +/- 5%) in the mean ploidy of megakaryocytes suggesting a role of p19(INK4D) in the endomitotic arrest.
- PRMT1- dependent methylation of RUNX1 at arginine residues 206 and 210 abrogates its association with SIN3A.
- Data of the current study do not confirm the universal and population independent susceptibility role of the SLC22A4 C6607T and RUNX1 G24658C variants for rheumatoid arthritis.
- In functional assays, corepressor ETO, but not AML1/ETO, augments SHARP-mediated repression in an histone deacetylase-dependent manner.
- AML1-Evi-1 specifically transforms hematopoietic stem cells through fusion of the entire Evi-1 sequence to AML1.
- Conclude that acute lymphoblastic leukemia TEL-AML1 gene status should be incorporated into risk classification schemes.
- study excludes occurrence and persistence of ETV6-RUNX1 transcript in most pregnancies between 6th and 10th week of development at levels of >/=10-4
- Point mutations to large genomic deletions of RUNX1 gene is associated with thrombocytopenia and mental retardation
- role of RUNX1 haploinsufficiency in megakaryopoiesis and predisposition to AML; leukemic clone had trisomy 21 resulting from duplication of chromosome 21 containing the RUNX1 deletion
- AML1-ETO fusion proteins have a selective preference for certain AML1 target genes that contain multimerized AML1 consensus sites in their regulatory elements
- AML1-ETO promotes leukemogenesis by blocking cell differentiation through inhibition of Sp1 transactivity.
- Novel cytogenetic mutation typical for childhood B-cell ALL: intrachromosomal amplification of chromosome 21, which requires high-risk therapy irrespective of other risk factors and is associated with a cryptic 12;21 translocation of good prognostic valu
- RUNX1/RUNX1T1 siRNAs compromise the engraftment and/or self-renewal capacities of t(8;21) leukaemia-initiating cells.
- Fanconi Anemia patient with AML1 gene amplification and monosomy 7 in pre-transplant myelodysplasia (MDS) relapsing 7 years after successful allo-SCT.
- TEL/AML1 fusion gene may have a role in childhood acute lymphoblastic leukemia
- RUNX1-MTG16 fusion gene in acute myeloblastic leukemia with t(16;21)(q24;q22) is reported.
- RUNX3 is found to be commonly repressed by the t(8;21) and inv(16) fusion proteins and might have an important role in core-binding factor AML
- Gene expression profiling identified several biological pathways downstream of RUNX1 in patients with FPD-AML.
- survivin gene acts as a critical mediator of AML1/ETO-induced late oncogeneic events.
- AML1 can regulate the c-mpl promoter both positively and negatively by changing the binding partner according to cell types
- interaction with PEBP2-beta leads to the phosphorylation of RUNX1, which in turn induces p300 phosphorylation
- It would appear prudent to screen young patients with myelodysplasia/AML for RUNX1 mutation, before consideration of sibling hematopoietic stem cell transplantation.
- Considering these results, AML1 point mutations might be a useful biomarker that differentiates radio-induced MDS/AML from spontaneous MDS/AML.
- hypothesis of the ETV6/RUNX1 leukemogenic model shows these secondary changes are necessary for leukemogenesis rather than progression of disease. This study also disclosed RUNX1 alterations in the ETV6/RUNX1-negative group
- array CGH performed on CD34(+) cells revealed cryptic partial deletions of RUNX1.
- genomic profile of ETV6-RUNX1 positive acute lymphoblastic leukemia highlights a recurrent deletion of TBL1XR1.
- Increased expression of p21/WAF/Cip1 in primary leukemic blasts suggests that elevated p21/WAF/Cip1 levels may contribute to specific features observed in AML1-positive leukemia.
- Histone H1 depletion and/or histone H3 hyperacetylation may have a linkage with an increase susceptibility of specific chromosomal regions to undergo translocations.
- crucial role of the NHR4 domain in determination of cellular fate during AML1-ETO-associated leukemogenesis.
- novel role for the leukemia-related AML1-ETO protein in epigenetic control of cell growth through upregulation of ribosomal gene transcription mediated by RNA Pol I.
- major role for the functional interaction of AML1/ETO with AML1 and HEB in transcriptional regulation determined by the fusion protein
- Four copies of RUNX1 were found.
- ETV6/RUNX1 fusion lacking prognostic effect in pediatric patients with acute lymphoblastic leukemia.
- miR-27a plays a regulatory role in megakaryocytic differentiation by attenuating Runx1 expression, and during megakaryopoiesis, Runx1 and miR-27a are engaged in a feedback loop involving positive regulation of miR-27a expression by Runx1.
- Marker chromosomes are a significant mechanism of high-level RUNX1 gene amplification in hematologic malignancies