The DOI matches its Crossref record; 82 of the 82 references it cites were found in a registry or an index; 3 of the 15 sources its claims cite were checked for support.
Subtype-specific 3D genome alteration in acute myeloid leukaemia
Open accessAbstract
Acute myeloid leukaemia (AML) represents a set of heterogeneous myeloid malignancies, and hallmarks include mutations in epigenetic modifiers, transcription factors and kinases 1 – 5 . The extent to which mutations in AML drive alterations in chromatin 3D structure and contribute to myeloid transformation is unclear. Here we use Hi-C and whole-genome sequencing to analyse 25 samples from patients with AML and 7 samples from healthy donors. Recurrent and subtype-specific alterations in A/B compartments, topologically associating domains and chromatin loops were identified. RNA sequencing, ATAC with sequencing and CUT&Tag for CTCF, H3K27ac and H3K27me3 in the same AML samples also revealed extensive and recurrent AML-specific promoter–enhancer and promoter–silencer loops. We validated the role of repressive loops on their target genes by CRISPR deletion and interference. Structural variation-induced enhancer-hijacking and silencer-hijacking events were further identified in AML samples. Hijacked enhancers play a part in AML cell growth, as demonstrated by CRISPR screening, whereas hijacked silencers have a downregulating role, as evidenced by CRISPR-interference-mediated de-repression. Finally, whole-genome bisulfite sequencing of 20 AML and normal samples revealed the delicate relationship between DNA methylation, CTCF binding and 3D genome structure. Treatment of AML cells with a DNA hypomethylating agent and triple knockdown of DNMT1 , DNMT3A and DNMT3B enabled the manipulation of DNA methylation to revert 3D genome organization and gene expression. Overall, this study provides a resource for leukaemia studies and highlights the role of repressive loops and hijacked cis elements in human diseases. Extensive genomic analyses of the chromatin architecture in acute myeloid leukaemia reveals several characteristics, including subtype-specific distal enhancers and silencers, that may represent new anticancer therapeutic targets.
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TL;DR
This study maps 3D genome organization in primary acute myeloid leukemia (AML) and identifies subtype-specific A/B compartment switches, TAD alterations, chromatin loops, and architectural stripes. It further shows that promoter-silencer loops and structural-variant-induced enhancer/silencer hijacking contribute to gene dysregulation, and that DNA hypomethylating treatment or DNMT triple knockdown can partially reverse AML-associated chromatin topology.
Key findings
- In 25 AML and 7 healthy donor samples, Hi-C identified recurrent and subtype-specific 3D alterations: on average 3.2% A-to-B and 2.9% B-to-A compartment switches versus HSPC; 391 of 622 curated COSMIC cancer/AML-related genes fell in altered TADs in at least one sample, with >100 recurrent.
- AML-specific loops averaged ~200 per AML sample; 42.4% were promoter-enhancer (P-E) and 11.2% promoter-silencer (P-S), with P-S loops accounting for 9.2% of all loops and averaging 169 kb. CRISPR deletion of an RTTN silencer increased RTTN expression 3-fold (p=5E-5), and CRISPRi de-repression of IKZF2-linked silencers increased IKZF2 expression >35-fold (P=0.00017).
- SV-induced neo-loops included enhancer hijacking (17.2% of neo-loops) and silencer hijacking (5.7%); CRISPRi screening of 74 neo P-E loops in Kasumi-1 cells identified 14 sgRNAs targeting 13 enhancers as significantly depleted, and hijacked silencer de-repression increased EXD1 and ALG10 expression by 5.97-fold and 2.70-fold, respectively.
- 5-AZA treatment reduced global methylation from 74% to 39%; 31.6% of AML-specific loops dissociated after treatment versus 2.5% of shared loops, and 55% of A-to-B altered compartments in an AML cell line were reversed to the A compartment.
Methods
- Primary samples: in situ Hi-C and RNA-seq in 32 primary samples (25 AML, 4 normal CD34+ HSPC, 3 PBMC), with ~600 million paired-end reads per Hi-C library; WGS at ~40x in 25 AML; ATAC-seq and CUT&Tag for H3K27ac, H3K27me3, and CTCF; WGBS in 18 AML and 2 PBMC at ~30X; 199 total genomic datasets.
- Functional validation: 4C-seq, 3D DNA FISH, HiChIP for H3K27me3, CRISPR deletion, CRISPRi/CRISPR activation, luciferase reporter assays, and a CRISPRi screen in Kasumi-1 cells; cell-line experiments in Kasumi-1, THP-1, HL60, U937, and K562.
- Perturbation: U937 cells treated with 0.5 μM 5-AZA for 12 days or subjected to inducible DNMT3A/3B/1 triple knockdown, followed by WGBS and Hi-C; computational analyses included Hi-C compartment/TAD/loop calling, NeoLoopFinder, stripe detection, and differential loop/compartment analyses.
Limitations
- The paper states that future experiments should aim to dissolve chromatin interactions without changing local chromatin status at cis-regulatory elements, and that phenotypic effects need deeper study, with animal models desirable.
- Evident from the text: the primary AML cohort is moderate in size (25 samples), and subtype-specific conclusions rest on small subgroups; functional validation of loops and hijacking is largely performed in AML cell lines rather than in vivo.
- Evident from the text: although the authors report that <4.8% of AML-specific loops were in CNV regions, structural variation and copy-number effects remain potential confounders in 3D genome analyses.
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114 Own result · 24 Own method · 11 Own interpretation · 9 Not checked yet · 2 No basis given · 1 Supported · 1 Partly supported · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“Clustering analysis by Hi-CRep49 showed that 5-AZA treated and DNMT TKD cells were more similar to each other than the DMSO treated cells (Fig. 6e).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > HMA/DNMT TKO reverses chromatin topology
What the sources say
- Supportedcites [49] Yang, T. et al. HiCRep: assessing the reproducibility of Hi-C data using a stratum-adjusted correlation coefficient. Genome Res. 27, 1939–1949 (2017). source
The citation identifies HiCRep as the method used for the citing paper’s clustering analysis. The source’s Results section (“Evaluating biological relevance by constructing cell lineages”) describes using HiCRep to assess similarities among cell types and construct a hierarchy. The 5-AZA, DNMT TKD, and DMSO comparison is the citing paper’s own result, attributed to its Figure 6e, not to this source. (LLM, conf=0.92)
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In the paper
“We noticed that a cluster of samples all contained mutations in the KMT2B gene, which has not been used as a dominant AML subtyping classifier before.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Subtype-specific compartmentalization
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In the paper
“However, as shown in Extended Data Fig. 3c, the majority of TAD alterations did not affect the expression of genes, consistent with a recent study in multiple cancer types26.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > TAD alteration and gene expression
What the sources say
- Not checked yetcites [26] Akdemir, K. C. et al. Disruption of chromatin folding domains by somatic genomic rearrangements in human cancer. Nat. Genet. 52, 294–305 (2020). source
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In the paper
“The samples were clustered into different groups, which accurately reflected the AML genetic subtypes (Fig. 1c), such as RUNX1 and CEBPA mutations.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Subtype-specific compartmentalization
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In the paper
“Similarly, we observed other compartment switch regions unique to AML or AML subgroups, containing known AML gens such as POUA2F1, FGF13, and BCL11 (Extended Data Fig. 2c).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Subtype-specific compartmentalization
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In the paper
“Moreover, the A/B compartment switching regions also grouped by their genetic mutation profile (Fig. 1f).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Subtype-specific compartmentalization
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In the paper
“We observed that CTCF binding sites in AML samples were hypomethylated (Extended Data Fig. 11c).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Altered DNA methylation and 3D genome
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In the paper
“Only less than 4.8% of the AML-specific loops were in the CNV regions (Extended Data Fig. 4a-b), suggesting that they were not confounded by copy number variations (CNVs).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > AML-specific chromatin loops
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In the paper
“We performed luciferase reporter assays to test the activity for five of them and all increased the luciferase expression (Fig. 4j).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Function of hijacked enhancers
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“Deletion of this silencer increased the RTTN expression by 3 folds (Extended Data Fig. 7g, p=5E-5), dramatically slowed cell proliferation (Extended Data Fig. 7h), and decreased the sizes of the colonies by colony formation assay (Extended Data Fig. 7i-j).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Validating promoter-silencer loops
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In the paper
“We identified 391 out of the 622 curated COSMIC cancer-related and AML-related genes located inside the altered TADs in at least one sample, and more than 100 are recurrent across multiple samples (Extended Data Fig. 3b)4,24,25.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > TAD alteration and gene expression
What the sources say
- Partly supportedcites [4] Papaemmanuil, E. et al. Genomic classification and prognosis in acute myeloid leukemia. N. Engl. J. Med. 374, 2209–2221 (2016). sourceExperimental — accuracy not yet measured
The Results section, “Driver-Mutation Landscape of AML” (page unavailable), identifies 76 AML driver genes or genomic regions, supporting the use of this paper for AML-related gene identification. It does not report a curated set of 622 genes, altered TADs, or the counts of 391 genes and more than 100 recurrent genes; those appear to be the citing authors’ own findings. (LLM, conf=0.78)
- Partly supportedcites [24] Sondka, Z. et al. The COSMIC Cancer Gene Census: describing genetic dysfunction across all human cancers. Nat. Rev. Cancer 18, 696–705 (2018). sourceExperimental — accuracy not yet measured
The Introduction describes the COSMIC Cancer Gene Census as a curated resource of cancer genes, supporting its use to identify such genes. But the Tier 2 section gives 719 genes in the August 2018 census, not the cited sentence’s combined set of 622 COSMIC cancer-related and AML-related genes. The 391 genes in altered TADs and their recurrence are presented as the citing authors’ own findings, not findings attributed to this source. (LLM, conf=0.84)
- Not checked yetcites [25] Metzeler, K. H. et al. Spectrum and prognostic relevance of driver gene mutations in acute myeloid leukemia. Blood 128, 686–698 (2016). source
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In the paper
“Genes located in the A-to-B or B-to-A switching regions showed decreased or increased expression, respectively (Fig. 1e).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Subtype-specific compartmentalization
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In the paper
“On average, there was 3.2% A-to-B compartment switch and 2.9% B-to-A switch comparing AML samples with HPSC controls (Fig. 1d).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Subtype-specific compartmentalization
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In the paper
“For example, the WT1 gene showed B-to-A switch and expression activation exclusively in samples with TET2 and/or FLT3-ITD mutations, accompanied by the gain of ATAC-seq and H3K27ac peaks (Extended Data Fig. 2a-b).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Subtype-specific compartmentalization
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In the paper
“Correspondingly, we observed multiple gained chromatin loops appeared in these AML samples across the lost CTCF binding sites, including a loop linking WDR66 promoter with distal regions.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Altered DNA methylation and 3D genome
plaincorrelationaln = 4- Asserted: passes — The authors put it forward as true.
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“For example, we observed in four AML samples (424, 018, 546, and 472) a lost binding of CTCF, the motif of which was hypermethylated in those samples (Bar plot in Extended Data Fig. 11g).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Altered DNA methylation and 3D genome
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“We observed variable methylation levels globally in AML samples (Extended Data Fig. 11a) and significantly higher methylation at CpG islands in AML compared with normal PBMC and HSPC (Fig. 6a), consistent with previous findings46.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Altered DNA methylation and 3D genome
What the sources say
- Not checked yetcites [46] Akalin, A. et al. Base-pair resolution DNA methylation sequencing reveals profoundly divergent epigenetic landscapes in acute myeloid leukemia. PLoS Genet. 8, e1002781 (2012). source
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In the paper
“As shown in Fig. 2e, 220 genes were significantly upregulated in AML and 88 genes were downregulated.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > AML-specific chromatin loops
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“Overall, we found 261 cancer-related genes whose promoters were located in the neo-loop anchors, 44 of which were recurrent across different samples.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Silencer hijacking
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“For example, MYCN formed a subtype-specific interaction with a cluster of co-occurring enhancers ~650Kb downstream, and this loop was only observed in AML samples with TET2/FLT3-ITD, CEBPA or STAG2/KRAS/NRAS mutations (Fig. 2d).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > AML-specific chromatin loops
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In the paper
“Across all samples, 42.4% of AML-specific loops were between gene promoter and enhancers (P-E), and 11.2% are between promoter and silencers (P-S) (Fig. 2g, Supplementary Table 2).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > AML-specific chromatin loops
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In the paper
“Overall, 5.7% of all the neo-loops in this study lead to silencer hijacking, while 17.2% of the neo-loops introduce enhancer-hijacking (Fig. 5e).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Silencer hijacking
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“A representative example was shown in Extended Data Fig. 9c, where there was a fusion between chr7 and chr11 in AML 270, but not in HSPC. This neo-loop connected the CDK5 gene (located on chr7) to several enhancers on chr11. In contrast, there were no such inter-chromosomal Hi-C signals in HSPC.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Detecting enhancer hijacking in AML
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In the paper
“We also identified the loss of CTCF binding sites in AML samples that were potentially due to hypermethylation (Extended Data Fig. 11d). There are in average 76 such sites in each AML samples.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Altered DNA methylation and 3D genome
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In the paper
“Similarly, the CBL gene was linked to enhancers on chr7 in sample 270, but in THP-1 cells, it was linked with enhancers on chr9 (Extended Data Fig. 9d);”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Detecting enhancer hijacking in AML
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In the paper
“The AML-specific loops also showed subtype-specific patterns and contained many known AML proto-oncogenes (such as MYCN, WT1, ERG, MEIS1, and RUNX1) in the loop anchors (Fig. 2c).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > AML-specific chromatin loops
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In the paper
“P-S loops account for 9.2% of all loops, with an average size of 169 kb (Extended Data Fig. 6a and 6b).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > AML-specific chromatin loops
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In the paper
“On average, each AML sample has 1.7 large deletions (>1 Mb), 2.1 inversions (>1 Mb), and 13.2 inter-chromosomal translocations (Supplementary Table 5).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Detecting enhancer hijacking in AML
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“For example, the MYC gene (located on chr8) was looped with a cluster of enhancers on chr14 in sample 1360 due to t(8;14), but was looped with a different set of enhancers on chr11 in HL-60 cells due to t(8;11) (Fig. 4b).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Detecting enhancer hijacking in AML
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In the paper
“The stable A compartments were slightly enriched for CpGi, while the stable B compartment regions were depleted of CpGi (Extended Data Fig. 13e).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > HMA/DNMT TKO reverses chromatin topology
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In the paper
“865 out of the 905 (95.5%) TKD-induced A-to-B reversion regions overlapped with the A-to-B revision regions induced by 5-AZA treatment, and the overlap is 79% for the B-to-A reversion regions (Fig. 6f).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > HMA/DNMT TKO reverses chromatin topology
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In the paper
“We demonstrated that the HMA exposure partially restored the chromatin structure, including reverting switched compartment and dissociating AML-specific loops.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Discussion
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In the paper
“We also showed the inter-chromosomal Hi-C map in the HSPC 213, where there is no visible inter-chromosomal interactions.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Extended Data
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The treatment slowed down the cell proliferation (Extended Data Fig. 12a).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > HMA/DNMT TKO reverses chromatin topology
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The diamond-shaped region between the two dashed lines resided the interactions across the lost CTCF sites.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Extended Data
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The loops are absent in all three PBMC samples (only one is plotted) and less frequent in the four HSPC samples (only one is plotted).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Extended Data
plainn = 4- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“AML sample 018 has the same loop but with less interacting signals and almost no H3K27me3 signals at the loop anchor.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Extended Data
plainSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the results showed that after 5-AZA treatment A/A and B/B interactions were decreased, while the interactions between A/B compartment were increased (Fig. 6i).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > HMA/DNMT TKO reverses chromatin topology
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We noticed that the CpGi originally in A compartment (A-to-A and A-to-B) were hypomethylated, while CpGi originally in B compartment (B-to-B and B-to-A) were hypermethylated.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > HMA/DNMT TKO reverses chromatin topology
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“5-AZA treatment dramatically decreased DNA methylation levels for all four regions, with the biggest changes in open sea (Extended Data Fig. 13c), as well as on CTCF binding motifs (Extended Data Fig. 13d).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > HMA/DNMT TKO reverses chromatin topology
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We observed increased interactions across the lost CTCF binding sites, suggesting that disruption of CTCF site might lead to loss of insulation and change the local chromatin interaction profile.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Altered DNA methylation and 3D genome
hedgedconditionaln = 4- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“SV calls from Delly and Speedseq were merged and only SVs detected by both methods were kept to reduce false positives.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Human blood samples were obtained with consent from AML patients or healthy donors under the Penn State Hershey IRB-approved protocol STUDY00005272.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Materials and Experiments
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The quantity and molecular size of the library was confirmed by Qubit HS DNA assay (ThermoFisher) and Tapestation 2200 system(Agilent).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Materials and Experiments
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“In two separate replicates of experiments, lentiviruses of sgRNA plasmids were then transfected into 2 million of the treated Kasumi-1 cells with an MOI<0.3.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Materials and Experiments
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Furthermore, the detected SVs were compared against the DGV database (version 2016-05-15) to reduce germline SV calls.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“This final set of point mutations was further used to confirm the clinical molecular diagnosis of our AML samples, and both results were used for optimizing the subtyping of the AML samples.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The qPCR was performed for RTTN RNA expression with the primer listed in Supplementary Table 11, using CRPSIR-processed Kasumi-1 cells without the deletion as the control.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Materials and Experiments
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All insertions have been verified by Sanger sequencing.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Materials and Experiments
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Each cloning was verified by Sanger sequencing.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Materials and Experiments
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Myeloblasts accounted for more than 90% of purified PBMC for most samples”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Materials and Experiments
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Two biological replications were applied to each of CRISPR interference, CRISPR deletion, and reporter assay with similar results.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“To control for cell number and transfection efficiency, firefly luciferase activity was normalized to renilla luciferase.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Materials and Experiments
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Read alignments were shifted +4bp on “+” strand and −5bp on “-” strand to account for Tn5 insertion before peak calling.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The Western Blots for yH2AX, Caspase-3, GAPDH, and β-actin under 5-AZA treatment were repeated for twice with similar results (Extended Data Fig. 12c-d).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Reads mapped to the same MboI restriction fragment are not informative to chromatin interactions and thus are removed for downstream analysis.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Each biological replicate contains three technical replicates.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The Western Blots for DNMT3A, DNMT3B, DNMT1, and GAPDH in the DNMT TKD experiment were repeated for three times with similar results (Fig. 7d).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Peakachu reports a probability score associated with each loop which demarcates confidence of loop calling. The probability score is also positively associated with the loop intensity, making it convenient for differential loop analysis.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
What the sources say
- Not checked yetcites [27] Salameh, T. J. et al. A supervised learning framework for chromatin loop detection in genome-wide contact maps. Nat. Commun. 11, 3428 (2020). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“To ensure specificity, we filter raw calls to retain stripes larger than 300kb (eight of 40Kb binds) to avoid calls that are less distinguishable from loop clusters or background noise.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“and minimal quality score of 20 was used to reduce false positive calls.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“To minimize the number of germline calls, point mutations that overlap with dbSNP150 mutations were removed.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“measurements were taken in triplicates.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Materials and Experiments
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Peakachu detects loops as CTCF or H3K27ac loops depending on a pre-trained CTCF model or H3K27ac model.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
What the sources say
- Not checked yetcites [27] Salameh, T. J. et al. A supervised learning framework for chromatin loop detection in genome-wide contact maps. Nat. Commun. 11, 3428 (2020). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The library passed QC by the following parameters: skew ratio = 2.53 (criterial <10); perfect match = 91.5 (>70%); undetected guides = 0 (<0.5%); Coverage = ~5,500 per sgRNA (>100).”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Materials and Experiments
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Peaks in the ENCODE hg38 blacklist regions (http://mitra.stanford.edu/kundaje/akundaje/release/blacklists/hg38-human/hg38.blacklist.bed.gz) were filtered out.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Cell proliferation was independently performed with three technical replicates every 24 hours.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Materials and Experiments
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“In this work, loops were first detected using both models and only those detected by both models were reported to reduce the false positive loop calls.”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Informatics analysis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
The paper relies on this without support.
AML is characterized by a global aberrant DNA methylation profile.
“AML is also characterized by a global aberrant DNA methylation profile.”
The paper relies on this without support.
Genome-wide enhancer hijacking in AML has not been studied.
“However, genome-wide enhancer hijacking in AML have not been studied.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“structural variations have the potential to rewire genes with ectopic regulatory elements”
From Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration (2023) · cites this paper as [24]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > HMA/DNMT TKO reverses chromatin topology
“In a parallel effort, we treated the U937 cells with DNA hypomethylating agent 5-AZA, at a low but effective dosage (0.5μM for 12 days)”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Methods > Materials and Experiments
“U937 cells were cultured in either 0.5M 5-AZA or the same volume of DMSO for 12 days with alternate day drug media readministering.”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Function of hijacked enhancers
“The CUT&Tag data showed specific depletion of H3K37ac signals at the two targeted loci (Extended Data Fig. 10c)”
§ Subtype-specific 3D genome alteration in acute myeloid leukemia > Extended Data
“c, H3K27ac at the sgRNA-targeted loci and the NSMCE3 gene promoter.”
Citations
Cites
Fast gapped-read alignment with Bowtie 2
Langmead, B., & Salzberg, S. L. (2012) · Nature Methods · doi:10.1038/nmeth.1923 · Cited by 56,400
STAR: ultrafast universal RNA-seq aligner
Dobin, A., Davis, C. A., Schlesinger, F., Drenkow, J., Zaleski, C., Jha, S., Batut, P., Chaisson, M., & Gingeras, T. R. (2013) · Bioinformatics · doi:10.1093/bioinformatics/bts635 · Cited by 51,709
RSEM: accurate transcript quantification from RNA-Seq data with or without a reference genome
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A 3D Map of the Human Genome at Kilobase Resolution Reveals Principles of Chromatin Looping
Rao, S. S. P., Huntley, M. H., Durand, N. C., Stamenova, E. K., Bochkov, I. D., Robinson, J. T., Sanborn, A. L., Machol, I., Omer, A. D., Lander, E. S., et al. (2014) · Cell · doi:10.1016/j.cell.2014.11.021 · Cited by 9,212
Comprehensive Mapping of Long-Range Interactions Reveals Folding Principles of the Human Genome
Lieberman-Aiden, E., van Berkum, N. L., Williams, L., Imakaev, M., Ragoczy, T., Telling, A., Amit, I., Lajoie, B. R., Sabo, P. J., Dorschner, M. O., et al. (2009) · Science · doi:10.1126/science.1181369 · Cited by 8,898
Topological domains in mammalian genomes identified by analysis of chromatin interactions
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Self-citationDöhner, H., Estey, E. H., Grimwade, D. J., Amadori, S., Appelbaum, F. R., Büchner, T., Dombret, H., Ebert, B. L., Fenaux, P., Larson, R. A., et al. (2016) · Blood · doi:10.1182/blood-2016-08-733196 · Cited by 5,938
Self-citationBismark: a flexible aligner and methylation caller for Bisulfite-Seq applications
Krueger, F., & Andrews, S. (2011) · Bioinformatics · doi:10.1093/bioinformatics/btr167 · Cited by 5,324
Research works printed but not linked: 1
- Spracklin, G. et al. Heterochromatin diversity modulates genome compartmentalization and loop extrusion barriers. Preprint at bioRxiv https://doi.org/10.1101/2021.08.05.455340 (2021). · DOI
Cited by
Sorted by citations
Items 101–200 of 213
Moeckel, C. M., Mouratidis, I., Chantzi, N., Uzun, Y., & Georgakopoulos‐Soares, I. (2024) · BioEssays · doi:10.1002/bies.202300210 · Cited by 4
“Studies have highlighted the value of CRISPR screens in general in identifying cis -regulatory elements associated with disease states, [130–133] including neurodevelopmental disorders and neurode-generativediseases [134,135] andhost-pathogeninteractionsforviruses such as COVID-19.”
BackgroundLoop Extrusion Machinery Impairments in Models and Disease
Ryzhkova, A. S., Maltseva, E., Баттулин, Н. Р., & Kabirova, E. (2024) · Cells · doi:10.3390/cells13221896 · Cited by 2
Liu, X., Wei, H., Zhang, Q., Zhang, N., Wu, Q., & Xu, C. (2024) · Nature Communications · doi:10.1038/s41467-024-55403-7 · Cited by 3
3D genome sequencing technology in its mid-teens: past, present, and future
Chai, H., & Ruan, Y. (2025) · Trends in Genetics · doi:10.1016/j.tig.2025.07.010 · Cited by 4
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sciMET-cap: High-throughput single-cell methylation analysis with a reduced sequencing burdenPreprint
Acharya, S. N., Nichols, R. V., Rylaarsdam, L. E., O’Connell, B. L., Braun, T. P., & Adey, A. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.07.12.548718 · Cited by 3
A fast and adaptive detection framework for genome-wide chromatin loop mapping from Hi-C dataPreprint
Chen, S., Wang, J., Jung, I., Qiu, Z., Gao, X., & Li, Y. (2024) · Genome Research · doi:10.1101/gr.279274.124 · Cited by 3
Hanafiah, A., Geng, Z., Liu, T., Tai, Y. T., Cai, W., Wang, Q., Christensen, N. D., Liu, Y., Yue, F., & Gao, Z. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.11.13.623456 · Cited by 3
Self-citationSingle-cell Multiome Analysis of Chromatin State and Transcriptome in the Human Basal GangliaPreprint
Chang, L., Li, K., Xie, Y., Zhong, G., Rink, J. A., Báez-Becerra, C. T., Lie, A., Indralingam, H. S., Dong, K., Loe, T. H., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.02.03.703645 · Cited by 5
Self-citationThree-dimensional chromatin landscapes in MLLr AML
Sui, P., Wang, Z., Zhang, P., & Pan, F. (2024) · Experimental Hematology and Oncology · doi:10.1186/s40164-024-00523-5 · Cited by 2
Supervised Chromatin Loop Detection Using Peakachu Version 2
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Chavan, A., Jones, C., Lawrence, W., & Choudhury, S. R. (2025) · Epigenetics & Chromatin · doi:10.1186/s13072-025-00610-9 · Cited by 2
“Recent studies have highlighted the critical role of chromatin looping and remodeling in shaping subtype-specific genetic and epigenetic landscapes in AML by linking promoters with enhancers and silencers [5, 6].”
The Biological Function of Genome Organization
Yang, X., Zhu, H., Liu, Y., Wang, J., Song, Y., Liao, S., & Dong, P. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26189058 · Cited by 3
“Genomic analyses of primary AML patient samples have revealed abnormal A/B compartment switching, which may induce the dysregulation of disease-related genes such as WT1 , ultimately leading to aberrant myeloid differentiation [151].”
Three-dimensional genome reorganization in hematopoietic stem cells
Nakajima, A., Kirito, K., Nakanishi, M., & Takayama, N. (2025) · Experimental Hematology · doi:10.1016/j.exphem.2025.105249 · Cited by 2
How structural variation shapes the cancer epigenome
MacLennan, S., & Marra, M. A. (2025) · Trends in cancer · doi:10.1016/j.trecan.2025.09.001 · Cited by 2
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Self-citationWu, X., & Zhang, J. (2026) · Current Proteomics · doi:10.1016/j.curpro.2026.100101 · Cited by 4
High Mobility Group A1 Chromatin Keys: Unlocking the Genome During MPN Progression
Resar, L. M. S., & Luo, L. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26052125 · Cited by 2
Targeting the 3D genome by anthracyclines for chemotherapeutic effects
Tan, M., Sun, S., Liu, Y., Perreault, A. A., Phanstiel, D. H., Dou, L., & Pang, B. (2025) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2500704122 · Cited by 5
“These abnormal 3D chromatin interactions could hijack the noncoding regulatory elements, such as silencers ( 8 ) and enhancers, to dysregulate gene expression, thereby promoting tumor development and progression ( 9 , 10 ).”
Xie, T., Danieli‐Mackay, A., Buccarelli, M., Barbieri, M., Papadionysiou, I., D’Alessandris, Q. G., Übelmesser, N., Vinchure, O. S., Lauretti, L., Fotia, G., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.04.20.537702 · Cited by 2
“Structural (SVs) and copy number variants (CNVs) in tumor cells can rewire the 3D genome in ways that allow for the aberrant activation of oncogenes (Hnisz et al., 2016; Weischenfeldt et al., 2017) or the repression of tumor suppressors (Xu et al., 2022a).”
BackgroundSelf-citationTracing the evolution of single-cell cancer 3D genomes: an atlas for cancer gene discoveryPreprint
Liu, M., Jin, S., Agabiti, S. S., Jensen, T. B., Yang, T., Radda, J. S. D., Ruiz, C. F., Baldissera, G., Rajaei, M., Townsend, J. P., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.07.23.550157 · Cited by 2
Probabilistic association of differentially expressed genes withcis-regulatory elementsPreprint
Roberts, B. S., Anderson, A. G., Partridge, E. C., Cooper, G. M., & Myers, R. (2024) · Genome Research · doi:10.1101/gr.278598.123 · Cited by 2
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Sheng, G., Tao, J., Jin, P., Li, Y., Jin, W., & Wang, K. (2024) · Biomedicines · doi:10.3390/biomedicines12092147 · Cited by 1
“This disease is marked by complex karyotypes and various molec‑ ular alterations [1,2], contributing to the underappreciated heterogeneity among AML co‑ horts.”
BackgroundEpigenomic Sequencing Technologies
Chen, J., Keshavarzian, T., & Lupien, M. (2024) · Royal Society of Chemistry eBooks · doi:10.1039/9781837674916-00109 · Cited by 1
Chromatin hubs drive key regulatory networks in leukemia
Swaroop, A., & Yue, F. (2025) · Molecular Cell · doi:10.1016/j.molcel.2024.12.011 · Cited by 1
Self-citationWu, C., Tianshu, Z., Ke, W., Xiong, W., Zhang, Z., Zhang, S., Wang, J., Deng, L., Yan, K., Wang, M., et al. (2025) · Genomics Proteomics & Bioinformatics · doi:10.1093/gpbjnl/qzaf054 · Cited by 1
Multivalent cannabinoid epigenotoxicities and multigenerational aging
Reece, A. S., & Hulse, G. K. (2025) · Elsevier eBooks · doi:10.1016/b978-0-443-13492-0.00001-3 · Cited by 1
3D Genome Engineering: Current Advances and Therapeutic Opportunities in Human Diseases
Jiang, X., Wang, X., Shen, S., Hou, S., & Chen, Y. (2025) · Research · doi:10.34133/research.0865 · Cited by 3
“Similar chromatin alterations have been observed in primary acute myeloid leukemia cells, where a significant proportion of genes exhibited A/B compartment switching accompanied by corresponding changes in gene expression [ 103 ].”
Self-citationBai, J., Wei, H., Hu, S., Guo, Y., Zhang, Q., Liu, X., & Xu, C. (2025) · Science Advances · doi:10.1126/sciadv.adw8040 · Cited by 1
Elucidating the risk factors and oncogene drivers of acute myeloid leukemia
Sanya, D. R. A., & Onésime, D. (2025) · Human Cell · doi:10.1007/s13577-025-01294-9 · Cited by 1
Wang, B., Wang, S., Ding, L., Li, H., Li, Y., & Wang, J. (2025) · Advanced Science · doi:10.1002/advs.202508110 · Cited by 1
Dysregulation of the ALDH1A3/PML–RARα axis promotes the progression of acute promyelocytic leukemia
Cai, J., Liang, C.-H., Han, L., Jiang, H.-Y., Duan, J., Li, F., Liu, J., Liang, C., Gao, L., & Yu, S.-C. (2026) · Cancer Letters · doi:10.1016/j.canlet.2026.218280 · Cited by 1
Targeting ZMIZ1 induces differentiation in acute myeloid leukemia via chromatin remodeling
Li, H., Liu, Y., Cui, J., Fu, Z., Xu, Y., Yang, S., Zhu, K., Xue, Y., Zhang, Y., Zhao, Y., et al. (2026) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-026-02766-6 · Cited by 1
Self-citationCHD4 is a copper sensor linking chromatin remodeling to cuproptosis
Wang, Y., Chi, R., Zhang, C., Liu, Z., Tian, X., Wang, A., Sun, Q., Miao, Y., Xia, J., Shi, Y., et al. (2026) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2026.05.314 · Cited by 1
Jin, M., Quan, K., Wang, H., Wang, H., Du, L., Li, T., Chu, M., Sun, D., & Wei, C. (2026) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2026.153008 · Cited by 1
cPRC1.2 and CTCF-mediated transition from poised to active chromatin loops at bivalent genes
Hanafiah, A., Geng, Z., Liu, T., Tai, Y. T., Cai, W., Wang, Q. Y., Christensen, N., Liu, Y., Yue, F., & Gao, Z. (2026) · EMBO Reports · doi:10.1038/s44319-026-00885-3 · Cited by 4
“Interest-ingly, a previous report has shown that CTCF binding is highly correlated with chromatin loops established by PRC2 (Xu et al, 2022), which catalyzes H3K27me3 as docking sites for cPRC1 binding (Fischle et al, 2003; Min et al, 2003).”
Self-citationXie, X., Tan, D., Mo, J., Xu, Y., Ni, Q., Liu, T., Wang, H., Chen, B., Liao, Y., Lin, Y., et al. (2026) · Nature Cell Biology · doi:10.1038/s41556-026-02063-y · Cited by 1
“…fills the gap left by previous 4DN cancer studies that were limited by the complexity of the background genome and a lack of temporal information 7,9 , as well as by studies focusing solely on normal cell fate transitions, such as early embryonic development 37,38 , differentiation 12 and…”
Zapilko, V., Moisio, S., Parikka, M., Heinäniemi, M., & Lohi, O. (2023) · Cancers · doi:10.3390/cancers15245821 · Cited by 2
Inferring the Cancer Cellular Epigenome Heterogeneity via DNA Methylation Patterns
Li, S. (2023) · Cancer treatment and research · doi:10.1007/978-3-031-45654-1_12 · Cited by 1
Dong, J., & Konopleva, M. Y. (2025) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2025.2500417 · Cited by 1
“Alterations in 3D genome topology, linking aberrant DNA methylation to enhancer-promoter loops bound by CCCTC-binding factor (CTCF), emphasize epigenetic dysfunction as a promising therapeutic target [101].”
Xu, K., Zong-yuan, Y., Sun, C., Gou, C., Zhu, J., Wang, J., Bo, X., Yu, G., Li, H., & Chen, H. (2025) · Advanced Science · doi:10.1002/advs.202504571 · Cited by 1
Li, B., Zhang, R., Wang, N., Liu, X., Li, N., Ding, J., Cao, Z., Qu, X., & Xing, C. (2025) · ACS Applied Bio Materials · doi:10.1021/acsabm.5c01152 · Cited by 1
CTCF Is Essential for the Development and Maintenance of CALM ‐ AF10 ‐Induced Leukemia
Kuroki, Y., Yamagata, K., Aikawa, Y., Shima, Y., Shioneri, H., & Kitabayashi, I. (2025) · Cancer Science · doi:10.1111/cas.70161 · Cited by 1
Reece, A. S., & Hulse, G. K. (2023) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2023.1182535 · Cited by 3
Pulice, J. L., & Meyerson, M. M. (2023) · SSRN Electronic Journal · doi:10.2139/ssrn.4612965 · Cited by 1
Defining the Rules of Biology in the Age of Genome Writing
Woolfson, A. (2023) · GEN Biotechnology · doi:10.1089/genbio.2023.29125.awo · Cited by 1
The 3D genome of pediatric B-cell precursor acute lymphoblastic leukemiaPreprint
Moura‐Castro, L. H., Aydın, E., Dushime, G. T., Woodward, E. L., Castor, A., Gunnarsson, R., Lilljebjörn, H., Olsson, L., Fioretos, T., Johansson, B., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.07.22.666073 · Cited by 1
HiCDOC: chromatin compartment prediction and differential analysis from Hi-C data with replicatesPreprint
Maigné, É., Kurylo, C., Zytnicki, M., & Foissac, S. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.18.677058 · Cited by 1
Subramanian, S., Thoms, J., Huang, Y., Cornejo, P., Koch, F. C., Jacquelin, S., Shen, S., Song, E., Joshi, S. M., Brownlee, C., et al. (2023) · bioRxiv · doi:10.1101/2023.04.18.537282
“…been developed to allow massively parallel interrogation of enhancer activity and specificity (Edginton-White et al., 2023; Hrvatin et al., 2019; Xu et al., 2022), our data provides a catalogue of putative enhancers already annotated with respect to spatiotemporal activity that could fast track…”
BackgroundSelf-citationFu, Y., Wang, X., & Yue, F. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.08.07.552228 · Cited by 1
Self-citationCUT&tag: A powerful epigenetic tool for chromatin profilingPreprint
Li, P., fu, Z., Jiang, S., Sun, Y., zheng, S., & Zong, L. (2023) · doi:10.22541/au.169203623.39699591/v1
Tumor Heterogeneity in Breast Cancer Progression
Mishra, Y. G., Kalali, S., Kizhuvedath, A., Indumathi, A., Adhikari, A., Tanisha, & Manavathi, B. (2023) · Springer eBooks · doi:10.1007/978-981-99-2196-6_16-1
DegCre: Probabilistic association of differential gene expression with regulatory regionsPreprint
Roberts, B. S., Cooper, G. M., & Myers, R. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.10.04.560923
“…the association of CREs to genes, whether through HiC approaches, correlational methods, or other techniques, often focus on static conditions, generating data of CRE activity and gene expression in a single context, with notable exceptions (Adamson et al. 2016; Reed et al. 2022; Xu et al. 2022).”
BackgroundMethodInfluentialChoppavarapu, L., Fang, K., Liu, T., & Jin, V. X. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.03.13.584872
“For example, Xu et al. identified AML subtype-specific changes in 3D genome features such as compartments, TAD boundaries and chromatin loops and further showed that repressive loops were widespread in the genome 17 .”
BackgroundResultInfluentialTargeted Treatment of Acute Myeloid Leukemia Based on Epigenetic Regulation Mechanism
Zhou, S. (2024) · MedScien · doi:10.61173/6yecxn21
Tumor Heterogeneity in Breast Cancer Progression
Mishra, Y. G., Kalali, S., Kizhuvedath, A., Indumathi, A., Adhikari, A., Tanisha, & Manavathi, B. (2024) · Springer eBooks · doi:10.1007/978-981-99-6263-1_16
Emerging Technologies for Epigenetic Drug Discovery
(2024) · Royal Society of Chemistry eBooks · doi:10.1039/9781837674916-part2
RNA in Stow, Leukemia on the Go: P-Bodies RNA Sequestration Drives Leukemogenesis
Germanos, A. A., Muthukumar, S., & Bellodi, C. (2025) · Cellular Reprogramming · doi:10.1089/cell.2024.0092
Xu, J. J., Scoca, V., Chen, Y., Zhan, Y. A., Fisher, A., Udoh, E.-O., Fernando, S., Alija, B., Pantazi, J., Sudunagunta, V. S., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.04.01.646632
Self-citationFunctional enhancers: concept, screening, and validation
Lin, H., Chen, F., & Huang, J. (2025) · Scientia Sinica Vitae · doi:10.1360/ssv-2025-0113
Techniques to detect physical interactions between genomic regions
Hata, T., & Fujii, H. (2025) · Epigenomics · doi:10.1080/17501911.2025.2523232
Chromatin Perturbation Promotes Susceptibility to Hypomethylating AgentsPreprint
Schneider, C., Alexe, G., Merickel, L. A., Meyer, A., Swift, M. L., Serafim, R. B., Basanthakumar, A. T., Taillon, A., Salhotra, S., Boniolo, F., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.07.28.666975
Reece, A. S., & Hulse, G. K. (2025) · Elsevier eBooks · doi:10.1016/b978-0-443-13492-0.00027-x
Zhang, T., Lin, L., Li, J., Li, C., Liang, S., Bai, X., Wang, F., Bao, Y., Guo, D., Bo, X., et al. (2025) · Advanced Science · doi:10.1002/advs.202410603
Zhou, Y., Hu, Y., Tan, L., Zhu, J., Fei, Y., Gu, M., & Tian, D. (2025) · BMC Genomics · doi:10.1186/s12864-025-11987-y
WITHDRAWN: A Druggable Tumor Suppressor and Leukemic Stem Cell MarkerPreprint
Pan, Y., Meng, X., Wang, C., Zhou, W., Chen, Y., Hammer, R., Zheng, H., Hildebrandt, G. C., & Kang, X. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.10.16.682831
Self-citationCRISPR-Cas9 in acute myeloid leukaemia: Current state-of-art and future perspectives
Zingarelli, F., Nanni, J., Cristiano, G., Zannoni, L., & Curti, A. (2025) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2025.102582
Moran, S., Fan, Z., Zanovello, M., Feng, F., Wang, X. Q. D., Lü, C., Liu, J., & Zhang, X. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.10.30.685561
“The publication of several large cancer 3D genomic datasets has allowed us to systematically survey for long Polycomb loops in a pan-cancer setting (19–25).”
Self-citationIdentification of the Role of NAT10 in the Regulation of Porcine Circovirus Type 2 Infection
Liu, Y., Zhou, G., Wang, G., & Wu, Z. (2025) · Veterinary Sciences · doi:10.3390/vetsci12121160
“Among these, methylation modifications such as m 6 A, m 1 A, m 5 C, guanosine methylation, and 2 ′ -O-methylation have been extensively characterized [34–38].”
Exploring multi-level microbial interactions from individual 3D genomes to community networksPreprint
Jiang, W.-J., Cai, K.-W., Sun, Y., Zheng, Z., Xu, F., Gao, R.-X., Wei, N., Zhu, H., Yu-Juan, W., Xia, Q., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2025.12.03.692222
Additional file 1 of Reprogramming of 3D genome structure underlying HSPC development in zebrafish
He, M., Li, X., Xu, B., Lu, Y., Lai, J., Ling, Y., Liu, H., An, Z., Zhang, W., & Li, F. (2024) · Figshare · doi:10.6084/m9.figshare.26735595
Acharya, S. N., Nichols, R. V., Rylaarsdam, L. E., O’Connell, B. L., Braun, T. P., & Adey, A. (2024) · Figshare · doi:10.6084/m9.figshare.26747744
Additional file 4 of Reprogramming of 3D genome structure underlying HSPC development in zebrafish
He, M., Li, X., Xu, B., Lu, Y., Lai, J., Ling, Y., Liu, H., An, Z., Zhang, W., & Li, F. (2024) · Figshare · doi:10.6084/m9.figshare.26735604
Acharya, S. N., Nichols, R. V., Rylaarsdam, L. E., O’Connell, B. L., Braun, T. P., & Adey, A. (2024) · Figshare · doi:10.6084/m9.figshare.26241330
Additional file 2 of Reprogramming of 3D genome structure underlying HSPC development in zebrafish
He, M., Li, X., Xu, B., Lu, Y., Lai, J., Ling, Y., Liu, H., An, Z., Zhang, W., & Li, F. (2024) · Figshare · doi:10.6084/m9.figshare.26735598
Additional file 5 of Reprogramming of 3D genome structure underlying HSPC development in zebrafish
He, M., Li, X., Xu, B., Lu, Y., Lai, J., Ling, Y., Liu, H., An, Z., Zhang, W., & Li, F. (2024) · Figshare · doi:10.6084/m9.figshare.26735607
Additional file 6 of Reprogramming of 3D genome structure underlying HSPC development in zebrafish
He, M., Li, X., Xu, B., Lu, Y., Lai, J., Ling, Y., Liu, H., An, Z., Zhang, W., & Li, F. (2024) · Figshare · doi:10.6084/m9.figshare.26735610
Acharya, S. N., Nichols, R. V., Rylaarsdam, L. E., O’Connell, B. L., Braun, T. P., & Adey, A. (2024) · Figshare · doi:10.6084/m9.figshare.26241192
Additional file 3 of Reprogramming of 3D genome structure underlying HSPC development in zebrafish
He, M., Li, X., Xu, B., Lu, Y., Lai, J., Ling, Y., Liu, H., An, Z., Zhang, W., & Li, F. (2024) · Figshare · doi:10.6084/m9.figshare.26735601
Additional file 7 of Reprogramming of 3D genome structure underlying HSPC development in zebrafish
He, M., Li, X., Xu, B., Lu, Y., Lai, J., Ling, Y., Liu, H., An, Z., Zhang, W., & Li, F. (2024) · Figshare · doi:10.6084/m9.figshare.26735613
Acharya, S. N., Nichols, R. V., Rylaarsdam, L. E., O’Connell, B. L., Braun, T. P., & Adey, A. (2024) · Figshare · doi:10.6084/m9.figshare.26747738
Acharya, S. N., Nichols, R. V., Rylaarsdam, L. E., O’Connell, B. L., Braun, T. P., & Adey, A. (2024) · Figshare · doi:10.6084/m9.figshare.26747741
Additional file 1 of Three-dimensional chromatin landscapes in MLLr AML
Sui, P., Wang, Z., Zhang, P., & Pan, F. (2024) · Figshare · doi:10.6084/m9.figshare.25884968
Genetic and epigenetic mechanisms underlying treatment-induced neuroendocrine prostate cancer
Keo, V., Lü, X., Zhao, J. C., & Yu, J. (2025) · Journal of the National Cancer Center · doi:10.1016/j.jncc.2025.11.001
Berico, P., Dunton, C. L., Almassalha, L. M., Yanke, A. F., Medina, K., Acosta, N., Muijlwijk, T., Do, C., Lee, S., Edmiston, S. N., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.02.05.702638
Bartalucci, N., Mannelli, F., Tarantino, D., Enderti, A., Romagnoli, S., Colazzo, D., Scappini, B., Gianfaldoni, G., Piccini, M., Signori, L., et al. (2026) · Blood Cancer Journal · doi:10.1038/s41408-026-01465-3
Peng, Y., Deng, Y., Liu, M., Liu, Z., Li, Y.-H., Zhao, X.-Y., Xing, D., Jia, J., & Ge, H. (2026) · Briefings in Bioinformatics · doi:10.1093/bib/bbag096 · Cited by 1
Phase separation of β-catenin assembles active loop hubs in colorectal cancer
Yang, J., Sun, J., Zhang, H., Yu, Y., Chen, F., Mo, J., Luo, S., Xu, Y., Zhong, L., Tan, D., et al. (2026) · Genome biology · doi:10.1186/s13059-026-04030-0
“S3a, b) [25], as higher DNA methylation level inhibits transcription factor binding and represent an effective strategy to disrupt chromatin loops [7, 8].”
DNA methylation changes CTCF binding and reorganizes 3D genome structure in breast cancer cells
Segueni, J. (2024) · theses.fr (ABES) · doi:10.70675/abf007fbz8adcz4c68zb9faz5f550f134b2a
Kamran, M., Nassar, N. N., & Cancelas, J. A. (2026) · Open Biology · doi:10.1098/rsob.260011
Connecting multiway enhancer-promoter interactions to changes in gene expression in cancerPreprint
Kumari, K., Shin, S., Shi, G., Reed, K. S. M., Misteli, T., & Thirumalai, D. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.04.25.720760
3D Chromatin Architecture During Early Development: New Methods and New Findings
Olais, E. B., Jácome-López, K., Pérez‐Molina, R., & Furlan-Magaril, M. (2026) · Methods in molecular biology · doi:10.1007/978-1-0716-5126-1_18
Interplay of the 3D genome and epigenome in androgen-driven prostate cancer
Campbell, E. M., Challis, D., Clark, S. J., & Achinger-Kawecka, J. (2026) · Epigenomics · doi:10.1080/17501911.2026.2676129
“…within the 3D chromatin landscape, where DNA hypermethylation at enhancers can directly constrain enhancer-promoter loop formation [17,89] and can be targeted with DNMT inhibition [20,90], suggesting an active or consolidating role of DNA methylation in the reorganization of 3D chromatin topology.”
Reddy, M. A., Bhattacharya, S., Tanwar, V. S., Malek, V., Chen, Z., Zhang, L., Lanting, L. L., Wu, X., Grant, M. B., Tompkins, J. D., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.05.27.727961
“Genetic studies have shown that most disease-associated variants reside in non-coding regions, with many mapping to cis-regulatory elements such as enhancers ( 42-44 ).”
Aberrant DNA methylation is co-regulated across the genome in leukemia and other types of cancerPreprint
Baranda, M. V., Liesenfelder, S., Kraft, F., Kuo, C., Perez-Correa, J.-F., Jost, E., Stiehl, T., & Wagner, W. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.06.05.729844
“…DNA methyltransferases (44), interactions between DNAm and histone modifications (45), higher-order three-dimensional chromatin organization (46), regulatory contributions from non-coding RNAs such as long non-coding RNAs (lncRNAs) or PIWI-interacting RNAs (piRNAs) (47); and potentially, by…”
Bhansali, R. S., Long, J. S., Pölönen, P., Isobe, T., Wang, S., Zhang, S., Geng, Z., Tausif, A., Antopia, M. C., Aboreden, N. G., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.06.29.733236
Self-citationIntracellular iron homeostasis-regulated epigenetic reprogramming contributes to −7/del(7q) leukemia
Zheng, J., Peng, Y., Deng, X., Zhang, L., Wang, Z., Chen, X., Li, H., Li, Y., Zhang, Q., Zheng, L., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-75292-2
Metadata
- Authors
- Xu, J., Song, F., Lyu, H., Kobayashi, M., Zhang, B., Zhao, Z., Hou, Y., Wang, X., Luan, Y., Jia, B., Stasiak, L., Wong, J. H.-Y., Wang, Q., Jin, Q., Jin, Q., Fu, Y., Yang, H., Hardison, R. C., Dovat, S., Platanias, L. C., Diao, Y., Yang, Y., Yamada, T., Viny, A. D., Levine, R. L., Claxton, D., Broach, J. R., Zheng, H., & Yue, F.
- Affiliations
- Northwestern University (US)
- Penn State Cancer Institute (US)
- Pennsylvania State University (US)
- Duke University (US)
- Columbia University Irving Medical Center (US)
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Zheng, Hong
- Yue, Feng
- ORCID
- Xu, Jie
- Song, Fan
- Lyu, Huijue
- Kobayashi, Mikoto
- Zhang, Baozhen
- Hou, Ye
- Wang, Xiaotao
- Luan, Yu
- Wong, Josiah Hiu-yuen
- Wang, Qixuan
- Jin, Qi
- Jin, Qiushi
- Fu, Yihao
- Yang, Hongbo
- Hardison, Ross C.
- Dovat, Sinisa
- Platanias, Leonidas C.
- Diao, Yarui
- Yang, Yue
- Yamada, Tomoko
- Viny, Aaron D.
- Levine, Ross L.
- Claxton, David
- Broach, James. R.
- Zheng, Hong
- Yue, Feng
- Venue
- Nature
- Published
- 2022-10-26
- Volume
- 611
- Issue
- 7935
- Pages
- 387-398
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC10060167
- OpenAlex
- W4307659092
- Semantic Scholar
- 132618fe8c2b6c087d9eae40298458947550ac3b
- Cited by
- 208
- References
- 78
- Citations by year
- 2026: 38 · 2025: 61 · 2024: 68 · 2023: 40 · 2022: 1
- FWCI
- 31.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Damon Runyon Cancer Research Foundation (DRG 117-15, P30 CA008748)
- Memorial Sloan-Kettering Cancer Center (CA008748, P30 CA008748, NIH P30CA008748)
- Edward P. Evans Foundation
- National Institutes of Health (CA008748, NIH P30 CA008748)
- National Institute on Drug Abuse (U01DA053691)
- National Human Genome Research Institute (R01HG011207, R01HG009906)
- National Cancer Institute (NIH P30 CA008748, R01CA213912, CA008748, U54CA143869, U01CA200060, R01CA216421, K08CA215317, P30CA008748, R35CA197594, P30CA014236)
- National Institute of General Medical Sciences (R35GM124820)
- National Institute of Diabetes and Digestive and Kidney Diseases (R24DK106766)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- acute myeloid leukemia, 3D genome organization, chromatin looping, A/B compartments, topologically associating domains, enhancer hijacking, CTCF binding, DNA methylation, DNMT1, DNMT3A, DNMT3B, hypomethylating agents, leukemia subtypes, CRISPR interference, CRISPR screen, cancer therapy targets
- MeSH terms
- CCCTC-Binding Factor, Chromatin, DNA (Cytosine-5-)-Methyltransferases, Enhancer Elements, Genetic, Humans, Promoter Regions, Genetic, Sulfites, Reproducibility of Results, Leukemia, Myeloid, Acute, Genome, Human, Gene Expression Regulation, Leukemic, Sequence Analysis, DNA Methylation, Gene Silencing, CRISPR-Cas Systems
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
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