The lncRNA-DOT1L-LAMP5 axis was measured on H3K79 in MOLM-13 alone: eight human samples, one fusion, no index-fusion arm
also called GSE150483 provenance · LAMP5-AS1 cell system · lncRNA DOT1L LAMP5 axis
An entry on the lncRNA LAMP5-AS1 notes that the MLL fusions used are not named. The deposited chromatin sequencing is eight human samples from a single cell line, MOLM-13, which carries MLL-AF9 - so the H3K79 part of the story was never measured in the infant fusion.
The same thing, for a scientist
`mechanism-lamp5-as1-lncrna-activates-dot1l` carries the caveat *"The MLL fusions used are not named in the abstract"* [E1]. GEO series **GSE150483** - found in the paper's data-availability statement, not by elink - resolves the chromatin arm. Eight *Homo sapiens* samples, every one `cell type: MOLM-13`, source name *Leukemia cell line*: paired shLAMP5-AS1 and control-siRNA ChIP for **H3K79me2** and **H3K79me3** with matched inputs [E2]. MOLM-13 is KMT2A::MLLT3 and myeloid, so the axis's H3K79 evidence carries a two-axis import. The full text additionally names MV4-11, THP-1, SEM and NOD/SCID xenografts, so the paper is broader than the deposition - but **none of those appear in the H3K79 arm**, which is the arm this graph's entry is built on [E3]. The distinction matters because LAMP5 was originally described as a DOT1L-activated bodyguard for MLL fusion proteins across several fusions, and an entry that reads the H3K79 result as fusion-general is reading past the two lines of sequencing that exist.
The H3K79 arm, sample by sample
| Sample | Antibody | Transfection |
|---|---|---|
| ChIP_ShLAMP5-AS1_H3K79me2 | H3K79me2 | shLAMP5-AS1 |
| ChIP_ShNC_H3K79me2 | H3K79me2 | control siRNA |
| input_ShLAMP5-AS1_H3K79me2 | none | shLAMP5-AS1 |
| input_ShNC_H3K79me2 | none | control siRNA |
| (the same four, H3K79me3) | H3K79me3 | as above |
Eight samples, all cell type: MOLM-13, all human 2. There is one biological replicate per condition and no dose series, so the effect size behind the axis is unbounded by the deposition. That is a limit the graph's entry does not currently state.
Where the paper is broader than its deposition
The open-access full text names MV4-11 (14 mentions), THP-1 (10), SEM (10), MOLM-13 (7) and NOD/SCID (7) 3. SEM is the index fusion, so the paper does touch KMT2A::AFF1 somewhere - but not in any deposited H3K79 experiment.
This is the inverse of the AHD-inhibitor case in the sibling entry ana-unstated-system-ahd-inhibitor-resolved, where the deposition also under-reported the paper. Two of this beat's sixteen resolutions have that shape, which is why the standing phrasing of the deposited sequencing is not a formality: reading a deposition as a study roster systematically narrows a paper, and this graph's failure mode has usually been the opposite.
| script | none - GEO accession-display text endpoint plus PMC data-availability statement |
|---|---|
| status | run |
| result summary | 8 of 8 deposited H3K79 samples are human MOLM-13 (KMT2A::MLLT3, myeloid), one replicate per condition. The paper's full text also names SEM, MV4-11 and THP-1, none of which appear in the deposited H3K79 arm. Accession recoverable only from the data-availability statement, not from elink. |
inputs
[ "PMID 38374003", "GSE150483", "PMC10877858" ]
counts — the numbers behind the chart
{
"samples_total": 8,
"samples_human": 8,
"cell_lines_deposited": 1,
"cell_lines_named_in_full_text": 4,
"replicates_per_condition": 1,
"index_fusion_samples_deposited": 0
}entries affected
[ "mechanism-lamp5-as1-lncrna-activates-dot1l" ]
import axes
[ "fusion: KMT2A::MLLT3 not KMT2A::AFF1", "lineage: myeloid not B-lymphoid" ]
- An autophagy-inducing strategy aimed at degrading the fusion protein would act on normal KMT2A and on much else besides, and a single-line chromatin experiment gives no read on that selectivity.
- If LAMP5 protection is a general DOT1L-output phenomenon rather than a fusion-specific one, then blocking the axis removes a protective mechanism from normal DOT1L-high progenitors too, which is a bite-back the deposited data cannot bound.
- The one-replicate design means a combination dose chosen from this axis rests on an unreplicated H3K79 measurement in the wrong fusion.
- Does LAMP5-AS1 knockdown change H3K79me2 in SEM? The paper appears to use SEM somewhere and deposited no H3K79 data from it, so the index-fusion version of this graph's own claim is untested.
- Is the autophagy-mediated fusion degradation the paper reports partner-dependent? MLL-AF9 and MLL-AF4 have very different protein stabilities and this deposition speaks only to the former.
- E1established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.paper
The LAMP5-AS1 paper reports that blockade of the lncRNA-DOT1L-LAMP5 axis enhances autophagy and promotes degradation of MLL fusion proteins, and its abstract does not name the MLL fusions used.
Blockade of the lncRNA-DOT1L-LAMP5 axis enhances autophagy and promotes degradation of MLL fusion proteins. · Chen TQ, Huang HJ, Zhu SX, Chen XT, Pu KJ, Wang D, An Y, Lian JY, Sun YM, Chen YQ, Wang WT · Exp Hematol Oncol 2024What this evidence cannot show
Identifiers taken from the NCBI esummary record fetched on 2026-09-19. Full text read from Europe PMC PMC10877858 (open access) on the same date.
Evidence that argues against this (1)
- LAMP5 was originally characterised as a DOT1L-activated protector of MLL fusion proteins across multiple fusions, so an axis demonstrated on H3K79 in a single MLLT3 line may be a general feature of DOT1L-high leukaemia rather than a fusion-specific mechanism. Wang WT et al. 2019
- E2established confidence 5 of 5: Multiple independent lines of evidence; treated as settled in the field.dataset
GEO series GSE150483 contains eight Homo sapiens samples, all annotated 'cell type: MOLM-13' with source name 'Leukemia cell line': paired shLAMP5-AS1 and control-siRNA ChIP for H3K79me2 and H3K79me3 with matched inputs.
Blockade of the lncRNA-DOT1L-LAMP5 axis: H3K79me2 and H3K79me3 ChIP in MOLM-13 (GSE150483) · GEO submitters · NCBI Gene Expression Omnibus 2024What this evidence cannot show
Read on 2026-09-19 from the GEO accession-display text endpoint. Submitter-entered. One biological replicate per condition, no dose series and no second cell line in the deposited chromatin arm. This accession was recovered from the paper's data-availability statement in PMC; elink dbfrom=pubmed&db=gds returns no GEO link for this PMID, so an elink-only search would have recorded this source as having no deposition.
Evidence that argues against this (1)
- A single-replicate ChIP comparison cannot support an effect-size claim, and submitter-entered GEO fields give no quality metrics, so the strength of the H3K79 change behind this axis is not recoverable from the deposition at all. Rogic S et al. 2026
- E3strong confidence 4 of 5: Replicated in peer-reviewed work by more than one group.paper
The paper's open-access full text names MV4-11, THP-1, SEM, MOLM-13 and NOD/SCID xenografts, so the study spans systems including the index fusion SEM that are absent from the deposited H3K79 arm.
Blockade of the lncRNA-DOT1L-LAMP5 axis enhances autophagy and promotes degradation of MLL fusion proteins. · Chen TQ, Huang HJ, Zhu SX, Chen XT, Pu KJ, Wang D, An Y, Lian JY, Sun YM, Chen YQ, Wang WT · Exp Hematol Oncol 2024What this evidence cannot show
Counted by regular-expression tally over the flattened PMC full text on 2026-09-19 (MV4-11 14, THP1 10, SEM 10, MOLM-13 7, NOD/SCID 7, MLL-AF9 10). A mention count is not an experiment inventory: a line named in an introduction or a reagent table is counted identically to one carrying a figure, and this entry does not claim which experiments used which line.
Evidence that argues against this (1)
- Mention counts can invert the truth in either direction, and this beat found the opposite shape elsewhere - a deposition naming systems the abstract omitted - so neither the paper nor the deposition should be treated as the authoritative roster on its own. Souren NY et al. 2022
the H3K79 arm is eight MOLM-13 samples, one replicate per condition
H3K79me2 and me3 ChIP deposited only in MOLM-13
- analogous to →The AHD inhibitor's deposited arm is MOLM-13 and its in vivo arm is nowhere: a half-resolution that names the limit exactly
both depositions are narrower than their papers, omitting arms the graph cites
resolved source in the unstated-system worklist