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The promyelocytic leukemia PML protein fuels immune suppression in triple-negative breast cancer

ABSTRACT: Tumors evade immune surveillance through diverse mechanisms that include modelling of the tumor microenvironment (TME) and impaired antigen presentation. Here, we identify the stress response protein PML as a key driver of immune evasion in triple-negative breast cancer (TNBC)

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ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Roberta Noberini

LAB HEAD: Tiziana Bonaldi

PROVIDER: PXD063630 | Pride | 2026-06-04

REPOSITORIES: Pride

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			Action	DRS
	QEP230126_CG_RB_ChIP_BP_R1_A.raw	Raw
	QEP230126_CG_RB_ChIP_BP_R1_B.raw	Raw
	QEP230126_CG_RB_ChIP_BP_R1_C.raw	Raw
	QEP230126_CG_RB_ChIP_BP_R1_D.raw	Raw
	QEP230126_CG_RB_ChIP_BP_R1_E.raw	Raw

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Monitoring post-translational modifications and associated proteomes of WT-PML-V and two mutants from acute promyelocytic leukaemia patients refractory for arsenic therapy: A216T-PML-V and L217F-PML-V

Project description:U2OS PML-/- cells were reconstituted with YFP-PML-V of three types: WT, A216T or L217F. These cell lines were used to purify YFP-PML bodies using anti-GFP nanobody beads from cells either treated or not with arsenic (1uM for 2h). Protein samples were monitored for PML post-translational modifications and associated proteomes to try to understand why people with acute promyelocytic leukaemia that is resistant to arsenic treatment have these mutations.

2025-03-27 | PXD051743 | Pride

Identifying chromatin associations with promyelocytic leukemia nuclear bodies using immunoTRAP

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2013-03-28 | E-GEOD-40554 | biostudies-arrayexpress

Chromatin modifications induced by PML-RARalpha repress critical targets in leukemogenesis as analyzed by ChIP-Chip.

Project description:A global view of PML-RAR? transcriptional functions was obtained by genome-wide binding and chromatin modification analyses, combined with genome wide expression data. Complete Abstract: The translocation t(15;17) generates the chimeric PML-RAR? transcription factor that is the initiating event of acute promyelocytic leukemia. A global view of PML-RAR? transcriptional functions was obtained by genome-wide binding and chromatin modification analyses, combined with genome wide expression data. ChIP-chip experiments identified 372 direct genomic PML-RAR? targets. A subset of these was confirmed in primary acute promyelocytic leukemia. Direct PML-RARá targets include regulators of global transcriptional programs as well as critical regulatory genes for basic cellular functions such as cell cycle control and apoptosis. PML-RAR? binding universally led to HDAC1 recruitment, loss of histone H3 acetylation, increased tri-methylation of histone H3 lysine 9 and unexpectedly increased tri-methylation of histone H3 lysine 4. The binding of PMLRAR? to target promoters and the resulting histone modifications resulted in mRNA repression of functionally relevant genes. Taken together our results reveal that the transcription factor PML-RAR? regulates key cancer related genes and pathways by inducing a repressed chromatin formation on its direct genomic target genes. Keywords: ChIP on Chip U937 transfected with an inducible PML-RAR?/empty vecor were induced, harvested and Chromatin-Ips for PML, AcH3 followed by microarray hybridasation were carried out. For detailed procedures see Hoemme et al. "Chromatin modifications induced by PML-RARalpha repress critical targets in leukemogenesis as analyzed by ChIP-Chip"

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Proteomic screening identifies HNRNPA2B1 as a novel factor that controls Epstein-Barr virus reactivation through chromatin regulation

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2026-05-01 | PXD074669 | Pride

Transcription profiling of human normal bone marrow CD34+ cells, promyelocytes, and neutrophils and PR9 cell line PML-RARA induction time series

Project description:To better understand the pathogenesis of acute promyelocytic leukemia (APL, FAB M3 AML), we identified genes that are expressed differently in APL cells compared to other acute myeloid leukemia subtypes, and to normal promyelocytes. Comparative gene expression analysis of 14 M3, 62 other AML (M0, M1, M2 and M4) and 5 enriched normal promyelocyte samples revealed a signature of 1,121 genes that are specifically dysregulated in M3 samples relative to other AML, and that do not simply represent normal promyelocyte expression (â??M3-specific signatureâ??). We used a novel, high throughput digital platform (Nanostring's nCounter system) to evaluate a subset of the most significantly dysregulated genes in 30 AML samples; 33 of 37 evaluable gene expression patterns were validated. In an additional analysis, we selected only genes that are dysregulated in M3 both compared to other AML subtypes, and to purified normal CD34+ cells, promyelocytes, and/or neutrophils, thereby isolating a 478 gene "composite M3 dysregulome". Surprisingly, the expression of only a few of these genes was significantly altered in PR-9 cells after PML-RARA induction, suggesting that most of these genes are not direct targets of PML-RARA. Comparison of the M3-specific signature to our previously described murine APL dysregulome revealed 33 commonly dysregulated genes, including JUN, EGR1, and TNF. Collectively, these results suggest that PML-RARA initiates a transcriptional cascade which generates a unique downstream expression signature in both primary human and mouse APL cells. Experiment Overall Design: 14 human APL/M3 AML samples were compared to 62 AML samples of other AML FAB subtypes (bone marrow aspirates collected at diagnosis, included in GSE10358), to fractionated cells from normal human bone marrow aspirates (5 CD34+ cells, 5 promyelocytes, 5 neutrophils/PMNs), and to PR9 cells before and after Zinc-induction of PML-RARA.

2008-10-26 | E-GEOD-12662 | biostudies-arrayexpress

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