# PML

Source: https://onco.cc/targets/pml/  
OnCo record `pml` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

PML (PML nuclear body scaffold) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a drug target, a tumour suppressor, a biomarker and a fusion partner, and an approved or late-stage drug is recorded against it. Tied to Leukaemia, Thyroid cancer, Lung cancer and 3 more.

## Summary

Functions via its association with PML-nuclear bodies (PML-NBs) in a wide range of important cellular processes, including tumour suppression, transcriptional regulation, apoptosis, senescence, DNA damage response, and viral defense mechanisms. Acts as the scaffold of PML-NBs allowing other proteins to shuttle in and out, a process which is regulated by SUMO-mediated modifications and interactions. Inhibits EIF4E-mediated mRNA nuclear export by reducing EIF4E affinity for the 5' 7-methylguanosine (m7G) cap of target mRNAs.

CIViC holds 7 clinical evidence items and 0 assertions across 6 variants, naming Tretinoin, Arsenic Trioxide and Tamibarotene. Open Targets scores its association with cancer at 0.75 (direct and indirect evidence; datatypes literature 0.99, affected pathway 0.87, genetic association 0.63, somatic mutation 0.80). IntOGen calls it a driver in 1 cohort (0 activating, 1 loss-of-function), covering Lung. In OnCo, 2 product records name it (Arsenic trioxide and Tretinoin (all-trans retinoic acid, ATRA)).

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: PML nuclear body scaffold; TRIM19; RNF71
- Tags: cancer-genes-wave
- Symbol: PML
- Class: tumor-suppressor
- Biology: Functions via its association with PML-nuclear bodies (PML-NBs) in a wide range of important cellular processes, including tumour suppression, transcriptional regulation, apoptosis, senescence, DNA damage response, and viral defense mechanisms. Acts as the scaffold of PML-NBs allowing other proteins to shuttle in and out, a process which is regulated by SUMO-mediated modifications and interactions. Inhibits EIF4E-mediated mRNA nuclear export by reducing EIF4E affinity for the 5' 7-methylguanosine (m7G) cap of target mRNAs. Isoform PML-4 has a multifaceted role in the regulation of apoptosis and growth suppression: activates RB1 and inhibits AKT1 via interactions with PP1 and PP2A phosphatases respectively, negatively affects the PI3K pathway by inhibiting MTOR and activating PTEN, and positively regulates p53/TP53 by acting at different levels (by promoting its acetylation and phosphorylation and by inhibiting its MDM2-dependent degradation). Isoform PML-4 also: acts as a transcriptional repressor of TBX2 during cellular senescence and the repression is dependent on a functional RBL2/E2F4 repressor complex, regulates double-strand break repair in gamma-irradiation-induced DNA damage responses via its interaction with WRN, acts as a negative regulator of telomerase by interacting with TERT, and regulates PER2 nuclear localisation and circadian function. Isoform PML-6 inhibits specifically the activity of the tetrameric form of PKM. Location: Nucleus; Nucleus, nucleoplasm; Cytoplasm; Nucleus, PML body (UniProt). Locus 15q24.1 (HGNC).
- Where found: Leukaemia: Open Targets association 0.58 with leukaemia (MONDO_0005059); Thyroid cancer: Open Targets association 0.57 with thyroid cancer (MONDO_0002108); Lung cancer: IntOGen driver in 1 cohort (LUNG); Skin cancer: Open Targets association 0.53 with skin cancer (MONDO_0002898); Myeloproliferative neoplasms: Open Targets association 0.52 with myeloproliferative neoplasm (MONDO_0020076); Acute promyelocytic leukaemia: CIViC evidence names this disease

## Notes

- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: CIViC lists 3 therapies; IntOGen calls it a loss-of-function (LoF) driver in 1 cohort; CIViC holds 7 clinical evidence items on its variants; UniProt disease notes describe a translocation or gene fusion involving the gene. Evidence tier "approved-drug" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.

## Sources

- HGNC HGNC:9113: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:9113
- UniProt P29590: https://www.uniprot.org/uniprotkb/P29590/entry
- NCBI Gene 5371: https://www.ncbi.nlm.nih.gov/gene/5371
- Ensembl ENSG00000140464: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000140464

## Connected records

- collections: [CIViC](https://onco.cc/collections/civic/), [IntOGen](https://onco.cc/collections/intogen/), [Open Targets Platform](https://onco.cc/collections/open-targets/)
- cancers: [Acute promyelocytic leukaemia](https://onco.cc/cancers/apl/), [Leukaemia (all types)](https://onco.cc/cancers/leukaemia/), [Lung cancer (all types)](https://onco.cc/cancers/lung-cancer/), [Myeloproliferative neoplasms (PV, ET, myelofibrosis)](https://onco.cc/cancers/myeloproliferative-neoplasms/), [Skin cancer (all types)](https://onco.cc/cancers/skin-cancer/), [Thyroid cancer](https://onco.cc/cancers/thyroid/)
- drugs: [Arsenic trioxide](https://onco.cc/drugs/arsenic-trioxide/), [Tretinoin (all-trans retinoic acid, ATRA)](https://onco.cc/drugs/tretinoin-atra/)

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JSON: https://onco.cc/api/v1/entities/pml.json