# SOCS1

Source: https://onco.cc/targets/socs1/  
OnCo record `socs1` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

SOCS1 (Suppressor of cytokine signalling 1) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Diffuse large B-cell lymphoma and Rectal cancer.

## Summary

Essential negative regulator of type I and type II interferon (IFN) signalling, as well as that of other cytokines, including IL2, IL4, IL6 and leukaemia inhibitory factor (LIF). Down-regulates cytokine signalling by inhibiting the JAK/STAT signalling pathway. Acts by binding to JAK proteins and to IFNGR1 and inhibiting their kinase activity.

CIViC holds 1 clinical evidence item and 0 assertions across 1 variant. Open Targets scores its association with cancer at 0.49 (direct and indirect evidence; datatypes literature 0.99, animal model 0.51, genetic association 0.04, somatic mutation 0.74). IntOGen calls it a driver in 5 cohorts (3 activating, 2 loss-of-function), covering Diffuse Large B-Cell Lymphoma, NOS, Malignant Lymphoma, Non-Hodgkin Lymphoma, Rectal Adenocarcinoma.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: suppressor of cytokine signaling 1; Suppressor of cytokine signaling 1; SOCS-1; SSI-1; TIP3; Cish1
- Tags: cancer-genes-wave
- Symbol: SOCS1
- Class: oncogene
- Biology: Essential negative regulator of type I and type II interferon (IFN) signalling, as well as that of other cytokines, including IL2, IL4, IL6 and leukaemia inhibitory factor (LIF). Down-regulates cytokine signalling by inhibiting the JAK/STAT signalling pathway. Acts by binding to JAK proteins and to IFNGR1 and inhibiting their kinase activity. In vitro, suppresses Tec protein-tyrosine activity. Regulates IFN-gamma (IFNG)-mediated sensory neuron survival. Probable substrate recognition component of an ECS (Elongin BC-CUL2/5-SOCS-box protein) E3 ubiquitin ligase complex which mediates the ubiquitination and subsequent proteasomal degradation of target proteins. Location: Nucleus; Cytoplasmic vesicle (UniProt). Locus 16p13.13 (HGNC).
- Where found: Non-Hodgkin lymphoma: Open Targets association 0.68 with non-Hodgkin lymphoma (MONDO_0018908); IntOGen driver in 2 cohorts (MLYM, NHL); Diffuse large B-cell lymphoma: Open Targets association 0.63 with diffuse large B-cell lymphoma (MONDO_0018905); CIViC evidence names this disease; Rectal cancer: IntOGen driver in 1 cohort (READ)

## 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: IntOGen calls it an activating (Act) driver in 3 cohorts; IntOGen calls it a loss-of-function (LoF) driver in 2 cohorts; CIViC holds 1 clinical evidence items on its variants. Evidence tier "clinical-evidence" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.
- Lymphoma, JAK-STAT, in NK/T-cell lymphoma and in Hodgkin lymphoma: STAT3 and STAT5B mutations lock the transcription factor in its phosphorylated form. The STAT5B N642H substitution increases the binding affinity of the phosphotyrosine for the mutant histidine, so the phosphorylated protein persists and binds its target sites far more, and the growth advantage it gives can be partly reversed by a JAK1/2 inhibitor in the laboratory (Kucuk 2015). In Hodgkin lymphoma and primary mediastinal B-cell lymphoma the pathway is switched on from the other end, by amplification of JAK2 inside the 9p24.1 amplicon and by loss of the brakes SOCS1 and PTPN1. Frequency: Activating STAT3 and STAT5B mutations across 51 NK/T-cell lymphomas and 43 gamma-delta T-cell lymphomas, with STAT5B N642H particularly frequent in the gamma-delta group (Kucuk 2015). JAK2 sits in the 9p24.1 amplicon in Hodgkin lymphoma and mediastinal large B-cell lymphoma, and its amplification raises both protein and activity and specifically induces PD-1 ligand transcription (Green 2010). What it changes about treatment: Not through an approved drug. JAK inhibitors have been tested in both settings without becoming standard; the practical consequence of the Hodgkin and mediastinal finding is that it explains why checkpoint blockade works there.

## Sources

- HGNC HGNC:19383: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:19383
- UniProt O15524: https://www.uniprot.org/uniprotkb/O15524/entry
- NCBI Gene 8651: https://www.ncbi.nlm.nih.gov/gene/8651
- Ensembl ENSG00000185338: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000185338
- Kucuk et al., Nat Commun 2015: activating STAT3 and STAT5B mutations in lymphomas derived from NK or gamma-delta T cells: https://doi.org/10.1038/ncomms7025
- Green et al., Blood 2010: selective 9p24.1 amplification and PD-1 ligand induction through JAK2 in Hodgkin lymphoma and mediastinal large B-cell lymphoma: https://doi.org/10.1182/blood-2010-05-282780

## 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: [Diffuse large B-cell lymphoma](https://onco.cc/cancers/dlbcl/), [Hodgkin lymphoma](https://onco.cc/cancers/hodgkin-lymphoma/), [Non-Hodgkin lymphoma (all types)](https://onco.cc/cancers/non-hodgkin-lymphoma/), [Primary mediastinal (thymic) large B-cell lymphoma](https://onco.cc/cancers/primary-mediastinal-b-cell-lymphoma/), [Rectal cancer](https://onco.cc/cancers/rectal-cancer/)
- pathways: [JAK-STAT signalling](https://onco.cc/pathways/jak-stat/)

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JSON: https://onco.cc/api/v1/entities/socs1.json