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STAT3 and lymphoma are reported together in 5 articles.
Gene
STAT3
- HGNC
- HGNC:11364
206articles
206mentions
4variants with confirmed gene link
Most co-reported phenotypes (articles)
breast cancer 25hepatocellular carcinoma 13lung cancer 13colorectal cancer 12diabetes mellitus 12autism spectrum disorder 11ulcerative colitis 9neurodevelopmental disorder 8
Reported variants (articles · ClinVar status)
Phenotype
Lymphoma
428articles
428mentions
12co-reported genes shown
Most co-reported genes (articles)
Counts are literature co-mentions in SaudiVarKB, not clinical or causal assertions. Gene details: HGNC; variant status: ClinVar via dbSNP.
Publications
5 records shown · first 60Expression of Bruton's Tyrosine Kinase Reflects Immune Cells Infiltration and Cell Proliferation in Breast Cancer.
PMID 41822319 | PMCID PMC12978404 | DOI 10.14740/wjon2708 · World journal of oncology · 2026 · 4 validated mentions
Evidence preview
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| gene | STAT3 | “Notably, BTK-high tumors showed robust enrichment of immune pathways (interferon gamma (IFN-γ) response, interleukin-6 (IL-6)/Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3), tumor necrosis factor-α (TNF-α) signaling) and exhibited elevated tumor-infiltrating leukocyte and lymphocyte fractions, increased cytolytic activity, and greater abundance of myeloid and lymphoid cell populations.” | 0.98 | hgnc_dict_v1 |
| phenotype | lymphoma | “BTK inhibitors are approved and in clinical use for hematological cancers such as lymphoma and leukemia, with testing underway in solid tumors.” | 0.98 | phenotype_alias_lexicon_v2 |
| phenotype | breast cancer | “Expression of Bruton's Tyrosine Kinase Reflects Immune Cells Infiltration and Cell Proliferation in Breast Cancer.” | 0.98 | phenotype_alias_lexicon_v2 |
| phenotype | leukemia | “BTK inhibitors are approved and in clinical use for hematological cancers such as lymphoma and leukemia, with testing underway in solid tumors.” | 0.98 | phenotype_alias_lexicon_v2 |
Gut-derived Endotoxin-TLR4 Signaling Drives MYC-Ig Translocation to Promote Lymphoproliferation through c-JUN and STAT3 Activation.
PMID 36287175 | PMCID PMC9898117 | DOI 10.1158/1541-7786.MCR-19-1209 · Molecular cancer research : MCR · 2023 · 6 validated mentions
Evidence preview
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| gene | STAT3 | “Gut-derived Endotoxin-TLR4 Signaling Drives MYC-Ig Translocation to Promote Lymphoproliferation through c-JUN and STAT3 Activation.” | 0.98 | hgnc_dict_v1 |
| phenotype | lymphoma | “UNLABELLED: Synergism between obesity and virus infection promotes the development of B-cell lymphoma.” | 0.98 | phenotype_alias_lexicon_v2 |
| gene | TLR4 | “TLR4 activation in turn caused c-JUN-dependent and STAT3-dependent translocations of MYC loci to suppress transactivation of CD95/FAS.” | 0.98 | hgnc_dict_v1 |
| gene | MYC | “TLR4 activation in turn caused c-JUN-dependent and STAT3-dependent translocations of MYC loci to suppress transactivation of CD95/FAS.” | 0.98 | hgnc_dict_v1 |
Whole Exome Sequencing reveals NOTCH1 mutations in anaplastic large cell lymphoma and points to Notch both as a key pathway and a potential therapeutic target.
PMID 32327503 | PMCID PMC8168516 | DOI 10.3324/haematol.2019.238766 · Haematologica · 2021 · 5 validated mentions
Evidence preview
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| gene | STAT3 | “Furthermore, we demonstrate that NPM-ALK promotes NOTCH1 expression through binding of STAT3 upstream of NOTCH1.” | 0.98 | hgnc_dict_v1 |
| phenotype | lymphoma | “Whole Exome Sequencing reveals NOTCH1 mutations in anaplastic large cell lymphoma and points to Notch both as a key pathway and a potential therapeutic target.” | 0.98 | phenotype_alias_lexicon_v2 |
| gene | NOTCH1 | “Whole Exome Sequencing reveals NOTCH1 mutations in anaplastic large cell lymphoma and points to Notch both as a key pathway and a potential therapeutic target.” | 0.98 | hgnc_dict_v1 |
| gene | ALK | “To understand disease pathology and to uncover novel targets for therapy, Whole-Exome Sequencing (WES) of Anaplastic Lymphoma Kinase (ALK)+ ALCL was performed as well as Gene-Set Enrichment Analysis.” | 0.98 | hgnc_dict_v1 |
Evodiamine Mitigates Cellular Growth and Promotes Apoptosis by Targeting the c-Met Pathway in Prostate Cancer Cells.
PMID 32183146 | PMCID PMC7144730 | DOI 10.3390/molecules25061320 · Molecules (Basel, Switzerland) · 2020 · 3 validated mentions
Evidence preview
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| gene | STAT3 | “We investigated the ability of EVO to affect hepatocyte growth factor (HGF)-induced c-Met/Src/STAT3 activation cascades in castration-resistant prostate cancer (CRPC).” | 0.98 | hgnc_dict_v1 |
| phenotype | lymphoma | “Then, we noted that EVO arrested the cell cycle, caused apoptosis, and downregulated the expression of various carcinogenic markers such as B-cell lymphoma 2 (Bcl-2), B-cell lymphoma-extra large (Bcl-xL), cyclin D1, cyclooxygenase 2 (COX-2), survivin, vascular endothelial growth factor (VEGF), and matrix metallopeptidases 9 (MMP-9).” | 0.98 | phenotype_alias_lexicon_v2 |
| phenotype | prostate cancer | “Evodiamine Mitigates Cellular Growth and Promotes Apoptosis by Targeting the c-Met Pathway in Prostate Cancer Cells.” | 0.98 | phenotype_alias_lexicon_v2 |
Hepato-protective effect of rutin via IL-6/STAT3 pathway in CCl4-induced hepatotoxicity in rats.
PMID 26062544 | PMCID PMC4477598 | DOI 10.1186/s40659-015-0022-y · Biological research · 2015 · 4 validated mentions
Evidence preview
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| gene | STAT3 | “Hepato-protective effect of rutin via IL-6/STAT3 pathway in CCl4-induced hepatotoxicity in rats.” | 0.98 | hgnc_dict_v1 |
| phenotype | lymphoma | “Expression of the following genes were monitored with real-time PCR: interleukin-6 (IL-6), dual-specificity protein kinase 5 (MEK5), Fas-associated death domain protein (FADD), epidermal growth factor (EGF), signal transducer and activator of transcription 3 (STAT3), Janus kinase (JAK), B-cell lymphoma 2 (Bcl2) and B-cell lymphoma-extra-large (Bcl-XL).” | 0.98 | phenotype_alias_lexicon_v2 |
| gene | FADD | “Expression of the following genes were monitored with real-time PCR: interleukin-6 (IL-6), dual-specificity protein kinase 5 (MEK5), Fas-associated death domain protein (FADD), epidermal growth factor (EGF), signal transducer and activator of transcription 3 (STAT3), Janus kinase (JAK), B-cell lymphoma 2 (Bcl2) and B-cell lymphoma-extra-large (Bcl-XL).” | 0.98 | hgnc_dict_v1 |
| gene | EGF | “Expression of the following genes were monitored with real-time PCR: interleukin-6 (IL-6), dual-specificity protein kinase 5 (MEK5), Fas-associated death domain protein (FADD), epidermal growth factor (EGF), signal transducer and activator of transcription 3 (STAT3), Janus kinase (JAK), B-cell lymphoma 2 (Bcl2) and B-cell lymphoma-extra-large (Bcl-XL).” | 0.98 | hgnc_dict_v1 |