KLHDC8B

gene
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Also known as MGC35097

Summary

KLHDC8B (kelch domain containing 8B, HGNC:28557) is a protein-coding gene on chromosome 3p21.31, encoding Kelch domain-containing protein 8B (Q8IXV7). Involved in pinching off the separated nuclei at the cleavage furrow and in cytokinesis.

This gene encodes a protein which forms a distinct beta-propeller protein structure of kelch domains allowing for protein-protein interactions. Mutations in this gene have been associated with Hodgkin lymphoma.

Source: NCBI Gene 200942 — RefSeq curated summary.

At a glance

  • Gene–disease (curated): classic Hodgkin lymphoma (Limited, GenCC)
  • GWAS associations: 14
  • Clinical variants (ClinVar): 192 total
  • Phenotypes (HPO): 4
  • MANE Select transcript: NM_173546

Identifiers

Gene identifiers

FieldValue
HGNC IDHGNC:28557
Approved symbolKLHDC8B
Namekelch domain containing 8B
Location3p21.31
Locus typegene with protein product
StatusApproved
AliasesMGC35097
Ensembl geneENSG00000185909
Ensembl biotypeprotein_coding
OMIM613169
Entrez200942

Gene structure

Transcript identifiers

Ensembl transcripts: 14 — 10 protein_coding, 3 protein_coding_CDS_not_defined, 1 retained_intron

ENST00000332780, ENST00000459846, ENST00000462582, ENST00000471811, ENST00000476495, ENST00000904821, ENST00000904822, ENST00000948545, ENST00000948546, ENST00000948547, ENST00000948548, ENST00000948549, ENST00000948550, ENST00000948551

RefSeq mRNA: 1 — MANE Select: NM_173546 NM_173546

CCDS: CCDS2791

Canonical transcript exons

ENST00000332780 — 6 exons

ExonStartEnd
ENSE000012988394917506249175163
ENSE000013321724917560549176486
ENSE000019045984917159849171685
ENSE000027244554917263649173145
ENSE000035184314917423949174403
ENSE000036857184917474249174966

Expression profiles

Bgee: expression breadth ubiquitous, 247 present calls, max score 98.78.

FANTOM5 (CAGE): breadth ubiquitous, TPM avg 12.6739 / max 280.1762, expressed in 1588 samples.

FANTOM5 promoters (2 alternative TSS)

Promoter IDTPM avgSamples expressed
3661611.22861541
366151.4453947

Top tissues by expression

253 total, by Bgee expression score (0-100, higher = more expressed):

TissueAnatomy IDExpression scoreQuality
right adrenal gland cortexUBERON:003582798.78gold quality
left adrenal gland cortexUBERON:003582598.77gold quality
adrenal cortexUBERON:000123598.69gold quality
adrenal tissueUBERON:001830398.66gold quality
right adrenal glandUBERON:000123398.64gold quality
left adrenal glandUBERON:000123498.63gold quality
apex of heartUBERON:000209898.24gold quality
left ventricle myocardiumUBERON:000656698.15gold quality
left ovaryUBERON:000211998.00gold quality
adrenal glandUBERON:000236997.96gold quality
right ovaryUBERON:000211897.61gold quality
cardiac muscle of right atriumUBERON:000337997.55gold quality
heart left ventricleUBERON:000208497.13gold quality
cardiac ventricleUBERON:000208297.05gold quality
lower esophagus mucosaUBERON:003583496.64gold quality
lower esophagusUBERON:001347396.58gold quality
lower esophagus muscularis layerUBERON:003583396.58gold quality
muscle layer of sigmoid colonUBERON:003580596.38gold quality
esophagogastric junction muscularis propriaUBERON:003584196.03gold quality
myocardiumUBERON:000234995.71gold quality
heartUBERON:000094895.57gold quality
ovaryUBERON:000099295.46gold quality
right lobe of thyroid glandUBERON:000111994.81gold quality
heart right ventricleUBERON:000208094.81gold quality
right atrium auricular regionUBERON:000663194.80gold quality
cardiac atriumUBERON:000208194.79gold quality
tibialis anteriorUBERON:000138594.78silver quality
esophagusUBERON:000104394.76gold quality
left lobe of thyroid glandUBERON:000112094.65gold quality
mucosa of stomachUBERON:000119994.50gold quality

Single-cell (SCXA)

Detected in 4 experiment(s), a significant marker in 3.

ExperimentMarker?Max mean expression
E-HCAD-10yes37.92
E-GEOD-93593yes6.60
E-ANND-3yes2.90
E-MTAB-10137no426.44

Regulation

Is transcription factor: no

miRNA regulators (miRDB)

67 targeting KLHDC8B, top 30 by miRDB confidence (max_score; target_count = how many genes the miRNA targets in total — lower means more specific):

miRNAMax scoreAvg scoremiRNA target_count
HSA-MIR-6758-5P100.0066.211470
HSA-MIR-6856-5P100.0065.471298
HSA-MIR-432-3P100.0067.86705
HSA-MIR-4476100.0068.182030
HSA-MIR-6876-5P100.0067.682126
HSA-MIR-450099.9972.722367
HSA-MIR-34A-5P99.9971.211784
HSA-MIR-449A99.9971.051776
HSA-LET-7A-5P99.9872.291790
HSA-LET-7B-5P99.9872.311790
HSA-LET-7C-5P99.9872.291790
HSA-LET-7E-5P99.9872.291790
HSA-LET-7F-5P99.9872.561784
HSA-LET-7G-5P99.9872.371784
HSA-LET-7I-5P99.9872.371788
HSA-MIR-98-5P99.9872.331787
HSA-LET-7D-5P99.9671.761632
HSA-MIR-445899.9671.641650
HSA-MIR-3605-5P99.9667.12932
HSA-MIR-6755-5P99.9565.59464
HSA-MIR-22-3P99.9368.13917
HSA-MIR-3682-5P99.9367.971163
HSA-MIR-497-5P99.9271.832674
HSA-MIR-15A-5P99.9072.802787
HSA-MIR-15B-5P99.9072.782798
HSA-MIR-16-5P99.9072.802780
HSA-MIR-195-5P99.9072.812805
HSA-MIR-6499-3P99.9066.381212
HSA-MIR-6838-5P99.8971.942690
HSA-MIR-424-5P99.8971.902641

Literature-anchored findings (GeneRIF, showing 3)

  • Depletion of KLHDC8B through RNA interference leads to an increase in binucleated cells, implicating its reduced expression in the formation of classical Hodgkin lymphoma’s signature Reed-Sternberg cell. (PMID:19706467)
  • Deficiency of KLHDC8B leads to binucleated cells, implicating its involvement in Reed-Sternberg cell formation (PMID:20107318)
  • kelch protein KLHDC8B guards against mitotic errors, centrosomal amplification, and chromosomal instability (PMID:22988245)

Cross-species orthologs

2 orthologs

OrganismSymbolGene ID
mus_musculusKlhdc8bENSMUSG00000032609
rattus_norvegicusKlhdc8bENSRNOG00000047867

Paralogs (54): KLHL13 (ENSG00000003096), KLHL20 (ENSG00000076321), KEAP1 (ENSG00000079999), KLHL42 (ENSG00000087448), KLHL22 (ENSG00000099910), KLHL4 (ENSG00000102271), KLHL2 (ENSG00000109466), KLHL5 (ENSG00000109790), BACH2 (ENSG00000112182), KLHL18 (ENSG00000114648), KLHL24 (ENSG00000114796), IVNS1ABP (ENSG00000116679), KLHL12 (ENSG00000117153), KLHL29 (ENSG00000119771), KBTBD7 (ENSG00000120696), KLHL7 (ENSG00000122550), KLHL31 (ENSG00000124743), KLHDC7B (ENSG00000130487), KLHL36 (ENSG00000135686), KLHL8 (ENSG00000145332), KLHL3 (ENSG00000146021), KLHL35 (ENSG00000149243), KLHL1 (ENSG00000150361), BACH1 (ENSG00000156273), KLHL40 (ENSG00000157119), KLHL10 (ENSG00000161594), KLHL21 (ENSG00000162413), KLHDC8A (ENSG00000162873), KBTBD8 (ENSG00000163376), KBTBD6 (ENSG00000165572), KLHL26 (ENSG00000167487), KLHL30 (ENSG00000168427), KBTBD2 (ENSG00000170852), KLHL6 (ENSG00000172578), KLHL15 (ENSG00000174010), KLHL38 (ENSG00000175946), KBTBD11 (ENSG00000176595), KLHDC7A (ENSG00000179023), KLHL28 (ENSG00000179454), KBTBD3 (ENSG00000182359)

Protein

Protein identifiers

Kelch domain-containing protein 8BQ8IXV7 (reviewed: Q8IXV7)

All UniProt accessions (1): Q8IXV7

UniProt curated annotations — full annotation on UniProt →

Function. Involved in pinching off the separated nuclei at the cleavage furrow and in cytokinesis. Required for mitotic integrity and maintenance of chromosomal stability. Protects cells against mitotic errors, centrosomal amplification, micronucleus formation and aneuploidy. Plays a key role of midbody function involving abscission of the daughter cells during cytokinesis and appropriate chromosomal and nuclear segregation into the daughter cells.

Subcellular location. Cytoplasm. Midbody.

Disease relevance. Lymphoma, Hodgkin, classic (CHL) [MIM:236000] A malignant disease characterized by progressive enlargement of the lymph nodes, spleen and general lymphoid tissue, and the presence of large, usually multinucleate, cells (Reed-Sternberg cells). Reed-Sternberg cells compose only 1-2% of the total tumor cell mass. The remainder is composed of a variety of reactive, mixed inflammatory cells consisting of lymphocytes, plasma cells, neutrophils, eosinophils and histiocytes. Disease susceptibility is associated with variants affecting the gene represented in this entry. A variant in the 5’-UTR of KLHDC8B, responsible for decreasing its expression, is associated with classic Hodgkin lymphoma and segregates with the disease in some families. A chromosomal aberration disrupting KLHDC8B has been found in a family with the nodular sclerosis type of Hodgkin lymphoma. Translocation t(2,3)(q11.2;p21.31).

RefSeq proteins (1): NP_775817* (*=MANE)

Domains & families (InterPro)

IDNameType
IPR006652Kelch_1Repeat
IPR015915Kelch-typ_b-propellerHomologous_superfamily
IPR051746Kelch_domain_containing_8Family

Pfam: PF01344, PF24681

UniProt features (9 total): repeat 8, chain 1

Structure

Experimental structures (PDB)

0 structures.

Predicted structure (AlphaFold)

ModelpLDDTFraction very-high
AF-Q8IXV7-F194.790.92

Function

Pathways and Gene Ontology

Reactome pathways

0 pathways

MSigDB gene sets: 115 (showing top): GOBP_MITOTIC_CYTOKINESIS, MEF2_02, GOBP_CYTOKINETIC_PROCESS, GGCNKCCATNK_UNKNOWN, GOBP_ORGANELLE_FISSION, GOBP_CYTOKINESIS, NF1_Q6_01, KINSEY_TARGETS_OF_EWSR1_FLII_FUSION_DN, GOBP_MITOTIC_NUCLEAR_DIVISION, GOBP_MITOTIC_CELL_CYCLE, GATA4_Q3, CTAWWWATA_RSRFC4_Q2, RODRIGUES_THYROID_CARCINOMA_POORLY_DIFFERENTIATED_DN, GOBP_NUCLEAR_CHROMOSOME_SEGREGATION, GOBP_CYTOSKELETON_DEPENDENT_CYTOKINESIS

GO Biological Process (4): nuclear chromosome segregation (GO:0098813), mitotic nuclear division (GO:0140014), mitotic cytokinetic process (GO:1902410), cell division (GO:0051301)

GO Molecular Function (1): protein binding (GO:0005515)

GO Cellular Component (5): cytoplasm (GO:0005737), cytosol (GO:0005829), midbody (GO:0030496), intercellular bridge (GO:0045171), cellularization cleavage furrow (GO:0110070)

GO top-level categories

Rollup of top GO terms by namespace:

CategoryTerms
cellular anatomical structure4
mitotic cell cycle2
mitotic cell cycle process2
chromosome segregation1
nuclear division1
mitotic cytokinesis1
cytokinetic process1
cellular process1
binding1
intracellular anatomical structure1
cytoplasm1
plasma membrane region1

Protein interactions and networks

STRING

526 interactions, top by confidence (×1000):

Protein AProtein BPartner UniProtScore
KLHDC8BBCL11AQ9H165648
KLHDC8BCBFA2T3O75081647
KLHDC8BPRR35P0CG20597
KLHDC8BFAM133AQ8N9E0536
KLHDC8BRRP36Q96EU6532
KLHDC8BSPMIP7A4D263517
KLHDC8BTRAPPC6BQ86SZ2500
KLHDC8BTIGD3Q6B0B8499
KLHDC8BCSF1P09603495
KLHDC8BTOGARAM1Q9Y4F4492
KLHDC8BKCNG3Q8TAE7477
KLHDC8BKBTBD12Q3ZCT8473
KLHDC8BSIPA1L2Q9P2F8472
KLHDC8BAKR1C3P42330470
KLHDC8BCSF1RP07333468

IntAct

28 interactions, top by confidence:

ABTypeScore
CCT2TXNDC9psi-mi:“MI:0914”(association)0.730
PDCL3PEX7psi-mi:“MI:0914”(association)0.640
CCT3TXNDC9psi-mi:“MI:0914”(association)0.640
CCT5TXNDC9psi-mi:“MI:0914”(association)0.640
CCT7TXNDC9psi-mi:“MI:0914”(association)0.640
IMPDH1BCAT2psi-mi:“MI:0914”(association)0.530
CCT7PEX7psi-mi:“MI:0914”(association)0.530
ZNRD2CCDC85Cpsi-mi:“MI:0914”(association)0.530
Dlg4KLHDC8Bpsi-mi:“MI:0407”(direct interaction)0.440
CCT3C6orf11psi-mi:“MI:0914”(association)0.350
CCT7C6orf11psi-mi:“MI:0914”(association)0.350
IMPDH1LCMT2psi-mi:“MI:0914”(association)0.350
CCT2WDR91psi-mi:“MI:0914”(association)0.350
NANOS1CNOT1psi-mi:“MI:0914”(association)0.350
CCT5TUBAL3psi-mi:“MI:0914”(association)0.350
CCT3TUBAL3psi-mi:“MI:0914”(association)0.350
CCT7WDR46psi-mi:“MI:0914”(association)0.350
SHOXPBX1psi-mi:“MI:0914”(association)0.350
PDCL3POTEFpsi-mi:“MI:0914”(association)0.350
CAMK2DPPM1Dpsi-mi:“MI:0914”(association)0.350
CD226TMED7-TICAM2psi-mi:“MI:0914”(association)0.350
DNAJA2ENC1psi-mi:“MI:0914”(association)0.350

BioGRID (11): KLHDC8B (Affinity Capture-MS), KLHDC8B (Affinity Capture-MS), KLHDC8B (Affinity Capture-MS), KLHDC8B (Affinity Capture-MS), KLHDC8B (Affinity Capture-MS), KLHDC8B (Affinity Capture-MS), KLHDC8B (Affinity Capture-MS), KLHDC8B (Affinity Capture-MS), KLHDC8B (Affinity Capture-MS), KLHDC8B (Affinity Capture-MS), KLHDC8B (Affinity Capture-MS)

ESM2 similar proteins: D4A2K4, O70277, O75382, O95294, P49593, P57775, Q08DS0, Q0D2K2, Q12788, Q2KJJ5, Q2TBI8, Q3U410, Q3USL1, Q4G0W2, Q501J2, Q5BK60, Q5E9V5, Q5RCW7, Q5RJL2, Q5SUV1, Q5U2W5, Q5XIA9, Q5ZJ37, Q6PF15, Q6RFH5, Q8BGY4, Q8BNV1, Q8BSF5, Q8C3F7, Q8C4J7, Q8IXV7, Q8IYD2, Q8IZ69, Q8K1S1, Q8N135, Q8NEP7, Q8WU66, Q91XA8, Q96AZ1, Q96I51

Diamond homologs: Q5E9V5, Q5RCW7, Q5XIA9, Q8IXV7, Q8IYD2, Q8N239, Q91XA8, Q9D2D9, O14682, Q0WW40, Q4KLM4, Q6DFF7, Q8R2P1, Q9H0H3, Q0D2A9, Q6NRH0

SIGNOR signaling

0 interactions.

Enriched among interaction partners

Reactome pathways and GO biological processes over-represented among this gene’s 28 IntAct physical interaction partners (hypergeometric vs the genome-wide background, BH-FDR, gene-set size 15–500, ranked by fold). A functional readout of the neighbourhood — distinct from this gene’s own memberships above, and biased toward well-studied / hub proteins, so read it as themes rather than proof.

Reactome pathways:

PathwayPartnersFoldFDR
Formation of tubulin folding intermediates by CCT/TriC5124.4×3e-08
Cooperation of Prefoldin and TriC/CCT in actin and tubulin folding5120.0×3e-08
Chaperonin-mediated protein folding588.4×8e-08
Protein folding576.3×1e-07

GO biological processes:

GO termPartnersFoldFDR
protein folding520.7×1e-04
protein stabilization513.4×8e-04

Disease & clinical

Clinical variants and AI predictions

ClinVar

192 variants total. Per-class counts are floors (≥ shown; pagination cap):

ClassificationCount (floor)
Pathogenic0
Likely pathogenic0
Uncertain significance114
Likely benign61
Benign4

Top pathogenic / likely-pathogenic (0)

SpliceAI

649 predictions. Top by Δscore:

VariantEffectΔscore
3:49171682:GCGG:Gdonor_gain1.0000
3:49172780:G:GTdonor_gain1.0000
3:49174237:A:AGacceptor_gain1.0000
3:49174237:AGAT:Aacceptor_gain1.0000
3:49174238:G:GGacceptor_gain1.0000
3:49174238:GATG:Gacceptor_gain1.0000
3:49174962:GCATG:Gdonor_gain1.0000
3:49174966:GGTGA:Gdonor_loss1.0000
3:49174967:G:Tdonor_loss1.0000
3:49174968:T:Adonor_loss1.0000
3:49175099:GGA:Gdonor_gain1.0000
3:49171681:GGCGG:Gdonor_gain0.9900
3:49171682:GCGGG:Gdonor_gain0.9900
3:49171683:CGGGT:Cdonor_loss0.9900
3:49171684:GG:Gdonor_gain0.9900
3:49171684:GGGT:Gdonor_loss0.9900
3:49171685:GG:Gdonor_gain0.9900
3:49171685:GGTGA:Gdonor_loss0.9900
3:49171686:G:GGdonor_gain0.9900
3:49171687:T:Gdonor_loss0.9900
3:49174234:TGCAG:Tacceptor_loss0.9900
3:49174235:GCA:Gacceptor_loss0.9900
3:49174236:CA:Cacceptor_loss0.9900
3:49174238:G:Aacceptor_loss0.9900
3:49174238:GAT:Gacceptor_gain0.9900
3:49174967:G:GGdonor_gain0.9900
3:49175060:AG:Aacceptor_gain0.9900
3:49175061:GG:Gacceptor_gain0.9900
3:49171714:G:Tdonor_gain0.9800
3:49172631:TCCA:Tacceptor_loss0.9800

AlphaMissense

2265 scored. Top likely-pathogenic:

VariantProtein changeam_pathogenicity
3:49174804:T:AW202R0.998
3:49174804:T:CW202R0.998
3:49174806:G:CW202C0.998
3:49174806:G:TW202C0.998
3:49174840:T:CF214L0.998
3:49174842:T:AF214L0.998
3:49174842:T:GF214L0.998
3:49174930:T:CF244L0.997
3:49174932:T:AF244L0.997
3:49174932:T:GF244L0.997
3:49175108:G:CR271S0.997
3:49175108:G:TR271S0.997
3:49175154:G:TG287W0.997
3:49175155:G:AG287E0.997
3:49175663:G:CW309C0.997
3:49175663:G:TW309C0.997
3:49173090:G:CW107C0.996
3:49173090:G:TW107C0.996
3:49174876:A:CS226R0.996
3:49174878:C:AS226R0.996
3:49174878:C:GS226R0.996
3:49174883:G:AG228D0.996
3:49174931:T:CF244S0.996
3:49175661:T:AW309R0.996
3:49175661:T:CW309R0.996
3:49174840:T:AF214I0.995
3:49174883:G:TG228V0.995
3:49174886:G:AG229D0.995
3:49175067:T:AW258R0.995
3:49175067:T:CW258R0.995

dbSNP variants (sampled 300 via entrez): RS1000172589 (3:49176504 T>G), RS1000315059 (3:49171639 G>A), RS1000620034 (3:49174220 A>G), RS1000667106 (3:49171874 C>A,T), RS1000690219 (3:49176203 G>A), RS1002826752 (3:49170001 G>A), RS1003064599 (3:49176744 G>A,T), RS1003123054 (3:49173761 G>T), RS1003455186 (3:49172057 G>A), RS1003660451 (3:49175288 C>T), RS1004244169 (3:49175359 C>T), RS1005659224 (3:49176912 C>A), RS1005936169 (3:49176275 G>A), RS1006529222 (3:49169644 C>T), RS1006571788 (3:49170551 T>C)

Disease associations

OMIM: gene MIM:613169 | disease phenotypes: MIM:236000

GenCC curated gene-disease

DiseaseClassificationInheritance
classic Hodgkin lymphomaLimitedAutosomal dominant

Mondo (1): classic Hodgkin lymphoma (MONDO:0009348)

Orphanet (1): Classic Hodgkin lymphoma (Orphanet:391)

HPO phenotypes

4 total (4 of 4 shown, HPO-id order):

HPOTerm
HP:0000007Autosomal recessive inheritance
HP:0003347Impaired lymphocyte transformation with phytohemagglutinin
HP:0003459Polyclonal elevation of IgM
HP:0012189Hodgkin lymphoma

GWAS associations

14 associations (top):

StudyTraitp-value
GCST000880_30Menarche (age at onset)3.000000e-08
GCST003818_48Resting heart rate3.000000e-13
GCST004131_23Inflammatory bowel disease1.000000e-33
GCST004132_17Crohn’s disease3.000000e-23
GCST004133_11Ulcerative colitis8.000000e-20
GCST007387_40Insomnia symptoms (never/rarely vs. sometimes/usually)5.000000e-09
GCST007388_28Insomnia symptoms (never/rarely vs. usually)2.000000e-09
GCST008840_1Depressive symptom (depressed mood) (binary trait)8.000000e-10
GCST010698_80Subcortical volume (min-P)3.000000e-24
GCST010699_110Brain morphology (min-P)4.000000e-08
GCST010701_52Cortical surface area (MOSTest)1.000000e-16
GCST010702_36Subcortical volume (MOSTest)1.000000e-10
GCST010703_262Brain morphology (MOSTest)2.000000e-13
GCST90020024_1147A body shape index2.000000e-08

EFO canonical traits (5, from GWAS)

EFO IDTrait name
EFO:0004703age at menarche
EFO:0007876insomnia measurement
EFO:0007006depressive symptom measurement
EFO:0004346neuroimaging measurement
EFO:0007789BMI-adjusted waist circumference

Drugs & pharmacology

Drug and pharmacology data

Is drug target: no

PharmGKB: 1 entry (VIP=true, CPIC=false)

CTD chemical–gene interactions

33 total (human), top 30 by PubMed support.

ChemicalActions (top 5)PubMed papers
Valproic Acidaffects cotreatment, decreases expression, affects expression, increases expression5
Benzo(a)pyreneincreases expression, decreases expression, decreases methylation4
Cadmium Chloridedecreases expression, increases abundance, increases expression3
Air Pollutantsincreases abundance, decreases expression2
Estradiolaffects cotreatment, decreases expression2
Nickeldecreases expression2
Cyclosporinedecreases expression2
Particulate Matterdecreases expression, increases abundance2
aristolochic acid Iincreases expression1
methylmercuric chloridedecreases expression1
triphenyl phosphateaffects expression1
bisphenol Adecreases expression, increases methylation1
trichostatin Adecreases expression1
sodium arseniteincreases expression1
S-(1,2-dichlorovinyl)cysteineaffects response to substance, increases expression, affects cotreatment, decreases expression1
beta-methylcholineaffects expression1
CGP 52608affects binding, increases reaction1
4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamideaffects cotreatment, decreases expression1
dorsomorphinaffects cotreatment, decreases expression1
Decitabineaffects expression1
Cadmiumincreases abundance, increases expression1
Cisplatinaffects expression1
Dichlorodiphenyl Dichloroethylenedecreases expression1
Doxorubicinincreases expression1
Lipopolysaccharidesdecreases expression, affects response to substance, increases expression, affects cotreatment1
Methyl Methanesulfonateincreases expression1
Niclosamideincreases expression1
Smokedecreases expression1
Tobacco Smoke Pollutionincreases expression1
Triclosandecreases expression1

Clinical trials (associated diseases)

101 trials via MONDO — disease-level, not drug-specific.

TrialPhaseStatusTitle
NCT02166463PHASE3ACTIVE_NOT_RECRUITINGBrentuximab Vedotin and Combination Chemotherapy in Treating Children and Young Adults With Stage IIB, Stage IIIB, IVA, or IVB Hodgkin Lymphoma
NCT02661503PHASE3ACTIVE_NOT_RECRUITINGHD21 for Advanced Stages
NCT02684708PHASE3COMPLETEDSecond International Inter-Group Study for Classical Hodgkin Lymphoma in Children and Adolescents
NCT03907488PHASE3ACTIVE_NOT_RECRUITINGImmunotherapy (Nivolumab or Brentuximab Vedotin) Plus Combination Chemotherapy in Treating Patients With Newly Diagnosed Stage III-IV Classic Hodgkin Lymphoma
NCT04342936PHASE3UNKNOWNStudy of Camrelizumab (SHR-1210) vs. Chemotherapy in Participants With Relapsed or Refractory Classical Hodgkin Lymphoma
NCT04486391PHASE3TERMINATEDTislelizumab Monotherapy Versus Salvage Chemotherapy for Relapsed/Refractory Classical Hodgkin Lymphoma
NCT05518318PHASE3UNKNOWNGLS-010 Monotherapy Versus Chemotherapy in Patients With Relapsed or Refractory Classical Hodgkin’s Lymphoma (R/R cHL)
NCT05711628PHASE3WITHDRAWNA Trial Comparing Chemotherapy Versus Novel Immune Checkpoint Inhibitor (Pembrolizumab) Plus Chemotherapy in Treating Relapsed/Refractory Classical Hodgkin Lymphoma
NCT06465446PHASE3NOT_YET_RECRUITINGA Study of IMM01 Plus Tiselizumab Versus Physician’s Choice Chemotherapy in PD(L)1-refractory Classical Hodgkin Lymphoma
NCT00654732PHASE2COMPLETEDCombination Chemotherapy With or Without Rituximab in Treating Participants With Stage III-IV Classic Hodgkin Lymphoma
NCT00742027PHASE2COMPLETEDPhase II Study of Oral Panobinostat in Adult Participants With Relapsed/Refractory Classical Hodgkin’s Lymphoma
NCT00967369PHASE2COMPLETEDCombination Chemotherapy With or Without Bortezomib in Treating Patients With Classical Hodgkin Lymphoma That Has Returned or Does Not Respond to Prior Treatment.
NCT02164500PHASE2COMPLETEDJAK-inhibition in Recurrent Classical Hodgkin Lymphoma
NCT02414568PHASE2COMPLETEDBendamustine Study in Classical Hodgkin Lymphoma Patients Over 60 Treated by Prednisone, Vinblastine and Doxorubicin
NCT02758717PHASE2ACTIVE_NOT_RECRUITINGNivolumab and Brentuximab Vedotin in Treating Older Patients With Untreated Hodgkin Lymphoma
NCT02824029PHASE2COMPLETEDIbrutinib in Treating Patients With Relapsed or Refractory Classical Hodgkin Lymphoma
NCT02940301PHASE2ACTIVE_NOT_RECRUITINGIbrutinib and Nivolumab in Treating Patients With Relapsed or Refractory Classical Hodgkin Lymphoma
NCT03004833PHASE2COMPLETEDNivolumab and AVD in Early-stage Unfavorable Classical Hodgkin Lymphoma
NCT03057795PHASE2ACTIVE_NOT_RECRUITINGNivolumab & Brentuximab Vedotin Consolidation After Autologous SCT in Patients With High-Risk Classical Hodgkin Lymphoma
NCT03209973PHASE2COMPLETEDA Study of Tislelizumab as Monotherapy in Relapsed or Refractory Classical Hodgkin Lymphoma
NCT03226249PHASE2UNKNOWNPET-Directed Therapy With Pembrolizumab and Combination Chemotherapy in Treating Patients With Previously Untreated Classical Hodgkin Lymphoma
NCT03233347PHASE2ACTIVE_NOT_RECRUITINGDoxorubicin, Vinblastine, Dacarbazine, Brentuximab Vedotin, and Nivolumab in Treating Patients With Stage I-II Hodgkin Lymphoma
NCT03480334PHASE2ACTIVE_NOT_RECRUITINGAbscopal Effect of Radiotherapy and Nivolumab in Relapsed Hodgkin Lymphoma After Anti-PD1 Therapy
NCT03527628PHASE2UNKNOWNOPTmizing Advanced Stage HodgkIn LymphoMa patIentS Therapy
NCT03580564PHASE2COMPLETEDAn Open, Multicenter Phase II Study to Evaluate the Safety and Efficacy of KL-A167 Injection in Relapsed or Refractory Classical Hodgkin’s Lymphoma
NCT03652441PHASE2COMPLETEDConsolidation Therapy With Brentuximab Vedotin After Allogeneic Stem Cell Transplantation for Relapsed or Refractory Hodgkin Lymphoma
NCT03655483PHASE2UNKNOWNStudy of GLS-010 Injection in the Treatment of Classical Hodgkin’s Lymphoma
NCT03712202PHASE2ACTIVE_NOT_RECRUITINGBrentuximab Vedotin and Nivolumab in Treating Patients With Early Stage Classic Hodgkin Lymphoma
NCT04067037PHASE2ACTIVE_NOT_RECRUITINGCamrelizumab Combined With AVD in the First-line Treatment for Patients With Advanced Classical Hodgkin’s Lymphoma
NCT04318080PHASE2COMPLETEDTislelizumab in Participants With Relapsed or Refractory Classical Hodgkin Lymphoma
NCT04510636PHASE2RECRUITINGStudy of Pembrolizumab With Bendamustine in Hodgkin Lymphoma
NCT04624984PHASE2UNKNOWNPD-1 Inhibitor or PD-1 Inhibitor Plus GVD for Relapsed/Refractory CHL
NCT04788043PHASE2ACTIVE_NOT_RECRUITINGStudy of Magrolimab and Pembrolizumab in Relapsed or Refractory Classic Hodgkin Lymphoma
NCT04837859PHASE2RECRUITINGPhase II Trial of Individualized Immunotherapy in Early-Stage Unfavorable Classical Hodgkin Lymphoma
NCT04838652PHASE2RECRUITINGPembrolizumab in Combination With Salvage Chemotherapy for First-relapsed or Refractory Classical Hodgkin Lymphoma
NCT05008224PHASE2COMPLETEDStudy of Safety and Efficacy of Pembrolizumab and Chemotherapy in Participants With Newly Diagnosed Classical Hodgkin Lymphoma (cHL) (MK-3475-C11/KEYNOTE-C11)
NCT05039073PHASE2RECRUITINGBrentuximab Vedotin and Nivolumab for the Treatment of Relapsed/Refractory Classic Hodgkin Lymphoma Previously Treated With Brentuximab Vedotin or Checkpoint Inhibitors
NCT05179603PHASE2TERMINATEDA Study of SAR444245 With or Without Other Anticancer Therapies for the Treatment of Adults and Adolescents With Relapsed or Refractory B Cell Lymphoma (Master Protocol) [Pegathor Lymphoma 205]
NCT05404945PHASE2ACTIVE_NOT_RECRUITINGFitness-adapted, Pembrolizumab-based Therapy for Untreated Classical Hodgkin Lymphoma Patients 60 Years of Age and Above
NCT05900765PHASE2RECRUITINGA Study of Zimberelimab(GLS-010) Combined With AVD for Newly Diagnosed Early-stage Hodgkin’s Lymphoma