SNPMiner Trials by Shray Alag

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SNPMiner SNPMiner Trials (Home Page)


Report for SNP rs1544410

Developed by Shray Alag, 2020.
SNP Clinical Trial Gene

There are 4 clinical trials

Clinical Trials


1 Vitamin D Supplementation Enhances Immune Response to BCG Vaccination in Infants

The purpose of this study is to determine whether a single oral dose of vitamin D given to infants prior to Bacille-Calmette-Guerin (BCG) vaccination will enhance the immune response to BCG vaccination.

NCT01288950
Conditions
  1. Tuberculosis
Interventions
  1. Dietary Supplement: Vitamin D3 (cholecalciferol)
MeSH:Tuberculosis

The investigators will also determine whether specific host genetic variants including the Fok-I(rs2228570T/C), Bsm-I(rs1544410A/G), GC(rs2282679A/C), DHCR7(rs12785878G/T) and CYP2R1 (rs10741657A/G) polymorphisms affect baseline vitamin D levels and alter the response to vitamin D supplementation.. Bacille-Calmette-Guerin (BCG) vaccine efficacy.

The investigators will determine whether specific host genetic variants including the Fok-I(rs2228570T/C), Bsm-I(rs1544410A/G), GC(rs2282679A/C), DHCR7(rs12785878G/T) and CYP2R1 (rs10741657A/G) polymorphisms affect the response to BCG vaccine in infants receiving either vitamin D or placebo.. Inclusion Criteria: - Healthy mothers > 18 years of age - Term, healthy infants eligible to receive the Bacille-Calmette- Guerin (BCG) vaccine Exclusion Criteria: - Recent maternal history of tuberculosis (within 1 year) or active tuberculosis - Known maternal human immuno-deficiency virus (HIV) infection - Maternal fever or chorio-amnionitis - Maternal use of vitamin D, steroids or immuno-regulatory medications - Household member with active tuberculosis Inclusion Criteria: - Healthy mothers > 18 years of age - Term, healthy infants eligible to receive the Bacille-Calmette- Guerin (BCG) vaccine Exclusion Criteria: - Recent maternal history of tuberculosis (within 1 year) or active tuberculosis - Known maternal human immuno-deficiency virus (HIV) infection - Maternal fever or chorio-amnionitis - Maternal use of vitamin D, steroids or immuno-regulatory medications - Household member with active tuberculosis Tuberculosis Tuberculosis In 2000, there were an estimated 884,000 cases of tuberculosis (TB) in children with many developing severe, disseminated disease.

Primary Outcomes

Description: BCG vaccine efficacy will be assessed by measuring the host immune response against BCG at 2 months, 6 months and one year after BCG immunization. A whole blood assay will be used to measure multiple cytokines and mycobacterial growth suppression.

Measure: Bacille-Calmette-Guerin (BCG) vaccine efficacy

Time: 2 months

Measure: Bacille-Calmette-Guerin (BCG) vaccine efficacy

Time: 6 months

Measure: Bacille-Calmette-Guerin (BCG) vaccine efficacy

Time: 1 year

Secondary Outcomes

Description: Serum 25 hydroxy (OH) vitamin D levels will be measured prior to vitamin D supplementation and at 2 months, 6 months and one year after BCG immunization. The investigators will also determine whether specific host genetic variants including the Fok-I(rs2228570T/C), Bsm-I(rs1544410A/G), GC(rs2282679A/C), DHCR7(rs12785878G/T) and CYP2R1 (rs10741657A/G) polymorphisms affect baseline vitamin D levels and alter the response to vitamin D supplementation.

Measure: Effect of a single dose of 50,000 IU vitamin D3 on serum vitamin D levels

Time: 2 months

Description: The investigators will determine whether specific host genetic variants including the Fok-I(rs2228570T/C), Bsm-I(rs1544410A/G), GC(rs2282679A/C), DHCR7(rs12785878G/T) and CYP2R1 (rs10741657A/G) polymorphisms affect the response to BCG vaccine in infants receiving either vitamin D or placebo.

Measure: Bacille-Calmette-Guerin (BCG) vaccine efficacy

Time: 1 year

2 Vitamin D Receptor and Megalin Gene Polymorphisms and Their Association With Obesity, Central Obesity and the Metabolic Syndrome

The link between metabolic disturbances and vitamin D receptor (VDR) and MEGALIN (or LRP2) gene polymorphisms remains unclear, particularly among African-American adults. The associations of single nucleotide polymorphisms (SNPs) for VDR [rs1544410(BsmI:G/A), rs7975232(ApaI:A/C), rs731236(TaqI:G/A)] and MEGALIN [rs3755166:G/A,rs2075252:C/T, rs2228171:C/T] genes with incident and prevalent metabolic disturbances, including obesity, central obesity and metabolic syndrome (MetS) were evaluated. From 1,024 African-Americans participating in the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS, Baltimore, MD, 2004-2013) study, 539 subjects were selected who had complete genetic data as well as covariates selected for metabolic outcomes at two consecutive examinations (visits 1 and 2) with a mean follow-up time of 4.64±0.93y. Haplotype (HAP) analyses generated polymorphism groups that were linked to incident and prevalent metabolic disturbances.

NCT03279432
Conditions
  1. Metabolic Syndrome
  2. Obesity
  3. Central Obesity
MeSH:Obesity Metabolic Syndrome Obesity, Abdominal Syndrome
HPO:Abdominal obesity Obesity Truncal obesity

The associations of single nucleotide polymorphisms (SNPs) for VDR [rs1544410(BsmI:G/A), rs7975232(ApaI:A/C), rs731236(TaqI:G/A)] and MEGALIN [rs3755166:G/A,rs2075252:C/T, rs2228171:C/T] genes with incident and prevalent metabolic disturbances, including obesity, central obesity and metabolic syndrome (MetS) were evaluated.

Primary Outcomes

Description: Obesity was defined as BMI≥30 kg/m2.

Measure: Obesity

Time: 2004-2013

Description: Central obesity was defined based on waist circumference (WC) ≥ 102 cm or 40 inches (men), ≥ 88 cm or 35 inches (women)

Measure: Central Obesity

Time: 2004-2013

Description: Participants who screened positive on at least 3 of 5 conditions ((1) central obesity (see above); (2) dyslipidemia: TAG≥1.695 mmol/L (150 mg/dl); (3) dyslipidemia: HDL-C<40 mg/dL (male), <50 mg/dL (female); (4) blood pressure≥130/85 mmHg; (5) fasting plasma glucose≥6.1 mmol/L (110 mg/dl).(39)) were classified as MetS-positive (2) Similarly, continuous annual rates of change (Δ) in metabolic outcomes were considered, specifically number of metabolic disturbances (MetD), BMI, WC, SBP, DBP, TAG, HDL-C, and Glucose. Binary incident outcomes included obesity, central obesity, MetS and other metabolic disturbance (i.e. hypertension, dyslipidemia-TAG, dyslipidemia-HDL and hyperglycemia).

Measure: Metabolic Syndrome

Time: 2004-2013

3 Vitamin D and Skin Pigmentation in Healthy Humans Exposed to UVB

Skin pigmentation (melanin) absorbs ultra violet type B (UVB) radiation found in sunlight and is believed to be responsible for darker-skinned persons' generally low 25(OH)D status. This phenomenon is found in immigrants living in Northern countries and their 25(OH)D responses to UVB-irradiation seem low. We hypothesized that objectively measured skin pigmentation and/or pigment genes influence UVB-induced 25(OH)D increase significantly in combination with other influential parameters. The influence of objectively measured constitutive and facultative skin pigmentation on UVB-induced 25(OH)D increase over time was investigated together with other possible influential parameters. These other influential parameters include sex, age, weight, height, BMI, number of fatty fish meals per week, Fitzpatrick Skin Type and 25(OH)D start level. The genetic parameters include 33 Vitamin D receptor and pigment SNPs. This is a single-centre, open and non-blinded clinical trial. No randomisation was used, as the participants were allocated into two groups based on their Fitzpatrick Skin type and ethnic origin. The light-skinned group included participants with Fitzpatrick Skin type II-IV and were of Northern origin (Denmark, the Faroe Islands and the UK). The darker-skinned included Fitzpatrick Skin Types V-VI originating from countries located at latitudes below 50 degrees N. Thus, it could be ensured that the participants represented a wide range of skin pigmentation. The light-skinned (N = 22) and the darker-skinned subjects (N = 18) were exposed to identical UVB doses on identical body areas over nine weeks with weekly measurements of 25(OH)D. The UVB-induced 25(OH)D synthesis was investigated in summer-pigmented skin with melanin throughout the epidermis and during winter when ambient UVB exposure is negligible. Demographic data (gender, age, weight, height, Fitzpatrick Skin Type, measured constitutive and facultative skin pigmentation (PPF)) was collected/measured and registered in prior to study start. The number of daily consumed fatty fish meals was recorded in a questionnaire. Serum 25(OH)D was analysed weekly.

NCT03409510
Conditions
  1. Healthy Volunteers
Interventions
  1. Radiation: UVB radiation

The influence of the vitamin D receptor gene was investigated by genotyping the two single nucleotide polymorphisms (SNP), rs1544410 (BsmI) and rs2228570 (FokI), located in the gene (ENSG00000111424, Chromosome 12q13) as previously described.

Primary Outcomes

Description: Serum 25(OH)D is a marker of vitamin D increase induced by UVB

Measure: Change in serum 25(OH)D

Time: Measured at study start and weekly over nine weeks

4 Personalization of AntiTB Treatment: Evaluation of Pharmacological Determinants of Treatment Response

The aim of the study is to investigate the possible correlation of plasma drug concentrations with Time To Positivity (TTP) in liquid culture in patients with active pulmonary multi sensitive TB in the first two weeks of treatment. Secondary aims are: the correlation between plasma drug concentrations and hepato/neuro toxicity; the impact of different allelic variants on PK data, toxicity and TTP in liquid culture; the feasibility of using dried blood/plasma spots to measure plasma concentrations of anti-TB drugs and determine genetic polymorphisms.

NCT03416309
Conditions
  1. Tuberculosis, Pulmonary
MeSH:Tuberculosis Tuberculosis, Pulmonary

Analyzed SNPs will be: ABCB1 3435C>T (rs1045642), OATP1B1 521T>C (rs4149056) e OATP1B1 85-7793T>C (rs4149032), PXR 63396C>T (rs2472677), BsmI G>A (rs1544410).

Primary Outcomes

Description: Investigate the correlation of plasma drug concentrations (Rifampicin, Isoniazid, Ethambutol and Pyrazinamide, HRZE) with the change in Time To Positivity (TTP) in liquid culture in patients with active pulmonary TB between the baseline and the first week of treatment.

Measure: Correlation between AUC of RHZE and TTP

Time: 1 week from start of treatment

Description: Investigate the correlation of plasma drug concentrations (Rifampicin, Isoniazid, Ethambutol and Pyrazinamide, HRZE) with the change in Time To Positivity (TTP) in liquid culture in patients with active pulmonary TB between the baseline and the second week of treatment.

Measure: Correlation between AUC of RHZE and TTP

Time: 2 weeks from start of treatment

Secondary Outcomes

Description: Investigate the correlation of plasma drug concentrations (Rifampicin, Isoniazid, Ethambutol and Pyrazinamide, HRZE) with hepatotoxicity (increase of AST and/or ALT) and neurotoxicity (peripheral neuropathy)

Measure: Correlation between AUC of RHZE and toxicity

Time: 1 week and 2 weeks from start of treatment

Description: Investigate the impact of different allelic variants of NAT2, SLCO1B1, ABCB1, VDR on AUC of RHZE toxicity and TTP in liquid culture

Measure: Correlation between PG and AUC of RHZE

Time: 1 week and 2 weeks from start of treatment

Description: Assess the consistency of using dried plasma spots to measure plasma concentrations of anti-TB drugs comparing to plasma samples

Measure: Assess the consistency of results using of DPS for measuring the plasma drug concentrations

Time: 1 week and 2 weeks from start of treatment

Description: A pharmacometric model will be develop to correlate pharmacokinetics (AUC of RHZE) with the anti-TB treatment response (clinical and TTP) of the standard first-line anti-TB regimen.

Measure: Correlate AUC of RHZE with antiTB response

Time: 6 months after end of treatment

Description: A pharmacometric model will be develop to correlate PG with the anti-TB treatment response (clinical and TTP) of the standard first-line anti-TB regimen.

Measure: Correlate PG with antiTB response

Time: 6 months after end of treatment


HPO Nodes


HP:0001513: Obesity
Genes 490
NR2E3 WT1 LMNA TBX3 POGZ PROK2 DCC MID2 SDCCAG8 ZNF41 RAB39B LIMK1 CNKSR2 PRPF4 PDE11A RP2 USP27X BBS10 CTNNB1 KIDINS220 FGFR3 XYLT1 PDE6B TOPORS GP1BB BBS7 GATA4 ARL2BP KCNJ11 MLXIPL HS6ST1 CEP290 GHRL EGF TAF1 PRKAR1A SEC24C PROM1 BBS12 POMC NPHP1 CARTPT C8ORF37 APOE DMD ZBTB20 BBS2 SYNE2 BLK UBE3A CCDC141 TMEM43 FTSJ1 HCFC1 FEZF1 SOX2 CACNA1S CDH23 BBS7 EMD ELN IFT172 CEL MAGEL2 TMEM67 JMJD1C UFD1 NIN ARMC5 CREBBP MKKS PDE6A BAP1 FHL1 GTF2I NEUROD1 USH2A SIN3A KIF7 RBMX PCARE CXORF56 EXOC6B MCM3AP LEP TBX1 HERC2 MED12 PDX1 OTX2 USP9X ARL6 LZTFL1 PWAR1 ADRB3 BBS9 RPE65 REEP6 RLBP1 HNF1A ERMARD TTC8 POMGNT1 INPP5E WDPCP CUL4B SAG SDCCAG8 SDC3 HESX1 KMT2A BLK RAD21 SEMA4A MOG ATP6AP2 CEP164 ARL6 BBS12 POMC MAN1B1 CTSH ALMS1 HSD11B1 NPAP1 CDHR1 RERE BLM HCRT ARNT2 FLRT3 BBS4 ROM1 SNORD116-1 ARHGEF6 ZNF711 ZNF513 GDI1 GNAS VPS13B RP1 FTO DDX6 PCNT POU3F4 TULP1 DUSP6 MC4R PNPLA6 SYP CREBBP SPATA7 LMNA GABRA3 H6PD CA4 NIPBL GNAS MKRN3 FMR1 SNORD115-1 RP9 MC3R MKS1 BBS2 PHF6 SUFU GNAS-AS1 WDR11 TSPAN7 MERTK GNAS MTTP PRPF6 NR0B2 GNAS BAP1 PRKAR1A MYT1L HNF4A RAI1 DYNC2I2 RPGR BBS9 SMARCB1 NKAP RAB23 GUCA1B LAS1L ZNF365 ALMS1 PAX6 HDAC8 ATRX TRAF3IP1 HDAC8 KIAA1549 CNNM2 PROKR2 MOG SEMA3A BBS5 PAX6 LEPR LZTFL1 SYNE1 SNRNP200 MKKS SMC1A PRMT7 CNGB1 MEGF8 CLRN1 TTC8 MAPK8IP3 TRAF7 AKT2 SETD2 IQSEC2 PCNT PPARG P2RY11 HESX1 BBS10 NDN POMC RAB23 MECP2 SOX10 PRPH2 PTCHD1 KCNJ18 BBS2 INS ACADVL LIPE KMT2D DHDDS WNT4 HLA-DQB1 MKRN3-AS1 KLF11 IDH3B TUB BBIP1 CCDC141 FRMPD4 CNGA1 ARL13B ADCY3 ACSL4 SNRPN PHF21A GNAS GNAS TBX3 STX16 ARL3 SH2B1 TUB SMO HUWE1 SHOX CYP7A1 NEK2 PRPF3 PAK3 RDH12 TCF20 USP8 IFT172 BBIP1 FGF8 ADNP IFT27 CYP19A1 ARHGEF18 RREB1 ABCA4 SLC10A7 PDGFB LRAT ARVCF PKDCC IQSEC2 MTFMT CLIP2 C8ORF37 SIM1 TBX1 BEST1 PIGT SETD5 PDSS1 EHMT1 SPG11 SCAPER ZNF408 RPS6KA3 SIM1 SH2B1 BAZ1B BRAF SLC25A4 P4HTM CEP290 C8ORF37 APPL1 UPF3B ENPP1 TRIM32 AFF4 SMARCE1 RFC2 AIP RNPC3 PRCD DHX38 UCP3 IFT172 BBS5 SLC7A14 PDE4D ATRX WT1 FAM161A ANOS1 SHANK3 IFT172 FGFR1 ZNF711 MC4R LEP DLG3 NSMF PNKP GNAS MAGEL2 RPS6KA3 KIZ SLC7A7 ADRB2 RAI1 MEGF8 AFF4 HDAC8 FXR1 GNAS CLCN4 PSMD12 PHF6 OFD1 PAX4 TRIP12 MAGEL2 GABRD EP300 TRAPPC9 SOX3 PHIP PTEN KCNAB2 WAC NDNF FGF17 ARMC5 HDAC4 SH3KBP1 IMPG2 LARS2 HACE1 ADNP AGRP LEPR PROK2 IL17RD AGBL5 USP8 TERT BPTF THOC2 PIK3CA SKI AHR TRAPPC9 CRX CRB1 PRMT7 KISS1R NF2 COMT TBX1 IMPDH1 SMAD4 BBS1 GTF2IRD1 EIF2S3 BBS1 PRPF31 PCSK1 KLHL7 DEAF1 COL10A1 AKT2 SMC3 CCDC28B CUL4B ABCC8 FLII DPYD PDE4D NRL PDE6G RBP3 MRAP2 AGTR2 VPS13B KDM6A IPW IGFALS PROKR2 MECP2 XRCC4 TRIM32 FGFR1 SPRY4 MKS1 ALG13 HGSNAT CERKL AKT1 RHO IDH3A RP1L1 EHMT1 EP300 PWRN1 IGF1 TACR3 SIN3A EYS EIF2S3 BBS4 IL1RAPL1 LAS1L IFT88 ARL6 CREBBP AHI1 CHD7 ELN CEP19 ARL6 PRPF8 SLC9A7 PCSK1 MAK SRY DNMT3A HACE1 HLA-DRB1 TTC8 TNFSF4 DYRK1B FOXP1 KIDINS220 OFD1 TBL2 BDNF RGR FSCN2 HIRA GHR NTRK2 IQSEC2 IFT74 ZNF81 XYLT1 ALB PRDM16 IFT140 IFT27 MAN1B1 ARX PDE4D SIM1 GCK IGF1R CANT1 SH2B1
Protein Mutations 3
G20210A P12A W64R