Dr Hugo Gallardo-Blanco, PhD - Universidad Autonoma de Nuevo Leon - Researcher

Dr Hugo Gallardo-Blanco

PhD

Universidad Autonoma de Nuevo Leon

Researcher

Monterrey, Nuevo Leon | Mexico

Main Specialties: Biology

Additional Specialties: Molecular biology, Genomic, GWAS, Molecular genetic, Diabetes, Cancer, Obesity

ORCID logohttps://orcid.org/0000-0002-7816-4967


Top Author

Dr Hugo Gallardo-Blanco, PhD - Universidad Autonoma de Nuevo Leon - Researcher

Dr Hugo Gallardo-Blanco

PhD

Introduction

Contributions in Research and Academics:
From 2013, 14 articles published in journals indexed in JCR and PubMed, with an impact factor greater than 1.0.

Evaluator of proposals:
"ConTex: Call for Collaborative Research Scholarships from the University of Texas-CONACYT System for Fiscal Year 18 (2017-2018)".
"Proposals of the Call for Projects of Scientific Development to Address National Problems (2017)".

He participated as Reviewer in prestigious journals and indexed in JCR: "International Journal of Dermatology," "Experimental and Therapeutic Medicine," "Clinical Genetics," and "Gaceta Medica de México."

Currently collaborates in four approved projects in Obesity, Cancer, and Diabetes. These projects have allowed continuity to the research line of metabolic disorders associated with cancer, as well as articles, lectures, and presentations. In these projects has participated in the direction, planning and experimental design, data analysis, bioinformatic analysis, biostatistics, bibliography, scientific writing and preparation of manuscripts.

Thanks to the dissemination of their experience through publications, other researchers have requested their advice for the analysis, data management and design of experiments.
Primary Affiliation: Universidad Autonoma de Nuevo Leon - Monterrey, Nuevo Leon , Mexico

Primary Affiliation: Universidad Autonoma de Nuevo Leon - Monterrey, Nuevo Leon , Mexico

Specialties:

Additional Specialties:

Research Interests:


View Dr Hugo Gallardo-Blanco’s Resume / CV

Education

Dec 2005
Universidad Autonoma de Nuevo Leon
Doctor in Sciences
Biotechnology
Mar 1998
Universidad Autonoma de Nuevo Leon
Master in Sciences
Molecular Biology and Genetic Engineering
Jun 1995
Universidad Autonoma de Nuevo Leon
Biologist
Aug 1989 - Jul 1993
Universidad Autónoma de Nuevo León Facultad de Ciencias Biológicas
Biologo

Experience

Jan 2019
SNI Level 1 (2019-2022)
Member
CONACYT
Oct 2018
Professor
Professor
UANL
Jan 2016
SNI Level 1 (2016-2018)
MEMBER
CONACYT
Sep 2006
Universidad Autónoma de Nuevo León Facultad de Medicina
Researcher and Professor
Genetica

Publications

31Publications

697Reads

261Profile Views

19PubMed Central Citations

Data set and results of regression analysis of gene variants in Prostate Cancer patients from Mexico-mestizo population.

Zenodo

Genotyping assays were performed using TaqMan SNP Genotyping Assays probes C_27532228_20 and C_2362601_10 (Life Technologies, Carlsbad, CA, USA). Thermalcycler: StepOnePlus™ Real-Time PCR (Thermo Fisher Scientific, Waltham, MA, USA). Sample: genomic DNA from blood. Subjects: Prostate cancer patients and controls (healthy and benign prostatic hyperplasia). Results of Regression Anlysis for clinical features of gene SRD5A2 variants (rs9282858 and rs523349) in prostate cancer patients from Mexican-mestizo population. Starting with the full model, successive models are created, each one using one less regressor (or covariate) than the previous model. Each of the regressors currently in the model is removed to create a "trial" model excluding that regressor. The p-value of the current model (or full model) versus the trial model (or reduced model) is calculated, and the model with the smallest p-value is used as the next model. This method removes the least significant variable from the current model. If every p-value is smaller than the p-value cut off specified, the backward elimination method stops. The method also stops if all variables have been removed from the model, or if all variables left are included in the original reduced model. From the standpoint of further analysis, the final model becomes the "full model" for this set of potential regressors Ethics approval and consent to participate in the study: The protocol and informed consent were approved by the Ethics and Research Committee of the School of Medicine (Universidad Autonoma de Nuevo Leon), with registration number UR16-00007. In the data set, no data was included that compromises the confidentiality of the participating subjetcs.

 

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July 2020

Database for Gene Variants and Metabolic Networks Implicated in Familial Gastroschisis

Data

Gastroschisis is one of the most prevalent human birth defects concerning the ventral body wall development. Recent research has given a better understanding of gastroschisis pathogenesis through the identification of multiple novel pathogenetic pathways implicated in ventral body wall closure. Deciphering the underlying genetic factors segregating among familial gastroschisis allows better detection of novel susceptibility variants than the screening of pooled unrelated cases and controls, whereas bioinformatic-aided analysis can help to address new insights into human biology and molecular mechanisms involved in gastroschisis. Technological advances in DNA sequencing (Next Generation Sequencing), computing power, and machine learning techniques provide opportunities to the scientific communities to assess significant gaps in research and clinical practice. Thus, in an effort to study the role of gene variation in gastroschisis, we employed whole exome sequencing in a Mexican family with recurrence for gastroschisis. Stringent bioinformatic analyses were implemented to identify and predict pathogenetic networks comprised of potential gastroschisis predispositions. This is the first database for gene variants and metabolic networks implicated in familial gastroschisis. The dataset provides information on gastroschisis annotated genes, gene variants, and metabolic networks and constitutes a useful source to enhance further investigations in gastroschisis.

http://dx.doi.org/10.3390/data4030097

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July 2019
10 Reads

Dataset of Pedigree, genotypes, clinical and biochemical characteristics of families of Northeastern Mexico

Zenodo

This dataset combines pedigree, genotypes, clinical and biochemical data of 37 families of Northeastern Mexico. Primary reference is the article: Gallardo‑Blanco, H.L., Villarreal‑Perez, J.Z., Cerda‑Flores, R.M., Figueroa, A., Sanchez‑Dominguez, C.N., Gutierrez‑Valverde, J.M. ... Martinez‑Garza, L.E. (2017). Genetic variants in KCNJ11, TCF7L2 and HNF4A are associated with type 2 diabetes, BMI and dyslipidemia in families of Northeastern Mexico: A pilot study. Experimental and Therapeutic Medicine, 13, 523-529. https://doi.org/10.3892/etm.2016.3990 If you use these data please cite the corresponding manuscript, which can be downloaded here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5348709/ https://www.spandidos-publications.com/10.3892/etm.2016.3990 This dataset contains genotypes for the following SNPs: rs2986742 rs4846051 rs1801131 rs1801133 rs6541030 rs12130799 rs11208654 rs1137100 rs12405556 rs3118378 rs3737576 rs10923931 rs7554936 rs3737787 rs2516839 rs1040404 rs4670767 rs7578597 rs13400937 rs10496971 rs2627037 rs1801262 rs1569175 rs2975760 rs3792267 rs10510228 rs1801282 rs3856806 rs4955316 rs9809104 rs4607103 rs6548616 rs734873 rs5400 rs2030763 rs4402960 rs1513181 rs9291090 rs10010131 rs10007810 rs385194 rs1799883 rs2504853 rs7754840 rs7745461 rs1800750 rs1800629 rs361525 rs12200998 rs2397060 rs192655 rs1044498 rs4463276 rs731257 rs864745 rs32314 rs2330442 rs4717865 rs3173798 rs10954737 rs854555 rs3917542 rs662 rs705308 rs3943253 rs751141 rs1471939 rs12544346 rs13266634 rs7844723 rs2242103 rs1408801 rs10811661 rs10511828 rs12779790 rs3793791 rs4746136 rs1111875 rs10885390 rs11196175 rs7903146 rs10885406 rs12255372 rs290487 rs4918842 rs2237892 rs10839880 rs1837606 rs5210 rs5218 rs5219 rs2946788 rs11227699 rs7930460 rs1800849 rs1387153 rs948028 rs2270031 rs2416791 rs7961581 rs2070586 rs1503767 rs2269793 rs8050136 rs818386 rs2966849 rs1879488 rs757210 rs2033111 rs11652805 rs10512572 rs2125345 rs12946618 rs12946115 rs12950541 rs1885088 rs3907047 rs2071023 rs2833479 rs2833483 rs2300386 rs2835370 rs1296819 rs1892848 rs4821004

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May 2019
8 Reads

Dataset for genes and gene variants from familial gastroschisis

Zenodo

The dataset consists of records from whole exome sequecing and bioinformatic analysis which includes genes and gene variants from a Mexican family with recurrence for gastroschisis (two affected half-sisters with gastroschisis, mother, and father of the proband). Release of this dataset was based on the Human Genome annotation, GRCh37/hg19. The full list of tables is described in the file READ ME and remain available in csv files.

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May 2019
10 Reads

A clinical-pathogenetic approach on associated anomalies and chromosomal defects supports novel candidate critical regions and genes for gastroschisis.

Pediatr Surg Int 2018 Sep 9;34(9):931-943. Epub 2018 Aug 9.

Departamento de Genética, Facultad de Medicina y Hospital Universitario José Eleuterio González, Universidad Autónoma de Nuevo León, Ave. Madero y Gonzalitos S/N Col. Mitras Centro, CP 64460, Monterrey, Nuevo León, México.

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http://dx.doi.org/10.1007/s00383-018-4331-4DOI Listing
September 2018
135 Reads
1.061 Impact Factor

Nanoparticles for death‑induced gene therapy in cancer (Review).

Mol Med Rep 2018 Jan 15;17(1):1413-1420. Epub 2017 Nov 15.

Department of Biochemistry and Molecular Medicine, Faculty of Medicine, Universidad Autonoma de Nuevo Leon, Monterrey, Nuevo Leon 64460, Mexico.

Due to the high toxicity and side effects of the use of traditional chemotherapy in cancer, scientists are working on the development of alternative therapeutic technologies. An example of this is the use of death?induced gene therapy. This therapy consists of the killing of tumor cells via transfection with plasmid DNA (pDNA) that contains a gene which produces a protein that results in the apoptosis of cancerous cells. The cell death is caused by the direct activation of apoptosis (apoptosis?induced gene therapy) or by the protein toxic effects (toxin?induced gene therapy). The introduction of pDNA into the tumor cells has been a challenge for the development of this therapy. The most recent implementation of gene vectors is the use of polymeric or inorganic nanoparticles, which have biological and physicochemical properties (shape, size, surface charge, water interaction and biodegradation rate) that allow them to carry the pDNA into the tumor cell. Furthermore, nanoparticles may be functionalized with specific molecules for the recognition of molecular markers on the surface of tumor cells. The binding between the nanoparticle and the tumor cell induces specific endocytosis, avoiding toxicity in healthy cells. Currently, there are no clinical protocols approved for the use of nanoparticles in death?induced gene therapy. There are still various challenges in the design of the perfect transfection vector, however nanoparticles have been demonstrated to be a suitable candidate. This review describes the role of nanoparticles used for pDNA transfection and key aspects for their use in death?induced gene therapy.

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http://dx.doi.org/10.3892/mmr.2017.8091DOI Listing
January 2018
13 Reads
1 Citation
1.484 Impact Factor

Candidate gene polymorphisms and risk of psoriasis: A pilot study.

Exp Ther Med 2016 Apr 9;11(4):1217-1222. Epub 2016 Feb 9.

Department of Genetics, University Hospital 'Dr. José Eleuterio González', Monterrey, Nuevo León 64460, México.

Psoriasis is a complex genetic disease, which has previously been associated with numerous single nucleotide polymorphisms (SNPs) that are implicated in various processes, including skin barrier functions and in the regulation of inflammatory and immune responses. The present study aimed to investigate the genotypic and allelic frequencies of 32 SNPs at 24 genetic loci, and their association with psoriasis in a Mexican population. These SNPs, which were associated with psoriasis in previous studies, included the following genes: Major histocompatibility complex class I-C (), interleukin ()-, , , , tumor necrosis factor ()-?, ring finger protein-114 (), cyclin-dependent kinase 5 regulatory subunit-associated protein 1-like 1, late cornified envelope 3B/3C, signal transducer and activator of transcription 4, , interferon induced with helicase C domain 1, , TNF-?-induced protein 3 (), interacting protein 1, endoplasmic reticulum aminopeptidase 1, TNF receptor-associated factor interacting protein 2, , nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha, F-box and leucine-rich repeat protein 19, nitric oxide synthase 2, cluster of differentiation 40, nuclear receptor coactivator 5, and metallopeptidase domain 33. A total of 32 male and 14 female subjects with a clinical diagnosis of chronic plaque psoriasis, as well as 103 control subjects, were analyzed. Molecular analyses were performed using TaqMan® assays in a TaqMan® OpenArray® Genotyping system. Results were analyzed using the Golden Helix SNP and Variation Suite 7 program. Of the 32 SNPs, six were associated with an increased risk of developing psoriasis, including: rs10484554 [allele T: odds ratio (OR) 3.51], rs3212227 (allele T: OR 1.88), IL-12B rs3213094 (allele C: OR 1.94), HLA complex group 27 rs1265181 (allele C: OR 2.83), annexin A6 rs17728338 (allele A: OR 2.41), and rs6125829 (allele G: OR 1.98). Fisher's exact test detected statistical significance; however, following false discovery rate and Bonferroni correction, this association was no longer significant (threshold for genome-wide significance, P<1.56×10). SNPs that were associated with an increased risk of psoriasis in the present study have previously been associated with psoriasis in European, American, and Asian populations. In order to establish genome-wide significance, future studies must analyze a greater sample size. To the best of our knowledge, the present pilot study is the first to investigate the association between these 32 SNPs and psoriasis in a Mexican Mestizo population.

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http://dx.doi.org/10.3892/etm.2016.3066DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4812537PMC
April 2016
26 Reads
8 Citations
1.410 Impact Factor

A pharmacogenetic pilot study reveals MTHFR, DRD3, and MDR1 polymorphisms as biomarker candidates for slow atorvastatin metabolizers.

BMC Cancer 2016 Feb 8;16:74. Epub 2016 Feb 8.

Departamento de Bioquímica y Medicina Molecular, Facultad de Medicina, Universidad Autónoma de Nuevo León, Monterrey, NL, México.

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http://dx.doi.org/10.1186/s12885-016-2062-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4746878PMC
February 2016
54 Reads
4 Citations
3.362 Impact Factor

Assessment of biochemical parameters and characterization of TNFα -308G/A and PTPN22 +1858C/T gene polymorphisms in the risk of obesity in adolescents.

Salinas-Santander MA, León-Cachón RB, Cepeda-Nieto AC, Sánchez-Domínguez CN, González-Zavala MA, Gallardo-Blanco HL, Esparza-González SC, González-Madrazo MÁ, Biomedical reports, 2016, vol. 4, no. 1, pp. 107-111

http://europepmc.org/abstract/med/26870345

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January 2016
20 Reads

The tumor necrosis factor α (-308 A/G) polymorphism is associated with cystic fibrosis in Mexican patients.

PLoS One 2014 6;9(3):e90945. Epub 2014 Mar 6.

Departamento de Bioquimica y Medicina Molecular, Facultad de Medicina, Universidad Autonoma de Nuevo Leon, Monterrey, Nuevo Leon, Mexico; Centro de Investigacion y Desarrollo en Ciencias de la Salud, Universidad Autonoma de Nuevo Leon, Monterrey, Nuevo Leon, Mexico.

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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0090945PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3946307PMC
February 2015
35 Reads
3.234 Impact Factor

Detection of Turner Syndrome by Quantitative PCR of SHOX and VAMP7 Genes.

Ibarra-Ramírez M, Zamudio-Osuna MJ, Campos-Acevedo LD, Gallardo-Blanco HL, Cerda-Flores RM, Rodríguez-Sánchez IP, Martínez-de-Villarreal LE, Genetic testing and molecular biomarkers, 2015, vol. 19, no. 2, pp. 88-92

http://europepmc.org/abstract/med/25535777

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February 2015
24 Reads

A pharmacogenetic pilot study reveals MTHFR, DRD3, and MDR1 polymorphisms as biomarker candidates for slow atorvastatin metabolizers.

León-Cachón RB, Ascacio-Martínez JA, Gamino-Peña ME, Cerda-Flores RM, Meester I, Gallardo-Blanco HL, Gómez-Silva M, Piñeyro-Garza E, Barrera-Saldaña HA, BMC cancer, 2015, vol. 16, no. 1, pp. 74

http://europepmc.org/abstract/med/26857559

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January 2015
21 Reads

An investigation into the MMP1 gene promoter region polymorphism--1607 2G with recessive dystrophic epidermolysis bullosa disease severity in northeastern Mexican patients.

Int J Dermatol 2014 Aug 5;53(8):985-90. Epub 2014 Jun 5.

Department of Dermatology, Universidad Autónoma de Nuevo León, Hospital Universitario "Jose E. González", Monterrey, Mexico.

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http://dx.doi.org/10.1111/ijd.12499DOI Listing
August 2014
65 Reads
1 Citation
1.230 Impact Factor

Nanoparticles vs cancer: a multifuncional tool.

Curr Top Med Chem 2014 Mar;14(5):664-75

Centro de investigacion en Materiales Avanzados, S. C. (CIMAV), Unidad Monterrey, Mexico.

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http://dx.doi.org/10.2174/1568026614666140118213316DOI Listing
March 2014
18 Reads
3 Citations
3.402 Impact Factor

Nanoparticles vs Cancer: A Multifuncional Tool.

Sanchez-Dominguez CN, Gallardo-Blanco HL, Rodriguez-Rodriguez AA, Vela-Gonzalez AV, Sanchez-Dominguez M, Current topics in medicinal chemistry, 2014, vol. 14, no. 5, pp. 664-675

http://europepmc.org/abstract/med/24444160

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March 2014
8 Reads

The Tumor Necrosis Factor α (-308 A/G) Polymorphism Is Associated with Cystic Fibrosis in Mexican Patients.

Sanchez-Dominguez CN, Reyes-Lopez MA, Bustamante A, Cerda-Flores RM, Villalobos-Torres Mdel C, Gallardo-Blanco HL, Rojas-Martinez A, Martinez-Rodriguez HG, Barrera-Saldaña HA, Ortiz-Lopez R, PloS one, 2014, vol. 9, no. 3, pp. e90945

http://europepmc.org/abstract/med/24603877

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January 2014
16 Reads

Following

Ricardo M Cerda-Flores
Ricardo M Cerda-Flores

Centro de Investigación Biomédica del Noreste

Hugo A Barrera-Saldana
Hugo A Barrera-Saldana

University of California

Minerva Gomez-Flores
Minerva Gomez-Flores

Colonia Mitras Centro

Augusto Rojas-Martinez
Augusto Rojas-Martinez

School of Medicine / Tecnológico de Monterrey

Andres Figueroa
Andres Figueroa

University of California

Andrew P South
Andrew P South

St John's Institute of Dermatology