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Prasanth Sundaraganesan

Prasanth Sundaraganesan

Vellore, Vellore district

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About Prasanth Sundaraganesan:

My name is Prasanth Sundaraganesan, with a formal background of Master program in Data Analytics, Master of Science in Biotechnology, PG Diploma in Genetic Diagnosis Technology (Molecular Genetics), and Bachelor of Science in Zoology, I am looking to transition into Research Scientist. I am confident that my proven credibility as a Molecular genetic technologist with analytical skills, communication ability, and problem-solving mindset, I would be a great fit for this position.


My intellectual curiosity and passion for research are what led me to apply for the Researcher. As my curriculum vitae demonstrates, I have worked on several relevant projects from my Postgraduate genetic diagnosis technology days that provided the needed skill sets to be an effective researcher. I would be excited to join your research group. It has an exceptional appeal to me because of its vital mission to foster interdisciplinary discussions and collaboration opportunities. As a Research Scientist candidate, I would relish the opportunity to leverage my past experiences for the project and ascertain the quality of my work with the guidance of a pioneer like yours. In the future description I would like to work with cancer biology, molecular genetics, stem cell biology, gene therapy, and genetic blood disorders.

Experience

Before serving as a Molecular genetic technologist, during my postgraduate diploma in Genetics Diagnosis Technology I had work experience in several Molecular Genetics diagnosis of Thalassemia, Hemophilia, Chimerism, Leukemia, and Flow Cytometry and During my postgraduate I have tried to evaluate the Anticancer activity of Terminalia chebula aqueous extract the growth and migration of human lung cancer cell line (A-549), in a Xenograft Model using Zebrafish. Currently, I’m working as a Molecular diagnosis of Fanconi Anaemia (FA), DNA repair pathway proteins functions primarily in DNA interstrand crosslink (ICL) repair. The proteins in the FA pathway monoubiquitinate FANCD2 and FANCI proteins which form a complex at the site of DNA damage. Mainly we are focusing on a FANCD2 Ubiquitination from FA Patients with a negative western blot in peripheral blood. We are currently investigating the status of FANCD2 Ubiquitination in Skin fibroblasts from patients with mosaic FA to confirm the diagnosis and We are performing Prenatal Diagnosis from fetus tissue to find out the FANCD2 Ubiquitination. Mutations in 22 distinct FA-Pathway genes can cause the disease, We standardized long amplicon-PCRs (LA-PCRs) for most common genes associated with the pathogenesis of FA-FANCA, FANCL, and FANCG genes are more prevalent in Indian Population, Library preparation and next-generation sequencing (NGS). In-house bioinformatics pipeline was used to identify the mutations, and the mutations identified by NGS were confirmed by sanger sequencing. For the cases that did not have point mutations in the FANCA genes, MLPA was performed to detect deletions and Duplication. FANCD2 ubiquitination is the critical event in ICL repair, and it is defective in ~95% of FA cases. I have been doing ALPHA, BETA and DELTA Thalassemia, In Beta Thalassemia DNA was extracted from the patient’s, the reverse dot blot (RDB) technique was used to screen for the most common mutation, The Bata-thalassemia allele in the Indian population. In ALPHA Thalassemia, Globin gene multiplication and deletion were analyzed by gene dosage PCR followed by genescan analysis. Rare mutation was screened by DNA sequencing analysis. Delta Beta thal deletion to identified by MLPA and Hereditary persistence of fetal hemoglobin (HPFH) rare deletion was identified using GAP PCR. Then I have been doing Hemoglobin variant analysis by HPLC. The Tosoh automated G11 hemoglobin analyzer to identified HBF, HBA0, HBA2, HBC, HBD, HBE, and HBS. I am focusing on the molecular diagnosis of Diamond blackfan anemia. We standardized long amplicon-PCRs (LA-PCRs) for the 9 most common genes associated with the pathogenesis of DBA-RPS19, RPL11, RPL5, RPS24, RPS26, RPL35A, RPS17, RPL15, and GATA1. the mutations identified by NGS were confirmed by sanger sequencing. For the cases that did not have point mutations in the selected genes, MLPA was performed to detect deletions and Duplication. I am focusing on molecular diagnosis of congenital dyserythropoietic anemia. The following genes involved in the pathogenesis of CDA were amplified using long amplicon-PCRs CDAN1, c15orf41, SEC23B, KIF23, KLF1, and GATA1 followed by Next-generation sequencing. In-house pipelines were used to identify causative mutation. Pathogenicity was established using online tools. Mutation obtained were confirmed by Sanger sequencing. I am focusing on Haemolytic anemia also like Membranopathies (RBC membrane disorders) most common genes ANK1, EPB42, SPTA1, SPTB, SLC4A1, and PIEZ01, and Enzymopathies (RBC enzyme disorders) long amplicon-PCRs for the two most common genes G6PD, and PKLR, the mutations identified by NGS were confirmed by sanger sequencing. For all the cases that did not have point mutations in the selected genes then we are performing whole exome sequencing to find out the pathogenic or likely pathogenic mutations. In the future description I would like to work with cancer biology, molecular genetics, stem cell biology, gene therapy, and genetic blood disorders.

Education

  • Received hands-on training for several Molecular Genetics Diagnosis of Thalassemia, Hemophilia, Chimerism, Leukemia, and HPLC drug assay.
  • Flow cytometry experience in leukemia, lymphoma, and the Enumeration of CD34 stem cells.
  • Perform experiments and develop assays to identify rare tumor cells in bone marrow aspirates, peripheral blood, and central cerebrospinal fluid (CSF).

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