Bio


Aditya is a medical molecular biology-bioinformatics scientist. He has worked with a diverse group of scientists throughout his career from various fields like microbiology, pathology, molecular biology, oncology, cardiology, virology, bioinformatics, and cell biology.

During his Ph.D., Aditya developed a novel method of knocking down the Philadelphia chromosome, a precursor to chronic myeloid leukemia, using CRISPR Cas13a. He also developed cost-effective targeted genetic screening tests based on next-generation sequencing, leading to the concrete diagnosis in many cases, and is still under use at his previous institute. He also developed an artificial intelligence-based technique to score found variants to decrease diagnosis false positive and false negative rates.

He is currently working in wet and dry labs and with the MoTrPAC consortium. His wet lab work involves the development of "super AAVs" for precise and effective payload delivery into the cardiomyocytes. Additionally, he is also working on establishing organ slice culture in the laboratory, which would help conduct a battery of live tissue experiments. Aditya has also developed several local and cloud-based data analysis and plotting tools. He is also involved with big data analysis and working on answering the question of the scientific link between aging and physical activity.

Stanford Advisors


All Publications


  • Effective Downregulation of BCR-ABL Tumorigenicity by RNA Targeted CURRENT GENE THERAPY Singh, A., Bhatia, P. 2021; 21 (3): 270-277

    Abstract

    To induce BCR-ABL gene silencing using CRISPR Cas13a.CML is a clonal myeloproliferative disorder of pluripotent stem cells driven by a reciprocal translocation between chromosomes 9 and 22 forming a BCR-ABL fusion gene. Tyrosine- kinase inhibitor drugs like imatinib are the mainstay of treatment and cases resistant to these drugs have a poor prognosis in the absence of a compatible stem-cell donor. However with rapid advancements in gene-editing technologies most studies are now focusing on developing a translational model targeting single-gene disorders with a prospective permanent cure.To explore the potential application of the RNA targeting CRISPR-Cas13a system for effective knockdown of BCR-ABL fusion transcript in a CML cell line K562.CRISPR Cas13a crRNA was designed specific to the chimeric BCR-ABL gene and the system was transfected as a two-plasmid system into a CML cell line K562. The effects were enumerated by evaluating the expression levels of downstream genes dependent on the expression of the BCR-ABL gene. Also next-generation sequencing was used to ascertain the effects of CRISPR on the gene.The CRISPR system was successfully able to lower the expression of downstream genes [pCRKL and pCRK] dependent on the activated BCR-ABL kinase signal by up-to 4.3 folds. The viability of the CRISPR-treated cells was also significantly lowered by 373.83-fold [p-value= 0.000891196]. The time-dependent kinetics also highlighted the significant in-vitro suppressive activity to last up to 8 weeks [p-value: 0.025]. As per the cDNA sequencing data from the Oxford MinION next-generation sequencer the CRISPR treated cells show 62.37% suspected cleaved reads.These preliminary results highlight an excellent potential application of RNA targeting CRISPRs in Haematological neoplasms like CML and should pave the way for further research in this direction.

    View details for DOI 10.2174/1566523221666210217155233

    View details for Web of Science ID 000687489500007

    View details for PubMedID 33596804

  • Systematic evaluation of paediatric cohort with iron refractory iron deficiency anaemia (IRIDA) phenotype reveals multiple TMPRSS6 gene variations. British journal of haematology Bhatia, P., Singh, A., Hegde, A., Jain, R., Bansal, D. 2017; 177 (2): 311-318

    Abstract

    Systematic screening identified patients with an iron refractory iron deficiency anaemia (IRIDA) phenotype and genotype in iron-deficient children in the Indian subcontinent. Cases of moderate to severe microcytosis and anaemia with no obvious cause and normal C-reactive protein, HbA2 and tissue transglutaminase antibody levels (n = 550) were put on a trial of oral iron for 4 weeks. Sixty of these 550 cases (11%) were variably refractory to oral iron therapy (<10 g/l Hb rise) at 4-6 weeks and were subsequently evaluated for plasma iron, ferritin and hepcidin levels. The mean age of this cohort was 2.06 years. Low-normal to normal ferritin and normal to high hepcidin levels were noted in 25/60 (41.6%) and 47/60 (78.3%), respectively. An IRIDA phenotype was noted in 38.3% (23/60) based on standard criteria. TMPRSS6 gene sequencing in 20 cases with IRIDA phenotype revealed 9 potentially deleterious intronic and two benign exonic variations in 12/20 cases (60%). Of these, 4 intronic and both exonic variations were noted in multiple cases and are likely to act synergistically leading to an IRIDA phenotype. However, given that only 38% (23/60 cases) of cases with iron refractoriness had IRIDA phenotype, a balanced approach is needed and other causes for refractoriness should be investigated before genetic studies for TMPRSS6 are undertaken.

    View details for DOI 10.1111/bjh.14554

    View details for PubMedID 28169443