Current challenges in the therapeutic use of induced pluripotent stem cells (iPSCs) in cancer therapy

Induced Pluripotent Stem Cells (iPSCs) technology has catapulted the field of stem-cell biology through ectopic expression of reprogramming factors. Ever since its discovery, the potential of iPSCs has been explored by many scientists to unravel the molecular mechanism responsible for cancer initiation and progression. Besides modeling cancer, the further applications of this technology includes high-throughput drug screening, epigenetic reprogramming of cancer cell state to normal, immunotherapy and regenerative cell therapies. Here, we review the current challenges on clinical applications of iPSCs with respect to understanding cancer and personalizing treatment for the disease (AU)

Review on Molecular Diagnostic Techniques in Friedreich’s Ataxia.

Friedreich’s ataxia is a commonly inherited neurodegenerative disease with an autosomal recessive pattern of inheritance, and was described by Nikolaus Friedreich first in 1863. Friedreich’s ataxia is caused due to hyperexpansion of the intronic GAA trinucleotide repeats or mutations in the FXN gene on chromosome 9q13. This gene codes for a mitochondrial protein, frataxin, which is highly conserved in many species and has functions in iron-sulfur cluster biosynthesis. Friedreich’s ataxia mainly results from a deficiency of the frataxin protein, due to mutations in the FXN gene. Formation of sticky DNA, formation of DNA-RNA hybrid and epigenetic changes, including methylation of DNA and histone modifications, are the proposed mechanisms for disruption of FXN gene expression. Most cases of Friedreich’s ataxia are homozygous and caused due to expansion of the GAA trinucleotide repeat in the first intron of the FXN gene, however, some cases can be heterozygous, with GAA expansion in one allele and point mutation or deletion in the FXN gene on the other allele. Therefore, diagnosis of the disease based on only the clinical symptoms becomes difficult. Molecular diagnosis is, therefore, important, in order to detect GAA repeat expansions as well as mutations in the FXN gene. This review represents an overview of the molecular diagnostic studies in Friedreich’s ataxia, including an overview of the disease, as well as the gene and protein involved in the disease and techniques that can be useful in diagnosis of the Friedreich’s ataxia. The described methods include tools that are based on analysis of DNA as well as analysis of mRNA and protein levels. A brief description of mutations found in compound heterozygous Friedreich’s ataxia patients, is also provided.