Hematopoietic Stem Cell Transplantation: Are We There Yet?
Poster Nov 08, 2014
Shalmali Pendse, Anuradha Vaidya
Hematopoietic stem cells (HSCs) have a remarkable potential to self-renew and differentiate into many blood cell types. Self-renewal is the property to retain the stem cell status following cell division whereas differentiation is the property to get committed to a more specific lineage. HSCs have been studied extensively for therapeutic purposes in the treatment of blood diseases, inherited blood disorders, and autoimmune diseases. Today hematopoietic stem cell transplantation (HSCT) is not only an established treatment for various malignant and non-malignant conditions, but it is the only acceptable therapeutic procedure using stem cells.
Thomas et al (1957) were the first to perform allogeneic HSCT to treat a patient suffering from a hematological malignancy. In 1968, severe combined immuno-deficient disease (SCID) patients treated with HSCT were the first reported long term survivors following transplantation using HSCs. The discovery by Till and McCulloch embarked on a new journey towards many investigations to clarify HSC biology, functional characterization, purification, cultivation and other aspects of stem cell research, and HSCT. Simultaneously, the use of various conditioning regimens prior to allogeneic HSCT also improved the probability of long-term remission.
Recently, the concept of using mesenchymal stem cells (MSCs) along with HSCs is becoming a promising factor in improving transplantation success rates. Furthermore, the identification of novel HSC specific markers has proved beneficial in selectively isolating and transplanting HSCs especially in allogeneic transplantation using bone marrow, thereby greatly reducing the chances of graft rejection.
In the poster review we will discuss the various advancements in HSC research and their contributions in improving HSCT outcomes.
Genome-wide association studies (GWAS) have identified more than 100 genetic loci associated with type 2 diabetes. The majority of these are located in the intergenic or intragenic regions suggesting that the implicated variants may alter chromatin conformation. This, in turn, is likely to influence the expression of nearby or more remotely located genes to alter beta cell function. At present, however, detailed molecular and functional analyses are still lacking for most of these variants. We recently analysed one of these loci and mapped five causal variants in an islet-specific enhancer cluster within the STARD10 gene locus. Here, we aimed to understand how these causal variants influence b-cell function by alteration of the chromatin structure of enhancer clusterREAD MORE