Study of microenvironment mediated chemoresistance in Chronic Myeloid Leukemia

Show simple item record Kumar, Atul 2019-07-15T05:16:07Z 2019-07-15T05:16:07Z 2016
dc.identifier.other ROLL NO.11610603
dc.description Supervisor: Bithiah Grace Jaganathan en_US
dc.description.abstract Chronic Myeloid Leukemia (CML) is a myelo proliferative disorder in which the leukemic stem cells (LSC) give rise to abnormally high number of myeloid cells. CML is initiated by BCRABL fusion (9;22) (q34;q11) which is the result of reciprocal translocation between chromosome 9 and chromosome 22. BCR-ABL fusion gene codes for Bcr-Abl fusion protein which is a constitutively active tyrosine kinase. Tyrosine kinase inhibitors (TKIs) such as Imatinib mesylate (IM) is the mainline drug used for the treatment of CML. CML responds to IM treatment efficiently, especially in the chronic phase. However, in several patients, CML relapses even after few years of remission, mainly upon discontinuation of IM intake. Mutations in the BCRABL kinase domain have been reported to be the main cause of IM resistance. However, persistent leukemic cells in the BM in spite of IM treatment play a major role in causing relapse in CML patients. BM stromal microenvironment has been implicated to be the major cause of this persistence, where mesenchymal stromal cells (MSC) and their derivatives provide chemoprotection to CML cells through secreted factors as well as direct cell-cell contact. en_US
dc.language.iso en en_US
dc.relation.ispartofseries TH-1829;
dc.title Study of microenvironment mediated chemoresistance in Chronic Myeloid Leukemia en_US
dc.type Thesis en_US

Files in this item

This item appears in the following Collection(s)

Show simple item record



My Account