Reach Us +447482877761
Clonogenic Multiple Myeloma Cells Have Shared Stemness Signature Associated With Patient Survival | 9345
ISSN: 0974-7230

Journal of Computer Science & Systems Biology
Open Access

Like us on:

Our Group organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations
700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)
Recommended Conferences

16th World Congress on Structural Biology

Amsterdam, Netherlands
Share This Page

Clonogenic multiple myeloma cells have shared stemness signature associated with patient survival

International Conference on Integrative Biology Summit

Renji Reghunathan, Chonglei Bi, Shaw Cheng Liu, Koh Tze Loong, Tae-Hoon Chung, Gaofeng Huang and Wee Joo Chng

ScientificTracks Abstracts: J Comput Sci Syst Biol

DOI: 10.4172/0974-7230.S1.002

Many cancers are hierarchically organized and sustained by a subpopulation of clonogenic cells that have self renewal capacity. Tumor re-growth following initial reductions in disease burden suggests that tumor cells capable of clonogenic growth are relatively drug resistant, and in several human cancers these functional properties have been attributed to cancer stem cells (CSC) that are derived from mutated adult stem cells. Multiple myeloma (MM) is a neoplastic clonal expansion of phenotypically heterogeneous population of plasma cells in the bone marrow that secrete abnormal amounts of monoclonal antibodies. Terminally differentiated CD138+ plasma cells constitute the majority of the tumor cells in MM but are unable to sustain the clonogenic growth indefinitely. Chemoresistant self-renewing population of CD138- cells, isolated from myeloma patient samples and cell lines have been reported earlier. Human MM cell lines RPMI8226 and NCI H929 contained 2-5% of CD138- population. In this study, we showed that CD138- cells have increased drug efflux and ALDH1 activities, hallmark of normal and neoplastic stem cells. ALDH+CD138- cells were more clonogenic than ALDH-CD138+ cells and only CD138- cells differentiated into CD138+ cells. In vivo tumor initiation and clonogenic potentials of the CD138- population were confirmed using NOG mice. Gene expression profiling showed that compared to CD138+ cells, CD138? cells have an expression signature enriched with genes expressed in normal and malignant stem cells such as common progenitor cells (PC), hematopoietic stem cells (HSC) and leukemic stem cell (LSC). Differentially expressed genes included components of the polycomb repressor complex 2 (PRC2) and their targets. The EZH2 inhibitor DZNep (3- Deazaneplanocin) treatment showed differential activity on CD138- and CD138+ populations, suggesting that CD138- cells were more dependent on PCR2 proteins on survival and self renewal. This ?stemness signature? derived from the CD138- population was associated with poorer survival in different clinical datasets.