Glucocorticoid and proteasome inhibitor impact on the leukemic lymphoblast: Multiple, diverse signals converging on a few key downstream regulators

  title={Glucocorticoid and proteasome inhibitor impact on the leukemic lymphoblast: Multiple, diverse signals converging on a few key downstream regulators},
  author={George I. Lambrou and Lina Papadimitriou and George P. Chrousos and Spiros A Vlahopoulos},
  journal={Molecular and Cellular Endocrinology},

Early and Very Early GRIM19 and MCL1 Expression Are Correlated to Late Acquired Prednisolone Effects in a T-Cell Acute Leukemia Cell Line.

A study of Prednisolone treatment using as a model a leukemia cell line with subsequent investigation of resistance-related gene expression to identify significant targets of resistance to GC-induced apoptosis in ALL cells is reported.

Drugs acting on homeostasis: challenging cancer cell adaptation

It is shown that pathways of proteostasis and energy generation regulate common transcription factors, which induce transcription factor proteins that control expression of cytokines and regulators of apoptosis, cell division, differentiation, metabolism, and response to hormones.

Dissecting pharmacological effects of chloroquine in cancer treatment: interference with inflammatory signaling pathways

The work addressing the role of chloroquines in the homeostasis of mammalian tissue, and the potential strengths and weaknesses concerning their use in cancer therapy are reviewed.

Anticancer Effect of AntiMalarial Artemisinin Compounds

  • Ak Das
  • Biology, Chemistry
    Annals of medical and health sciences research
  • 2015
Experimental evidences suggest that artemisinin compounds may be a therapeutic alternative in highly aggressive cancers with rapid dissemination, without developing drug resistance, and specific interactions with established chemotherapy need to be further investigated in different cancer cells and their phenotypes.

AKT1 has dual actions on the glucocorticoid receptor by cooperating with 14-3-3

Cancer as a defective network for NF-κB

The role of the transcription factor NF-κB, which interacts with chromatin modulators by cell-specific dynamics, controls cell interactions during inflammation, and its abnormal feedback regulation is implicated in cancer, is addressed.

Differential network analysis and protein-protein interaction study reveals active protein modules in glucocorticoid resistance for infant acute lymphoblastic leukemia

Differential co-expression analysis is a promising approach to incorporate the dynamic context of gene expression profiles into the well-documented protein interaction networks and allows the detection of relevant protein modules that are highly enriched with DC gene pairs.

Inflammation and tissue homeostasis: the NF-κB system in physiology and malignant progression

Disruption of key feedback modules for NF-κB in certain cell types facilitates the survival of clones with genomic aberrations, and protects them from being recognized and eliminated by the immune system, to enable thereby carcinogenesis.

Lactacystin: first-in-class proteasome inhibitor still excelling and an exemplar for future antibiotic research

New and innovative uses are regularly being found for lactacystin, including as a model to study dementia, while new formulations and delivery systems may facilitate its use clinically as an anticancer agent, providing yet more evidence that a comprehensive, collaborative and coordinated programme is needed to fully investigate all new and existing chemical compounds, especially those of microbial origin.



c-Myc does not prevent glucocorticoid-induced apoptosis of human leukemic lymphoblasts

The data indicate that c-myc downregulation is not critical for induction of cell-death by GC in this system, and support the notion thatc-Myc sensitizes cells to apoptosis-inducing agents.

Jak/STAT pathways in cytokine signaling and myeloproliferative disorders: approaches for targeted therapies.

The results suggest the possibility that additional mutational events might be associated with the development of these neoplasms, and indicate the need for combination therapies as the nature and significance of these additional molecular events is better understood.

Identification of genes leading to glucocorticoid-induced leukemic cell death

Gene microarray analysis found the network of genes involved in GC-evoked cell death, using three clones derived from the CEM lymphoid leukemia cell line, and suggested that primary gene targets for GC often lack a classic GC response element.

New insights into role of microenvironment in multiple myeloma

Biology of acute lymphoblastic leukemia (ALL): clinical and therapeutic relevance.

  • C. Graux
  • Biology, Medicine
    Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis
  • 2011

Genomewide identification of prednisolone-responsive genes in acute lymphoblastic leukemia cells.

Biologic characterization of genes and pathways identified on 3 and 8 hours of prednisolone exposure in leukemic cells of 13 children might elucidate the action of glucocorticoids in ALL cells, possibly suggesting causes of glucOCorticoid resistance and new potential targets for therapy.

Epigenetic silencing of BIM in glucocorticoid poor-responsive pediatric acute lymphoblastic leukemia, and its reversal by histone deacetylase inhibition.

Findings provide a novel therapeutic strategy to reverse glucocorticoid resistance and improve outcome for high-risk pediatric ALL, as well as a therapeutic approach to reverse resistance in vivo.