scholarly journals https://researchopenworld.com/development-of-synthetic-cell-differentiation-agent-formulations-for-the-prevention-and-therapy-of-cancer-via-targeting-of-cancer-stem-cells/#

2019 ◽  
Vol 4 (1) ◽  
Keyword(s):  
Stem Cells ◽  
Cell Differentiation ◽  
Cancer Stem Cells ◽  
Synthetic Cell ◽  
Prevention And Therapy

A 3D Cellular Automaton for Cell Differentiation in a Solid Tumor with Plasticity

2018 ◽  
Vol 13 (01) ◽  
pp. 19-28 ◽  
Author(s):  
David H. Margarit ◽  
Lilia Romanelli ◽  
Alejandro J. Fendrik
Keyword(s):  
Stem Cells ◽  
Cell Differentiation ◽  
Cancer Stem Cells ◽  
Cellular Automaton ◽  
Solid Tumor ◽  
Spherical Symmetry ◽  
Differentiated Cells ◽  
Previous State

A model with spherical symmetry is proposed. We analyze the appropriate parameters of cell differentiation for different kinds of cells (Cancer Stem Cells (CSC) and Differentiated Cells (DC)). The plasticity (capacity to return from a DC to its previous state of CSC) is taken into account. Following this hypothesis, the dissemination of CSCs to another organ is analyzed. The location of the cells in the tumor and the plasticity range for possible metastasis is discussed.

scholarly journals Metabolic Targeting of Cancer Stem Cells

2020 ◽  
Vol 10 ◽  
Author(s):  
Anna Mukha ◽  
Anna Dubrovska
Keyword(s):  
Stem Cells ◽  
Cell Differentiation ◽  
Cancer Stem Cells ◽  
Clonal Evolution ◽  
Cancer Therapies ◽  
Intrinsic Resistance ◽  
Anti Cancer ◽  
Target Tumor Cell ◽  
High Degree ◽  
Metabolic Targeting

Most human tumors possess a high heterogeneity resulting from both clonal evolution and cell differentiation program. The process of cell differentiation is initiated from a population of cancer stem cells (CSCs), which are enriched in tumor‐regenerating and tumor‐propagating activities and responsible for tumor maintenance and regrowth after treatment. Intrinsic resistance to conventional therapies, as well as a high degree of phenotypic plasticity, makes CSCs hard-to-target tumor cell population. Reprogramming of CSC metabolic pathways plays an essential role in tumor progression and metastatic spread. Many of these pathways confer cell adaptation to the microenvironmental stresses, including a shortage of nutrients and anti-cancer therapies. A better understanding of CSC metabolic dependences as well as metabolic communication between CSCs and the tumor microenvironment are of utmost importance for efficient cancer treatment. In this mini-review, we discuss the general characteristics of CSC metabolism and potential metabolic targeting of CSC populations as a potent strategy to enhance the efficacy of conventional treatment approaches.

scholarly journals A Case of Identity: HOX Genes in Normal and Cancer Stem Cells

Cancers ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 512 ◽  
Author(s):  
Smith ◽  
Zyoud ◽  
Allegrucci
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cell Differentiation ◽  
Cancer Stem Cells ◽  
Adult Stem Cells ◽  
Hox Genes ◽  
Embryonic Stem ◽  
Stem Cell Differentiation ◽  
Embryonic Stem Cell Differentiation ◽  
Hox Gene

Stem cells are undifferentiated cells that have the unique ability to self-renew and differentiate into many different cell types. Their function is controlled by core gene networks whose misregulation can result in aberrant stem cell function and defects of regeneration or neoplasia. HOX genes are master regulators of cell identity and cell fate during embryonic development. They play a crucial role in embryonic stem cell differentiation into specific lineages and their expression is maintained in adult stem cells along differentiation hierarchies. Aberrant HOX gene expression is found in several cancers where they can function as either oncogenes by sustaining cell proliferation or tumor-suppressor genes by controlling cell differentiation. Emerging evidence shows that abnormal expression of HOX genes is involved in the transformation of adult stem cells into cancer stem cells. Cancer stem cells have been identified in most malignancies and proved to be responsible for cancer initiation, recurrence, and metastasis. In this review, we consider the role of HOX genes in normal and cancer stem cells and discuss how the modulation of HOX gene function could lead to the development of novel therapeutic strategies that target cancer stem cells to halt tumor initiation, progression, and resistance to treatment.

scholarly journals Correction: By promoting cell differentiation, miR-100 sensitizes basal-like breast cancer stem cells to hormonal therapy

Oncotarget ◽  
2019 ◽  
Vol 10 (48) ◽  
pp. 5003-5004 ◽  
Author(s):  
Annalisa Petrelli ◽  
Rosachiara Carollo ◽  
Marilisa Cargnelutti ◽  
Flora Iovino ◽  
Maurizio Callari ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cell Differentiation ◽  
Cancer Stem Cells ◽  
Hormonal Therapy ◽  
Breast Cancer Stem Cells ◽  
Basal Like Breast Cancer

Cancer Stem Cell Activity in Mantle Cell Lymphoma Is Inhibited by TLR9 Activation

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 884-884
Author(s):  
Sarah Brennan ◽  
Brooke Meade ◽  
Qiuju Wang ◽  
George Weiner ◽  
William Matsui
Keyword(s):  
Stem Cells ◽  
Multiple Myeloma ◽  
Stem Cell ◽  
Cell Differentiation ◽  
Cancer Stem Cells ◽  
Cell Lines ◽  
Plasma Cell ◽  
Cell Lymphoma ◽  
Cpg Odn ◽  
Mantle Cell

Abstract Patients with Mantle Cell Lymphoma (MCL) often respond to initial cytotoxic therapy, but invariably relapse. This clinical pattern suggests that standard therapies fail to eliminate a population of chemoresistant cells responsible for tumor regrowth and disease relapse. Studies in myeloid leukemias and multiple myeloma have suggested that cancer stem cells (CSC) are relatively quiescent and that this property promotes drug resistance. Therefore, the induction of CSC proliferation may increase their susceptibility to anti-cancer treatment. Unmethylated CpG DNA sequences induce the activation and differentiation of normal B cells through toll like receptor 9 (TLR9), and synthetic CpG oligonucleotides (ODN) are currently undergoing clinical trials in MCL and other B cell non-Hodgkin’s lymphomas. We initially examined the effects of TLR9 agonists on the clonogenic growth of the human MCL cell lines Granta 519, Jeko-1, and Rec-1 and found that the unmethylated CpG ODN 2006 (5ug/mL, 48 hours) significantly inhibited the ability of each of these cell lines to form colonies in methylcellulose (p<0.01). We previously demonstrated that clonogenic CSC in multiple myeloma and Hodgkin’s lymphoma may be identified based on the relative activity of the intracellular detoxification enzyme aldehydedehydrogenase (ALDH). Similarly, each of the MCL cell lines contained small populations (0.5−2.3%) of ALDH+ cells that were enriched for in vitro clonogenic growth upon primary and secondary plating in methylcellulose. Following treatment with CpG ODN 2006, the population of ALDH+ cells was significantly reduced in each cell line (p<0.05). The self-renewal potential of normal and cancer stem cells is lost through the process of differentiation, and treatment of the MCL cell lines with CpG ODN 2006 resulted in the loss of CD19 and CD20 expression and induction of the plasma cell antigen CD138 by FACS. Similarly, RT-PCR for regulators of B cell differentiation revealed decreased PAX-5 and BCL-6 expression coupled with increased transcription of BLIMP-1 and XBP-1. We hypothesized that the plasma cell differentiation induced by TLR9 agonists may improve the efficacy of anti-tumor agents with known activity against plasma cells, specifically the proteosome inhibitor bortezomib. Treatment with CpG ODN 2006 or bortezomib (10–100nM, 48 hours) alone induced apoptosis in a small percentage of cells within each MCL line, but the combination of these agents synergistically increased the proportion of Annexin V+ cells. In summary, cellular activation by CpG ODN 2006 reduces MCL clonogenicity and stem cell function through the induction of differentiation. In turn, plasma cell maturation appears to increases the sensitivity of MCL to bortezomib and suggests a novel mechanism for the anti-tumor activity of CpG ODN.

Effects of melatonin on apoptosis and cell differentiation in MCF-7 derived cancer stem cells

2018 ◽  
Vol 64 (12) ◽  
pp. 56 ◽  
Author(s):  
Nadir Koçak ◽  
Hüseyin Dönmez ◽  
İbrahim Halil Yildirim
Keyword(s):  
Stem Cells ◽  
Cell Differentiation ◽  
Cancer Stem Cells ◽  
Mcf 7
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