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Statements

Subject Item
n2:RIV%2F00216208%3A11310%2F12%3A10126299%21RIV13-GA0-11310___
rdf:type
n8:Vysledek skos:Concept
rdfs:seeAlso
http://dx.doi.org/10.4149/neo_2012_093
dcterms:description
Cancer stem cells (CSCs) form a small proportion of tumor cells that have stem cell properties: self-renewal capacity, the ability to develop into different lineages and proliferative potential. The interest in CSCs emerged from their expected role in initiation, progression and recurrence of many tumors. They are generally resistant to conventional chemotherapy and radiotherapy. There are two hypotheses about their origin: The first assumes that CSCs may arise from normal stem cells, and the second supposes that differentiated cells acquire the properties of CSCs. Both hypotheses are not mutually exclusive, as it is possible that CSCs have a diverse origin in different tumors. CD133+ cells (CD133 is marker of CSC in some tumors) isolated from NBL, osteosarcoma and Ewing sarcoma cell lines are resistant to cisplatin, carboplatin, etoposide and doxorubicin than the CD133- ones. Being resistant to chemotherapy, there were many attempts to target CSCs epigenetically including the use of histone deacetylase inhibitors. The diverse influence of valproic acid (histone deacetylase inhibitor) on normal and cancer stem cells was proved in different experiments. We have found an increase percentage of CD 133+ NBL cells after their incubation with VPA in a dose that does not induce apoptosis. Further researches on CSCs and clinical application for their detection are necessary: (i) to define the CSC function in carcinogenesis, cancer development and their role in metastasis; (ii) to find a specific marker for CSCs in different tumors; (iii) to explain the role of different pathways that determine their behavior and (iv) to explain mechanisms of chemoresistance of CSCs. Cancer stem cells (CSCs) form a small proportion of tumor cells that have stem cell properties: self-renewal capacity, the ability to develop into different lineages and proliferative potential. The interest in CSCs emerged from their expected role in initiation, progression and recurrence of many tumors. They are generally resistant to conventional chemotherapy and radiotherapy. There are two hypotheses about their origin: The first assumes that CSCs may arise from normal stem cells, and the second supposes that differentiated cells acquire the properties of CSCs. Both hypotheses are not mutually exclusive, as it is possible that CSCs have a diverse origin in different tumors. CD133+ cells (CD133 is marker of CSC in some tumors) isolated from NBL, osteosarcoma and Ewing sarcoma cell lines are resistant to cisplatin, carboplatin, etoposide and doxorubicin than the CD133- ones. Being resistant to chemotherapy, there were many attempts to target CSCs epigenetically including the use of histone deacetylase inhibitors. The diverse influence of valproic acid (histone deacetylase inhibitor) on normal and cancer stem cells was proved in different experiments. We have found an increase percentage of CD 133+ NBL cells after their incubation with VPA in a dose that does not induce apoptosis. Further researches on CSCs and clinical application for their detection are necessary: (i) to define the CSC function in carcinogenesis, cancer development and their role in metastasis; (ii) to find a specific marker for CSCs in different tumors; (iii) to explain the role of different pathways that determine their behavior and (iv) to explain mechanisms of chemoresistance of CSCs.
dcterms:title
Neuroblastoma stem cells - mechanisms of chemoresistance and histonedeacetylase inhibitors Neuroblastoma stem cells - mechanisms of chemoresistance and histonedeacetylase inhibitors
skos:prefLabel
Neuroblastoma stem cells - mechanisms of chemoresistance and histonedeacetylase inhibitors Neuroblastoma stem cells - mechanisms of chemoresistance and histonedeacetylase inhibitors
skos:notation
RIV/00216208:11310/12:10126299!RIV13-GA0-11310___
n8:predkladatel
n10:orjk%3A11310
n3:aktivita
n7:P n7:I
n3:aktivity
I, P(GAP301/10/0356)
n3:cisloPeriodika
6
n3:dodaniDat
n14:2013
n3:domaciTvurceVysledku
n19:8486573
n3:druhVysledku
n9:J
n3:duvernostUdaju
n20:S
n3:entitaPredkladatele
n16:predkladatel
n3:idSjednocenehoVysledku
153870
n3:idVysledku
RIV/00216208:11310/12:10126299
n3:jazykVysledku
n11:eng
n3:klicovaSlova
progenitor cells; valproic acid; hematopoietic stem; distinct side population; tumor-initiating cells; histone deacetylase inhibitors; neuroblastomam; CD 133; cancer stem cells
n3:klicoveSlovo
n13:histone%20deacetylase%20inhibitors n13:progenitor%20cells n13:valproic%20acid n13:hematopoietic%20stem n13:distinct%20side%20population n13:cancer%20stem%20cells n13:tumor-initiating%20cells n13:CD%20133 n13:neuroblastomam
n3:kodStatuVydavatele
SK - Slovenská republika
n3:kontrolniKodProRIV
[9EDF5F57F70F]
n3:nazevZdroje
Neoplasma
n3:obor
n21:CE
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
6
n3:projekt
n4:GAP301%2F10%2F0356
n3:rokUplatneniVysledku
n14:2012
n3:svazekPeriodika
59
n3:tvurceVysledku
Cipro, Šimon Stiborová, Marie Vícha, Aleš Eckschlager, Tomáš Khalil, Mohamed Hraběta, Jan
n3:wos
000310820200018
s:issn
0028-2685
s:numberOfPages
10
n18:doi
10.4149/neo_2012_093
n12:organizacniJednotka
11310