Gene expression profiling of tumor-initiating stem cells from mouse Krebs-2 carcinoma using a novel marker of poorly differentiated cells

Potter, Ekaterina A.; Долгова, Е. В.; Proskurina, Anastasia S.; Efremov, Yaroslav R.; Minkevich, Alexandra M.; Розанов, А. С.; Peltek, S. E.; Николин, В. П.; Попова, Н. А.; Seledtsov, Igor; Молодцов, В. В.; Zavyalov, Evgeniy L.; Taranov, Oleg S.; Байбородин, С. И.; Ostanin, А. А.; Черных, Е. Р.; Kolchanov, Nikolay А.; Богачев, С. С.

doi:10.18632/oncotarget.14116

Cited by 18 publications

(24 citation statements)

References 107 publications

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“…Yet, several scenarios appear likely, for instance extracellular DNA may interfere with the processing of NER and homology repair DNA intermediates; alternatively, double-stranded DNA ends may exhaust the pool of repair machinery proteins or launch distinct repair cascades. Whichever the case may be, this interference leads to eradicate TISCs from the tumor site [ 1 – 8 ].…”

Section: Introductionmentioning

confidence: 99%

Efficacy of a new cancer treatment strategy based on eradication of tumor-initiating stem cells in a mouse model of Krebs-2 solid adenocarcinoma

et al. 2018

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Krebs-2 solid carcinoma was cured using a new “3+1” strategy for eradication of Krebs-2 tumor-initiating stem cells. This strategy was based on synchronization of these cells in a treatment-sensitive phase of the cell cycle. The synchronization mechanism, subsequent destruction of Krebs-2 tumor-initiating stem cells, and cure of mice from a solid graft were found to depend on the temporal profile of the interstrand cross-link repair cycle. Also, the temporal profile of the Krebs-2 interstrand repair cycle was found to have a pronounced seasonal cyclicity at the place of experiments (Novosibirsk, Russia). As a result, the therapeutic effect that is based on application of the described strategy, originally developed for the “winter repair cycle” (November−April), is completely eliminated in the summer period (June−September). We conclude that оne of the possible and the likeliest reasons for our failure to observe the therapeutic effects was the seasonal cyclicity in the duration of the interstrand repair cycle, the parameter that is central to our strategy.

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Section: Introductionmentioning

confidence: 99%

Efficacy of a new cancer treatment strategy based on eradication of tumor-initiating stem cells in a mouse model of Krebs-2 solid adenocarcinoma

et al. 2018

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“…Tumor-initiating stem cells (TISCs) were first described by Lapidot and Bonnet and Dick. 8 , 9 These cells are primarily responsible for tumor engraftment, and they provide high proliferative capacity of cancer cell population, contributing to the tumor structure 10 , 11 , 12 and metastasis. 13 – 15 Our recent studies have shown that eliminating such TISCs from the cancer cell population leads to tumor eradication and full recovery of tumor-engrafted mice (ascites and solid forms of murine Krebs-2 adenocarcinomas).…”

Section: Introductionmentioning

confidence: 99%

Novel Cancer Stem Marker and Its Applicability for Grading Primary Human Gliomas

Долгова

Мишинов

Proskurina

et al. 2018

Technol Cancer Res Treat

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Poorly differentiated cell populations including tumor-initiating stem cells have been demonstrated to display a unique ability to natively internalize fragmented double-stranded DNA. Using this feature as a marker, we show that 0.1% to 6% of human glioblastoma cells from the bioptates can effectively internalize a fluorescently labeled DNA probe. Of these, using samples from 3 patients, 66% to 100% cells are also positive for CD133, a well-established surface marker of tumor-initiating glioma stem cells. Using the samples from primary malignant brain lesions (33 patients), we demonstrate that tumor grading significantly correlates (R = .71) with the percentage of DNA-internalizing cells. No such correlation is observed for relapse samples (18 patients).

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“…Ранее мы проанализировали 167 генов, демонстрирующих повышенную экспрессию в клетках асцитной карциномы Кребс2, проявляющих все свойства СРК [25] и на основании литературных данных определили 96 из них, являющихся потенциальными индукторами «плюрипотентного» фенотипа этих клеток [26]. В данной работе мы предприняли попытку проанализировать условия и механизмы активации экспрессии этих генов.…”

Section: Introductionunclassified

Cancer Stem Cells: «Emergency Service» for Tumors Under Generalized Cellular Stress

Efremov¹,

Proskurina²,

Potter³

et al. 2019

Math.Biol.Bioinf.

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The analysis of conditions and possible mechanisms of activation of 96 genes providing a malignant/pluripotent phenotype of Krebs-2 cancer stem cells have been performed. Three stress factors combined into the single concept of "generalized cellular stress", which are supposed to regulate the expression of these genes, are determined. Additionally, for these genes, the presence of binding sites for transcription factors that are being activated in response to factors of generalized cellular stress has been established. The data obtained suggest the existence of a mechanism for the de novo formation of a pluripotent/stem-like phenotype of tumor cells under conditions of generalized cellular stress.

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Gene expression profiling of tumor-initiating stem cells from mouse Krebs-2 carcinoma using a novel marker of poorly differentiated cells

Abstract: ABSTRACT

Cited by 18 publications

References 107 publications

Efficacy of a new cancer treatment strategy based on eradication of tumor-initiating stem cells in a mouse model of Krebs-2 solid adenocarcinoma

Efficacy of a new cancer treatment strategy based on eradication of tumor-initiating stem cells in a mouse model of Krebs-2 solid adenocarcinoma

Novel Cancer Stem Marker and Its Applicability for Grading Primary Human Gliomas

Cancer Stem Cells: «Emergency Service» for Tumors Under Generalized Cellular Stress

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