Relevant bibliographies by topics / Stemness

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Stemness'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 June 2025

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Journal articles on the topic "Stemness"

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Weitzman, Jonathan B. ""Stemness"." Genome Biology 3 (2002): spotlight—20020918–01. http://dx.doi.org/10.1186/gb-spotlight-20020918-01.

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Bowman, Teresa V., and Eirini Trompouki. "Sensing Stemness." Current Stem Cell Reports 7, no. 4 (2021): 219–28. http://dx.doi.org/10.1007/s40778-021-00201-w.

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Abstract Purpose of Review Hematopoietic stem cells (HSCs) are formed embryonically during a dynamic developmental process and later reside in adult hematopoietic organs in a quiescent state. In response to their changing environment, HSCs have evolved diverse mechanisms to cope with intrinsic and extrinsic challenges. This review intends to discuss how HSCs and other stem cells co-opted DNA and RNA innate immune pathways to fine-tune developmental processes. Recent Findings Innate immune receptors for nucleic acids like the RIG-I-like family receptors and members of DNA sensing pathways are expressed in HSCs and other stem cells. Even though the “classic” role of these receptors is recognition of foreign DNA or RNA from pathogens, it was recently shown that cellular transposable element (TE) RNA or R-loops activate such receptors, serving as endogenous triggers of inflammatory signaling that can shape HSC formation during development and regeneration. Summary Endogenous TEs and R-loops activate RNA and DNA sensors, which trigger distinct inflammatory signals to fine-tune stem cell decisions. This phenomenon could have broad implications for diverse somatic stem cells, for a variety of diseases and during aging.
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Bilodeau, Mélanie, and Guy Sauvageau. "Uncovering stemness." Nature Cell Biology 8, no. 10 (2006): 1048–49. http://dx.doi.org/10.1038/ncb1006-1048.

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Alderton, Gemma. "Rethinking stemness." Science 362, no. 6417 (2018): 905.18–907. http://dx.doi.org/10.1126/science.362.6417.905-r.

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Westphal, Heiner. "Restoring stemness." Differentiation 73, no. 9-10 (2005): 447–51. http://dx.doi.org/10.1111/j.1432-0436.2005.00034.x.

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Visan, Ioana. "Memory stemness." Nature Immunology 15, no. 9 (2014): 832. http://dx.doi.org/10.1038/ni.2976.

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Mikkers, Harald, and Jonas Frisén. "Deconstructing stemness." EMBO Journal 24, no. 15 (2005): 2715–19. http://dx.doi.org/10.1038/sj.emboj.7600749.

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Yang, Jihong, Hao Xu, Congshu Li, Zhenhao Li, and Zhe Hu. "An explorative study for leveraging transcriptomic data of embryonic stem cells in mining cancer stemness genes, regulators, and networks." Mathematical Biosciences and Engineering 19, no. 12 (2022): 13949–66. http://dx.doi.org/10.3934/mbe.2022650.

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<abstract><p>Due to the exquisite ability of cancer stemness to facilitate tumor initiation, metastasis, and cancer therapy resistance, targeting cancer stemness is expected to have clinical implications for cancer treatment. Genes are fundamental for forming and maintaining stemness. Considering shared genetic programs and pathways between embryonic stem cells and cancer stem cells, we conducted a study analyzing transcriptomic data of embryonic stem cells for mining potential cancer stemness genes. Firstly, we integrated co-expression and regression models and predicted 820 stemness genes. Results of gene enrichment analysis confirmed the good prediction performance for enriched signatures in cancer stem cells. Secondly, we provided an application case using the predicted stemness genes to construct a breast cancer stemness network. Mining on the network identified CD44, SOX2, TWIST1, and DLG4 as potential regulators of breast cancer stemness. Thirdly, using the signature of 31,028 chemical perturbations and their correlation with stemness marker genes, we predicted 67 stemness inhibitors with reasonable accuracy of 78%. Two drugs, namely Rigosertib and Proscillaridin A, were first identified as potential stemness inhibitors for melanoma and colon cancer, respectively. Overall, mining embryonic stem cell data provides a valuable way to identify cancer stemness regulators.</p></abstract>
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Chen, Jen-Lung, Yun-Shen Tai, Hsin-Yi Tsai та ін. "Betulinic Acid Inhibits the Stemness of Gastric Cancer Cells by Regulating the GRP78-TGF-β1 Signaling Pathway and Macrophage Polarization". Molecules 28, № 4 (2023): 1725. http://dx.doi.org/10.3390/molecules28041725.

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Cancer stemness is the process by which cancer cells acquire chemoresistance and self-renewal in the tumor microenvironment. Glucose-regulated protein 78 (GRP78) is a biomarker for gastric cancer and is involved in cancer stemness. By inducing cancer stemness in various types of cancer, the polarization of macrophages into tumor-associated macrophages (TAMs) controls tumor progression. Betulinic acid (BA) is a bioactive natural compound with anticancer properties. However, whether GRP78 regulates TAM-mediated cancer stemness in the tumor microenvironment and whether BA inhibits GRP78-mediated cancer stemness in gastric cancer remain unknown. In this study, we investigated the role of GRP78 in gastric cancer stemness in a tumor microenvironment regulated by BA. The results indicated that BA inhibited not only GRP78-mediated stemness-related protein expression and GRP78-TGF-β-mediated macrophage polarization into TAMs, but also TAM-mediated cancer stemness. Therefore, BA is a promising candidate for clinical application in combination-chemotherapy targeting cancer stemness.
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Wu, Qiong, Anders E. Berglund, Robert J. MacAulay, and Arnold B. Etame. "A Novel Role of BIRC3 in Stemness Reprogramming of Glioblastoma." International Journal of Molecular Sciences 23, no. 1 (2021): 297. http://dx.doi.org/10.3390/ijms23010297.

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Stemness reprogramming remains a largely unaddressed principal cause of lethality in glioblastoma (GBM). It is therefore of utmost importance to identify and target mechanisms that are essential for GBM stemness and self-renewal. Previously, we implicated BIRC3 as an essential mediator of therapeutic resistance and survival adaptation in GBM. In this study, we present novel evidence that BIRC3 has an essential noncanonical role in GBM self-renewal and stemness reprogramming. We demonstrate that BIRC3 drives stemness reprogramming of human GBM cell lines, mouse GBM cell lines and patient-derived GBM stem cells (GSCs) through regulation of BMP4 signaling axis. Specifically, BIRC3 induces stemness reprogramming in GBM through downstream inactivation of BMP4 signaling. RNA-Seq interrogation of the stemness reprogramming hypoxic (pseudopalisading necrosis and perinecrosis) niche in GBM patient tissues further validated the high BIRC3/low BMP4 expression correlation. BIRC3 knockout upregulated BMP4 expression and prevented stemness reprogramming of GBM models. Furthermore, siRNA silencing of BMP4 restored stemness reprogramming of BIRC3 knockout in GBM models. In vivo silencing of BIRC3 suppressed tumor initiation and progression in GBM orthotopic intracranial xenografts. The stemness reprograming of both GSCs and non-GSCs populations highlights the impact of BIRC3 on intra-tumoral cellular heterogeneity GBM. Our study has identified a novel function of BIRC3 that can be targeted to reverse stemness programming of GBM.
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Dissertations / Theses on the topic "Stemness"

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Jurczak, Daniel. "Stemness in human embryonic stem cells." Thesis, University of Skövde, School of Life Sciences, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-3509.

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<p>Stem cells are cells that have a unique ability to divide for an indefinite period. Additionally, they can give rise to a plethora of specialized cell types. The advent of high-throughput technologies made it possible to investigate gene expression on a large scale. This enabled scientists to perform comprehensive gene profiling studies of stem cells. Several authors have suggested that there might be a common set of genes that control the stemness of stem cells. In this study, we suggest that ”stemness” genes that are related to ”stemness” characteristics show a statistically significant down-regulation between undifferentiated and differentiated cells. For this we have analyzed microarray data from five different cell lines and compared their global expression profiles. Common down-regulated transcripts among those data sets were de- rived by using a well-established gene expression analysis procedure called Significance Analysis of Microarrays. Since all three data sets were provided by Cellartis AB, the derived list of common transcripts was subsequently compared with an external study. Moreover, we also performed a comparison with down-regulated genes derived from mouse embryonic stem cells. This was done to determine if there is a common set of stemness genes even across distinct species. Re- sults were further evaluated using a comprehensive data-set from a study by Skottman et al. (2005). All results where compared uti- lizing using a range of false discovery rate threshold values and the results were subsequently used for gene ontology term enrichment. GO terms where utilized to functionally annotate and classify those embryonic stem cell transcripts, that were found to be common in all data-sets and identify over-represented biological processes related to those genes.</p>
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GARULLI, Chiara. "BMP4: the crossroad between stemness and cancer." Doctoral thesis, Università degli Studi di Camerino, 2014. http://hdl.handle.net/11581/401773.

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Increasing evidence supports the theory that tumor growth, maintenance, and recurrence are dependent on a small subset of cells with stem properties, redefined cancer initiating cells (CIC) or cancer stem cells (CSC). Bone morphogenetic proteins (BMPs)are extracellular signalling molecules, member of the transforming growth factor β (TGF‐β)superfamily. These factors control various cellular processes, such as proliferation, differentiation, apoptosis and migration. Moreover they are involved in cell‐fate specification during embryogenesis, in the maintenance of developmental potency in embryonic and adult stem cells and may contribute to sustain CIC populations in breast carcinoma. Using the mouse A17 cell model previously related to mesenchymal cancer stem cells and basal-­like breast cancer, we investigated the role of BMPs in the control of breast cancer cell plasticity. We showed an autocrine activation of BMPs signaling pathway in A17 cells that seems to be crucial for the maintenance of their mesenchymal and stem-‐like phenotype. Pharmacological inhibition of BMPs signaling cascade by Dorsomorphin, a small molecule inhibitor of BMP Type I Receptor kinases, induced loss of A17s mesenchymal features, by downregulating Snail and Slug transcriptional factors and COX2 expression, resulting in the acquirement of epithelial­‐like traits. Dorsomorphin treatment led also to a decrease of stem cell markers expression, resulting in the loss of self­‐renewal ability. This phenotypic switch compromised A17 cells motility, invasion ability and in vitro tumor growth through inhibition of cell cycle progression. Transient transfection with a pool of four different synthetic siRNA molecules targeting specifically BMP4 gave similar results supporting the specificity of pharmacological treatment evidencing BMP4 crucial role. Taken together these results reveal that BMPs family, and in particular BMP4, can be considered the key molecules at the crossroad between stemness and cancer.
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Khan, Zarine. "Stemness status in differentiated and undifferentiated glioma cells." Thesis, University of Central Lancashire, 2011. http://clok.uclan.ac.uk/2814/.

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Undifferentiated cancer stem cells (CSCs) with their unique potential of self-renewal and multi-lineage differentiation fuel tumour growth and relapse. Efficacy of glioma therapy can be considerably improved if the target is focused towards successful identification and elimination of CSCs. The aim of this research lies in defining specific and selective marker(s) to isolate glioma stem cells, to explore the differentiation state of brain tumour cells and to determine the protein profile changes that assist tumour cells to sustain stem cell-like characteristics. The three stem cell-related protein (CD133, Oct4-A and BMP3) expressions were investigated in control, hypoxic and serum-deprived U87-MG cells in order to shed light on the influence the micro-environment has in generating stem cells. Hypoxia offered a rapid state of undifferentiation as compared to serum deprivation by expressing a basal level of CD133 protein, a designated stem cell marker. Subsequent measurements of chemosensitivity and cell cycle analysis under undifferentiation conditions added to the cytotoxic potential of Taxol and showed an enhanced sensitivity of serum-deprived cells towards chemotherapeutic drugs. Moreover, proteomic analysis produced a wide dataset, depicting the changes that occur at the proteomic level in the differentiated and undifferentiated U87-MG cells. With ingenuity pathway analysis (IPA), human protein research database (HPRD) and the literature review, several proteins were proposed to be tested as potential biomarkers. They included Uracil DNA glycosylase (UDG), Phosphoglycerate kinase 1 (PGK1), Heterogeneous nuclear riboprotein K (HNRNPK) and moesin that can be used as differentiated markers for glioma cells. Vimentin, Eukaryotic translation initiation factor 4e (EIF4e), Casein kinase II alpha 1 (CSNK2A1) should be further investigated to study their precise role in gliomagenesis. Laminin binding protein associated with Integrin α6β1 and BMP2 should also be explored as a potential biomarker for isolation of glioma stem cells. This novel study envelops diverse aspects related to CSCs such as biomarkers, stem cell niche, chemoresistance, cell cycle and proteomics and also suggests the existence of two sub-types of CSCs within glioma population. It can be concluded that the finding thus obtained may be a step in the right direction in helping treat brain tumours.
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Gandhi, Shaan-Chirag Chandrahas. "Regulation of stemness and differentiation in colorectal cancer." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:a32fd55a-4b1e-4a15-9f79-9fdbd986774a.

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The cancer stem cell (CSC) model of carcinogenesis and progression posits that within a tumor lies a subpopulation of cells that solely possess the ability to initiate a tumor and to differentiate into tumor cell lineages. Although the behavior of such cells is known, the challenge is to identify factors that characterize the CSC subpopulation. In this thesis, cell lines were identified that, when grown in three-dimensions, gave rise to organized colonies containing lumens originating from differentiating cells (“lumen lines”) and to densely-packed, spherical colonies originating from non-differentiating cells (“dense lines”). A microarray comparison of the pair identified genes upregulated in dense lines, including CD55 and BMI1, and in lumen lines, including CDX1 (Chapter 3). CD55 was used to isolate CD55high CSCs via flow cytometry that are able to self-renew, differentiate, initiate more colonies, proliferate more rapidly and exhibit an increased G2/M cell cycle population as opposed to unfractionated cells. Furthermore, the CD55high cells were able to give rise to more differentiated, lumen colonies in vitro, indicating that CD55 enriches for cells possessing a capacity to differentiate, and were able to enrich the CD24highCD44high putative CSC population further (Chapter 4). CDNA induction of BMI1 and CDX1 expression led to increased clonogenicity/proliferation and decreased clonogenicity/proliferation, respectively, and incorporation of a CDX1 reporter construct into the SW1222 cell line identified CDX1+ cells as a low-expressing population of CD55 (Chapter 5). Finally, co-culture of cell lines in an in vivo-like environment with intestinal myofibroblasts promoted the CSC population by enhancing clonogenicity, proliferation and expression of CD55 (Chapter 6). The results of this thesis implicate CD55 as a potent marker of colorectal cancer stemness, link the expression of BMI1 and CDX1 to cancer stemness and differentiation, respectively, and identify a role for the in vivo stem cell niche in maintaining the CSC population.
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Adorno-Cruz, Valery. "Identifying Stemness and Metastasis Drivers in Breast Cancer." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case158687657816132.

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García-Prat, Laura 1987. "Stemness maintenance in skeletal muscle : a focus on aging." Doctoral thesis, Universitat Pompeu Fabra, 2015. http://hdl.handle.net/10803/482052.

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During aging, muscle stem cell regenerative function declines, being maximal at advanced geriatric age, due to a quiescence-to-senescence transition. How quiescence is maintained over long periods of time remains largely unknown. Here we demonstrate that basal autophagy is indispensable for muscle stem cell quiescence maintenance. Physiological failure of autophagy in aging muscle stem cells or forced genetic impairment in young cells causes senescence entry by loss of proteostasis and increased ROS, resulting in numerical and functional stem cell decline. Autophagy reestablishment reverses senescence and restores regenerative functions in geriatric muscle stem cells from mouse and humans. Furthermore, we also show that FoxO transcription factors are critical for muscle stem cell quiescence through repression of the myogenic differentiation program. Indeed, FoxO deficiency impairs postnatal establishment and life maintenance of the stem cell pool by allowing inappropriate differentiation. These findings uncover new regulatory mechanisms decisive for homeostatic and regenerative functions of muscle stem cells.<br>Durante el envejecimiento, la capacidad regenerativa de las células madre musculares disminuye por mecanismos desconocidos que implican una transición desde la quiescencia a la senescencia. Este trabajo demuestra que la autofagia es indispensable en el mantenimiento de la quiescencia. El declive fisiológico de la autofagia en células madre musculares a edad geriátrica o su inhibición forzada genéticamente en células jóvenes provoca una pérdida de proteostasis y la acumulación de estrés oxidativo que reduce su número y funcionalidad. El restablecimiento del flujo autofágico revierte la senescencia y restaura la capacidad regenerativa en células geriátricas de ratones y humanos. Además, identificamos los factores de transcripción FoxO como esenciales para mantener la quiescencia mediante represión del programa de diferenciación miogénica. De hecho, la ausencia de FoxO impide la formación y mantenimiento de la población de células madre musculares al permitir una diferenciación inapropiada. Estos hallazgos descubren mecanismos moleculares decisivos para mantener la homeostasis de las células madre del músculo esquelético.
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Hewabostanthirige, Dhanushka. "Loss of Id4 Promotes Stemness In Prostate Cancer Cells." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2019. http://digitalcommons.auctr.edu/cauetds/182.

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Inhibitor of differentiation 4 (ID4), a member of the helix-loop-helix family of transcriptional regulators has emerged as a tumor suppressor in prostate cancer (PCa). Recent studies have shown that Id4 is highly expressed in the normal prostate and decreases in prostate cancer due to epigenetic silencing. Id4 knockdown in androgen sensitive LNCaP cells has been shown to lead to castration resistant prostate cancer (CRPC) in vitro and in vivo. Id4-/- mice leads to underdeveloped prostate with PIN like lesions without the loss of Androgen Receptor (AR) expression. In this study we demonstrate that the loss of ID4 expression in PCa cell line LNCaP and DU145 may promote tumorigenesis by promoting stemness. LNCaP cells with stably silenced ID4 ((-)ID4) using retroviral based shRNA and LNCaP transfected with non-specific shRNA were used to perform colony forming assay and prostatosphere formation using matrigel. Expression of cancer stem cell markers was determined using western blotting and immunocytochemistry (ICC). FACS analysis was used to sort stem cells and determine the ID4 expression. Xenograft study was performed on SCID mice using CD133 positive LNCaP cells. LNCaP(-)ID4 and DU145 cells lacking ID4 showed increased holoclone as well as decreased paraclone formation, which are believed to be derived from stem cells and differentiated cells respectively, as compared to non-silencing control in the colony forming assay. There was also an increase in prostatosphere development in the LNCaP (-) ID4 cells indicating that the loss of ID4 is responsible for promoting the LNCaP cells towards cancer stem cells. The results were further validated via western blotting and ICC using known cancer stem cell markers on the holoclones and paraclones formed by these cells. Xenograft study showed that 10,000 cells from CD133 positive LNCaP cells developed tumor on SCID mice. This study reports for the first time that loss of ID4 increases holoclone and prostatosphere formation indicating that Id4 may contribute to promoting stemness in prostate cancer cells.
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López, Arribillaga Erika 1986. "Notch signalling in intestinal homeostasis and cancer: orchestrator of stemness." Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/664090.

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Wnt/β-catenin and Notch signalling cooperate in regulating the transcription of various genes specifically in the small intestinal stem and progenitor cell compartments. We characterized Bmi1 functionally in this context and showed that it contributes to ISC self-renewal capacity. We postulated that it does so by regulating its classical locus Cdkn2a and probably also by supporting DNA damage repair. Yet another level of Notch and Wnt/β-catenin crosstalk was found in colorectal cancer where tumour-associated β-catenin induced Jagged 1 (Jag1) transcription, thus leading to Notch activation. We also investigated which is the contribution of intestinal epithelial Jag1-mediated Notch activation on tumour initiating activity. We found that intestinal-specific deletion of Jag1 greatly decreases tumour formation in the ApcMin/+ background, likely due to reduced stemness. Jag1 deletion in preformed spheroids abrogates stemness-related gene expression and proliferation leading to spheroid failure. Jag1 is dispensable for normal stem cells, which rely on Dll1/4 Notch ligands for their maintenance. Together, these results open a new path in personalised CRC therapy, presumably involving Notch inhibition from specific ligands.<br>Las vías de señalización de Wnt/β-catenina y de Notch cooperan en la regulación transcripcional de varios genes específicamente en las células madre / progenitoras del epitelio intestinal. Hemos caracterizado la funcionalidad de Bmi1 en este contexto y demostrado que contribuye a la capacidad de auto-renovación de las células madre intestinales. Postulamos que lleva a cabo esta función mediante la regulación de su diana clásica, Cdkn2a, pero probablemente también llevando a cabo funciones alternativas ayudando a la reparación del daño en el ADN. Sin embargo, existe otro nivel de cooperación entre las vías de señalización de Wnt/β-catenina y de Notch en el contexto del cáncer colorectal. Aquí, la β-catenina asociada al tumor es capaz de inducir la transcripción de Jagged1 (Jag1), resultando en la activación de la vía de Notch. También hemos investigado cuál es la contribución a la iniciación tumoral de la activación de Notch mediada por Jag1 epitelial. Encontramos que delecionando Jag1 específicamente en el epitelio intestinal se reducía la formación tumoral en el modelo animal ApcMin/+, probablemente debido a una pérdida de las características de célula madre. La deleción de Jag1 en esferoides previamente formados abroga la expresión de genes de célula madre y la proliferación, llevando al colapso de los esferoides. Jag1 es dispensable para las células madre normales, que dependen de los ligandos de Notch Dll1/4 para su supervivencia. En conjunto, estos resultados abren un nuevo camino a las terapias personalizadas en el tratamiento del cáncer colorectal, presumiblemente mediante la inhibición de Notch a partir de ligandos específicos.
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Mohammadalipour, Ameneh. "Mechanical Properties of Cancer Cells: A Possible Biomarker for Stemness." Ohio University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1420642948.

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Annett, Stephanie Louise. "The role of FKBPL and its peptide derivatives in targeting stemness." Thesis, Queen's University Belfast, 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.725332.

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FKBPL is a secreted protein with well-established anti-angiogenic activity and a novel therapeutic peptide, ALM201, derived from the protein has entered Phase l/ll clinical trial in ovarian cancer patients. Ovarian cancer is the most lethal gynaecologic cancer with a high incidence of recurrent chemo-resistant disease and this has been attributed to a subpopulation of cancer stem cells (CSCs), which escape standard therapies and drive metastatic spread. ALM201 binds to the cell surface receptor antigen, CD44, a classic marker of CSCs, and for the first time, we demonstrate ALM201's ability to target ovarian CSCs. Tumoursphere assays have demonstrated that ALM201 is effective at reducing ovarian CSCs in a range of cell lines and primary patient samples in vitro and reduced the CD44+CD117+ ovarian CSC subpopulation. Clonogenic assays suggest that ALM201 mediates ovarian CSC differentiation; a similar observation was previously noted in breast cancer. In vitro ALM201 displayed potent anti-CSC activity in the high grade serous (HGS) ovarian cancer cell line, OVCAR3, however, it displayed no anti-angiogenic or anti-CSC efficacy in in vivo models. In contrast, ALM201 treatment of Kuramochi xenografts resulted in significant growth delay and a 10 fold decrease in CSCs in in vivo experiments. Upon CD31/PAS staining, the Kuramochi xenografts displayed an extensive CD31+ vasculature network, which was disrupted by treatment with ALM201. On the other hand, the OVCAR3 xenografts had relatively few CD31+ blood vessels but had extensive PAS+ vasculogenic mimicry (VM) networks; which ALM201 did not target. Furthermore, OVCAR3 xenografts dramatically up regulated the inflammatory cytokines IL-6 and IL-8, in comparison to the Kuramochi xenografts, and as a result ALM201 had no effect on the CSC sub-population. In a tissue microarray of HGS ovarian cancer patients, high FKBPL expression correlated with an increase in progression free interval thus indicating a role for FKBPL as a prognostic biomarker in the clinic. Endocrine therapies are commonly used to prevent ER+ breast cancer release however, findings suggest that they may be increasing treatment resistant breast CSCs. FKBPLs preclinical peptide AD-01 has previously shown potent anti-CSC activity in the breast cancer setting and here we demonstrate its ability to abrogate endocrine enrichment of CSCs in both cell lines and patient samples. Furthermore, we demonstrate using in vivo limiting dilution models that ALM201 alone or in combination with tamoxifen was effective at delaying tumour recurrence by 12 days and 21 days, respectively. FKBPL and its peptide derivatives down regulate the DLL4/Notch pathway, a regulator of CSC self-renewal, thus indicating a novel mechanism of action. In the haemopoietic setting, ALM201 inhibited migration of chronic lymphocytic leukaemia (CLL) - like cell lines without inducing apoptosis. In an in vivo model of CLL, treatment of ALM201 resulted in a compartmental shift of the cells from the bone marrow to the peripheral blood and spleen. Furthermore, in vitro studies of acute lymphocytic leukaemia (AML) cell lines show that the combination of ALM201 and all trans retinoic acid (ATRA) significantly reduces cell viability, compared to ATRA alone. Analysis of AML cell morphology indicates that ALM201 may be inducing cellular differentiation and thus overcoming the characteristic maturation arrest of this disease. In summary, high FKBPL levels is associated with progression free survival in HGS ovarian cancer patients and the clinical FKBPL peptide, ALM201, effectively targets angiogenesis and CSCs in well-vascularised HGS ovarian cancer thus enhancing the efficacy of this agent in the clinic. In addition, we have demonstrated additional indications for ALM201 in treating endocrine resistance in breast cancer and a novel role in haematopoietic malignancies.
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Books on the topic "Stemness"

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Khersonskiĭ, B. G. Poka ne stemnelo. Novoe literaturnoe obozrenie, 2010.

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Anaerobiosis and Stemness. Elsevier, 2016. http://dx.doi.org/10.1016/c2013-0-15565-1.

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Ivanovic, Zoran, and Marija Vlaski-Lafarge. Anaerobiosis and Stemness: An Evolutionary Paradigm for Therapeutic Applications. Elsevier Science & Technology Books, 2015.

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Ivanovic, Zoran, and Marija Vlaski-Lafarge. Anaerobiosis and Stemness: An Evolutionary Paradigm for Therapeutic Applications. Elsevier Science & Technology Books, 2015.

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Book chapters on the topic "Stemness"

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Pavlović, Mirjana, and Ksenija Radotić. "Stemness and Stem Cell Markers." In Animal and Plant Stem Cells. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47763-3_5.

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Zhang, Yan, Zongjin Li, and Na Liu. "The Stemness of Perinatal Stem Cells." In Perinatal Stem Cells. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-2703-2_3.

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Suo, Zhenhe, Jian-Guo Wen, and Jahn M. Nesland. "Stemness Regulation of Somatic Cancer Cells." In Stem Cells and Cancer Stem Cells, Volume 11. Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7329-5_12.

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Yun, Zhong, and Qun Lin. "Hypoxia and Regulation of Cancer Cell Stemness." In Advances in Experimental Medicine and Biology. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5915-6_2.

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Ray, Suman Kumar, and Sukhes Mukherjee. "Hypoxia and Regulation of Cancer Cell Stemness." In Hypoxia and Tumor Microenvironment. Springer Nature Singapore, 2025. https://doi.org/10.1007/978-981-96-1016-7_8.

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Coyle, Krysta M., Margaret L. Thomas, Mohammad Sultan, and Paola Marcato. "Targeting Key Stemness-Related Pathways in Human Cancers." In Cancer Stem Cells: Emerging Concepts and Future Perspectives in Translational Oncology. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-21030-8_15.

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Su, Zhaohui, and Guillaume Bourque. "Retrotransposon-Derived Regulatory Regions and Transcripts in Stemness." In Human Retrotransposons in Health and Disease. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48344-3_8.

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Taniguchi, Hiroaki, and Kohzoh Imai. "PRDM14, a Zinc Finger Protein, Regulates Cancer Stemness." In Methods in Molecular Biology. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8799-3_1.

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Das, Bikul, Rika Tsuchida, Sylvain Baruchel, David Malkin, and Herman Yeger. "The Idea and Evidence for the Tumor Stemness Switch." In Regulatory Networks in Stem Cells. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-227-8_35.

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Arreba-Tutusaus, Patricia, and Florian H. Heidel. "Signaling Pathways Maintaining Stemness in Adult Hematopoietic Stem Cells." In Adult Stem Cells. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9569-7_1.

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Conference papers on the topic "Stemness"

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Dolgasheva, D. S., E. A. Kravtsova, I. A. Tsydenova, et al. "EFFECT OF THE NUMBER OF STEMNESS GENE AMPLIFICATIONS ON THEIR EXPRESSION LEVEL AND SUBPOPULATION COMPOSITION OF CELL LINES AND TUMORS OF BREAST CANCER PATIENTS." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-314.

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Metastatic disease is the main cause of death in cancer patients; therefore, it is relevant to study various mechanisms of metastasis. The aim of this work is to study the influence of the number of stemness gene amplifications on the subpopulation composition of tumor cell lines, as well as to establish the dependence of the level of stemness gene expression on the number of amplifications in cell lines and tumors of breast cancer patients.
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Gaptulbarova, K. A., K. V. Nevskaya, D. S. Tsydenova, D. S. Dolgasheva, A. G. Pershina, and N. V. Litviakov. "ALTERATION OF THE TRANSCRIPTOME OF GENETICALLY MODIFIED BREAST CANCER LINES." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-307.

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We have previously shown an association of the ability of tumour cells to dedifferentiate to stem cells depending on the number of stemness gene amplifications that account for their overexpression. The breast cancer cell line BT549 has a single KLF5 stemness gene amplification and the lowest ability to dedifferentiate to form mammospheres of any standard breast tumour line. In due course, the MDA-MB231 cell line was characterised by the presence of MYC gene amplifications and a high ability to dedifferentiate to form mammospheres. Using CRISPER/Cas9 method, genetically modified BT549 and MDA-MB231 cell lines with high and low MYC gene expression, respectively, were obtained.
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Kang Li, Eric D. Miller, Mei Chen, Takeo Kanade, Lee E. Weiss, and Phil G. Campbell. "Computer vision tracking of stemness." In 2008 5th IEEE International Symposium on Biomedical Imaging (ISBI 2008). IEEE, 2008. http://dx.doi.org/10.1109/isbi.2008.4541129.

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Hanauske-Abel, Hartmut, Sukwinder Singh, Mainul Hoque, et al. "411 Cancer cell stemness and collagen regulators of stemness in uterine serous carcinoma (USC) mirror ovarian serous cancer (OSC) cell stemness: evidence emerging from ARK1-USC." In ESGO SoA 2020 Conference Abstracts. BMJ Publishing Group Ltd, 2020. http://dx.doi.org/10.1136/ijgc-2020-esgo.73.

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Karthaus, Wouter, Matan Hofree, Danielle Choi, et al. "Abstract 5722: Acquired stemness by luminal cells." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5722.

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Herlyn, Meenhard, Alexander Roesch, Mizuho Fukunaga-Kalabis, and Raj Somasundaram. "Abstract SY12-02: Dynamic stemness in melanoma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-sy12-02.

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Odarenko, K. V., O. V. Salomatina, N. F. Salakhutdinov, M. A. Zenkova, and A. V. Markov. "SEARCH FOR REGULATORY GENES AND SMALL-MOLECULAR INHIBITORS OF THE HIGHLY AGGRESSIVE PHENOTYPE OF GLIOBLASTOMA." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-279.

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Four sets of RNA-sequencing data were re-analyzed, and INHBA and VEGFC were found to be novel regulators of the highly aggressive mesenchymal phenotype of glioblastoma; their expression was validated in vitro. In the library of amide derivatives of soloxolone, the compound Jil-46 was identified, which blocked glial‑mesenchymal transition (GMT), inhibited stemness, and induced apoptosis in U87 glioblastoma cells.
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Malta, Tathiane, Artem Sokolov, Andrew J. Gentles, et al. "Abstract LB-004: Molecular hallmarks of cancer: Stemness." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-004.

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Malta, Tathiane M., Artem Sokolov, Andrew J. Gentles, et al. "Abstract LB-373: Comprehensive analysis of cancer stemness." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-lb-373.

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srivastava, Chitrangda, Khushboo Irshad, Arpit Sahu, et al. "Abstract 2077: Snail modulates stemness properties in hypoxic Glioblastoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2077.

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Reports on the topic "Stemness"

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Wu, Fangting. Exosome Mediates Stemness Transfer from Prostate Epithelial Progenitors to Prostate Cancer Cells. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada590430.

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จันทรวิสูตร, นพัต. การใช้ Differentiation Therapy ในการเปลี่ยนแปลงสภาวะเหนือพันธุกรรมและความรุนแรงของเซลล์มะเร็งในการรักษามะเร็งสมองชนิดกลัยโอบลาสโตมา. คณะแพทยศาสตร์ จุฬาลงกรณ์มหาวิทยาลัย, 2018. https://doi.org/10.58837/chula.res.2018.38.

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มะเร็งสมองชนิดกลัยโอบาสโตมา (Glioblastoma) เป็นมะเร็งสมองชนิดที่พบมากที่สุด และมีความรุนแรงมากที่สุดชนิดหนึ่งเมื่อเทียบกับมะเร็งชนิดอื่น ๆ โดยมีอัตราการรอดชีวิตของผู้ป่วยต่ำ เนื่องจากทางเลือกของวิธีการรักษามีน้อย และผู้ป่วยมักเกิดการกลับเป็นซ้ำ นำมาซึ่งความจำเป็นในการศึกษาเพิ่มเติมเกี่ยวกับชีววิทยาของเซลล์มะเร็งชนิดนี้ เพื่อเพิ่มความเข้าใจที่จะทำให้นำไปสู่หนทางการรักษาได้ในอนาคต การศึกษาวิจัยนี้ต้องการศึกษาความสัมพันธ์ระหว่างความรุนแรงของมะเร็งสมองชนิดกลัยโอบลาสโตมา กับการแสดงออกของยีนที่มีความเกี่ยวข้องกับความเป็นเซลล์ต้นกำเนิด (Stemness-related genes) โดยเฉพาะ LIN28/let-7 pathway และวิถีการส่งสัญญาณในเซลล์มะเร็ง โดยมุ่งเน้นศึกษาวิถีเอ็มทอร์สอง (Mtorc2 signaling pathway) นอกจากนี้ ยังต้องการวิเคราะห์ความสัมพันธ์ระหว่าง Mtorc2 signaling pathway ในเซลล์มะเร็งสมองกับยีนดังกล่าว โดยในการศึกษานี้ได้ทำการเปรียบเทียบคุณสมบัติของเซลล์มะเร็งกลัยโอมาชนิดเกรดสูง (U87MG) และเกรดต่ำ (H4) ได้แก่ ความสามารถในการเจริญ ความสามารถในการเคลื่อนที่การแสดงออกของยีนและการแสดงออกของโปรตีนที่เกี่ยวข้อง ซึ่งพบว่า ปริมาณการแสดงออกของโปรตีน LIN28B และระดับกิจกรรมของโปรตีนในวิถี mTORC2 ในเซลล์ U87MG มีความสอดคล้องกับความสามารถในการเคลื่อนที่ และความมีลักษณะคล้าย mesenchymal cells นอกจากนี้ ยังพบว่าตำแหน่งของกลุ่มโปรตีน mTORC2 ในเซลล์ น่าจะเป็นปัจจัยสำคัญที่ทำให้เซลล์มะเร็งสมองชนิดกลัยโอบลาสโตมามีความรุนแรงมากกว่าเซลล์มะเร็งกลัยโอมาระยะเริ่มต้น ทั้งนี้ ในประชากรของ U87MG พบว่ามีลักษณะของความหลากหลายทางกายภาพสูง โดยมีเซลล์ที่มี ขนาดต่างๆ กันอยู่ในประชากร ซึ่งสามารถแบ่งออกเป็นสองกลุ่ม ได้แก่ ประชากรเซลล์ขนาดใหญ่ และประชากรเซลล์ขนาดเล็ก ซึ่งเมื่อทำการแยกเซลล์ทั้งสองประชากรออกจากกัน ก็พบว่าการแสดงออกของยีนที่เกี่ยวข้องกับความเป็นเซลล์ต้นกำเนิด (OCT4, SOX2 และ LIN28B) และยีนที่เกี่ยวข้องกับ mTORC2 (RICTOR) มีการแสดงออกที่เปลี่ยนแปลงไป และส่งผลต่อความสามารถในการเจริญ โดยหากเซลล์ประชากร ขนาดต่าง ๆ อยู่แยกจากกัน จะทำให้ความเป็นเซลล์ต้นกำเนิดและอัตราการเจริญลดน้อยลงอย่างมีนัยสำคัญ ซึ่งเป็นข้อมูลที่จะสามารถนำไปต่อยอดในการศึกษาได้ในอนาคตเพื่อเข้าใจถึงพื้นฐานและการสื่อสารภายใน เซลล์มะเร็งสมองชนิดกลัยโอบลาสโตมา รวมไปถึงมะเร็งชนิดอื่น ๆ ที่มีความรุนแรง เพื่อใช้สำหรับการพัฒนาวิธีการรักษาแบบใหม่โดยไม่มุ่งเน้นที่การทำลายเซลล์มะเร็งเป็นหลักแต่เป็นการปรับให้ความรุนแรงของเซลล์มะเร็งลดลง
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