Готові списки джерел за темами / Lung Stem Cell

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Добірка наукової літератури з теми "Lung Stem Cell"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "Lung Stem Cell"

Kim, Carla F. "Paving the road for lung stem cell biology: bronchioalveolar stem cells and other putative distal lung stem cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 5 (November 2007): L1092—L1098. http://dx.doi.org/10.1152/ajplung.00015.2007.

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New discoveries in stem cell biology are making the biology of solid tissues increasingly complex. Important seminal studies demonstrating the presence of damage-resistant cell populations together with new isolation and characterization techniques suggest that stem cells exist in the adult lung. More detailed in vivo molecular and cellular characterization of bronchioalveolar stem cells (BASCs), other putative lung stem and progenitor cells, and differentiated cells is needed to determine the lineage relationships in adult lung. Lung diseases such as cystic fibrosis or chronic obstructive pulmonary disease, as well as the most common form of lung cancer in the United States, all involve apparent bronchiolar and alveolar cell defects. It is likely that the delicate balance of stem, progenitor, and differentiated cell functions in the lung is critically affected in patients with these devastating diseases. Thus the discovery of BASCs and other putative lung stem cells will lay the foundation for new inroads to understanding lung biology related to lung disease.

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Sentek, Hanna, and Diana Klein. "Lung-Resident Mesenchymal Stem Cell Fates within Lung Cancer." Cancers 13, no. 18 (September 16, 2021): 4637. http://dx.doi.org/10.3390/cancers13184637.

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Lung-resident mesenchymal stem cells (LR-MSCs) are non-hematopoietic multipotent stromal cells that predominately reside adventitial within lung blood vessels. Based on their self-renewal and differentiation properties, LR-MSCs turned out to be important regulators of normal lung homeostasis. LR-MSCs exert beneficial effects mainly by local secretion of various growth factors and cytokines that in turn foster pulmonary regeneration including suppression of inflammation. At the same time, MSCs derived from various tissues of origins represent the first choice of cells for cell-based therapeutic applications in clinical medicine. Particularly for various acute as well as chronic lung diseases, the therapeutic applications of exogenous MSCs were shown to mediate beneficial effects, hereby improving lung function and survival. In contrast, endogenous MSCs of normal lungs seem not to be sufficient for lung tissue protection or repair following a pathological trigger; LR-MSCs could even contribute to initiation and/or progression of lung diseases, particularly lung cancer because of their inherent tropism to migrate towards primary tumors and metastatic sites. However, the role of endogenous LR-MSCs to be multipotent tumor-associated (stromal) precursors remains to be unraveled. Here, we summarize the recent knowledge how ‘cancer-educated’ LR-MSCs impact on lung cancer with a focus on mesenchymal stem cell fates.

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Ionescu, Lavinia, Roisin N. Byrne, Tim van Haaften, Arul Vadivel, Rajesh S. Alphonse, Gloria J. Rey-Parra, Gaia Weissmann, Adam Hall, Farah Eaton, and Bernard Thébaud. "Stem cell conditioned medium improves acute lung injury in mice: in vivo evidence for stem cell paracrine action." American Journal of Physiology-Lung Cellular and Molecular Physiology 303, no. 11 (December 1, 2012): L967—L977. http://dx.doi.org/10.1152/ajplung.00144.2011.

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Mortality and morbidity of acute lung injury and acute respiratory distress syndrome remain high because of the lack of pharmacological therapies to prevent injury or promote repair. Mesenchymal stem cells (MSCs) prevent lung injury in various experimental models, despite a low proportion of donor-derived cell engraftment, suggesting that MSCs exert their beneficial effects via paracrine mechanisms. We hypothesized that soluble factors secreted by MSCs promote the resolution of lung injury in part by modulating alveolar macrophage (AM) function. We tested the therapeutic effect of MSC-derived conditioned medium (CdM) compared with whole MSCs, lung fibroblasts, and fibroblast-CdM. Intratracheal MSCs and MSC-CdM significantly attenuated lipopolysaccharide (LPS)-induced lung neutrophil influx, lung edema, and lung injury as assessed by an established lung injury score. MSC-CdM increased arginase-1 activity and Ym1 expression in LPS-exposed AMs. In vivo, AMs from LPS-MSC and LPS-MSC CdM lungs had enhanced expression of Ym1 and decreased expression of inducible nitric oxide synthase compared with untreated LPS mice. This suggests that MSC-CdM promotes alternative macrophage activation to an M2 “healer” phenotype. Comparative multiplex analysis of MSC- and fibroblast-CdM demonstrated that MSC-CdM contained several factors that may confer therapeutic benefit, including insulin-like growth factor I (IGF-I). Recombinant IGF-I partially reproduced the lung protective effect of MSC-CdM. In summary, MSCs act through a paracrine activity. MSC-CdM promotes the resolution of LPS-induced lung injury by attenuating lung inflammation and promoting a wound healing/anti-inflammatory M2 macrophage phenotype in part via IGF-I.

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Kuo, Ming-Han, Pei-Yu Chen, Yi-Ping Yang, Ming-Yi Zheng, Chia-Cheng Miao, Kuo-Chang Wen, Kuo-Ming Chang, et al. "Cytokine and Epigenetic Regulation of Programmed Death-Ligand 1 in Stem Cell Differentiation and Cancer Cell Plasticity." Stem Cells 39, no. 10 (June 28, 2021): 1298–309. http://dx.doi.org/10.1002/stem.3429.

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Abstract Programmed death-ligand 1 (PD-L1), an immune checkpoint ligand, is recognized as a potential target for cancer immunotherapy as well as for the induction of transplantation tolerance. However, how the crosstalk between stem cell programming and cytokine signaling regulates PD-L1 expression during stem cell differentiation and cancer cell plasticity remains unclear. Herein, we reported that PD-L1 expression was regulated by SOX2 during embryonic stem cell (ESC) differentiation and lung cancer cell plasticity. PD-L1 was induced during ESC differentiation to fibroblasts and was downregulated during SOX2-mediated reprogramming of fibroblasts to induced pluripotent stem cells (iPSCs). Furthermore, SOX2 activation affected cancer cell plasticity and inhibited PD-L1 expression in lung cancer cells. We discovered that the H3K27ac signal at the PD-L1 locus was enhanced during ESC differentiation to fibroblasts as well as during cancer plasticity of SOX2-positive lung cancer cells to SOX2-negative counterparts. Romidepsin, an epigenetic modifier, induced PD-L1 expression in lung cancer cells, whereas TGF-β stimulation downregulated SOX2 but upregulated PD-L1 expression in lung cancer cells. Furthermore, in addition to PD-L1, the expressions of EGFR and its ligand HBEGF were downregulated by activation of endogenous SOX2 expression during lung cancer cell plasticity and iPSC reprogramming, and the activation of EGFR signaling by HBEGF upregulated PD-L1 expression in lung cancer cells. Together, our results reveal the crosstalk between SOX2 programming and cytokine stimulation influences PD-L1 expression, and these findings may provide insights into PD-L1-mediated therapeutics.

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Kotton, Darrell N., and Alan Fine. "Lung stem cells." Cell and Tissue Research 331, no. 1 (September 6, 2007): 145–56. http://dx.doi.org/10.1007/s00441-007-0479-2.

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Omar, Said A., Amal Abdul-Hafez, Sherif Ibrahim, Natasha Pillai, Mohammed Abdulmageed, Ranga Prasanth Thiruvenkataramani, Tarek Mohamed, Burra V. Madhukar, and Bruce D. Uhal. "Stem-Cell Therapy for Bronchopulmonary Dysplasia (BPD) in Newborns." Cells 11, no. 8 (April 9, 2022): 1275. http://dx.doi.org/10.3390/cells11081275.

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Premature newborns are at a higher risk for the development of respiratory distress syndrome (RDS), acute lung injury (ALI) associated with lung inflammation, disruption of alveolar structure, impaired alveolar growth, lung fibrosis, impaired lung angiogenesis, and development of bronchopulmonary dysplasia (BPD) with severe long-term developmental adverse effects. The current therapy for BPD is limited to supportive care including high-oxygen therapy and pharmacotherapy. Recognizing more feasible treatment options to improve lung health and reduce complications associated with BPD is essential for improving the overall quality of life of premature infants. There is a reduction in the resident stem cells in lungs of premature infants with BPD, which strongly suggests a critical role of stem cells in BPD pathogenesis; this warrants the exploration of the potential therapeutic use of stem-cell therapy. Stem-cell-based therapies have shown promise for the treatment of many pathological conditions including acute lung injury and BPD. Mesenchymal stem cells (MSCs) and MSC-derived extracellular vesicles (EVs) including exosomes are promising and effective therapeutic modalities for the treatment of BPD. Treatment with MSCs and EVs may help to reduce lung inflammation, improve pulmonary architecture, attenuate pulmonary fibrosis, and increase the survival rate.

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Wu, Huijuan, and Nan Tang. "Stem cells in pulmonary alveolar regeneration." Development 148, no. 2 (January 15, 2021): dev193458. http://dx.doi.org/10.1242/dev.193458.

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ABSTRACTThe lungs are constantly exposed to the external environment and are therefore vulnerable to insults that can cause infection and injury. Maintaining the integrity and barrier function of the lung epithelium requires complex interactions of multiple cell lineages. Elucidating the cellular players and their regulation mechanisms provides fundamental information to deepen understanding about the responses and contributions of lung stem cells. This Review focuses on advances in our understanding of mammalian alveolar epithelial stem cell subpopulations and discusses insights about the regeneration-specific cell status of alveolar epithelial stem cells. We also consider how these advances can inform our understanding of post-injury lung repair processes and lung diseases.

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OTTO, W. R. "Lung stem cells." International Journal of Experimental Pathology 78, no. 5 (October 30, 2003): 291–310. http://dx.doi.org/10.1046/j.1365-2613.1997.370366.x.

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MAIUTHED, ARNATCHAI, WIPA CHANTARAWONG, and PITHI CHANVORACHOTE. "Lung Cancer Stem Cells and Cancer Stem Cell-targeting Natural Compounds." Anticancer Research 38, no. 7 (July 2018): 3797–809. http://dx.doi.org/10.21873/anticanres.12663.

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Yin, Huijing, Bo Jing, Dongliang Xu, Wenzheng Guo, Beibei Sun, Jie Zhang, Yueling Liao, et al. "Identification of Active Bronchioalveolar Stem Cells as the Cell of Origin in Lung Adenocarcinoma." Cancer Research 82, no. 6 (March 15, 2022): 1025–37. http://dx.doi.org/10.1158/0008-5472.can-21-2445.

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Abstract While initiation is established as a critical step in tumorigenesis, the identity of the cell of origin for lung adenocarcinoma and the mechanism controlling susceptibility to initiation remain elusive. Here we show that lung tumor suppressor Gprc5a-knockout (KO) mice are susceptible to initiation of lung tumorigenesis. Bronchioalveolar stem cells (BASC) and alveolar type 2 (AT2) cells were aberrantly expanded in Gprc5a-KO mouse lungs compared with those in wild-type (WT) mice, suggesting that Gprc5a-KO might confer susceptibility to initiation by increasing the cell of origin in mouse lungs. BASCs from Gprc5a-KO mice (KO-BASC) exhibited significantly increased stemness and self-renewal potential and reduced differentiation capacity compared with BASCs from WT mice (WT-BASC). AT2 cells did not possess self-renewal potential regardless of Gprc5a status. KO-BASCs expressed a stem-like gene profile with upregulated Abcg2, EGFR, and NF-κB signaling compared with WT-BASCs. Blockade of EGFR and NF-κB signaling inhibited both expansion of BASC and AT2 cells and lung tumorigenesis. Abcg2 was expressed in active KO-BASCs as well as in lung tumor cells but not in quiescent WT-BASCs or AT2 cells, supporting that lung adenocarcinoma cells are derived from Abcg2-positive KO-BASCs (active). Taken together, Gprc5a deletion leads to expansion of active BASCs via dysregulated EGFR and NF-κB signaling that confers susceptibility to initiation of lung tumorigenesis, marking Abcg2-positive BASCs as candidate cell of origin for lung adenocarcinoma. Significance: Identification of active bronchioalveolar stem cells as lung adenocarcinoma cells of origin provides insights into mechanisms of lung tumorigenesis and could facilitate development of effective strategies for cancer prevention and therapy. See related commentary by Osborne and Minna, p. 972

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Більше джерел

Дисертації з теми "Lung Stem Cell"

Sarvi, Sana. "Small cell lung cancer and cancer stem cell-like cells." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9542.

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Small cell lung cancer (SCLC) is a highly aggressive malignancy with extreme mortality and morbidity. Although initially chemo- and radio-sensitive, almost inevitable recurrence and resistance occurs. SCLC patients often present with metastases, making surgery not feasible. Current therapies, rationally designed on underlying pathogenesis, produce in vitro results, however, these have failed to translate into satisfactory clinical outcomes. Recently, research into cancer stem cells (CSCs) has gained momentum and form an attractive target for novel therapies. Based on this concept, CSCs are the cause of neoplastic tissue development that are inherently resistant to chemotherapy, explaining why conventional therapies can shrink the tumour but are unable to eliminate the tumour completely, leading to eventual recurrence. Here I demonstrate that SCLC H345 and H69 cell lines contain a subset of cells expressing CD133, a known CSC marker. CD133+ SCLC sub-population maintained their stem cell-like phenotype over a prolonged period of culture, differentiated in appropriate conditions and expressed the embryonic stem cell marker Oct-4 indicating their stem-like phenotype. Additionally, these cells displayed augmented clonogenic efficacy, were chemoresistant and tumorigenic in vivo, distinct from the CD133- cells. Thus, the SCLC CD133 expressing cells fulfil most criteria of CSClike definition. The molecular mechanisms associated with CD133+ SCLC chemoresistance and growth is unknown. Up-regulated Akt activity, a known promoter of resistance with survival advantage, was observed in CD133+ SCLC cells. Likewise, these cells demonstrated elevated expression of Bcl-2, an anti-apoptotic protein compared to their negative counterpart explaining CD133+ cell chemoresistance phenotype. Additionally, CD133+ cells revealed greater expression of neuropeptide receptors, gastrin releasing peptide (GRP) and V1A receptors compared to the CD133- cells. Addition of exogenous GRP and arginine vasopressin (AVP) to CD133+ SCLC cells promoted their clonogenic growth in semi-solid medium, illustrating for the first time neuropeptide dependent growth of these cells. A novel peptide (peptide-1) was designed based on the known structure of the substance P analogues that have shown benefit in animal models and in early clinical trials. This compound inhibited the growth of SCLC cells in in vitro with improved potency and stability compared to previous analogues and reduced tumorigenicity in vivo. Interestingly, peptide-1 was more effective in CD133+ cells due to increased expression of neuropeptide receptors on these cells. In conclusion, my results show that SCLC cells retain a sub-population of cells that demonstrate CSC-like phenotype. Preferential activation of Akt and Bcl-2 survival pathways and enhanced expression of neuropeptide receptors contribute to CD133+ SCLC chemoresistance and growth. Therefore, it can be proposed that CD133+ cells are the possible cause of SCLC development, treatment resistance and disease recurrence. Despite being chemoresistant, CD133+ cells demonstrated sensitivity to peptide-1. The identification of such new analogue that demonstrates efficacy towards resistant CD133+ SCLC cells is a very exciting step forward in the identification of a potential new therapy for resistant disease.

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Ismail, Siti N. "Stem cell bioprocessing : the bioengineering of lung epithelium in 3D from embryonic stem cells." Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/9013.

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Stem cell therapies and tissue engineering strategies are required for the clinical treatment of respiratory diseases. Previous studies have established protocols for the differentiation of airway epithelium from stem cells but have involved costly and laborious culture methods. The aim of this thesis was to achieve efficient and reproducible maintenance and differentiation of embryonic stem cells to airway epithelium, in 2D and 3D culture, by developing appropriate bioprocessing technology. Firstly, the 2D differentiation process of human and murine ES cells into pulmonary epithelial cells was addressed. The main finding in was that the proportion of type II pneumocytes, the major epithelial component of the gas-exchange area of lung, differentiated with this method was higher than that obtained in previous sudies, 33% of resultant cell expressed the specific marker surfactant protein C (SPC) compared with up to 10%. Secondly, the maintenance and differentiation was carried out in 3D. A protocol was devised that maintained undifferentiated human ES cells in culture for more than 200 days encapsulated in alginate without any feeder layer or growth factors. For ES cell differentiation in 3D, a method was devised to provide a relatively cheap and simple means of culture and use medium conditioned by a human pneumocyte tumour cell line (A549). The differentiation of human and murine ES cells into pulmonary epithelial cells, particularly type II pneumocytes, was found to be upregulated by culture in this conditioned medium, with or without embryoid body formation. The third step was to test whether this differentiation protocol was amenable to scale-up and automation in a bioreactor using cell encapsulation. It was possible to show that encapsulated murine ES cells cultured in static, co-culture or rotating wall bioreactor (HARV) systems, differentiate into endoderm and, predominantly, type I and II pneumocytes. Flow cytometry revealed that the mean yield of differentiated type II pneumocytes was around 50% at day 10 of cultivation. The final stage of the work was to design and produce a perfusion system airlift bioreactor to mimic the pulmonary microenvironment in order to achieve large scale production of biologically functional tissue. The results of these studies thus provide new protocols for the maintenance of ES cells and their differentiation towards pulmonary phenotypes that are relatively simple and cheap and can be applied in bioreactor systems that provide for the kind of scale up of differentiated cell production needed for future clinical applications.

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Baothman, Bandar. "Regulation of human lung mast cell responses by stem cell factor." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/20426/.

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Stem Cell Factor (SCF) is widely recognised as a crucial growth factor for mast cells and has been shown to mediate the development, differentiation and proliferation of mast cells from precursors. These effects of SCF are thought to be mediated by the c-KIT receptor. Whether SCF directly activates mast cells is more contentious and most of the data suggests that SCF can ‘prime’ mast cells for enhanced responses to IgE-dependent activation. The principal aim of the present work was to determine whether SCF activates human lung mast cells. Our studies showed that SCF was an effective direct activator of human lung mast cells. Although not as effective as anti-IgE at inducing histamine release, nonetheless, in about a third of all mast cell preparations, SCF induced substantial levels of release. Even more strikingly, SCF was as effective as anti-IgE at inducing prostaglandin D2 (PGD2) generation from mast cells. By contrast, SCF was relatively ineffective at inducing cytokine generation from human lung mast cells, a feature shared by other stimuli such as anti-IgE. The effects of SCF on histamine and PGD2 release were blocked by the c-KIT inhibitors imatinib, dasatinib and nilotinib suggesting that SCF acts through the c-KIT receptor to activate mast cells. Further studies were performed to evaluate the mechanism by which SCF and anti-IgE drive PGD2 generation from mast cells. In particular, the role of the enzyme cyclooxygenase (COX) on PGD2 generation was evaluated. Studies utilising COX-1 and COX-2 selective inhibitors demonstrated that COX-1 was the isoform that drives PGD2 generation from mast cells. This finding was further supported by Western blotting studies showing that COX-1 is the principal isoform expressed by mast cells. In total, these findings indicate that SCF can directly activate human lung mast cells through the c-KIT receptor to generate substantial amounts of PGD2 and variable amounts of histamine. The data also show that COX-1 is the principal isoform involved in PGD2 generation from human lung mast cells. Overall these studies indicate that SCF is a far more effective activator of human lung mast cells than hitherto appreciated.

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Alaqel, Abdullah. "The directed differentiation of human embryonic stem cells to lung cell lineages." Thesis, University of Bath, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.760955.

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Human embryonic stem cells (hESCs) show significant therapeutic potential in treating degenerative disorders. This is in part because of their ability to produce a limitless supply of starting cells and their potential to differentiate into more than 200 different cell types. The aim of the current research was to generate a robust stage wise protocol for the differentiation of hESCs to respiratory epithelial cells. The epithelial cells could then be used either for transplantation studies or, as an in vitro model for drug toxicity testing. In order to achieve this goal, we must identify the key steps in lung development and apply these to the differentiation protocol. In this study, we maintained Shef3 hESCs in their undifferentiated pluripotent state to expand the cells prior to the differentiated towards the definitive endoderm (DE) lineage. I used a two-stage protocol based on culture with a novel glycogen synthase kinase-3 (GSK-3) inhibitor (termed 1m), along with Activin-A. We confirmed the status of the cells by a combination of immunostaining and PCR. We showed loss of the pluripotency markers (Sox2 and Oct3/4) and gain of DE markers (Sox17, FoxA2 and CXCR4). After the induction of DE from hESCs, we then treated the cells with transforming growth factor (TGF)-β and bone morphogenetic protein (BMP) pathway inhibitors (SB431542 and Noggin respectively). This combinatorial treatment resulted in the differentiation into the anterior foregut endoderm (AFE) lineage based on expression of Pax9 and FoxA2 plus the up-regulation of Sox2. Further differentiation of AFE derivatives into more mature epithelial cells, termed lung progenitor cells (LPCs), was achieved following the treatment of AFE cells with a cocktail of trophic factors (BMP4, EGF, bFGF, FGF10, KGF and Wnt3a) yielded a population of NKX2.1-positive and FoxA2-positive cells that potentially corresponded to the lung lineage. Finally, prolonged treatment with FGF10 and FGF2 on LPC derived hESCs induced proximal (CC10, MUC5AC) and distal (SPB, SPC) airway epithelial cells. In addition, we also utilised the ectopic expression of an adenovirus expressing NKX2.1 to promote lung maturation. In conclusion, we have generated a protocol for the differentiation of hESCs into mature lung-like cells. The generation of these cells in vitro could potentially lead to a better in vitro model for toxicity testing and the development of novel therapies for promoting regeneration of lungs in patients with severe lung disorders.

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Wong, Kit-man Sunny, and 王傑民. "Isolation and characterization of cancer stem cells in non-small cell lung cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47250665.

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Tumor heterogeneity has long been observed and recognized as a challenge to cancer therapy. The cancer stem cell (CSC) model is one of the hypotheses proposed to explain such a phenomenon. A specific cancer stem cell marker has not been determined for non-small cell lung cancers (NSCLC), preventing the definitive evaluation of whether the biology of NSCLC is governed by the CSC model. This study aimed to analyze the expression of candidate CSC markers and using the identified putative marker, to isolate CSC and determine the applicability of the CSC model in NSCLC. The expression or activities of four putative stem cell markers, CD24, CD44, CD133 and aldehyde dehydrogenase 1 (ALDH1) were measured by flow cytometry in eight NSCLC cell lines before and after chemotherapy for 24 hours. Markers with increased expression after treatment were considered potential CSC markers and used for isolating tumor cell subpopulations from the untreated cell lines by fluorescence-activated cell sorting (FACS). Confirmatory analyses using widely acceptable methodology were performed to test for CSC properties in the marker+ and marker- subpopulations. Isolated subpopulations were further characterized by functional and phenotypic studies. Flow cytometry showed amongst the 4 markers, only ALDH1 expression was significantly enhanced by chemotherapeutic treatment, suggesting ALDH1 could be a CSC marker. Untreated ALDH1+ cells formed significantly more and larger cell spheres in non-adherent, serum-free conditions than ALDH1- cells. Likewise, higher in vitro tumorigenic ability was observed in ALDH1+ subset using colony formation assay. Furthermore, a higher resistance to cytotoxic drugs was observed in ALDH1+ compared to ALDH1- cells. In vivo studies also showed ALDH1+ cells showed higher tumorigenicity than ALDH1- cells; as few as 2,500 ALDH1+ cells formed tumor in SCID mice which were serially transplantable to 2nd and 3rd recipients, while no tumor was formed from ALDH- cells with even ten times the number of cells. Also, expression analysis revealed higher expression of the pluripotency genes, OCT4, NANOG, BMI1 and SOX9, in ALDH1+ cells. In view of previous studies reporting CD44 as a CSC marker in lung cancer, double marker selection of putative CSC was performed to compare ALDH1+CD44+ and ALDH1-CD44+ subpopulations. Results of the spheroid body formation assay and cisplatin treatment experiments revealed the ALDH1+CD44+ subpopulation possessed higher self-renewal ability and chemo-resistance. Cell migration and invasion assays showed differences between the ALDH1+CD44+ and ALDH1- CD44+ subpopulations. The significance of these observations require further investigation. In conclusion, the result showed that ALDH1 could be a marker for NSCLC stem cells as evidenced by enhanced self-renewal and differentiation abilities in ALDH1+ subpopulation. Furthermore, this study observed the presence of at least two potential stem cell subpopulations in NSCLC cells with differential selfrenewal, chemotherapy resistance and cell mobility properties. Further investigations are required to validate these observations and to investigate the underlying mechanisms. Better understanding of these issues would help to solve the challenges brought by tumor heterogeneity in lung cancer therapy.
published_or_final_version
Pathology
Master
Master of Philosophy

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Gadepalli, Venkat Sundar. "ISOLATION AND CHARACTERIZATION OF MULTIPOTENT LUNG STEM CELLS FROM p53 MUTANT MICE MODELS." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3644.

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Recent advances in understanding lung biology have shown evidence for the existence of resident lung stem cells. Independent studies in identifying and characterizing these somatic lung stem cells have shown the potential role of these cells in lung repair and regeneration. Understanding the functional characteristics of these tissue resident stem/progenitor cells has gained much importance with increasing evidence of cancer stem cells, cells in a tumor tissue with stem cell characteristics. Lung cancer is most commonly characterized by loss of p53 function which results in uncontrolled cell divisions. Incidence of p53 point mutations is highest in lung cancer, with a high percentage of missense mutations as a result of tobacco smoking. Certain point mutations in p53 gene results in its oncogenic gain of functions (GOF), with enhanced tumorigenic characteristics beyond the loss of p53 function. However, there are no available data on characterization of lung stem cells carrying GOF mutations and correlating them with those of normal stem cells, in this study, for the first time we show that percentage of Sca-1 expressing subpopulation is significantly higher in the lungs of mice carrying p53 GOF mutations than those in lungs isolated from p53+/+ wild type mice. Further, we successfully established lung cells differentially expressing two cell surface markers, Sca-1 and PDGFR-α, with results demonstrating existence of different subpopulations of cells in the lung. Results from our project demonstrate the importance of p53 GOF mutations as correlated with specific lung cell subpopulations.

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Svensson, Susanne. "In vitro and in vivo inhibition of Chk1 sensitize lung cancer stem cells to chemotherapy." Thesis, Universita' degli Studi di Catania, 2011. http://hdl.handle.net/10761/98.

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Development of resistance to radiation and chemotherapy turns the treatment of solid cancers into a therapeutic challenge. One of the most exciting breakthroughs being explored in cancer research today is the concept of cancer stem cells (CSCs). CSCs are a minority of cells within a tumor that are the source of tumor cell renewal and thereby determine the behavior of tumors, including proliferation, spreading and response to therapy. CSCs are highly resistant to conventional treatment and are therefore emerging as the preferred target of drug therapies in order to obtain eradication of tumors. In this study, we examined the activation of the DNA damage response pathway in CSCs derived from non-small cell lung cancer (NSCLC-CSCs) and their differentiated counterparts after treatment with chemotherapeutic agents commonly used in clinic for lung cancer treatment. Our data show that NSCLC-CSCs possess a highly active DNA damage pathway compared to differentiated progeny and preferentially activate the checkpoint kinase Chk1 in response to DNA damage caused by chemotherapy. This indicates that Chk1 is most likely the main player of drug resistance in NSCLC-CSCs and its targeting might yield significant therapeutic gains. We demonstrate that chemical Chk1 inhibitors dramatically induce NSCLC-CSC death in vitro in combination with DNA damaging drugs. Cell death is induced through a premature activation of the cell cycle regulatory proteins Cdc2 and Cyclin B1, which in turn forces cells with damaged DNA to enter aberrant mitosis, a mechanism known as mitotic catastrophe. Moreover, our results indicate that final cell death occurs through apoptosis. Combination therapy studies have been successfully carried out also in vivo. Chk1 inhibition enhanced the antitumoral effect of conventional chemotherapy in mice xenograft tumor models by increasing tumor latency, potently abrogating tumor growth and reducing tumor mass. We also found a significant reduction of NSCLC-CSCs in xenograft-derived cells, confirming that combination treatment actually targets and reduces the NSCLC-CSCs compartment in vivo. The importance of DNA repair as a resistance mechanism in cancer is a clinically relevant topic and we believe that the combination of selective Chk1 inhibitors with anti-cancer drugs could represent a new therapeutic approach for targeting NSCLC-CSCs and thereby for effective treatment of lung tumors.

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MONTERISI, SIMONA. "HOXB7 IN LUNG CANCER: A NOVEL ROLE IN STEM CELL AND IPS BIOLOGY." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/362619.

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Current diagnostic tools do not allow prognostic evaluation of patients with early stage lung cancer or selection of patients that might benefit from adjuvant chemotherapy. Therefore, the identification of novel prognostic markers in early-stage lung cancer is paramount. In this scenario, the transcription factor HOXB7, belonging to the homeobox family, has been shown to correlate with poor prognosis in different types of cancer and recently also in stage I lung adenocarcinoma. To better understand the prognostic implication of alterations in HOXB7 expression in lung cancer, we performed a bioinformatics analysis of multiple lung cancer expression datasets in order to identify gene sets representing cancer-relevant biological functions enriched in high-HOXB7 expressing tumors. We found several gene sets enriched in high-HOXB7 expressing tumors representing molecular mechanisms involved in epithelial to mesenchymal transition, in cancer progression, and, interestingly, in stemness and cellular reprogramming. Based on these results, we hypothesized that HOXB7 may have a role in the expansion of the stem cell compartment in cancer, a mechanism that has been shown to be a hallmark of enhanced tumorigenicity and of increased metastatic potential. Analysis of the stem-related surface marker CD90 revealed that overexpression of HOXB7 in lung cells increases the CD90high sub population. CD90high, but not CD90low cells, are able to form spheroids, which is an hallmark of stemness. Indeed, the sphere forming efficiency of normal lung BEAS-2B cells was 22% and 1.64% in CD90high and CD90low populations, respectively. In addition, we found that silencing of LIN28B counteracts the expansion of the CD90high population. LIN28B was recently described as an oncogene that regulates the cancer stem cell compartment. We found that LIN28B is under the direct transcriptional control of HOXB7. Therefore, we propose a novel molecular mechanism driven by HOXB7 and can increase stem-like properties in lung cells. We further demonstrated that the HOXB7-LIN28B axis plays an important role in reprogramming of adult cells into induced pluripotent stem cells (iPS). Indeed, HOXB7 may enhance the reprogramming efficiency achieved by the three genes OCT4, KLF4, SOX2 in both mouse embryonic fibroblast and human epithelial BEAS-2B cells by substituting MYC in the transcription factor cocktail of reprogramming factors used by Yamanaka. Of note, LIN28B silencing strongly decreases the number of reprogrammed colonies in high-HOXB7 expressing cells. These findings suggest that HOXB7, through transcriptional induction of the LIN28B gene, activates a program relevant for stem/iPS cell biology and for tumor progression, possibly opening a new line of research for the development of more effective therapies for metastatic lung cancer patients.

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Akunuru, Shailaja. "Regulation of cancer stem cell activity and epithelial mesenchymal transition by Rac1 in Human lung adenocarcinoma cells." University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1314301864.

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Ng, Alvin Vincent Yi Kwan. "Side population in human lung cancer cell lines and tumours is enriched with stem-like cancer cells." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/31784.

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An emerging concept in cancer initiation and development is that cells with characteristics of the stem cell phenotype drive tumour growth and progression. Accumulating evidence reveals that solid tumours such as brain and breast cancer contain primitive cancer stem cells that have high repopulation capacity. Recent studies have demonstrated that adult stem cells can be identified by a side population (SP) phenotype. The work in this thesis was the first in investigating the existence of cancer stem cells in human lung cancer. This study used flow cytometry and the Hoechst 33342 dye efflux assay to isolate and characterise SP cells from various human lung cancer cell lines. In addition, the existence of SP cells in lung cancer tissues obtained from surgical resection was also investigated. Results indicated that all six human lung cancer cell lines contained an SP that could be reliably detected under the experimental conditions used. Evidence was found for asymmetric division by the SP to generate a population resembling the original unsorted population. SP cells and non-SP cells were characterised at the molecular level to compare mRNA expression between the two populations. SP cells from each cell line displayed elevated expression of ATP-Binding Cassette (ABC) transporters associated with multi-drug resistance. In particular, expression of ABCG2 (BRCP1) defines the SP phenotype. Human telomerase reverse transcriptase (hTERT) expression was higher in the SP cells, suggesting this fraction may represent a reservoir with high proliferative potential for generating cancer cells. mRNA levels of MCM7, a member of the mini-chromosome maintenance (MCM) family of proteins, a critical component of the DNA replication complex, was lower in SP cells suggesting that a majority of the cells from the SP fraction were in G₀ of the cell cycle. Levels of mRNA expression of BMI-1, a pathway associated with stem cell self-renewal, were higher in the SP cells compared to the non-SP cells in four of the six cell lines. The Notch-1 pathway was another self-renewal pathway that had increased mRNA expression in five of six cell lines. Functional characterisation of the SP and non-SP were investigated in both in vitro and in vivo. The Matrigel [Trademark] invasion assay demonstrated SP cells as having higher potential for invasiveness than non-SP cells, suggesting there exist a population of stem-like cells within a lung tumour that is involved in the initiation of invasion and metastasis. Non-obese diabetic/severe combined immunodeficiency (NOD/SCID) xenograft transplant experiments showed that SP cells were more tumourigenic compared to non-SP cells. Using a cell viability assay, SP cells were determined to exhibit higher resistance to drugs used to treat lung cancer, some of which are substrates for ABC transporters. Staining patterns of other putative stem cell-related surface markers such as CD24, CD34, CD44 and nestin were also examined and compared between the SP and non-SP. Using the Hoechst efflux assay, SP cells were also isolated from patient tissues, which contained a low but persistent percentage (0.025 - 1.08) of SP cells. Taken together, these studies suggested that SP is an enriched source of tumour re-initiating cells with stem cell properties and may be an important target for effective therapy and a useful tool to investigate the tumourigenic process.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate

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Книги з теми "Lung Stem Cell"

El-Hashash, Ahmed. Lung Stem Cell Behavior. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95279-6.

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Cell therapy for lung disease. London: Imperial College Press, 2010.

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Burgess, Janette K., and Irene H. Heijink, eds. Stem Cell-Based Therapy for Lung Disease. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-29403-8.

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Pham, Phuc Van. Liver, lung and heart regeneration. Cham: Springer, 2017.

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Stem cells in the respiratory system. New York: Humana Press, 2010.

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Bertoncello, Ivan, ed. Stem Cells in the Lung. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-21082-7.

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Okudela, Koji. Cancer stem cells in lung cancer. Hauppauge, N.Y: Nova Science Publishers, 2010.

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Nikolić, Marko Z., and Brigid L. M. Hogan, eds. Lung Stem Cells in Development, Health and Disease. Sheffield, United Kingdom: European Respiratory Society, 2021. http://dx.doi.org/10.1183/2312508x.erm9121.

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Firth, Amy, and Jason X. J. Yuan, eds. Lung Stem Cells in the Epithelium and Vasculature. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16232-4.

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El-Hashash, Ahmed. Lung Stem Cell Behavior. Springer, 2019.

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Частини книг з теми "Lung Stem Cell"

El-Hashash, Ahmed. "Lung Stem Cells in Lung Repair and Regeneration." In Lung Stem Cell Behavior, 61–65. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95279-6_7.

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El-Hashash, Ahmed. "Lung Stem Cell Plasticity." In Lung Stem Cell Behavior, 57–59. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95279-6_6.

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El-Hashash, Ahmed. "Brief Overview of the Human Respiratory System Structure and Development." In Lung Stem Cell Behavior, 1–3. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95279-6_1.

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El-Hashash, Ahmed. "Diversity of Lung Stem and Progenitor Cell Types." In Lung Stem Cell Behavior, 5–13. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95279-6_2.

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El-Hashash, Ahmed. "Signals and Molecular Mechanisms Controlling Lung Stem/Progenitor Cell Development and Behavior." In Lung Stem Cell Behavior, 15–25. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95279-6_3.

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El-Hashash, Ahmed. "Signals and Molecular Mechanisms Regulating Stem Cell Behavior in Other Systems (e.g., Hematopoietic Stem Cells)." In Lung Stem Cell Behavior, 27–34. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95279-6_4.

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El-Hashash, Ahmed. "Mode of Cell Division as a Regulatory Mechanism for Lung Stem Cell Behavior Compared to Other Systems." In Lung Stem Cell Behavior, 35–55. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95279-6_5.

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El-Hashash, Ahmed. "Stem Cell-Based Organoid Models in Lung Development and Diseases." In Lung Stem Cell Behavior, 67–75. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95279-6_8.

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Cooke, Kenneth R., and Gregory Yanik. "Lung Injury after Hematopoietic Stem Cell Transplantation." In Hematopoietic Stem Cell Transplantation, 495–536. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-438-4_22.

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Prabavathy, D., and Niveditha Ramadoss. "Heterogeneity of Small Cell Lung Cancer Stem Cells." In Stem Cells Heterogeneity in Cancer, 41–57. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14366-4_3.

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Тези доповідей конференцій з теми "Lung Stem Cell"

Gray, Alice L., Scott M. Palmer, Robert D. Davis, Judith A. Voynow, Rebecca Buckley, Paul Szabolcs, and David Zaas. "Successful Staged Combined Lung-Stem Cell Transplant." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1134.

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Ptasinski, V., S. Monkley, M. Tammia, K. Öst, C. Overed-Sayer, P. Hazon, D. E. Wagner, and L. A. Murray. "Modeling idiopathic pulmonary fibrosis using induced pluripotent stem cell-derived alveolar epithelial organoids." In ERS Lung Science Conference 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/23120541.lsc-2021.62.

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Byrne, RN, TJ van Haaften, G. Rey-Parra, FC Eaton, LI Coltan, and B. Thebaud. "Stem Cell-Derived Paracrine Activity Prevents Lung Injury." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2009.

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Mckeon, F., W. Xian, S. Niroula, S. Wang, W. Rao, J. F. Engelhardt, K. R. Parekh, M. L. Metersky, and K. Goller. "Lung Stem Cell Heterogeneity in Advanced Cystic Fibrosis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2665.

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Goldsteen, P., P. Mulder, L. Kistemaker, J. Soeiro, K. Mathwig, A. Dolga, and R. Gosens. "Pluripotent stem cell derived airway cholinergic neurons for disease modelling of neuroplasticity in asthma." In ERS Lung Science Conference 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/23120541.lsc-2021.7.

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Selvam, Anjan Panneer, and Shalini Prasad. "Single Molecule Analysis Tool (SMAT) for Multiplexed Label-Free Assessment of Rare Cell Populations." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-40225.

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A nanowell sensor for single molecular proteomic analysis of lung cancer has been designed. The nanowell sensor is an electrochemical immunoassay and comprises of a heterogenous nanoporous arrays integrated on to a gold microelectronic platform. The sensor operates on the principle of electrochemical impedance spectroscopy (EIS). Our approach to classification of lung cancer is based on screening for levels of expression of specific proteomic biomarkers associated with lung cancer stem cells. Proteomic activity for two lung cancer cell lines for two specific markers (ALDH1A1 and ALDH1A3) was quantified. Test samples prepared by synthetically spiking human pooled serum were tested and quantified for cancer stem cell marker activity. The lowest proteomic activity measured with (a) ALDH1A3 was 0.01 ng/mL and (b) ALDH1A1 was 1 ng/mL correlating to the detection of unit stem cell count.

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Farhat, R., A. C. Miller, and D. Picker. "Polymicrobial Lung Abscess Complicating Autologous Hematopoietic Stem Cell Transplant." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6855.

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Liu, H. Y., Y. W. Chen, and H. W. E. Snoeck. "Human Pluripotent Stem Cell-Derived Lung Distal Tip Progenitors." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7462.

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Chen, Wan-Jiun, Huei-Wen Chen, Chao-Chi Ho, Hsuan-Yu Chen, and Pan-Chyr Yang. "Abstract 501: Characterization of lung cancer stem/initiating cells from non-small-cell lung cancer patients." 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.am2011-501.

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Young, Peter, Penny Roberts, Xiaolin Xu, Jeff Hooley, Doug Smith, Paul A. Moore, and Jennie Mather. "Abstract 502: Development of lung cancer cell lines exhibiting cancer stem cell properties through application of stem-cell culturing techniques." 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.am2011-502.

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Звіти організацій з теми "Lung Stem Cell"

Watabe, Kounosuke. Roles of microRNA-Mediated Drug Resistance in Tumor Stem Cells of Small Cell Lung Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada614451.

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Watabe, Kounosuke. Roles of MicroRNA-mediated Drug Resistance in Tumor Stem Cells of Small Cell Lung Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada598410.

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