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Дисертації з теми "Malignant Cells - Molecular Characetrization"

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Автор: Grafiati

Опубліковано: 7 вересня 2023

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Endaya, Berwini B. "Detecting Proliferating Tumor Cells for their Molecular Characterisation." Thesis, Griffith University, 2016. http://hdl.handle.net/10072/367491.

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Uncontrolled proliferation is a fundamental trait that defines all malignant neoplasms. The acquisition of such ability for unrestrained growth is governed by mechanisms encompassing a multitude of complementary molecular events that include somatic mutations, epigenetic alterations, and constant phenotypic changes driven by the ever changing tumour microenvironment. In time, while going through the evolutionary process of tumourigenesis, tumours acquire and adapt unique sets of these molecular events driving proliferation and growth. As a result, a multitude of growth pathways, each unique in its molecular makeup, yet similar in conferring unlimited proliferative capacity can potentially arise. A major challenge therefore is to establish a way to pinpoint the specific molecular alterations actively driving proliferation and tumour growth. In this study, we design a method that has the ability to detect and isolate the proliferating tumour cells for their molecular characterisation.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Au, Wing-yan. "Pathogenesis and progression of malignant B cell neoplasms /." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31540892.

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Joseloff, Elizabeth 1969. "AP-1 regulation during malignant progression of mouse keratinocyte cells." Diss., The University of Arizona, 1997. http://hdl.handle.net/10150/282562.

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The mouse skin model that has been used to study skin carcinogenesis can be divided into three stages: initiation, promotion, and progression. One genetic change observed during tumor promotion and malignant progression is increased transactivation of the transcription factor AP-1. AP-1 consists of Jun (c-Jun, Jun B, Jun D) and Fos (c-Fos, Fos B, Fra-1, Fra-2) proteins that form Jun:Jun homodimers or Jun:Fos heterodimers. AP-1 binds to a consensus cis-promoter element, the TRE, and transcriptionally regulate a number of genes with various biological functions. By studying the benign mouse keratinocyte cells, 308, and its malignant variant, 10Gy5, it has been shown that 10Gy5 cells have elevated AP-1 activity compared to 308 cells. Reduced AP-1 transactivation in 10Gy5 cells has been correlated with suppression of its malignant phenotype. This research examined the differential AP-1 transactivation in benign 308 and malignant 10Gy5 cells. By examing mechanisms of AP-1 regulation in the two cell lines, differences were observed with post-translational modifications of AP-1. There were differences in phosphorylation of one of the AP-1 family members, Jun B. In addition, AP-1 proteins in 10Gy5 cells appear to be in a fully reduced state, unlike AP-1 proteins in 308 cells. A third difference that was observed was in Jun B steady state protein levels, with decreased Jun B protein in malignant 10Gy5 compared to benign 308 cells. Reduced Jun B protein in 10Gy5 cells was the result of decreased Jun B protein synthesis. Jun B protein may inhibit AP-1 transactivation and cell proliferation. Experiments were performed to determine whether Jun B protein could modulate AP-1 transactivation, cell growth, and tumor formation in 308 and 10Gy5 cells. Altering Jun B protein levels in these keratinocytes affected AP-1 transactivation. Overexpression of Jun B protein in malignant 10Gy5 cells corresponded to an inhibition of cell growth and tumor development. However, overexpression of Jun B protein in 10Gy5 cells was not sufficient to reverse the malignancy, indicating that additional genetic changes are involved in malignant conversion of these keratinocytes. The results of this research suggest that Jun B protein levels may be important during malignant progression of mouse skin.

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Kårehed, Karin. "Signal Transduction in Malignant Cells – Transformation, Activation and Differentiation." Doctoral thesis, Uppsala University, Department of Genetics and Pathology, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6346.

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All aspects of cell life are regulated by signal transduction mechanisms. This thesis describes the regulatory roles of a few key signal transduction molecules involved in three major biological responses. The studied pathways include platelet derived growth factor (PDGF)-BB induced transformation of murine fibroblasts, interferon (IFN)-γ stimulated monocyte activation and all-trans retinoic acid (ATRA) induced myeloid differentiation.

We found that intact phosphoinositide 3OH-kinase (PI3K) activity is essential in the signaling pathway that leads to the morphological alterations and migration pattern characteristic of PDGF-BB transformed NIH/sis and NIH/COL1A1 fibroblasts. Furthermore, our data indicated that the small Rho-GTPase, Rac1 is the predominant mediator of these signals downstream of PI3K.

The study of the IFN-γ induced activation of monocytic U-937 cells showed that upregulation of the high affinity receptor for IgG (FcγRI) is dependent on the coordination of several regulatory events: the PKR-mediated serine 727 phosphorylation of Stat1, the expression of the hematopoietic lineage specific transcription factor PU.I, and the activation of the NFκB pathway.

ATRA-induced differentiation and cell cycle arrest are impaired in U-937 sublines expressing phosphorylation deficient Stat1 (Stat1Y701F and Stat1S727A). The findings in paper III indicated that the expression pattern of the myeloid specific transcription factors Stat2, ICSBP and c/EBPε was altered in the sublines and that intact Stat1 activation is critical for maintaining the balance of the transcriptional network during ATRA induced terminal differentiation.

Finally, ATRA-induced differentiation and growth arrest were blocked by treatment with the IKKα/β inhibitor BMS345541 or by ectopic expression of the NFκB super repressor IκBα (S32A/S36A). The fact that IκB(AA) sublines differentiated normally in response to vitamin D3, showed that NFκB inhibition specifically affected ATRA induced responses. Notably we suggest that the activity of the NFκB pathway may interfere with the differentiation process via a direct effect on the RAR/RXR mediated transcription.

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Bouralexis, Stelios. "Molecular mechanisms of Apo2L/TRAIL induced apoptosis in normal and malignant cells /." Title page, contents and synopsis only, 2003. http://web4.library.adelaide.edu.au/theses/09PH/09phb766.pdf.

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Au, Wing-yan, and 區永仁. "Pathogenesis and progression of malignant B cell neoplasms." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45007676.

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Solomon, Cynthia 1974. "Mechanisms of 1,25-dihydroxyvitamin D resistance in tumor cells as they progress from the normal to the malignant phenotype." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36710.

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Human retinoid X receptor alpha (hRXRalpha) plays a critical role in DNA binding and transcriptional activity through its heterodimeric association with several members of the nuclear receptor superfamily, including the vitamin D receptor (VDR). Several cancer cell lines derived from many tissues have been shown to be resistant to the growth inhibitory action of 1,25-dihydroxyvitamin D3, (1,25(OH)2D3), the biologically active metabolite of vitamin D3. In the malignant ras-transformed human keratinocyte cell line, HPK1Aras, 10--100 fold higher concentrations of 1,25(OH)2D3 are required than the non-malignant normal human epidermal keratinocytes to achieve comparable inhibition of cell growth. Here we show that in ras-transformed keratinocytes, ser260 of hRXRalpha is phosphorylated through the Ras-Raf-MAP kinase cascade. This phosphorylation event results in the inhibition of vitamin D signaling via VDR/hRXRalpha heterodimers. Strategies to reverse this resistance include the use of the MAP kinase inhibitor, PD098059, and a non-phosphorylatable hRXRalpha mutant, ala260, which completely abolishes RXR phosphorylation and restores the function of both 1,25(OH)2D3 and a specific RXR ligand, LG1069 (4-[1-(5,6,7,8-tetrahydro-3,5,5,8,8-pentamethyl-2-naphtalenyl)ethenyl]-benzoic acid). In addition, we show that a vitamin D analog with low calcemic activity (EB1089) is more potent than 1,25(OH)2D3 in inhibiting cancer cell growth in this system. Targeted therapy with selective analogs such as EB1089, in combination with the inhibition of phosphorylation of the RXR, could play a critical role in the therapeutic strategies of cancer biology. In addition, we also demonstrate that resistance to 1,25(OH)2D 3 can be acquired through genetic alterations in the VDR, implying that both components of the VDR/RXR heterodimer are potential targets for the induction of cellular resistance to 1,25(OH)2D3 and present two distinct mechanisms through which tumour cells can escape the growt

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Corradi, Giulia <1990&gt. "Molecular and functional characterization of the interplay between malignant and stromal cells in acute myeloid leukemia and myelodysplastic syndrome." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2019. http://amsdottorato.unibo.it/8812/1/Corradi_Giulia_Tesi.pdf.

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In this thesis, we studied the cross-talk between malignant cells and stromal cells, with the aim to elucidate the respective contribution to myeloid neoplasm onset and progression. First, we characterized and compared mesenchymal stromal cells (MSCs) isolated from myelodysplastic syndrome (MDS-MSCs) and acute myeloid leukemia (AML-MSCs) patients. We demonstrated that, despite some unaltered functions, patient-derived MSCs show also intrinsic, distinct functional abnormalities, which could all potentially favor a leukemia-protective bone marrow (BM) niche in vivo. Second, we investigated the ability of AML cells to modulate the AML-MSC functions. In a GEP-screening, we found that 40% of BM-derived AML samples show a higher IFN-γ expression, compared to the mean IFN-γ expression in healthy BM-derived cells. We demonstrated that in co-culture experiments, IFN-γ+ AML cells modify AML-MSC gene expression and function, inducing the up-regulation of IDO1, and consequently the generation of T regulatory cells. Finally, we wondered if the transcriptome of stromal cells could be influenced by the hematopoietic-specific alterations, i.e. Dnmt3a and Asxl1 mutations, which occur early in MDS/AML patients. We found that Dnmt3a- and Asxl1-null BM cells, when transplanted in wild-type mice, induce profound and deletion-specific modifications in the transcriptome of wild-type BM stromal cells, suggesting the ability of Dnmt3a- and Asxl1-null BM cells to shape the niche. Furthermore, we compared the transcriptome of wild-type BM stromal cells, obtained from transplantation experiments, with that of MSCs isolated from low-risk MDS patients with DNMT3A and ASXL1 mutations, and we highlighted some common modifications, which could be potentially relevant for human disease and specific for DNMT3A/ASXL1 mutations. In conclusion, this thesis pointed out that there is a bi-directional cross-talk, in which stromal cells can influence malignant cells, and in turn malignant/pre-malignant cells can alter stromal cell gene expression and function. Both mechanisms could potentially contribute to the pathogenesis of myeloid malignancies.

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Li, Ge. "Cell physiology, biochemistry, and molecular biology of 5-aminolevulinic acid-induced protoporphyrin IX in normal, immortalized, transfected, and malignant cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0005/NQ27837.pdf.

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Eliasson, Pernilla. "Live and Let Die : Critical regulation of survival in normal and malignant hematopoietic stem and progenitor cells." Doctoral thesis, Linköpings universitet, Experimentell hematologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-52932.

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The hematopoietic stem cell (HSC) is characterized by its ability to self-renew and produce all mature blood cells throughout the life of an organism. This is tightly regulated to maintain a balance between survival, proliferation, and differentiation. The HSCs are located in specialized niches in the bone marrow thought to be low in oxygen, which is suggested to be involved in the regulation of HSC maintenance, proliferation, and migration. However, the importance of hypoxia in the stem cell niche and the molecular mechanisms involved remain fairly undefined. Another important regulator of human HSCs maintenance is the tyrosine kinase receptor FLT3, which triggers survival of HSCs and progenitor cells. Mutations in FLT3 cause constitutively active signaling. This leads to uncontrolled survival and proliferation, which can result in development of acute myeloid leukemia (AML). One of the purposes with this thesis is to investigate how survival, proliferation and self-renewal in normal HSCs are affected by hypoxia. To study this, we used both in vitro and in vivo models with isolated Lineage-Sca-1+Kit+ (LSK) and CD34-Flt3-LSK cells from mouse bone marrow. We found that hypoxia maintained an immature phenotype. In addition, hypoxia decreased proliferation and induced cell cycle arrest, which is the signature of HSCs with long term multipotential capacity. A dormant state of HSCs is suggested to be critical for protecting and preventing depletion of the stem cell pool. Furthermore, we observed that hypoxia rescues HSCs from oxidative stress-induced cell death, implicating that hypoxia is important in the bone marrow niche to limit reactive oxidative species (ROS) production and give life-long protection of HSCs. Another focus in this thesis is to investigate downstream pathways involved in tyrosine kinase inhibitor-induced cell death of primary AML cells and cell lines expressing mutated FLT3. Our results demonstrate an important role of the PI3K/AKT pathway to mediate survival signals from FLT3. We found FoxO3a and its target gene Bim to be key players of apoptosis in cells carrying oncogenic FLT3 after treatment with tyrosine kinase inhibitors. In conclusion, this thesis highlights hypoxic-mediated regulation of normal HSCs maintenance and critical effectors of apoptosis in leukemic cells expressing mutated FLT3.

On the day of the defence date the title of article II was "Hypoxia, via hypoxia-inducible factor (HIF)-1, mediates low cell cycle activity and preserves the engraftment potential of mouse hematopoietic stem cells" and one of the authors is no longer included in the article.

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Hershberger, Courtney E. "The Impact of Mutations and Downmodulation of LUC7L2 and Other Splicing Factors on Alternative Splicing Landscapes in Leukemic Cells and Malignant Bone Marrow." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1592313710172514.

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Mahller, Yonatan Y. "Development of Oncolytic HSV-1 as an Anticancer Therapeutic for Extracranial Neural Tumors and Cancer Stem Cells." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1190588795.

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Chen, Rong-Jane, and 陳容甄. "Studies on the Molecular Mechanisms of Antifungal Agents-induced Human Malignant Cells Growth Arrest." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/47277382283745518819.

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碩士
台北醫學院
醫學研究所
88
Abstract In this study, we demonstrated that Ketoconazole (KT) and Terbinafine (TB), two widely used oral-antifungal agents inhibit cell cycle progression in human colorectal and hepatic cancer cell lines in G0/G1 phase. Human cancer cells with various p53 statuses were used to investigate the mechanisms of KT- and TB-induced G0/G1 arrest. The results of flow cytometry and cell growth curve analyses revealed that KT and TB-induced growth arrest was more profound in COLO 205 (with wild-type p53) than in HT 29 (p53 His273 mutant) and Hep 3B (with deleted p53). By the way, TB induced apoptosis in HL 60 cells. KT and TB increased the expression of p53, p21, and p27 in cancer cells, and inhibited the expression of CyclinD3 and CDK4 proteins leaded to the growth arrest in human cancer cells. In contrast, the expression of PCNA, as well as cyclin A, D1, and E levels in human cancer cells were not significant change as compared with untreated cells. CDK4 and CDK2 kinase activity from cells treated with KT and TB was markedly inhibited. In nude mice experiments, treated with KT or TB inhibit the growth of human COLO 205 tumor. Taken together, these results suggest universality of KT and TB in cessation of cell proliferation, also make them very attractive agents for use as potential cancer chemotherapeutic agents.

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Bouralexis, Stelios. "Molecular mechanisms of Apo2L/TRAIL induced apoptosis in normal and malignant cells / by Stelios Bouralexis." Thesis, 2003. http://hdl.handle.net/2440/21918.

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Bibliography: leaves 220-257.
xxix, 257 leaves : ill. (some col.) ; 30 cm.
Describes research into Apo2L/TRAIL, a member of the tumour necrosis factor (TNF) superfamily, which is seen as a possible treatment for a relatively uncommon malignant bone tumour, Osteogenic sarcoma. When tested on fresh isolates of bone related tumors, such as OS and Giant cell tumours, it was found that whilst chemotherapy was, at best, moderately effective in terms of induction of cell death, and Apo2L/TRAIL had no effect on any of the bone related tumour or sarcome in culture, combining the two agents together produced a significant increase in malignant cell death.
Thesis (Ph.D.)--University of Adelaide, Dept. of Orthopaedics and Trauma

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Li, Yi Chen, and 李宜珍. "Cellular and molecular mechanisms of malignant transformation in cancer cells of upper digestive track chronically exposed to areca nut." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/22upac.

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