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Characterizing prostate cancer stem-like cells and their contribution to prostate cancer tumorigenesisYan, Judy 11 1900 (has links)
On average, 65 Canadian men will be diagnosed with prostate cancer (PC) every day, making it the most common male cancer in Canada. Despite the prevalence, the etiology of PC is unknown. Evidence nonetheless supports the role of prostate cancer stem cells (PCSCs) in PC initiation and metastasis. In spite of almost a decade worth of research on PCSCs our knowledge on their biology remains fragmented. By taking advantage of the availability of DU145 cell-derived PCSCs in our laboratory, this thesis research focuses on investigating the unique properties of PCSCs and their function in promoting PC tumorigenesis.
We identified two PCSC-specific proteins, ALDH3A1 and CNTN1. In mouse models of xenograft tumors, ALDH3A1 was expressed at higher levels in PCSC-derived tumors than in DU145 non-PCSC-produced tumors and in lung metastases than local tumors. In clinical settings, elevation of ALDH3A1expression was observed from normal prostate tissues to carcinomas and from local PCs to the paired lymph node metastases. Additionally, ALDH3A1 was clearly detected in bone metastases. Similar to ALDH3A1, CNTN1 expression associates with PC progression and biochemical recurrence following radical prostatectomy. The clear presence of CNTN1 in lymph node and bone metastases was also demonstrated. Furthermore, CNTN1 expression promoted PC metastasis to the lungs and tumor initiation in NOD/SCID mice. Mechanistically, CNTN1 increased AKT activation and reduced E-cadherin expression. Collectively, our research revealed important roles of both PCSC proteins in promoting PC tumorigenesis and progression.
PC develops chemotherapy resistance in which PCSCs play a major role. In supporting this knowledge, we demonstrated that PCSCs are innately more resistant to the chemotherapeutic drugs, etoposide and docetaxel and that this resistance was in part attributable to their enhanced DNA damage response. Taken together, the findings of this thesis advances our knowledge on two specific PCSC markers and their association with prostate cancer progression and metastasis. As well as to the mechanism whereby PCSCs promote resistance to chemotherapeutic drugs. / Thesis / Doctor of Philosophy (PhD)
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The Clinical Significance of Either Extraprostatic Extension or Microscopic Bladder Neck Invasion Alone Versus Both in Men With pT3a Prostate Cancer Undergoing Radical ProstatectomyA Proposal for a New pT3a Subclassification / 前立腺癌pT3a期における前立腺外進展および膀胱頸部浸潤の臨床的意義―新たなpT3aサブクラスの提案Teramoto, Yuki 23 January 2023 (has links)
京都大学 / 新制・課程博士 / 博士(医学) / 甲第24317号 / 医博第4911号 / 新制||医||1062(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 小林 恭, 教授 溝脇 尚志, 教授 松田 道行 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Evasion of Tak1-p38α/β-Stat1/2 non-canonical Activin A signalling leads to aberrant mouse prostate epithelial cell proliferation in vitro and in vivo.Foletto, Veronica 12 June 2020 (has links)
Tgf-β ligands induce cell cycle arrest in a variety of mammalian epithelia, including in the prostate. Genetic deregulation of the downstream canonical Smad-dependent pathway is an early well-studied event in tumorigenesis, yet, in prostate cancer such mutations are rare, leaving unexplained how Tgf-β represses prostate cell proliferation.
Here, we adopted a variety of pharmacological and genetic approaches to dissect the pathways controlling proliferation in mouse prostate organoids.
We found that Egf signalling is a potent proliferative stimulus through the concomitant activation of both Pi3k/Akt and Mapk/Erk pathways. However, the autocrine release of the Tgf-β family ligand Activin A has a dominant role over Egf-induced proliferation by promoting the non-canonical Tak1-p38α/β axis, which leads to Mapkapk2, p16, p21, and Stat1/2 activation and cell-cycle arrest.
Bypass of the proliferation barrier can spontaneously occur upon long-term culture and it is associated to aberrant Activin A signalling and DNA replication stress. Finally, orthotopic transplantation of adapted organoids into immunocompetent hosts, leads to aberrant outgrowth and the emergence of prostatic intraepithelial neoplasia (PIN).
Overall, our experiments unveil how Activin A limits mouse prostate progenitor cells proliferation and provide a rationale for the frequent MAP3K7 (TAK1) and ACVR2A (Activin A type II receptor) deletions observed in human primary prostate cancers (20% in the TCGA 2015 dataset).
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Targeting Metabolism to Overcome Enzalutamide Resistance in Prostate CancerBhattacharjee, Sayani January 2022 (has links)
No description available.
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Relation Between the Selenoprotein Gene, Selenium, and Prostate CancerSchumacher, Fredrick R. January 2006 (has links)
No description available.
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The effect of the Wilms' tumor gene 1 (WT1) on E-cadherin regulation and migration of prostate cancer cellsBrett, Adina R. 06 January 2012 (has links)
No description available.
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Studies of Lipoxygenase FunctionMcCabe, Noel Patrick 18 January 2005 (has links)
No description available.
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PROSTATIC REGULATION OF THE ANDROGEN RECEPTOR BY CYCLIN D1: FUNCTION AND DYSFUNCTIONBURD, CRAIG J. 13 July 2006 (has links)
No description available.
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Stragegies to overcome progression of androgen refractory prostate cancer – targeting BCL-XL and androgen receptorYang, Chih-Cheng 05 January 2007 (has links)
No description available.
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Bicistronic vectors for animal models of breast and prostate cancerMorarescu, Diana 12 1900 (has links)
The improving of our understanding of cancer development still depends
on cancer research at the molecular level. In his project, bigenic vectors for
animal models of breast and prostate cancer are created.
Bigenic constructs are useful because they create animals expressing two
genes of interest at a time, with one injection step and no need for crossings. In
order to produce these vectors, previous animal models have been analyzed, and
the elements that worked successfully in previous models were gathered in a new
arrangement for the creation of an improved model. In order to create a bigenic
vector, the viral internal ribosomal entry site was utilized, as a means of obtaining
two protein products from one transcript.
One vector, the MMTV-Neu1842-IRES-Cre was successful in generating
a line of transgenic mice. Female founders of this line already express the
expected phenotype, tumors of the mammary tissue. Once this line is established,
it can be crossed with the Rosa26 line, to determine the pattern of Cre expression.
Other vectors were created for models of prostate cancer, using the
probasin promoter and the MT oncogene. While transgenic mice were attempted,
there were no phenotype differences between wild type and transgenic mice.
All created vectors were tested for expression ofthe two genes carried in
tissue culture experiments. All the experiments were successful, indicating a
working oncogene (by means of a focus assay) and Cre activity (by excission
assay).
The new breast cancer animal model carrying the MMTV-Neu1842-IRESCre
construct is promising and can be used in combination with existing models
to answer some of the remaining questions regarding breast cancer signaling
pathways. / Thesis / Master of Science (MSc)
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