Relevant bibliographies by topics / 111201 Cancer Cell Biology

Academic literature on the topic '111201 Cancer Cell Biology'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "111201 Cancer Cell Biology"

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Muffly, Lori S., Qian Li, Elysia Alvarez, Justine M. Kahn, Lena E. Winestone, Rosemary Cress, Dolly Penn, and Theresa H. M. Keegan. "Hematopoietic Cell Transplantation in First Remission Amongst Adolescent and Young Adult Acute Lymphoblastic Leukemia: A Population-Level Analysis across the United States." Blood 132, Supplement 1 (November 29, 2018): 3965. http://dx.doi.org/10.1182/blood-2018-99-111205.

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Abstract Background: The optimal role of allogeneic hematopoietic cell transplantation (HCT) for adolescents and young adults (AYA) with acute lymphoblastic leukemia (ALL) is an area of clinical debate. In this population-based evaluation of AYA ALL patients across the United States (US), we sought to describe recent patterns of care and outcomes regarding HCT in first complete remission (CR1) amongst AYAs with ALL. Methods: Data were abstracted from the National Cancer Institute Surveillance, Epidemiology, and End Results (SEER) Patterns of Care (POC) study focused on AYA cancers. AYAs (15-39 years) with ALL newly diagnosed between January 1, 2012 through December 31, 2013 and registered in the SEER program were included. Allogeneic HCT in CR1 was defined as occurrence of HCT without relapse/progression prior to the HCT date; HCT was considered a time-dependent variable in survival models. Multivariable logistic regression was used to evaluate associations with HCT in CR1; cox proportional hazards regression was used to evaluate associations with survival. Results: Three-hundred and ninety-nine AYAs (15-39 years) with newly diagnosed ALL between 2012-2013 were included; median follow-up for survival was 19 months (range, 0-35 months). The median age was 24 years; 85% had B-cell ALL, 27% had high risk ALL cytogenetics. One-third of AYA ALL patients received care from pediatric oncologists while two-thirds were treated by adult hematologist/oncologists; a majority (86%) received care at a teaching hospital. Fifty-eight percent received an asparaginase-containing ALL front-line regimen, 32% received hyperCVAD; 5.9% and 4.5% received another/unknown regimens, respectively. One-hundred and two (29%) AYAs underwent allogeneic HCT in CR1. Excluding patients with relapse/progression or death within three months of diagnosis (n=32), older age, high-risk ALL cytogenetics, treatment by an adult hematologist/oncologist, and front-line therapy with hyperCVAD were variables significantly associated (all P< 0.05) with increased odds of HCT in CR1 in univariate analysis, while Hispanic ethnicity and public or no/other insurance were associated with significantly lower odds of HCT in CR1. In multivariate adjusted analysis, only high-risk cytogenetics (odds ratio (OR) 4.84, 95% confidence interval (CI) 2.99-7.83) and receipt of hyperCVAD (OR 1.84, 95% CI 1.07-3.16) retained significant associations with HCT in CR1. The two-year cumulative incidence of relapse, relapse-free survival (RFS), and overall survival (OS) of the entire cohort were 28.3% (95% CI 23.4%-33.4%), 69.3% (95% CI, 63.6%-74.3%), and 84.1% (95% CI 79.7%-87.5%), respectively. Two-year cumulative incidence of relapse was significantly lower in patients receiving HCT in CR1 as opposed to those not receiving HCT in CR1 (15.1%, 95% CI 8.1%-24.1% vs 32.8%, 95% CI 26.9%-38.9%). This translated into a significant improvement in 2-year RFS (83.6%, 95% CI 72.6%-90.5% vs 64.3%, 95% CI 57.5%-70.3%), but no statistically significant differences in 2-year OS (88.9%, 95% CI 80.8%-93.7% vs 82.5%, 95% CI 77.2%-86.7%). Among all patients, receipt of care at a non-teaching hospital (hazard ratio (HR) 2.14, 95% CI 1.22-3.75) and use of another/unknown regimen (HR 9.08, 95% CI, 4.83-17.06) were significantly associated with inferior OS. Conclusions: In the US, allogeneic HCT in CR1 is most commonly administered to AYA ALL with high risk cytogenetics and as consolidation therapy for those who receive front-line hyperCVAD, as opposed to asparaginase-containing ALL regimens. Consistent with prior studies, AYA ALL patients treated at non-teaching hospitals have inferior survival. Although the landscape of ALL therapy is changing, these data provide an important snapshot of the modern state of HCT in CR1 for AYA ALL. Disclosures Muffly: Shire Pharmaceuticals: Research Funding; Adaptive Biotechnologies: Research Funding.
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Osman, Afaf, Brian Yu, Nancy Glavin, Tamar S. Polonsky, James K. Liao, and Richard A. Larson. "ABL Tyrosine Kinase Inhibitors (TKIs) Are Associated with Increased Rho-Associated Kinase (ROCK) Activity That May Contribute to Vascular Toxicity in Patients with Chronic Myeloid Leukemia (CML)." Blood 132, Supplement 1 (November 29, 2018): 1739. http://dx.doi.org/10.1182/blood-2018-99-111201.

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Abstract Introduction The use of 2nd or 3rd generation ABL TKIs in patients with CML is associated with vascular toxicity, including peripheral arterial occlusive disease and cardiovascular and cerebrovascular events. However, Imatinib, a 1st generation TKI, has not been shown to increase risk of cardiovascular events (Douxfils J et al. JAMA Oncol 2016;2:625). Therefore, there is a need to identify risk factors and predictors of vascular toxicity for patients receiving these TKIs. In mice, inhibition of the Abl kinases results in activation of Rho and its downstream target Rho kinase (ROCK) (Zandy et al. Proc Natl Acad Sci USA 2007;104:17686). Growing evidence suggests that elevated ROCK activity plays a central role in the pathogenesis of cardiovascular disease and stroke in both animal and clinical studies. TKIs used in CML are potent inhibitors of ABL1 and ABL2 kinases. We hypothesized that CML patients receiving 2nd or 3rd generation BCR/ABL1 TKIs have higher ROCK activity than patients not receiving these TKIs, providing a putative mechanism for the vascular toxicity observed in clinical studies. Methods We measured leukocyte ROCK activity in CML patients and analyzed results based on their last TKI dose. We isolated fresh peripheral blood leukocytes from 38 patients (17 females, 21 males) with a median age of 53 years (range, 24-90 years). 4 patients had newly diagnosed untreated CML at the start of the study. One male was receiving Dasatinib for Ph+ ALL and was also included. ROCK activity was assessed in leukocytes by measuring the ratio of phospho-myosin-binding subunit (p-MBS) on myosin light-chain phosphatase, a downstream target of ROCK, to total MBS using an automated Western blotting system (Wes, ProteinSimple, San Jose, CA) (Hata T et al. Atherosclerosis 2011; 214:117). Each patient had 1-6 measurements of leukocyte ROCK activity over 1 - 18 months (n=78 measurements). Information about cardiovascular risk factors, concomitant medications, CML status, and total duration of TKI therapy was collected. For patients with multiple samples over time, ROCK activity was calculated as the mean of all samples taken while receiving the same TKI. Patients in treatment-free remission (TFR) were considered off-TKI, but those in TFR < 1 month were excluded from the analysis to reduce potential confounding effects. Results We analyzed blood samples from 4 untreated CML patients, 8 while in TFR, and 31 who were actively receiving one of the 5 TKIs (7 Imatinib, 12 Dasatinib, 9 Nilotinib, 2 Ponatinib, 1 Bosutinib). 3 patients developed acute coronary syndrome during the study and required coronary revascularization for myocardial infarction. We found no significant difference in ROCK activity when comparing all patients receiving TKIs to those not receiving TKIs. However, we found higher leukocyte ROCK activity when comparing all patients receiving 2nd and 3rd generation TKIs to those not receiving any TKI (Welch's t test, mean leukocyte ROCK activity 1.00 ± 0.06 vs 0.80 ± 0.06; p=0.03). We also found higher leukocyte ROCK activity when comparing patients receiving Dasatinib to patients receiving Imatinib (mean leukocyte ROCK activity 1.05 ± 0.09 vs 0.75 ± 0.10; p=0.04). The comparison of Imatinib to all 2nd and 3rd generation TKIs was not significant (p=0.06). Conclusions We found that patients on 2nd and 3rd generation TKIs have higher leukocyte ROCK activity compared to those not receiving TKIs, and higher leukocyte ROCK activity in patients on Dasatinib compared with patients receiving Imatinib. These results are consistent with the known lower-risk of cardiovascular side-effects observed with Imatinib in comparison to the next generation ABL TKIs. Limitations include small sample size and heterogeneity in the patient population in terms of age, cardiovascular risk factors, specific TKI used, and total duration and sequencing of TKI agents. The study continues to accrue CML subjects in order to follow individual patients over time on TKI therapy. Disclosures Larson: Ariad/Takeda: Consultancy, Research Funding; BristolMyers Squibb: Consultancy, Research Funding; Novartis: Consultancy, Research Funding; Pfizer: Consultancy, Research Funding.
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Zelenkova, N. P. "Cancer cell biology." Kazan medical journal 43, no. 6 (October 19, 2021): 74–76. http://dx.doi.org/10.17816/kazmj83368.

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Bebber, Christina M., Fabienne Müller, Laura Prieto Clemente, Josephine Weber, and Silvia von Karstedt. "Ferroptosis in Cancer Cell Biology." Cancers 12, no. 1 (January 9, 2020): 164. http://dx.doi.org/10.3390/cancers12010164.

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A major hallmark of cancer is successful evasion of regulated forms of cell death. Ferroptosis is a recently discovered type of regulated necrosis which, unlike apoptosis or necroptosis, is independent of caspase activity and receptor-interacting protein 1 (RIPK1) kinase activity. Instead, ferroptotic cells die following iron-dependent lipid peroxidation, a process which is antagonised by glutathione peroxidase 4 (GPX4) and ferroptosis suppressor protein 1 (FSP1). Importantly, tumour cells escaping other forms of cell death have been suggested to maintain or acquire sensitivity to ferroptosis. Therefore, therapeutic exploitation of ferroptosis in cancer has received increasing attention. Here, we systematically review current literature on ferroptosis signalling, cross-signalling to cellular metabolism in cancer and a potential role for ferroptosis in tumour suppression and tumour immunology. By summarising current findings on cell biology relevant to ferroptosis in cancer, we aim to point out new conceptual avenues for utilising ferroptosis in systemic treatment approaches for cancer.
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Colaco, Camilo A. L. S. "Cancer immunotherapy: simply cell biology?" Trends in Molecular Medicine 9, no. 12 (December 2003): 515–16. http://dx.doi.org/10.1016/j.molmed.2003.10.006.

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Ray, L. B. "Cancer Cell Vulnerability." Science Signaling 4, no. 202 (December 6, 2011): ec338-ec338. http://dx.doi.org/10.1126/scisignal.4202ec338.

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Kroemer, Guido. "Tetraploid cancer cell precursors." Nature Reviews Molecular Cell Biology 11, no. 8 (June 23, 2010): 539. http://dx.doi.org/10.1038/nrm2924.

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Momeny, Majid, Tiina Arsiola, and Jukka Westermarck. "Cancer stem cell phosphatases." Biochemical Journal 478, no. 14 (July 28, 2021): 2899–920. http://dx.doi.org/10.1042/bcj20210254.

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Cancer stem cells (CSCs) are involved in the initiation and progression of human malignancies by enabling cancer tissue self-renewal capacity and constituting the therapy-resistant population of tumor cells. However, despite the exhausting characterization of CSC genetics, epigenetics, and kinase signaling, eradication of CSCs remains an unattainable goal in most human malignancies. While phosphatases contribute equally with kinases to cellular phosphoregulation, our understanding of phosphatases in CSCs lags severely behind our knowledge about other CSC signaling mechanisms. Many cancer-relevant phosphatases have recently become druggable, indicating that further understanding of the CSC phosphatases might provide novel therapeutic opportunities. This review summarizes the current knowledge about fundamental, but yet poorly understood involvement of phosphatases in the regulation of major CSC signaling pathways. We also review the functional roles of phosphatases in CSC self-renewal, cancer progression, and therapy resistance; focusing particularly on hematological cancers and glioblastoma. We further discuss the small molecule targeting of CSC phosphatases and their therapeutic potential in cancer combination therapies.
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Ray, L. B. "Fueling the Cancer Cell." Science Signaling 3, no. 122 (May 18, 2010): ec153-ec153. http://dx.doi.org/10.1126/scisignal.3122ec153.

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Nishino, Hiroshi. "Interleukin-6 affects cancer cell biology." Journal of Japan Society of Immunology & Allergology in Otolaryngology 34, no. 1 (2016): 13–18. http://dx.doi.org/10.5648/jjiao.34.13.

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Dissertations / Theses on the topic "111201 Cancer Cell Biology"

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Bair, Elisabeth Laurine. "Cell-cell and cell-matrix interactions involved in cancer invasion." Diss., The University of Arizona, 2004. http://hdl.handle.net/10150/280673.

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In order for a cancer to metastasize, it must first invade through the basement membrane that surrounds it, invade blood vessels and travel through the bloodstream to a new location where it extravasates the vessel and begins growing at the new site. The mechanisms by which a cancer becomes able to invade and metastasize are currently under intense study. Interactions of the cell with its environment via cell-cell contacts, extracellular matrix (ECM) interactions, and circulating proteins are thought to play a major role in signaling for these invasive processes to occur. Upregulation of proteolytic enzymes, such as the matrix metalloproteases, is suspected of being involved in the metastatic process. Cell-cell and cell-matrix contacts via integrins and cadherins are necessary for upregulation of the matrix metalloprotease matrilysin in oral squamous cell carcinoma. In an effort to identify the factors involved in upregulation of matrilysin expression detected in a co-culture of oral squamous cell carcinoma (SCC) cells and fibroblast cells, a coculture model designed to represent the actual tumor environment, we show that inhibition of beta1 integrin, E-cadherin, and N-cadherin with blocking antibodies thoroughly decreases the induction of matrilysin in the co-culture model. This demonstrates that interactions between cancer cells and normal cells surrounding them may allow for invasion and metastasis. The protein 90K may also play a role in the invasive process of prostate cancer. It functions as an immune modulator upregulating cytokines that induce MMPs and we show that it can induce matrilysin expression in prostate cancer cells. It also functions in cell aggregation, which can help cells survive during metastasis. For this reason, expression of 90K in prostate cancer, which we examined, may be indicative of aggressive disease, making 90K a potentially useful tumor marker. Cell-matrix contacts are also important for the transmembrane matrix metalloprotease MT1-MMP cleavage of laminin-10. We demonstrate that recombinant MT1-MMP is able to cleave human laminin-10 into four distinct products. This allows for prostate cancer cell migration on laminin-10 coated substrates, which can be inhibited with the addition of MT1-MMP antisense oligonucleotides. Ln-10 cleavage also occurs in vivo in human prostate tissue, indicating that this cell-matrix interaction has in vivo relevance in human prostate cancer.
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Krubasik, Davia Regina Editla. "The role of Metalloproteinases in cancer cell biology." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612722.

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Ng, Sheng Rong. "CRISPR-mediated interrogation of small cell lung cancer." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/117782.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2018.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged student-submitted from PDF version of thesis. Vita.
Includes bibliographical references.
Small cell lung cancer (SCLC) is a highly aggressive neuroendocrine lung carcinoma that remains among the most lethal of solid tumor malignancies. Despite decades of research, treatment outcomes for SCLC remain very poor, highlighting the need for novel approaches to target the disease. Recent genomic sequencing studies have identified multiple recurrently altered genes in human SCLC tumors, many of which remain to be functionally validated. Genetically engineered mouse models (GEMMs) of SCLC have been developed that recapitulate many key features of human SCLC. These models have been used extensively to investigate various aspects of SCLC biology, including tumor initiation, progression and metastasis. The development of the CRISPR-Cas9 system has greatly facilitated genome editing in mammalian cells, leading to its widespread adoption for various applications in cancer biology. We have utilized this system in two complementary ways to investigate the molecular mechanisms involved in SCLC initiation, progression and maintenance. Firstly, we have adapted the CRISPR-Cas9 system for use in GEMMs of SCLC, to enable rapid modeling and functional validation of candidate tumor suppressor genes in vivo. Using this system, we have demonstrated that p107, a member of the retinoblastoma family that is mutated in a significant fraction of human SCLC tumors, is a functional tumor suppressor in SCLC. Notably, loss of p107 in SCLC tumors resulted in significant phenotypic differences compared with loss of its close relative, p130. We also demonstrated that CRISPR-induced mutations can be used to infer lineage relationships between primary and metastatic tumors in the same animal. Secondly, we have performed a CRISPR-based genetic screen, utilizing a custom sgRNA library targeting the druggable genome, to identify novel SCLC-specific genetic vulnerabilities. We found that SCLC cells displayed enhanced sensitivity towards disruption of several key metabolic pathways, including the de novo pyrimidine biosynthesis pathway. Pharmacological inhibition of Dhodh, a key enzyme in this pathway, reduced the viability of SCLC cells in vitro and strongly suppressed SCLC tumor growth in vivo, validating this pathway as a promising therapeutic target in SCLC. Taken together, the work presented here demonstrates the utility of the CRISPR-Cas9 system for performing functional interrogation of SCLC.
by Sheng Rong Ng.
Ph. D.
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Kay, Sophie Kate. "Cell fate mechanisms in colorectal cancer." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:f19bf73d-0c0e-4fff-9589-bf43f9ff12f0.

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Colorectal cancer (CRC) arises in part from the dysregulation of cellular proliferation, associated with the canonical Wnt pathway, and differentiation, effected by the Notch signalling network. In this thesis, we develop a mathematical model of ordinary differential equations (ODEs) for the coupled interaction of the Notch and Wnt pathways in cells of the human intestinal epithelium. Our central aim is to understand the role of such crosstalk in the genesis and treatment of CRC. An embedding of this model in cells of a simulated colonic tissue enables computational exploration of the cell fate response to spatially inhomogeneous growth cues in the healthy intestinal epithelium. We also examine an alternative, rule-based model from the literature, which employs a simple binary approach to pathway activity, in which the Notch and Wnt pathways are constitutively on or off. Comparison of the two models demonstrates the substantial advantages of the equation-based paradigm, through its delivery of stable and robust cell fate patterning, and its versatility for exploring the multiscale consequences of a variety of subcellular phenomena. Extension of the ODE-based model to include mutant cells facilitates the study of Notch-mediated therapeutic approaches to CRC. We find a marked synergy between the application of γ-secretase inhibitors and Hath1 stabilisers in the treatment of early-stage intestinal polyps. This combined treatment is an efficient means of inducing mitotic arrest in the cell population of the intestinal epithelium through enforced conversion to a secretory phenotype and is highlighted as a viable route for further theoretical, experimental and clinical study.
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Neal, Corey Lekeil. "Snail mediates epithelial mesenchymal transition and cell adhesion in human prostate cancer cell lines." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2011. http://digitalcommons.auctr.edu/dissertations/233.

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Snaill (Snail) transcription factor induces Epithelial Mesenchymal Transition (EMT), in which epithelial cells down-regulate cell adhesion genes such as E-cadherin and up-regulate mesenchymal genes such as vimentin, leading to increased invasion and migration. Maspin is a putative tumor suppressor that is down-regulated in breast and prostate cancer and has been associated with decreased cell motility, while Snail is increased in breast cancer and associated with increased tumor motility and invasion. Very little is known about the role of Snail in cellular adhesion to the extracellular matrix (ECM) and its role in regulation of maspin expression has not been explored. We hypothesized that Snail will lead to decreased cellular adhesion to the extracellular matrix through integrin regulation, concomitant with increased cell migration. Our studies showed that Snail decreases cell adhesion to fibronectin (FN) and collagen I (CGN) matrix through inhibition of cL5 (fibronectin receptor), c~2 (collagen receptor), ~3 1 integrins, while migration to FN and CON was increased. We have also identified an inverse relationship between Snail and rnaspin in normal prostate epithelial cells and prostate cancer cells and shown for the first time that Snail can inhibit maspin expression. This work utilized normal prostate epithelial cells (PrEC), androgen-dependent LNCaP cells, androgen-independent C4-2, DU145, 22Rvl, ARCaP and PC3 prostate cancer cell lines. Cells with either the endogenous, overexpression or knockdown of the Snail transcription factor were utilized to observe the role of Snail in cell adhesion and migration and to establish its molecular mechanism(s) of action. We have provided direct evidence that the Snail transcription factor negatively impacts prostate cancer cell adhesion and migration to fibronectin and collagen matrices. This activity was regulated through integrins and the mitogen-activated protein kinase (MAPK) signaling pathway. Additionally, we have shown that Snail negatively regulates maspin expression by inhibiting activity at the maspin promoter. Collectively, these studies define a new role for Snail in cell adhesion to the ECM. Therefore, targeting of Snail may be useful to re-induce expression of maspin putative tumor suppressor, increase cell adhesion to ECM, decrease cell migration and prevent prostate cancer tumor progression and metastasis.
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McNae, Fiona. "The cell biology of non-genotoxic hepatocarcinogens." Thesis, University of Surrey, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260350.

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Weitzel, Douglas H. "Modulation of cell cycle checkpoints by anti-cancer agents /." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu148820531851081.

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Horlock, Nigel. "The cell biology of basal cell carcinoma : relationship to histology and clinical outcome." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391606.

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Poluri, Raghavendra Tejo Karthik. "Using bioinformatic analyses to understand prostate cancer cell biology." Master's thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/66803.

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Le cancer de la prostate (CaP) affecte 1 homme sur 7 au cours de sa vie. C’est le cancer numéro un diagnostiqué chez l'homme. Il s'agit du quatrième cancer le plus fréquent au Canada. Le CaP est une maladie hormonodépendante diagnostiquée chez l'homme. Les androgènes jouent un rôle vital dans la progression de la maladie. La première ligne de traitement, suivant une intervention chirurgicale ou un traitement de radiothérapie, est la thérapie de déprivation aux androgènes. Malgré une réponse initiale positive à l'inhibition des androgènes, la progression de la maladie vers un cancer de la prostate résistant à la castration (CRPC) est presque inévitable. Aux différentes étapes du CaP, le récepteur des androgènes joue un rôle majeur. Ainsi, cette thèse décrit les méthodes développées et utilisées pour mieux comprendre la biologie du CaP et le rôle joué par les androgènes dans cette maladie. Le travail démontré dans cette thèse se compose principalement d'analyses bioinformatiques effectuées sur des ensembles de données accessibles au public et d'un « pipeline » construit pour analyser des données RNA-Seq. Un pipeline RNA-Seq a été développé pour comprendre l'impact des androgènes et des gènes régulés lors du traitement aux androgènes dans les modèles de cellules de CaP. Ce pipeline bioinformatique se compose de divers outils qui ont été décrits ci-dessous dans le chapitre 1. L'objectif principal de ce projet était de développer un pipeline pour analyser les données RNA-Seq qui aide à comprendre et à définir les voies et les gènes métaboliques qui sont régulés par les androgènes, et qui jouent un rôle important dans la progression du CaP. Le flux de travail expérimental consistait en deux lignées cellulaires positives aux récepteurs aux androgènes LNCaP et LAPC4. Toutes les données utilisées dans ce projet ont été rendues publiques pour que la communauté de recherche puisse effectuer diverses autres études et analyses comparatives pour comprendre les fonctions des androgènes dans un sens beaucoup plus profond afin de développer de nouvelles thérapies pour traiter le CaP. Dans un autre projet décrit au chapitre 2, des analyses bioinformatiques ont été réalisées sur des données accessibles au public pour comprendre la fréquence de la perte et de l'altération génomique du gène PTEN localisé à 10q23. Ces analyses ont mis en évidence la fréquence d'altération génomique de PTEN qui est beaucoup plus élevée dans le CRPC que dans le CaP localisé. Ces analyses ont également aidé à identifier d'autres gènes altérés dans le CaP. Ces gènes n’ont pas été beaucoup étudiés dans la littérature, mais il semble que certains d’entre eux possèdent des caractéristiques de suppresseurs de tumeurs. Ces résultats pourraient être un bon début pour des analyses plus approfondies concernant la perte de gènes.La compréhension des fonctions de AR et de la suppression de PTEN aidera à développer de nouvelles stratégies et approches pour diagnostiquer et traiter le CaP. L'intégration des analyses bioinformatiques à la recherche clinique ouvre une nouvelle perspective dans le domaine de la recherche du CaP.
Prostate Cancer (PCa) affects 1 in 7 men in their lifetime and is the number one diagnosed cancer in men. It is the 4th most common cancer in Canada. PCa is a hormone-dependent disease diagnosed in men. Androgens play a vital role in the disease progression. The standard of care to treat PCa, following surgery or radiation therapy, is the androgen deprivation therapy (ADT). In spite of initial positive response to androgen inhibition, the progression of the disease to castration-resistant prostate cancer (CRPC) is almost inevitable. Across the various stages of PCa, the androgen receptor (AR) plays a major role. This thesis portrays the methods developed and used to understand PCa biology. The work demonstrated in this thesis majorly consists of bioinformatic analyses performed on publicly available data sets and a pipeline built to analyse RNA-Seq data. An RNA-Seq pipeline has been developed to understand the impact of androgens and the genes regulated upon androgen treatment in PCa cell models. This bioinformatic pipeline consists of various tools which have been described below in chapter 1. The major goal of this project was to develop a pipeline to analyse the RNA-Seq data which helps to understand and define the metabolic pathways and genes regulated by androgens which play an important role in PCa disease progression. The experimental workflow consisted of two androgen receptor positive cell lines LNCaP and LAPC4. All the data used in this project has been made publicly available for the research community to perform various other comparative studies and analyses to understand the functions of androgens in a much deeper sense to develop novel therapies to treat PCa. In another project described in chapter 2, bioinformatic analyses have been performed on publicly available data to understand the loss and genomic alteration frequency of the gene PTEN occurring at 10q23. These analyses highlighted that the genomic alteration frequency of PTEN is much higher in CRPC than in localised PCa, and also helped in identifying other genes which are lost along with PTEN. The lost genes have not been studied much in literature, but few studies demonstrated that they might possess tumor suppressor characteristics. These results might be a good start for further deeper analyses regarding the lost of genes. Understanding the functions of AR and the deletion of PTEN will help for the development of novel strategies and approaches to diagnose and treat PCa. Integration of bioinformatic analyses with clinical research open up a new perspective in the PCa research domain.
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Popovic, Predrag. "Cisplatin resistance in nonsmall cell lung cancer: Role of platinum accumulation and cell membranes." Thesis, University of Ottawa (Canada), 1994. http://hdl.handle.net/10393/9662.

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A cisplatin resistant cell line named E-8/0.7 was derived from the nonsmall cell lung cancer HTB 56 cell line. According to IC$\sb{50}$ estimations, E-8/0.7 cells were approximately 7.7 times more resistant to cisplatin than were HTB 56 cells. Uptake of cisplatin 100 $\mu$M over 1 hour was measured by atomic absorption spectrophotometry, and showed around a 30% lower uptake in E-8/0.7 cells compared to HTB 56 cells. Barotropic behaviour was analyzed by pressure tuning infrared spectroscopy. In the CH symmetric stretching region, we found a lower break point (and consequently lower membrane fluidity) in E-8/0.7 cells compared to the parent cell line. Lipid analyses of the two cell lines showed a higher cholesterol to phospholipid molar ratio in E-8/0.7 than in HTB 56 cells. Moreover, concentration of sphingomyelin was higher in E-8/0.7 cells than in HTB 56 cells.
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Books on the topic "111201 Cancer Cell Biology"

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Christian, Sherri L., ed. Cancer Cell Biology. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2376-3.

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Cancer biology. 3rd ed. New York: Oxford University Press, 1995.

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Cancer biology. 2nd ed. New York: Oxford University Press, 1987.

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Cancer biology. 4th ed. Oxford: Oxford University Press, 2007.

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Fior, Rita, and Rita Zilhão, eds. Molecular and Cell Biology of Cancer. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11812-9.

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Scatena, Roberto, Alvaro Mordente, and Bruno Giardina, eds. Advances in Cancer Stem Cell Biology. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-0809-3.

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Scatena, Roberto, Alvaro Mordente, and B. Giardina. Advances in cancer stem cell biology. New York: Springer, 2012.

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Schatten, Heide. Cell and molecular biology of breast cancer. New York: Humana Press, 2013.

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1939-, Wilson Samuel H., and Hoagland Mahlon B, eds. Cancer biology and biosynthesis. Boca Raton, Fla: CRC Press, 1991.

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Schatten, Heide, ed. Cell and Molecular Biology of Breast Cancer. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-634-4.

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Book chapters on the topic "111201 Cancer Cell Biology"

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Acconcia, Filippo, and Rakesh Kumar. "Cell Biology." In Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_992-2.

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Acconcia, Filippo, and Rakesh Kumar. "Cell Biology." In Encyclopedia of Cancer, 892–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_992.

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Hamerlik, Petra. "Cancer Stem Cells and Glioblastoma." In Glioma Cell Biology, 3–22. Vienna: Springer Vienna, 2014. http://dx.doi.org/10.1007/978-3-7091-1431-5_1.

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Ribatti, Domenico, and Enrico Crivellato. "Mast Cells, Angiogenesis and Cancer." In Mast Cell Biology, 270–88. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-9533-9_14.

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Enderling, Heiko. "Cancer Stem Cell Kinetics." In Encyclopedia of Systems Biology, 193–95. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_1386.

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Santra, Debarpita. "Cell Biology and Cell Behavior in Cancer." In Cancer Diagnostics and Therapeutics, 13–41. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-4752-9_2.

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Hann, Christine L. "Small Cell Lung Cancer: Biology Advances." In Lung Cancer, 197–211. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-74028-3_9.

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Barata, João T., and Mariana L. Oliveira. "Cell Signaling in Cancer." In Molecular and Cell Biology of Cancer, 31–49. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11812-9_3.

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Mathonnet, M., A. Perraud, S. Blondy, N. Christou, H. Akil, S. Battu, and M. O. Jauberteau. "Cancer Stem Cell Niche." In Stem Cell Biology and Regenerative Medicine, 197–209. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-21702-4_9.

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Adlung, Lorenz. "Cancer." In Cell and Molecular Biology for Non-Biologists, 103–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-65357-9_9.

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Conference papers on the topic "111201 Cancer Cell Biology"

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Gentles, Andrew J., Ajit J. Nirmal, Laura M. Heiser, Emma Lundberg, and Aaron M. Newman. "Single Cell Spatial Biology for Precision Cancer Medicine." In Pacific Symposium on Biocomputing 2023. WORLD SCIENTIFIC, 2022. http://dx.doi.org/10.1142/9789811270611_0052.

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Truong, Danh D., Emre Arslan, Margarita Divenko, Sandhya Krishnan, Alexander Lazar, Kunal Rai, and Joseph Ludwig. "Unraveling the Biology of Desmoplastic Small Round Cell Tumor." In Leading Edge of Cancer Research Symposium. The University of Texas at MD Anderson Cancer Center, 2022. http://dx.doi.org/10.52519/00091.

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Kim, Carla F. "Abstract SY12-01: Stem cell approaches dissect lung cancer biology." 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-sy12-01.

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Ciccolella, Simone, Murray D. Patterson, Paola Bonizzoni, and Gianluca Della Vedova. "Effective Clustering for Single Cell Sequencing Cancer Data." In BCB '19: 10th ACM International Conference on Bioinformatics, Computational Biology and Health Informatics. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3307339.3342149.

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Ding, XiaoFei, Ismael Sagredo, Gilbert Bustamante, Lu-Zhe Sun, Jing Yong Ye, and Frank DeLuna. "Label-free in vitro prostate cancer cell detection via photonic-crystal biosensor." In Biophysics, Biology and Biophotonics III: the Crossroads, edited by Adam Wax and Vadim Backman. SPIE, 2018. http://dx.doi.org/10.1117/12.2288019.

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Lucarini, G., V. Iacovacci, L. Ricotti, N. Comisso, P. Dario, and A. Menciassi. "Magnetically driven microrobotic system for cancer cell manipulation." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7319179.

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Kazmar, Tomáš, Matĕj Šmid, M. Fuchs, B. Luber, and J. Mattes. "Learning cellular texture features in microscopic cancer cell images for automated cell-detection." In 2010 32nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC 2010). IEEE, 2010. http://dx.doi.org/10.1109/iembs.2010.5626299.

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"Recombinant lactaptin analogon RL2 inhibits TRAIL-induced cell death in breast cancer cell lines by mitophagy." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-608.

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Roberts, Penny, Peter Young, Doug Smith, Jeff Hooley, Jonathan Li, Francine Chen, Deryk Loo, Jennie Mather, and Paul A. Moore. "Abstract 5211: Development of a panel of colon cancer cell lines with cancer stem cell properties: a tool for cancer biology and target discovery." 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.am2011-5211.

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Wan, Yuan, Young-tae Kim, Li Na, Andrew D. Ellington, and Samir M. Iqbal. "Aptamer-Based Lab-on-Chip for Cancer Cell Isolation and Detection." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13195.

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The isolation and detection of circulating tumor cells (CTCs), when these are few in number or small in mass, can enable early cancer detection [1]. Currently, most research endeavors to isolate circulating tumor cells rely on antibodies and immunohistochemistry [2,3]. Aptamer are alternative molecules that have affinities and specificities that are comparable to those of antibodies [4,5], but these can be more readily adapted to many applications [6–9], including lab-on-a-chip devices. Here, we report use of a novel epidermal growth factor receptor (EGFR) aptamer biochip to identify and isolate cancer cells that overexpress EGFR. These results provide a solid basis for the development of diagnostic devices that can readily identify and isolate CTCs.
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Reports on the topic "111201 Cancer Cell Biology"

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Park, M. S. Competency development in antibody production in cancer cell biology. Office of Scientific and Technical Information (OSTI), December 1998. http://dx.doi.org/10.2172/290996.

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Daley, George. Ovarian Cancer and Reproductive System Biology: A Harvard Stem Cell Institution Consortium. Fort Belvoir, VA: Defense Technical Information Center, December 2010. http://dx.doi.org/10.21236/ada542144.

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Chen, Changmao, Yunfeng Chen, and Lian Chen. The Effects of TCM Combined with Chemotherapy in Patients with Non-small Cell Lung Cancer: An Overview of Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0114.

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Review question / Objective: The aim of this overview is to comprehensive summary and critically evaluate the current evidence from systematic reviews (SR)/Meta-analysis pertaining to risk of bias and quality of evidence and methodological quality of systematic reviews of TCM combined with chemotherapy in patients with non-small cell lung cancer (NSCLC). Information sources: Five international electronic databases(Web of Science, The Cochrane Library, PubMed, MEDLINE, and EMBASE) and 4 Chinese electronic databases (China National Knowledge Infrastructure (CNKI), the Chinese Science and Technology Periodical Database (VIP), China Biology Medicine disc (CBM), and Wan Fang Digital Journals).
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Kang, Jing, Jun Zhang, Zongsheng Tian, Ye Xu, Jiangbi Li, and Mingxina Li. The efficacy and safety of immune-checkpoint inhibitor plus chemotherapy versus chemotherapy for non-small cell lung cancer: an updated systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0156.

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Review question / Objective: Population: histologically confirmed advanced NSCLC patients; Intervention: received immune-checkpoint inhibitor plus chemotherapy; Comparison:received chemotherapy; Outcome: reported OS, PFS, ORR and TRAEs; Study design: RCT. Condition being studied: Lung cancer is the primary cause of cancer-related deaths, with an estimated 2.20 million new cases and 1.79 million deaths every year, and 85% of all primary lung cancers are non-small cell lung cancer. Eligibility criteria: Studies were considered eligible if they met the following criteria: (1) being an randomized controlled trial published in English, (2) histologically confirmed advanced NSCLC patients, (3) reported OS, PFS, ORR and TRAEs, (4) the intervention group received immune-checkpoint inhibitor plus chemotherapy, while the control group received chemotherapy, (5) When numerous papers reporting the same trial were found, the most current or most complete publications were chosen. The following were the exclusion criteria: (1) duplicate articles, (2) reviews, meta-analyses, case reports, editorials and letters, (3) molecular biology or animal research, (4) retrospective or prospective observational cohort studies.
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Jarron, Matthew, Amy R. Cameron, and James Gemmill. Dundee Discoveries Past and Present. University of Dundee, November 2020. http://dx.doi.org/10.20933/100001182.

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A series of self-guided walking tours through pioneering scientific research in medicine, biology, forensics, nursing and dentistry from the past to the present. Dundee is now celebrated internationally for its pioneering work in medical sciences, in particular the University of Dundee’s ground-breaking research into cancer, diabetes, drug development and surgical techniques. But the city has many more amazing stories of innovation and discovery in medicine and biology, past and present, and the three walking tours presented here will introduce you to some of the most extraordinary. Basic information about each topic is presented on this map, but you will ­find more in-depth information, images and videos on the accompanying website at uod.ac.uk/DundeeDiscoveriesMap For younger explorers, we have also included a Scavenger Hunt – look out for the cancer cell symbols on the map and see if you can ­find the various features listed along the way!
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