Relevant bibliographies by topics / Cancer cells

Contents

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

Academic literature on the topic 'Cancer cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Cancer cells"

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Fernández-Lázaro, Diego, César Ignacio Fernández-Lázaro, and Martínez Alfredo Córdova. "Cell Death: Mechanisms and Pathways in Cancer Cells." Cancer Medicine Journal 1, no. 1 (August 31, 2018): 12–23. http://dx.doi.org/10.46619/cmj.2018.1-1003.

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Programmed cell death is an essential physiological and biological process for the proper development and functioning of the organism. Apoptosis is the term that describes the most frequent form of programmed cell death and derives from the morphological characteristics of this type of death caused by cellular suicide. Apoptosis is highly regulated to maintain homeostasis in the body, since its imbalances by increasing and decreasing lead to different types of diseases. In this review, we aim to describe the mechanisms of cell death and the pathways through apoptosis is initiated, transmitted, regulated, and executed.
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Srivastava, A. N., Neema Tiwari, Shailendra Yadav, and Suryakant . "LUNG CANCER STEM CELLS-AN UPDATE." Era's journal of medical research 4, no. 1 (June 1, 2017): 22–31. http://dx.doi.org/10.24041/ejmr2017.4.

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Fujimoto, Naohiro, Bin Han, Masayoshi Nomura, and Tetsuro Matsumoto. "WS1-1-1 Nitrogen-Containing Bisphosphonates Inhibit the Growth of Renal Cell Carcinoma Cells(Renal Cell Cancer)." Japanese Journal of Urology 99, no. 2 (2008): 142. http://dx.doi.org/10.5980/jpnjurol.99.142_1.

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MAS, Bezerra, Ferreira LAM, Kawasaki-Oyama RS, Nascimento MCA, Cuzziol CI, Castanhole-Nunes MMU, Pavarino EC, Maniglia JM, and Goloni-Bertollo EM. "Effectiveness of Hypoxia-Induced Accumulation of Cancer Stem Cells in Head and Neck Squamous Cell Carcinoma." Cancer Medicine Journal 3, S1 (November 30, 2020): 13–23. http://dx.doi.org/10.46619/cmj.2020.3.s1-1003.

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INTRODUCTION: The small number of cancer stem cells, which correspond to only 0.01% - 0.1% of total tumor cells, has been the biggest obstacle in understanding their biology and role in the origin and maintenance of tumors, their metastatic and recurrence potentials, and resistance to radio-chemotherapy. Therefore, promoting its accumulation will enable further studies and future advances in the diagnosis and treatment of head and neck cancer squamous cell carcinoma. OBJECTIVE: To induce cancer stem cell accumulation in primary cell cultures of head and neck squamous cell carcinoma using a hypoxia chamber. METHODS: Head and neck squamous cell carcinoma samples were cultured and subjected to hypoxia. Oxygen deprivation aimed to induce cancer stem cell accumulation. RESULTS: Immediately after hypoxia, the percentage of O2-deprived cancer stem cells increased 2-fold as compared to control. Surprisingly, new phenotyping performed 45 days after hypoxia showed a 9-fold increase in cancer stem cell percentage in cells that suffered hypoxia. Hypoxic cells showed an increase in spheroid formation when compared to control cells, as well as enhanced abilities in invasion and migration. CONCLUSION: Hypoxia was efficient in cancer stem cell accumulation. As cancer stem cells are a small number of cells within the tumor, promoting their accumulation will enable further studies and future advances in the diagnosis and treatment of head and neck cancer.
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Yin, Wen, Jialing Wang, Linling Jiang, and Y. James Kang. "Cancer and stem cells." Experimental Biology and Medicine 246, no. 16 (April 5, 2021): 1791–801. http://dx.doi.org/10.1177/15353702211005390.

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Being the second leading cause of death globally, cancer has been a long-standing and rapidly evolving focus of biomedical research and practice in the world. A tremendous effort has been made to understand the origin of cancer cells, the formation of cancerous tissues, and the mechanism by which they spread and relapse, but the disease still remains mysterious. Here, we made an attempt to scrutinize evidences that indicate the role of stem cells in tumorigenesis and metastasis, and cancer relapse. We also looked into the influence of cancers on stem cells, which in turn represent a major constituent of tumor microenvironment. Based on current understandings of the properties of (cancer) stem cells and their relation to cancers, we can foresee that novel therapeutic approaches would become the next wave of cancer treatment.
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Pratap, Dr Pushpendra D. "CANCER STEM CELLS IN CERVICAL CANCER AS BENEFICIAL GOALS AND BIOMARKERS: A COMPREHENSIVE." Era's Journal of Medical Research 10, no. 2 (December 2023): 51–55. http://dx.doi.org/10.24041/ejmr2023.36.

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The fourth most prevalent gynaecological malignancy affecting females globally is cervical cancer (CC). HPV (high-risk) infection has been related to the majority of CC cases. Owing to efficient screening through Pap smear and vaccination delivery, the commonness and death rate of CC have significantly decreased. Nevertheless, not all societies have access to this equally. A better therapeutic outcome may be achieved by targeting CSCs, which might play a significant impact in carcinogenesis, metastasis, recurrence, and radio / chemo –resistance of CC. The majority of tumours are made up of a tiny subset of tumour cells called CSCs that have the capability to self-renew and develop into a variety of tumour cell types. Cervical CSCs (CCSC) are challenging to recognise, which has prompted the hunt for other markers. The potential indicators of CSCs in CC are described in the current review. These CCSC indicators might be used as molecular goals to improve the effectiveness and lessen the negative effects of chemotherapy in HR-HPV-positive CC.
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Moorthy, Rajesh Kannan, Chandhru Srinivasan, Sridharan Jayamohan, Mahesh Kumar Kannan, Siva Sankari Thirugnanam, Janaki Sankar Ganesh, and Antony Joseph Velanganni Arockiam. "Knockdown of microRNA-375 suppresses cell proliferation and promotes apoptosis in human breast cancer cells." Indian Journal of Science and Technology 14, no. 43 (November 12, 2021): 3199–209. http://dx.doi.org/10.17485/ijst/v14i43.1719.

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Lee, Cheong J., Joseph Dosch, and Diane M. Simeone. "Pancreatic Cancer Stem Cells." Journal of Clinical Oncology 26, no. 17 (June 10, 2008): 2806–12. http://dx.doi.org/10.1200/jco.2008.16.6702.

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Cellular heterogeneity in cancer was observed decades ago by studies in mice which showed that distinct subpopulations of cells within a tumor mass are capable of driving tumorigenesis. Conceptualized from this finding was the stem-cell hypothesis for cancer, which suggests that only a specific subset of cancer cells within each tumor is responsible for tumor initiation and propagation, termed tumor initiating cells or cancer stem cells (CSCs). Recent data has been provided to support the existence of CSCs in human blood cell–derived cancers and solid organ tumors of the breast, brain, prostate, colon, and skin. Study of human pancreatic cancers has also revealed a specific subpopulation of cancer cells that possess the characteristics of CSCs. These pancreatic cancer stem cells express the cell surface markers CD44, CD24, and epithelial-specific antigen, and represent 0.5% to 1.0% of all pancreatic cancer cells. Along with the properties of self-renewal and multilineage differentiation, pancreatic CSCs display upregulation of important developmental genes that maintain self-renewal in normal stem cells, including Sonic hedgehog (SHH) and BMI-1. Signaling cascades that are integral in tumor metastasis are also upregulated in the pancreatic CSC. Understanding the biologic behavior and the molecular pathways that regulate growth, survival, and metastasis of pancreatic CSCs will help to identify novel therapeutic approaches to treat this dismal disease.
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Elgaly, Maher E., Mohamed E. El Ghareeb, and Farha El shennawy. "Cord Blood Mesenchymal Stem Cells Conditioned Media Suppress Epithelial Ovarian Cancer Cells in Vitro." International Journal of Trend in Scientific Research and Development Volume-2, Issue-5 (August 31, 2018): 1783–88. http://dx.doi.org/10.31142/ijtsrd18182.

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SK, Deshmukh. "Immune Cells in the Tumor Microenvironment and Cancer Stem Cells: Interplay for Tumor Progression." Journal of Embryology & Stem Cell Research 2, no. 2 (2018): 1–2. http://dx.doi.org/10.23880/jes-16000109.

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Dissertations / Theses on the topic "Cancer cells"

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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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Fruka, Tayra. "An evaluation of cancer biomarkers in normal ovarian epithelial cells and ovarian cancer cell lines." University of the Western Cape, 2019. http://hdl.handle.net/11394/6920.

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Philosophiae Doctor - PhD
Introduction: Globally, there are over 190,000 new reported cases of ovarian cancers per annum. This comprises 3% to 4% of all cancers in women. Ovarian cancer is one of the leading causes of deaths in women. Ovarian cancer is the second most diagnosed gynaecological malignancy and over all the fifth cause leading to death among all types of cancer in the UK in 2004. More than 70% of epithelial ovarian cancers are diagnosed at an advanced stage. Consequently, the prognosis is poor and the mortality rate high. Thus, the survival rate is affected by how far the disease has progressed or spread. A dire need exists to identify ovarian cancer biomarkers, which could be used as good indicators of expression in ovarian cancer cells in vitro Aim: The aim of this study was to analyse selected cancer biomarkers, which are currently under intense investigation for their suitability to diagnose epithelial ovarian cancer at an early stage. These biomarkers were analysed in terms of their in vitro expression in normal epithelial cells and ovarian cancer cell lines, which allows for their genomic and proteomic classification. The expression analysis of each biomarker is related to the malignancy of a tumour and, therefore, advocates its use for potential future improvement of sensitive tumour markers. Methods: The primary human ovarian surface epithelial cell line (HOSEpiC), SKOV-3 cells and the OAW42 human epithelial ovarian tumour cell lines were used to evaluate the selected cancer biomarkers. Cells were cultured using appropriate media and supplements, and real-time quantitative polymerase chain reaction (RT-PCR) utilized to validate expression levels of the following genes: HDAC1, HDAC2, HDCA3, HDAC5, HDAC6, HDAC7, HDAC8, LPAR1, LPAR2, MUC16 and FOSL1, against normal housekeeping genes GAPDH and HPRT. In addition, immunocytochemistry was also used in the validation process of the aforementioned genes. Significance: ovarian cancer cells express gene signatures, which pose significant challenges for cancer drug development, therapeutics, prevention and management. The present study is an effort to explore ovarian cancer biomarkers to provide a better diagnostic method that may offer translational therapeutic possibilities to increase five- year survival rate. Results: HDAC5, HDAC6, LPAR1, LPAR2 and MUC16 expressed distinctively in ovarian cancers matched to other tissues or cancer types have already been identified by RT-QPCR and confirmed by immunocytochemistry and efforts to generate monoclonal antibodies to the other six genes (HDAC1, HDAC2, HDAC3, HDAC7, HDAC8 and FOSL1) encoded proteins are underway. Conclusions: here we provide strong evidence suggesting that HDAC5, HDAC6, LPAR1, LPAR2, except MUC16 are up regulated in ovarian cancer. These data were confirmed by examining Human Protein Atlas (HPA) databases, in addition to protein expression of HDAC5, HDAC6, LPAR1, LPAR2 and MUC16 in cells cytoplasm. For future prospective, using other techniques that assess the variant expression that could explain the release of these gene candidates into the circulation with serum tumour markers, and protein expression will be strengthened.
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Sasaki, Naoya. "Alpha-fetoprotein-producing pancreatic cancer cells possess cancer stem cell characteristics." Kyoto University, 2012. http://hdl.handle.net/2433/157414.

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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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Liu, Qing. "Curcumin induces cell inhibition in breast cancer cells." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B38688608.

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Liu, Qing, and 劉晴. "Curcumin induces cell inhibition in breast cancer cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38688608.

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Oshima, Nobu. "Induction of Cancer Stem Cell Properties in Colon Cancer Cells by Defined Factors." Kyoto University, 2014. http://hdl.handle.net/2433/192147.

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Oshima N, Yamada Y, Nagayama S, Kawada K, Hasegawa S, et al. (2014) Induction of Cancer Stem Cell Properties in Colon Cancer Cells by Defined Factors. PLoS ONE 9(7): e101735. doi:10.1371/journal.pone.0101735
Kyoto University (京都大学)
0048
新制・課程博士
博士(医学)
甲第18547号
医博第3940号
新制||医||1006(附属図書館)
31447
京都大学大学院医学研究科医学専攻
(主査)教授 千葉 勉, 教授 野田 亮, 教授 武藤 学
学位規則第4条第1項該当
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Coulson-Gilmer, Camilla Lucette. "Cancer stem cells and chemoresistance in ovarian cancer." Thesis, University of Leeds, 2017. http://etheses.whiterose.ac.uk/18470/.

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The high mortality rate associated with epithelial ovarian cancer (EOC) is due to its insidious onset, leading to late diagnosis as well as eventual development of chemoresistance in the majority of patients. Cancer stem-like cells (CSCs) are thought to contribute to development of multi-drug resistant (MDR) tumours partly through their high level of ABC-transporter expression, which enables them to survive chemotherapy. ABC-transporter (MRP1, MRP2, BCRP, Pgp) and putative CSC-marker (ALDH1A1, CD44) expression was therefore evaluated by immunohistochemistry in a paraffin-embedded cohort of 57 high-grade EOC tumours. Typically 9-12% of cells in tumours expressed CD44 / ALDH1A1. These may represent a population enriched for CSCs. ABC-transporters were expressed in 10- 43% of cells on average. Using Spearman rank test, there was no correlation between CSC- marker and ABC-transporter expression, however correlation was observed between many of the ABC-transporters, suggesting existence of highly drug-resistant populations within tumours. Expression of CA125 (a glycoprotein expressed by EOC cells and used clinically to detect EOC relapse) and EpCAM (a cell adhesion molecule expressed by EOC cells) was also investigated. Interestingly, patient tumours with the highest level of EpCAM had longer overall survival by Kaplan-Meier analysis. In addition, increased expression of MRP1 and CD44 predicted poorer patient outcome by Cox regression analysis. In vitro functional assays were also used to identify CSCs. Cells derived from ascites samples had a mean colony-forming efficiency (CFE) or 6.3%, and in unsorted tumours this was 11.4%. Cancer cells were then isolated from primary ascites and tumour samples (using CA125 and EpCAM). On average, self-renewing assays revealed a 2.2-2.4-fold increase in CFE for CA125 or EpCAM positive sorted cells compared to CA125 or EpCAM negative cells. Future studies could characterise these self-renewing populations, which may lead to identification of novel CSC targets for use in EOC treatment.
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Choi, Mi-Yon. "P53 mediated cell motility in H1299 lung cancer cells." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/109.

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Studies have shown that gain-of- function mutant p53, AKT, and NFκB promote invasion and metastasis in tumor cells. Signals transduced by AKT and p53 are integrated via negative feedback between the two pathways. Tumor derived p53 was also indicated to induce NFκB gene expression. Due to the close relationship between p53/AKT and p53/NFκB, we hypothesized that AKT and NFκB can enhance motility in cells expressing mutant p53. Effects on cell motility were determined by scratch assays. CXCL5- chemokine is also known to induce cell motility. We hypothesized that enhanced cell motility by AKT and NFκB is mediated, in part, by CXCL5. CXCL5 expression levels in the presence and absence of inhibitors were determined by qRT-PCR. We also hypothesized that gain-of-function mutant p53 contributes to the activation of AKT. The effect of mutant p53 on AKT phosphorylation was investigated with a Ponasterone A- inducible mutant cell line (H1299/R175H) and vector control. These results indicated that AKT and NFκB enhance motility in cells expressing mutant p53 and this enhanced motility is, in part, mediated by CXCL5. However, AKT phosphorylation was independent of mutant p53.
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Kapeleris, Joanna C. "Circulating tumour cells in non-small cell lung cancer." Thesis, Queensland University of Technology, 2022. https://eprints.qut.edu.au/228607/1/Joanna_Kapeleris_Thesis.pdf.

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Circulating tumour cells (CTCs) have the potential to transform the management of patients with non-small cell lung cancer (NSCLC). The applications of CTCs can identify clinically actionable targets to predict treatment response and to better understand metastasis. CTCs isolated using microfluidics can be used as prognostic indicators of NSCLC as well as characterizing for markers of immunotherapy (PD-L1), molecular targets (ALK, EGFR). Short term cultures were successfully expanded in 9/70 NSCLC patients and cultured for up to 3 months. Optimization of this novel CTC culture model provides opportunity to identify new therapeutics for NSCLC patients in a precision medicine approach.
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Books on the topic "Cancer cells"

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Farrar, William L., ed. Cancer Stem Cells. Cambridge: Cambridge University Press, 2009. http://dx.doi.org/10.1017/cbo9780511605536.

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Yu, John S., ed. Cancer Stem Cells. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-280-9.

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Rajasekhar, Vinagolu K., ed. Cancer Stem Cells. Hoboken, NJ: John Wiley & Sons, 2014. http://dx.doi.org/10.1002/9781118356203.

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Wiestler, O. D., B. Haendler, and D. Mumberg, eds. Cancer Stem Cells. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-70853-7.

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Papaccio, Gianpaolo, and Vincenzo Desiderio, eds. Cancer Stem Cells. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7401-6.

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Bapat, Sharmila, ed. Cancer Stem Cells. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2008. http://dx.doi.org/10.1002/9780470391594.

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Pat, Moyer Mary, and Poste George, eds. Colon cancer cells. San Diego: Academic Press, 1990.

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Papaccio, Federica, and Gianpaolo Papaccio, eds. Cancer Stem Cells. New York, NY: Springer US, 2024. http://dx.doi.org/10.1007/978-1-0716-3730-2.

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Sharmila, Bapat, ed. Cancer stem cells. Hoboken, N.J: John Wiley & Sons, 2008.

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L, Farrar William, ed. Cancer stem cells. Cambridge: Cambridge University Press, 2009.

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Book chapters on the topic "Cancer cells"

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Ishii, Hideshi, Naotsugu Haraguchi, Keisuke Ieta, Koshi Mimori, and Masaki Mori. "Cancer Stem Cells: Gastrointestinal Cancers." In Stem Cells and Cancer, 155–63. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-933-8_12.

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Sazeides, Christos, and Anne Le. "Metabolic Relationship Between Cancer-Associated Fibroblasts and Cancer Cells." In The Heterogeneity of Cancer Metabolism, 189–204. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_14.

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AbstractCancer-associated fibroblasts (CAFs), a major component of the tumor microenvironment (TME), play an important role in cancer initiation, progression, and metastasis. Recent findings have demonstrated that the TME not only provides physical support for cancer cells but also directs cell-to-cell interactions (in this case, the interaction between cancer cells and CAFs). As cancer progresses, the CAFs also coevolve, transitioning from an inactivated state to an activated state. The elucidation and understanding of the interaction between cancer cells and CAFs will pave the way for new cancer therapies [1–3].
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Chowdhury, Suchandra, and Shyamasree Ghosh. "Cancer Stem Cells." In Stem Cells, 177–202. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-1638-9_7.

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Li, Ting, Christopher Copeland, and Anne Le. "Glutamine Metabolism in Cancer." In The Heterogeneity of Cancer Metabolism, 17–38. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_2.

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AbstractMetabolism is a fundamental process for all cellular functions. For decades, there has been growing evidence of a relationship between metabolism and malignant cell proliferation. Unlike normal differentiated cells, cancer cells have reprogrammed metabolism in order to fulfill their energy requirements. These cells display crucial modifications in many metabolic pathways, such as glycolysis and glutaminolysis, which include the tricarboxylic acid (TCA) cycle, the electron transport chain (ETC), and the pentose phosphate pathway (PPP) [1]. Since the discovery of the Warburg effect, it has been shown that the metabolism of cancer cells plays a critical role in cancer survival and growth. More recent research suggests that the involvement of glutamine in cancer metabolism is more significant than previously thought. Glutamine, a nonessential amino acid with both amine and amide functional groups, is the most abundant amino acid circulating in the bloodstream [2]. This chapter discusses the characteristic features of glutamine metabolism in cancers and the therapeutic options to target glutamine metabolism for cancer treatment.
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Jung, Jin G., and Anne Le. "Metabolism of Immune Cells in the Tumor Microenvironment." In The Heterogeneity of Cancer Metabolism, 173–85. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_13.

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AbstractThe tumor microenvironment (TME) is a complex biological structure surrounding tumor cells and includes blood vessels, immune cells, fibroblasts, adipocytes, and extracellular matrix (ECM) [1, 2]. These heterogeneous surrounding structures provide nutrients, metabolites, and signaling molecules to provide a cancer-friendly environment. The metabolic interplay between immune cells and cancer cells in the TME is a key feature not only for understanding tumor biology but also for discovering cancer cells’ vulnerability. As cancer immunotherapy to treat cancer patients and the use of metabolomics technologies become more and more common [3], the importance of the interplay between cancer cells and immune cells in the TME is emerging with respect to not only cell-to-cell interactions but also metabolic pathways. This interaction between immune cells and cancer cells is a complex and dynamic process in which immune cells act as a determinant factor of cancer cells’ fate and vice versa. In this chapter, we provide an overview of the metabolic interplay between immune cells and cancer cells and discuss the therapeutic opportunities as a result of this interplay in order to define targets for cancer treatment. It is important to understand and identify therapeutic targets that interrupt this cancerpromoting relationship between cancer cells and the surrounding immune cells, allowing for maximum efficacy of immune checkpoint inhibitors as well as other genetic and cellular therapies.
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Jung, Jin G., and Anne Le. "Targeting Metabolic Cross Talk Between Cancer Cells and Cancer-Associated Fibroblasts." In The Heterogeneity of Cancer Metabolism, 205–14. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_15.

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AbstractAlthough cancer has classically been regarded as a genetic disease of uncontrolled cell growth, the importance of the tumor microenvironment (TME) [1, 2] is continuously emphasized by the accumulating evidence that cancer growth is not simply dependent on the cancer cells themselves [3, 4] but also dependent on angiogenesis [5–8], inflammation [9, 10], and the supporting roles of cancer-associated fibroblasts (CAFs) [11–13]. After the discovery that CAFs are able to remodel the tumor matrix within the TME and provide the nutrients and chemicals to promote cancer cell growth [14], many studies have aimed to uncover the cross talk between cancer cells and CAFs. Moreover, a new paradigm in cancer metabolism shows how cancer cells act like “metabolic parasites” to take up the high-energy metabolites, such as lactate, ketone bodies, free fatty acids, and glutamine from supporting cells, including CAFs and cancer-associated adipocytes (CAAs) [15, 16]. This chapter provides an overview of the metabolic coupling between CAFs and cancer cells to further define the therapeutic options to disrupt the CAF-cancer cell interactions.
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Hung, Jaclyn Y. "Cancer Stem Cells: Lung Cancer." In Stem Cells and Cancer, 177–84. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-933-8_14.

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Dosch, Joseph, Cheong Jun Lee, and Diane M. Simeone. "Cancer Stem Cells: Pancreatic Cancer." In Stem Cells and Cancer, 185–97. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-933-8_15.

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Saucedo, Leslie. "Cancer." In Getting to Know Your Cells, 79–84. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-30146-9_14.

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Georgiadis, Konstantinos L., Kathryn Simpson, Mahmood Ayub, Ged Brady, Juan Valle, Claus Jorgensen, and Caroline Dive. "Circulating Tumor Cells." In Pancreatic Cancer, 1325–60. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7193-0_62.

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Conference papers on the topic "Cancer cells"

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Yoshimoto, T., T. Ishikawa, N. Matsuki, H. Fujiwara, Y. Imai, H. Ueno, M. Takeda, and T. Yamaguchi. "Rheology of Cancer Cells With Different Metastatic Properties." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206593.

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Cancer is the leading cause of death in Japan as well as many other countries. One of the most serious problem of cancer is that cancer cells often migrate to a distant part of the body, referred to as metastasis. The rheological properties of cancer cells have been investigated by some reserchers [1,2]. However, the correlations between the metastasis and the rheological properties are still unclear, because of limited number of experimental cases reported so far. In this study, we used two kinds of human breast cancer cell lines, MCF-7 and KPL-4. It is known that KPL-4 has much higher metastatic property than MCF-7. The rheological properties of these cells were measured by a micropipette aspiration method [3,4]. By comparing Young’s modulus between two kinds of cancer cells, we discuss the correlations between the metastasis and the cell deformability.
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Salmanzadeh, Alireza, Harsha Kittur, Michael B. Sano, Mark A. Stremler, P. Christopher Roberts, Eva M. Schmelz, and Rafael V. Davalos. "Investigating Dielectrophoretic Signature of Mouse Ovarian Surface Epithelial Cells, Macrophages and Fibroblasts." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80872.

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Epithelial ovarian carcinomas are the fourth leading cause of death in women in the United States among all cancers and the leading cause of death from gynecological malignancies1. The main reason for this high rate of mortality is the inability to properly detect these carcinomas early. Investigations for diagnosing ovarian cancer in early stages have been hindered by two major obstacles: lack of adequate cell models to study different cancer stages and lack of a reliable technique to isolate these cancer cells from peritoneal fluid. In trying to solve the first challenge, Dr. Schmelz and collaborators presented a transformed mouse ovarian surface epithelial (MOSE) cell model by isolating different transitional stages of ovarian cancer as cells progressed from a premalignant nontumorigenic phenotype to a highly aggressive malignant phenotype2, 3. In this model four stages of transformed cells, namely early (MOSE-E), early-intermediate (MOSE-E/I), intermediate (MOSE-I) and late (MOSE-L) cells, were distinguishable3. In the current study, we attempt to solve the second challenge of isolating cancer cells from macrophages and fibroblasts, which are found in the peritoneal fluid. Based on differences in cells’ intrinsic electrical properties, a new cell manipulation technique, contactless dielectrophoresis (cDEP), was implemented.
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Kitagawa, H., N. Yamamoto, G. Kosaki, and H. Yamazaki. "AN IMPORTANT ROLE OF CARBOHYDRATE MOIETIES ON CANCER CELL MEMBRANE GLYCOPROTEINS IN CANCER CELL-INDUCED PLATELET AGGREGATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644667.

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Platelet aggregation induced by cancer cells may be an essential process in the development of hematogenous metastasis of cancers. A mechanism in HMV-I (human vaginal melanoma cell line)-induced platelet aggregation was studied by using monoclonal antibodies against membrane proteins of cancer cells or platelets. HMV-I cells or their membrana ractions induced platelet aggregation of human heparinized PRP, to which hirudin had no inhibitory effect. The platelet aggregation by HMV-I was completely lost after the pretreatment of the cells with 0.3U/ml neuraminidase for 60 min at 37°C. Preincubation of platelets with monoclonal antibodies against platelet GP lb or GP Ilb/lIIa inhibited HMV-I induced aggregation. A monoclonal antibody MB3 (igM) against another human melanoma (HMMB) which had been transplanted in nude mice was produced by hybridoma technique. Screening studies by cell binding ELISA revealed that MB3 antibody reacted with not only HMMB cells but also many other cells including HMV-I, M7609 (colon carcinoma cell line) and normal fibroblasts. Western-blot analyses showedthat MB3 antibody reacted with multiple, more than ten, proteins with molecular weights ranging from UO to 200 kDa in unreduced SDS-PAGE of HMV-I, HMMB or M7609. In contrast, when .these cells pretreated with neuraminidase were used in Western-blot, MB3 reactivity were all lost. MB3 reacted with at least three glycoproteins of human red cell membrane in Western-blot, but it did not react with human platelets. Immune adherent asgay with trypsin-treated HMV-I or HMMB cells as target cells showed negative reactivity. MB3 antibody inhibited HMV-I-induced aggregation of platelets, but did not inhibit M7609-induced aggregation which depended on thrombin generation.These results suggest that MB3 antibody may be against sialic acid-containing carbohydrate moieties of membrane glycoproteins on these cancercells and that the carbohydrate(s) may play a critical role in' cancer cell-platelet interaction.
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Zielinski, Rachel, Cosmin Mihai, and Samir Ghadiali. "Multi-Scale Modeling of Cancer Cell Migration and Adhesion During Epithelial-to-Mesenchymal Transition." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53511.

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Cancer is a leading cause of death in the US, and tumor cell metastasis and secondary tumor formation are key factors in the malignancy and prognosis of the disease. The regulation of cell motility plays an important role in the migration and invasion of cancer cells into surrounding tissues. The primary modes of increased motility in cancerous tissues may include collective migration of a group of epithelial cells during tumor growth and single cell migration of mesenchymal cells after detachment from the primary tumor site [1]. In epithelial cancers, metastasizing cells lose their cell-cell adhesions, detach from the tumor mass, begin expressing mesenchymal markers, and become highly motile and invasive, a process known as epithelial-to-mesenchymal transition (EMT) (Fig. 1) [2]. Although the cellular and biochemical signaling mechanisms underlying EMT have been studied extensively, there is limited information about the biomechanical mechanisms of EMT. In particular, it is not known how changes in cell mechanics (cell stiffness, cell-cell adhesion strength, traction forces) influence the detachment, migration and invasion processes that occur during metastasis.
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Cohen-Armon, Malka. "An Unveiled Cell Death Mechanism Exclusive to Human Cancer Cells." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021014.

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Patel, Sagar S., Ramesh Natarajan, and Rebecca L. Heise. "Mechanotransduction of Primary Cilia in Lung Adenocarcinoma." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80435.

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Lung cancer causes more than 1 million deaths worldwide annually [1]. In a recent study by the American Cancer Society in 2011, more than 221,000 new cases of lung cancers were reported [2]. Out of these, the mortality rate was found in roughly 70% of the cases [2]. Lung cancer is divided into two major categories: small cell and non-small cell. In the United States, non-small cell lung cancer accounts for 85% of all lung cancers and is considered the most common type of lung cancer [2]. It is usually resistant to chemotherapy, therefore making it extremely difficult to treat [3]. Furthermore adenocarcinomas, a type of non-small cell lung cancer, occur towards the periphery of the lungs and are the most common type accounting for 40–45% of all lung cancer cases [3]. Epithelial cells in the healthy lungs undergo stresses during inhalation and expiration of normal breathing. In addition to the forces of normal breathing, lung cancer cells may also experience abnormal mechanical forces due to pre-existing lung diseases such as asthma, bronchitis and chronic obstructive pulmonary disease or other tumor associated structural changes. These conditions can significantly alter the structure of the lungs and cell phenotype [4]. The change in the structure of the lungs affects the mechanical environment of the cells. Changes in extracellular (ECM) stiffness, cell stretch, and shear stress influence tumorigenesis and metastasis [5]. One mechanism through which the cells sense and respond to the cellular mechanical environment is through the primary cilia [6–7]. Primary cilia are non-motile, solitary structures formed from the cellular microtubules and protrude out of each cell. They have also been shown to play an important role in facilitating common cancer signaling pathways such as Sonic Hedgehog and Wnt/β-catenin signaling [8–9]. The objective of this study was to test the hypothesis that lung cancer cells respond to mechanical stimuli with the formation of primary cilia that are necessary for 3 hallmarks of tumor progression: proliferation, epithelial mesenchymal-transition, and migration.
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Tang, Xin, Tony Cappa, Theresa Kuhlenschmidt, Mark Kuhlenschmidt, and Taher A. Saif. "A Novel Way to Characterize the Non-Specific Surface Adhesion of Cancer Cells and Understand Cancer Metastasis." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-11953.

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Cancer deaths are mostly caused by the metastasis of the malignant cells, not by the primary tumor itself. During metastasis, cancer cells detach from the primary tumor, spread to different tissues via blood circulation or lymph system, and reattach to invade new tissues and organs. In this project, we hypothesize that cancer cells manage their invasion by changing their surface adhesivity. To study the cell surface adhesivity, a novel and versatile microelectromechanical systems (MEMS) force sensor is developed to quantify the strength of adhesion between living cancer cells and a probe. The Silicon sensors consist of a probe and 2 flexible cantilever beams, while the probe is used to contact the cancer cell and the flexible beams are used to measure the cell force response in the range from nN to uN. The spring constant of the sensor is 14 nN/ μm. Our results demonstrate that the aggressive HCT-8 cells (from human colon adenocarcinoma) show high nonspecific adhesivity when they aggregate into cell islands, and low surface non-specific adhesivity after they disassociate from the cell islands. The surface adhesivity of less aggressive Caco-2 cells (from human colon carcinoma) and normal MA104 cell (from monkey kidney) are found to be lower than that of before-disassociation HCT-8 cells. Furthermore, the adhesion force response of cancer cells is found to show 2-slope force behavior, which is different from previous results of focal-adhesion detachment experiments. The 2-stage force bearing model is proposed to interpret the underlying mechanism.
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Di Donato, Marzia, Pia Giovannelli, Antimo Migliaccio, and Gabriella Castoria. "New Approaches Targeting the Invasive Phenotype of Prostate Cancer-Associated Fibroblasts." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021001.

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Regenbrecht, Christian. "Implication of Intra-Tumor Heterogeneity on Colorectal Cancer Response to MEK Inhibition." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021019.

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Benammar, Sarra, Fatima Mraiche, Jensa Mariam Joseph, and Katerina Gorachinova. "Glucose and Transferrin Liganded PLGA Nanoparticles Internalization in Non-Small Lung Cancer Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0227.

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Introduction: Recently, after a decade of confusing results, several studies pointed out that overexpression of GLUT1 (glucose transporter 1) is a biomarker of worse prognosis in NSCLC. Nonetheless, the presence of transferrin (Tf receptor), which is overexpressed in most cancer tissues and most lung cancers as well, in NSCLC is also an indicator of very poor prognosis. Therefore, these ligands can be used for active targeting of lung cancer cells and improved efficacy of internalization of cancer therapy using nanomedicines. Objectives: Having the background, the main goal of the project was the assessment of the influence of the glucose and transferrin ligands on the efficacy of internalization of the designed (i) glucose decorated PLGA (poly lactic-coglycolic acid) nanoparticles (Glu-PLGA NPs) and (ii) transferrin decorated PLGA nanoparticles (Tf-PLGA NPs) in comparison to (iii) non-liganded PLGA NPs using a A549 lung cancer cells. Methods: Glu-PLGA NPs, Tf-PLGA NPs and PLGA NP - fluorescently labelled), were designed using a sonication assisted nanoprecipitation method. Further, physicochemical properties characterization (particle size analysis, zeta potential, FTIR analysis, DSC analysis), cytotoxicity evaluation using MTT test, and cell internalization studies of DTAF labelled NPs using fluorimetry in A549 NSCLC cell line were performed. Results: The results pointed to a significantly improved internalization rate of the liganded compared to PLGA NPs. Glu-PLGA NPs showed higher internalization rate compared to Tf-PLGA and PLGA NPs, in the serum-supplemented and serumfree medium even at normal levels of glucose in the cell growth medium. Conclusion: The developed nanocarriers offer unique advantages of enhanced targetability, improved cell internalization and decreased toxicity, which makes them promising solution for current therapeutic limitations.
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Reports on the topic "Cancer cells"

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Alessa, Mohammed, Tayba Wahedi, Jumanah Alsairafi, Nouf Almatrafi, Wisal Shuaib, Johara Alnafie, Fatimah Alzubaidi, and Soha Elmorsy. Prevalence of Thyroid cancer in Saudi Arabis: Systematic review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0088.

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Review question / Objective: What is the prevalence of Thyroid cancer among population in kingdom of Saudi Arabia?. The aim of this systematic review is to scrutinize the prevalence of thyroid cancer (TC) in Saudi Arabia and assess the relative frequency of subgroups related to types of thyroid cancer, age, and gender. Condition being studied: Thyroid cancer is an abnormal growth of cells that starts in the thyroid gland. There is four types of differentiated thyroid cancer, three of these cancer develop from the follicular cells, the papillary thyroid cancer, follicular thyroid cancer, Hürthle cell carcinoma, and one rare type develops from the thyroid’s C cells called medullary thyroid cancer. There is one undifferentiated thyroid cancer called anaplastic thyroid cancer.
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Jones, Jonathan. Cell-Matrix Interactions in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, August 1995. http://dx.doi.org/10.21236/ada300395.

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Brooks, James D. Single Cell Characterization of Prostate Cancer-Circulating Tumor Cells. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada596639.

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Brooks, James B. Single Cell Characterization of Prostate Cancer Circulating Tumor Cells. Fort Belvoir, VA: Defense Technical Information Center, August 2011. http://dx.doi.org/10.21236/ada550987.

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Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells with a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, February 2003. http://dx.doi.org/10.21236/ada415526.

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Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells With a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, February 2004. http://dx.doi.org/10.21236/ada423810.

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Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells with a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada476353.

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Markovic, Dubravka, and Edward P. Cohen. Treatment of Breast Cancer with Immunogenic Cells Transfected with DNA from Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396744.

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Fridman, Rafael A. Cell Surface Regulation of Matrix Metalloproteinases in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada395379.

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Fridman, Rafael A. Cell Surface Regulation of Matrix Metalloproteinases in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada396698.

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