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Relevant bibliographies by topics / Cancer research; Cell death

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Academic literature on the topic 'Cancer research; Cell death'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Cancer research; Cell death"

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Catalano, Veronica, Miriam Gaggianesi, Valentina Spina, Flora Iovino, Francesco Dieli, Giorgio Stassi, and Matilde Todaro. "Colorectal Cancer Stem Cells and Cell Death." Cancers 3, no. 2 (April 11, 2011): 1929–46. http://dx.doi.org/10.3390/cancers3021929.

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Brancolini, Claudio, and Luca Iuliano. "Proteotoxic Stress and Cell Death in Cancer Cells." Cancers 12, no. 9 (August 23, 2020): 2385. http://dx.doi.org/10.3390/cancers12092385.

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To maintain proteostasis, cells must integrate information and activities that supervise protein synthesis, protein folding, conformational stability, and also protein degradation. Extrinsic and intrinsic conditions can both impact normal proteostasis, causing the appearance of proteotoxic stress. Initially, proteotoxic stress elicits adaptive responses aimed at restoring proteostasis, allowing cells to survive the stress condition. However, if the proteostasis restoration fails, a permanent and sustained proteotoxic stress can be deleterious, and cell death ensues. Many cancer cells convive with high levels of proteotoxic stress, and this condition could be exploited from a therapeutic perspective. Understanding the cell death pathways engaged by proteotoxic stress is instrumental to better hijack the proliferative fate of cancer cells.

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Zhu, Shan, Qiuhong Zhang, Xiaofan Sun, Herbert J. Zeh, Michael T. Lotze, Rui Kang, and Daolin Tang. "HSPA5 Regulates Ferroptotic Cell Death in Cancer Cells." Cancer Research 77, no. 8 (January 27, 2017): 2064–77. http://dx.doi.org/10.1158/0008-5472.can-16-1979.

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Philchenkov, Alex. "Preface: Focus on Cell Death." Critical Reviews™ in Oncogenesis 21, no. 3-4 (2016): v—vii. http://dx.doi.org/10.1615/critrevoncog.2016017027.

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Macintosh, Robin L., and Kevin M. Ryan. "Autophagy in tumour cell death." Seminars in Cancer Biology 23, no. 5 (October 2013): 344–51. http://dx.doi.org/10.1016/j.semcancer.2013.05.006.

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Sonnenschein, Carlos, and Ana M. Soto. "The Death of the Cancer Cell." Cancer Research 71, no. 13 (April 20, 2011): 4334–37. http://dx.doi.org/10.1158/0008-5472.can-11-0639.

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Carpinteiro, Alexander, Claudia Dumitru, Marcus Schenck, and Erich Gulbins. "Ceramide-induced cell death in malignant cells." Cancer Letters 264, no. 1 (June 2008): 1–10. http://dx.doi.org/10.1016/j.canlet.2008.02.020.

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Wang, Tzu-Hao, Hsin-Shih Wang, and Yung-Kwei Soong. "Paclitaxel-induced cell death." Cancer 88, no. 11 (June 1, 2000): 2619–28. http://dx.doi.org/10.1002/1097-0142(20000601)88:11<2619::aid-cncr26>3.0.co;2-j.

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Greenwood, Emma. "MUCking up cell death." Nature Reviews Cancer 4, no. 4 (April 2004): 249. http://dx.doi.org/10.1038/nrc1325.

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Bangham, Jenny. "Checking in cell death." Nature Reviews Cancer 5, no. 1 (January 2005): 5. http://dx.doi.org/10.1038/nrc1538.

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Dissertations / Theses on the topic "Cancer research; Cell death"

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Dremann, David Michael. "Pluronic Activity in Hyperthermia-induced Cancer Cell Death." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1247425426.

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Ongkeko, Weg M. "The role of Cdc2 and p53 in cell cycle checkpoints and apoptosis." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244848.

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McGuire, Karen M. "Characterization of Apatone and Tolecine Induced Cell Death Mechanisms in Bladder and Ovarian Cancer." Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1334356592.

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Rong, Yiping. "Bcl-2 Regulates Proapoptotic Calcium Signals by Interacting with the Inositol 1, 4, 5-Trisphosphate Receptor." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1228322705.

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Dhillon, Harsharan. "Mechanisms of Piperlongumine-Induced Cancer Cell Death." Diss., North Dakota State University, 2015. http://hdl.handle.net/10365/25178.

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Piperlongumine (PPLGM), a bioactive agent obtained from long pepper plants, possesses potent antitumor activity by inducing reactive oxygen species (ROS). However, the mechanisms for PPLGM?s antitumor actions are not well defined. We investigated PPLGM?s antitumor effects and molecular mechanisms against pancreatic and colon cancer, two of the leading causes of cancer death for both men and women in the U.S. We found that PPLGM activated a ROSmediated DNA damage pathway that lead to pancreatic cancer cell death in vitro. Further, mice treated with PPLGM showed reduced pancreatic tumor volume, which was associated with a decrease in tumor cell proliferation and enhanced oxidative stress levels. To elucidate the target pathways responsible for PPLGM-mediated cell death, RNA sequencing was performed. 684 genes were differentially expressed in pancreatic cancer cells treated with PPLGM compared to the control. Genes related to ER-stress and UPR pathways were activated in PPLGM-treated pancreatic cancer cells. To determine the therapeutic efficacy of PPLGM in combination with currently used chemotherapy in vivo, an orthotopic mouse model of pancreatic cancer was used. The combination of PPLGM with gemcitabine resulted in greater reduction of tumor weight and volume than either agent alone, and PPLGM-treated mouse tumors showed decreased expression of Ki-67, a proliferation marker. In vitro studies supported the in vivo results where the combination of PPLGM with gemcitabine and erlotinib significantly decreased pancreatic cancer cell viability and survival, and induced apoptosis compared to control cells or cells treated with the chemotherapeutic agents alone. PPLGM inhibited the growth of colorectal cancer cells to a greater degree than normal colon cells and activated p-ERK protein expression. The use of a MEK inhibitor attenuated the activation of p-ERK and partially blocked PPLGM-mediated cell death, indicating the involvement of the MEK/ERK pathway in colon cancer cell death. These results suggest PPLGM holds potential as a therapeutic agent to treat pancreatic and colon cancer in the clinics.
North Dakota State University. Department of Biological Sciences
NDSU Graduate School Doctoral Dissertation Fellowship
NDSU Center for Protease Research COBRE (NIH 2P20 RR015566, P30 GM103332-01)
NDSU Development Foundation Centennial
Engebretson Family Research Endowments

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Giampazolias, Evangelos. "Investigating non-apoptotic cell death in cancer." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8056/.

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Prokop, Katherine Jane. "Cell Death Characterization In Tumor Constructs Using Irreversible Electroporation." Thesis, Virginia Tech, 2013. http://hdl.handle.net/10919/51655.

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Pancreatic and prostate cancer are both prevalent cancers in the United States with pancreatic being one of the most aggressive of all cancers and prostate cancer being one of the most common, ranking as the number one cancer in men. Treatment of both cancers can be quite challenging as the anatomy of the pancreas and prostate, as well as the development and diagnosis of the disease can greatly limit treatment options. Therefore, it is necessary to develop new cancer treatments to help manage and prevent these cancers. Irreversible electroporation is a new non-thermal focal ablation therapy utilizing short, pulsed electric fields to damage cell membranes leading to cell death. The therapy is minimally invasive, involving the insertion of needle electrodes into the region of interest and lasts less than two minutes. Heat sink effects that thermal therapies experience near large blood vessels do not affect irreversible electroporation. This allows the treatment to be used on tumors near vasculature as well as critical structures without harming these vital regions. While irreversible electroporation is a promising new cancer therapy, further developments are necessary to improve treatment planning models. This work aims to further understand the electric field thresholds necessary to kill different types of cancer cells with a focus on pancreatic and prostate cancer. The work is done using an in vitro tumor (hydrogel) model as this model is better than traditional cell suspension studies, with added benefits over the immediate use of tissue and animal models.
Master of Science

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Świdziński, Jodi A. "Programmed cell death in Arabidopsis thaliana." Thesis, University of Oxford, 2003. http://ora.ox.ac.uk/objects/uuid:6e2580fc-8873-4722-89f7-b206d4be2a5f.

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Programmed Cell Death (PCD) describes an orderly cellular breakdown that occurs in both plants and animals throughout development and in response to biotic and abiotic stresses. The molecular machinery that functions in the induction and execution of animal PCD has been characterised in great detail. Conversely, few genes and proteins involved in plant PCD have been identified. While certain features of animal PCD may be conserved, the induction and execution of plant PCD is also likely to involve novel proteins and mechanisms. The aim of the work presented in this thesis was to investigate experimental approaches for studying plant PCD and to gain an understanding of the molecular mechanisms involved. To this end, an Arabidopsis thaliana cell suspension system was developed in which PCD could be induced by both a heat treatment (55°C, 10 min) and senescence (13 to 14 days-old). This system allowed for the molecular responses related to programmed cell death to be distinguished from those that were a specific response to the inducing stimulus. The Arabidopsis cell suspension system was utilised for an analysis of transcriptomic and proteomic changes that occur following the induction of PCD. A custom cDNA microarray analysis of ~100 putative cell death-related genes was used to measure the abundance of transcripts of these genes during PCD, and this work was extended to a whole-genome transcriptomic analysis of PCD. A number of candidate genes that may play a role in plant PCD were identified. These included those encoding antioxidant enzymes, cytosolic heat shock proteins, the mitochondrial adenine nucleotide translocase, ion transporters, a two-component response regulator (ARR4), several pathogenesis-related proteins, phospholipases and proteases, extracellular glycoproteins and enzymes (including a subtilisin-like protease, chitinases, and glucanases), and transcriptional regulators such as a homeobox leucine zipper and NAC-domain proteins. The induction and execution of plant PCD is also likely to involve mechanisms that are not transcriptionally regulated. A proteomic analysis of changes in the total cellular protein profile during heat- and senescence-induced PCD was therefore used to identify 12 proteins that are modulated in both systems and may play a PCD-specific role. These included the mitochondrial voltage-dependent anion channel (Athsr2), catalase, mitochondrial superoxide dismutase, an extracellular glycoprotein, and aconitase. Selected genes and proteins identified in the transcriptomic and proteomic analyses were further investigated in an attempt to define their role in plant PCD. Since PCD is difficult to quantitatively analyse at the whole-plant level, initially a strategy of transient expression of genes of interest in Arabidopsis protoplasts was adopted. However, it proved to be technically difficult to accurately quantify the number of dead cells in this system. As an alternative, Arabidopsis T-DNA insertional mutants within genes of interest were investigated for PCD-related phenotypes. Mutants in Senescence-Related Gene 3, the mitochondrial voltage-dependent anion channel (Athsr2), and cytosolic Heat shock protein 70-3 were isolated. The mutant lines were not visibly affected in their development, formation of xylem, onset and progression of senescence, or responses to abiotic and biotic stresses. This indicated that these genes are either not involved in the PCD pathway or that their functional role can be fulfilled by other gene products.

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Li, Fangfang. "Regulation of pancreatic β-cell death and cancer cell migration by TPRM2 channels." Thesis, University of Leeds, 2016. http://etheses.whiterose.ac.uk/13374/.

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Hoopes, Justin Darrel. "Mechanisms of Induced Cell Death in Bluetongue Virus Challenged Human Cell Lines." DigitalCommons@USU, 2009. https://digitalcommons.usu.edu/etd/252.

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Bluetongue virus (BTV) is a pathogenic member of the Reoviridae family. BTV does not cause disease in humans, but is capable of selectively infecting and killing certain transformed human cell lines. Understanding BTV's oncotrophism may lead to new therapeutics for treating cancer. This study focused on the underlying mechanisms of BTV-induced cell death in carcinoma cell lines. It was our hypothesis that BTV infects human carcinoma transformed cells, produces mRNA and protein, induces a strong inflammatory response, induces mitogen activated protein kinase (MAPK)-based pro-apoptotic signaling, inhibits PKB-based signaling, and eventually kills the cell by inducing apoptosis. Three carcinoma cell lines (A498, HEP-G2, and A549) were independently infected with BTV. In each cell line we determined: (1) cell viability over the course of infection; (2) BTV induced cytokine expression profile and magnitude of expression; (3) BTV viral RNA expression profile and magnitude of expression; (4) BTV viral protein expression profile and magnitude of expression; (5) changes in BTV induced cell death and cytokine expression in cells with protein kinase B (PKB), p38-MAPK, extracellular receptor kinase (ERK-1/2), stress-activated protein kinase (SAPK-JNK), Src kinase, platelet-derived growth factor receptor (PDGFR) kinase, epidermal growth factor receptor (EDGFR) kinase, or Janus kinase (JAK) activity inhibited; (6) intracellular changes in PKB, p38-MAPK, ERK-1/2, and SAPK-JNK phosphorylation as a result of BTV infection; and (7) BTV-induced changes in tyrosine phosphorylation. We determined that BTV infects and kills all three cell lines in a cell line dependent manner. Relative cell death between cell lines was proportional to cytokine expression, but inversely proportional to viral protein expression. Only tyrosine kinase inhibitors influenced BTV-induced cell death and cytokine expression. Both A498 and A549 cells constitutively expressed phosphorylated PKB and p38 MAPK, of which both were de-phosphorylated during BTV infection. Tyrosine phosphorylation remained active, with elevated tyrosine phosphorylation exclusively in infected cells. We conclude that BTV-induced cell death and cytokine expression are a function of the cell's response to infection and are directly related through intracellular signaling. These pathways are only partially poly I:C inducible, but include PKB and tyrosine kinase signaling.

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Books on the topic "Cancer research; Cell death"

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service), ScienceDirect (Online, ed. Programmed cell death: General principles for studying cell death. San Diego, Calif: Academic Press, 2008.

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LaFond, Richard E. Cancer: The outlaw cell. 3rd ed. Oxford: American Chemical Society/Oxford University Press, 2011.

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service), ScienceDirect (Online, ed. Programmed cell death: The biology and therapeutic implications of cell death. San Diego, Calif: Academic Press/Elsevier, 2008.

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The immortal cell: Why cancer research fails. Garden City Park, N.Y: Avery Pub. Group, 1994.

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Johnson, Daniel Eric. Cell death signaling in cancer biology and treatment. New York: Humana Press, 2013.

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Khosravi-Far, Roya, and Eileen White. Programmed Cell Death in Cancer Progression and Therapy. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6554-5.

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Johnson, Daniel E., ed. Cell Death Signaling in Cancer Biology and Treatment. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5847-0.

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One renegade cell: How cancer begins. New York, NY: Basic Books, 1998.

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Resende, Rodrigo R., and Henning Ulrich, eds. Trends in Stem Cell Proliferation and Cancer Research. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6211-4.

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Maureen, Bowen Sandra, ed. Programmed cell death in tumours and tissues. London: Chapman and Hall, 1990.

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Book chapters on the topic "Cancer research; Cell death"

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Mehrpour, Maryam, Ahmed Hamaï, and Patrice Codogno. "Autophagy, Cell Death, and Cancer." In Trends in Stem Cell Proliferation and Cancer Research, 359–90. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6211-4_14.

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Ruirui, Kong, Payal Ray, Mengxue Yang, Pushuai Wen, Li Zhu, Jianghong Liu, Kazuo Fushimi, et al. "Alternative Pre-mRNA Splicing, Cell Death, and Cancer." In Cancer Treatment and Research, 181–212. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-31659-3_8.

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Yamazaki, Takahiro, Claire Vanpouille-Box, Sandra Demaria, and Lorenzo Galluzzi. "Immunogenic Cell Death Driven by Radiation—Impact on the Tumor Microenvironment." In Cancer Treatment and Research, 281–96. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-38862-1_10.

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Reed, John C., Toshiyuki Miyashita, Stanislaw Krajewski, Shinichi Takayama, Christine Aime-Sempe, Shinichi Kitada, Takaaki Sato, et al. "Bcl-2 family proteins and the regulation of programmed cell death in leukemia and lymphoma." In Cancer Treatment and Research, 31–72. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1261-1_3.

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Zarisfi, Mohammadreza, Tu Nguyen, Jessie R. Nedrow, and Anne Le. "The Heterogeneity Metabolism of Renal Cell Carcinomas." In The Heterogeneity of Cancer Metabolism, 117–26. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_8.

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AbstractAccording to data from the American Cancer Society, cancer is one of the deadliest health problems globally. Annually, renal cell carcinoma (RCC) causes more than 100,000 deaths worldwide [1–4], posing an urgent need to develop effective treatments to increase patient survival outcomes. New therapies are expected to address a major factor contributing to cancer’s resistance to standard therapies: oncogenic heterogeneity. Gene expression can vary tremendously among different types of cancers, different patients of the same tumor type, and even within individual tumors; various metabolic phenotypes can emerge, making singletherapy approaches insufficient. Novel strategies targeting the diverse metabolism of cancers aim to overcome this obstacle. Though some have yielded positive results, it remains a challenge to uncover all of the distinct metabolic profiles of RCC. In the quest to overcome this obstacle, the metabolic oriented research focusing on these cancers has offered freshly new perspectives, which are expected to contribute heavily to the development of new treatments.

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Bennett, Jason, Marta Moretti, Anil K. Thotakura, Laura Tornatore, and Guido Franzoso. "The Regulation of the JNK Cascade and Programmed Cell Death by NF-κB: Mechanisms and Functions." In Trends in Stem Cell Proliferation and Cancer Research, 297–336. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6211-4_12.

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Zhivotovsky, Boris. "Systems Biology Analysis of Cell Death Pathways in Cancer: How Collaborative and Interdisciplinary Research Helps." In Cancer Systems Biology, Bioinformatics and Medicine, 267–96. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1567-7_10.

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Vaux, David L. "Cell Death and Cancer." In Cell Death, 121–34. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9302-0_6.

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Matsuhashi, Sachiko, and Iwata Ozaki. "Programmed Cell Death 4." In Encyclopedia of Cancer, 2995–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4761.

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Matsuhashi, Sachiko, and Iwata Ozaki. "Programmed Cell Death 4." In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_4761-3.

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Conference papers on the topic "Cancer research; Cell death"

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Qu, Ang, Hao Wang, Jinna Li, Junjie Wang, Jingjia Liu, Yuzhu Hou, Li Huang, and Yong Zhao. "Direct effects of 125I seeds radiation on A549 lung cancer cells: G2/M arrest and enhanced cell death." In Annual International Conference on Advances in Cancer Medical Research. Global Science & Technology Forum (GSTF), 2013. http://dx.doi.org/10.5176/2345-7821_acmr13.04.

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Thiyagarajan, Magesh. "Portable Plasma Biomedical Device for Cancer Treatment." In ASME 2011 6th Frontiers in Biomedical Devices Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/biomed2011-66030.

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This research study examined the effect of non-thermal portable atmospheric air plasma system on leukemia cancer cells. Acute monocytic leukemia cells (THP-1) were exposed to atmospheric pressure non-thermal plasma. To assess death caused by plasma exposure, cells were subjected to trypan blue exclusion assays and a kill-curve and assessment of death overtime were compiled using data from the assays. In addition to this, DNA was harvested from treated and untreated samples to determine if apoptotic ladders were present. Results have indicated that non-thermal plasma can cause cell death in THP-1 cells overtime, and the death that occurs corresponds directly to the amount of time that the cells were exposed to ionized plasma. Preliminary fluorescent imaging of the treated cells revealed that higher treatment doses are not only more likely to induce cellular death but are likely to induce necrotic death, while lower treatment doses that are capable of inducing death may induce apoptotic or programmed cellular death. Ideally the results obtained from these experiments will allow for further investigation of the effects of ionized non-thermal plasma on melanoma cell lines and will lead to an inexpensive method for treating early stage skin cancer and cancerous lesions.

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Singh, Preeti, Madan Godbole, Geeta Rao, Vishwamohan Saxena, Sanjay Annarao, Raja Roy, Kalyan Mitra, VK Bajpai, and Arvind Ingle. "Abstract B98: Chloroquin converts molecular iodine induced autophagy in MDAMB231 to apoptotic cell death: Implications for overcoming chemotherapeutic resistance." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-b98.

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Polotskaia, Alla, and Jill Bargonetti. "Abstract C30: p53-independent 8-amino-adenosine mediated breast cancer cell death." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-c30.

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Zhang, Xiaolong, Xiaolin Chen, and Hua Tan. "A Numerical Study on Highly Viscous Compound Cancer Cell Microfiltration." In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-66953.

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Cancer is a leading cause of death worldwide. There has been extensive research on cancer in recent decades, with many studies focusing on Circulating Tumor Cells (CTCs), i.e., cancer cells shed into the circulating bloodstream from a primary tumor site. CTCs are mainly responsible for initiating metastases, and can be used as an indicator for early cancer detection. Investigating CTCs and the related detection methods such as microfiltration is of great importance. CTCs as well as other cells are normally composed of highly viscous nucleus and cytoplasm which are encapsulated by the outermost layer of cortical membrane. In order to account for the effects of viscous nucleus and cytoplasm on the microfiltration process and study the dynamic characteristics comprehensively, a realistic model is preferred. In this research, we employ the compound droplet model consisting of three layers, the layer of cell membrane, cytoplasm and nucleus, to capture the full range of CTCs behavior during the microfiltration process. The compound cell deformation and pressure signature during microfiltration are studied numerically. Also discussed are the effects of nucleus-cytoplasm ratio (N/C ratio), their viscosity as well as surface tension on the cell behavior when it squeezing through the filter channel. Our results can gain insight into the physics behind the filtering process and provide some guidance to the design and optimization of such devices.

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Huang, Shengbing, and Frank A. Sinicrope. "Abstract B46: Celecoxib induces autophagy and apoptosis in human colorectal cancer cells: Strategies to enhance cell death." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Dec 6–9, 2009; Houston, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-09-b46.

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Kapur, Arvinder, Mayur Kajla, Susan Paskewitz, Allegra Cappuccini, Pooja Mehta, Geeta Mehta, and Manish Patankar. "Abstract A16: A novel death receptor ligand fabclavine inhibits cancer and cancer stem cell proliferation by extrinsic apoptosis." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research; September 13-16, 2019; Atlanta, GA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.ovca19-a16.

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Zhu, Shan, Tina N. Davis, and Andrew L. Kung. "Abstract A69: Activation of PI3K p110α by minocycline leads to cell dysfunction and cell death in 9L glioma." In Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-a69.

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Rello-Varona, S., M. Fuentes-Guirado, R. López-Alemany, A. Contreras-Pérez, N. Mulet-Margalef, S. Garcia-Monclús, X. Garcia del Muro, and OM Tirado. "PO-477 BCL-Xl inhibition enhances dinaciclib-induced cell death in soft-tissue sarcoma cell lines." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.496.

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Saadatzadeh, Mohammad Reza, Khadijeh Bijangi Vishehsaraei, Haiyan Wang, Aaron Cohen-Gadol, Karen E. Pollok, and Ahmad R. Safa. "Abstract B18: Targeting histone deacetylase 6 (HDAC6) depresses proliferation and induces caspase-associated cell death in glioblastoma multiforme (GBM) cells and GBM stem cell-like spheroids." In Abstracts: AACR Special Conference: Advances in Brain Cancer Research; May 27-30, 2015; Washington, DC. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.brain15-b18.

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Reports on the topic "Cancer research; Cell death"

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Distelhorst, Clark W. Programmed Cell Death in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 1995. http://dx.doi.org/10.21236/ada300581.

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Distelhorst, Clark W. Programmed Cell Death in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 1997. http://dx.doi.org/10.21236/ada340671.

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Kornbluth, Sally. Metabolic Regulation of Ovarian Cancer Cell Death. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada570124.

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Kornbluth, Sally. Metabolic Regulation of Ovarian Cancer Cell Death. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada597625.

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Kaini, Ramesh. Molecular Basis of Autophagic Cell Death in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2009. http://dx.doi.org/10.21236/ada540723.

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Kaini, Ramesh. Molecular Basis of Autophagic Cell Death in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2009. http://dx.doi.org/10.21236/ada506319.

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Quinn, Timothy. Killing Breast Cancer Cells With a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada478599.

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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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Abstract:

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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Levenson, Victor V. Lysosome-mediated Cell Death and Autophagy-Dependent Multidrug Resistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada495800.

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Cowburn, David. Rational Design of Regulators of Programmed Cell Death in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada395357.

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