Gotowa bibliografia na temat „Malignancy - Cytotoxicity”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „Malignancy - Cytotoxicity”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Artykuły w czasopismach na temat "Malignancy - Cytotoxicity"
Santos-Pirath, I. M., L. O. Walter, M. F. Maioral, P. D. Neuenfeldt, R. J. Nunes i M. C. Santos-Silva. "Apoptosis induced by synthetic compounds containing a 3,4,5-trimethoxyphenyl fragment against lymphoid immature neoplasms". Biochemistry and Cell Biology 97, nr 5 (październik 2019): 630–37. http://dx.doi.org/10.1139/bcb-2018-0316.
Pełny tekst źródłaSun, Xin, Yang Yu, Li Ma, Xin Xue, Zhenkui Gao, Juan Ma i Man Zhang. "T cell cytotoxicity toward hematologic malignancy via B7-H3 targeting". Investigational New Drugs 38, nr 3 (3.07.2019): 722–32. http://dx.doi.org/10.1007/s10637-019-00819-y.
Pełny tekst źródłaSmyth, Mark J., Kevin Y. T. Thia, Shayna E. A. Street, Duncan MacGregor, Dale I. Godfrey i Joseph A. Trapani. "Perforin-Mediated Cytotoxicity Is Critical for Surveillance of Spontaneous Lymphoma". Journal of Experimental Medicine 192, nr 5 (5.09.2000): 755–60. http://dx.doi.org/10.1084/jem.192.5.755.
Pełny tekst źródłaBanerjee, Kaushik, Satyajit Das, Pritha Choudhury, Sarbari Ghosh, Rathindranath Baral i Soumitra Kumar Choudhuri. "A Novel Approach of Synthesizing and Evaluating the Anticancer Potential of Silver Oxide Nanoparticles in vitro". Chemotherapy 62, nr 5 (2017): 279–89. http://dx.doi.org/10.1159/000453446.
Pełny tekst źródłaWang, Jiaan-Der, Ya-Yu Wang, Shih-Yi Lin, Cheng-Yi Chang, Jian-Ri Li, Shi-Wei Huang, Wen-Ying Chen, Su-Lan Liao i Chun-Jung Chen. "Exosomal HMGB1 Promoted Cancer Malignancy". Cancers 13, nr 4 (19.02.2021): 877. http://dx.doi.org/10.3390/cancers13040877.
Pełny tekst źródłaGottlieb, DJ, HG Prentice, HE Heslop, C. Bello-Fernandez, AC Bianchi, AR Galazka i MK Brenner. "Effects of recombinant interleukin-2 administration on cytotoxic function following high-dose chemo-radiotherapy for hematological malignancy". Blood 74, nr 7 (15.11.1989): 2335–42. http://dx.doi.org/10.1182/blood.v74.7.2335.2335.
Pełny tekst źródłaGottlieb, DJ, HG Prentice, HE Heslop, C. Bello-Fernandez, AC Bianchi, AR Galazka i MK Brenner. "Effects of recombinant interleukin-2 administration on cytotoxic function following high-dose chemo-radiotherapy for hematological malignancy". Blood 74, nr 7 (15.11.1989): 2335–42. http://dx.doi.org/10.1182/blood.v74.7.2335.bloodjournal7472335.
Pełny tekst źródłaLee, Han Bi, Jae-Ho Yoon, Gi June Min, Sung-Soo Park, Silvia Park, Sung-Eun Lee, Ki-Seong Eom i in. "Natural-Killer Cell Cytotoxicity Is a Diagnostic and Prognostic Marker in Adult Patients with Secondary Hemophagocytic Lymphohistiocytosis: Results from a Prospective Phase II Observational Study". Blood 134, Supplement_1 (13.11.2019): 2331. http://dx.doi.org/10.1182/blood-2019-129676.
Pełny tekst źródłaSoiffer, RJ, MJ Robertson, C. Murray, K. Cochran i J. Ritz. "Interleukin-12 augments cytolytic activity of peripheral blood lymphocytes from patients with hematologic and solid malignancies". Blood 82, nr 9 (1.11.1993): 2790–96. http://dx.doi.org/10.1182/blood.v82.9.2790.2790.
Pełny tekst źródłaSoiffer, RJ, MJ Robertson, C. Murray, K. Cochran i J. Ritz. "Interleukin-12 augments cytolytic activity of peripheral blood lymphocytes from patients with hematologic and solid malignancies". Blood 82, nr 9 (1.11.1993): 2790–96. http://dx.doi.org/10.1182/blood.v82.9.2790.bloodjournal8292790.
Pełny tekst źródłaRozprawy doktorskie na temat "Malignancy - Cytotoxicity"
Padilla, Roberto. "Discovering the Potential of Photoluminescent Ruthenium(II) Complexes as Photodynamic Therapy Agents". Diss., Virginia Tech, 2016. http://hdl.handle.net/10919/78190.
Pełny tekst źródłaPh. D.
Craperi, Delphine. "Thérapie génique des gliomes : caractérisation des voies cytotoxiques déclenchées par le système thymidine kinase herpétique/ganciclovir". Université Joseph Fourier (Grenoble ; 1971-2015), 1998. http://www.theses.fr/1998GRE10073.
Pełny tekst źródłaChen, Yi-Chen, i 陳亦禎. "Investigation of Methylation Status of FLT4 and MGMT in Cancers and Enhancement of Temozolomide-Induced Cytotoxicity for Malignant Glioma". Thesis, 2014. http://ndltd.ncl.edu.tw/handle/jj3z56.
Pełny tekst źródła國立中正大學
生物醫學研究所
102
Oral cancer is the fourth most common cancer type among men in Taiwan, and about 94% of oral cancers are oral squamous cell carcinoma (OSCC). In cancer pathogenesis, epigenetic modification such as DNA methylation driven gene silencing of tumor suppressor genes is recognized as a key event. Therefore, we employed the Illumina GoldenGate Methylation array, which included 1,505 CpG sites covering 807 genes to analyze oral samples from OSCC patients. Among them, Fms-related tyrosine kinase 4 (FLT4) was highly methylated in most of the OSCC samples. In addition, we employed bisulfite pyrosequencing analysis to validate the methylation level of FLT4 in OSCC lines and patient samples. We found hyper-methylation levels were observed in OSCC lines. We also treated OSCC lines with 5-aza-dC, and found that the methylation level of FLT4 was reduced. Furthermore, we examined FLT4 methylation level in patient samples and found that FLT4 was significantly hyper-methylated in OSCC samples than in normal samples. Next, we used real-time PCR and found the expression level of FLT4 in OSCC lines and OSCC samples were low, but significantly higher expression of FLT4 was found in normal oral tissues. Taken DNA methylation and gene expression profiles together, we found FLT4 was hyper-methylated in oral cancer and thus it may hold diagnostic and predictive value as a biomarker. In addition to understanding the methylation profile of OSCC, we are also interested in exploring the methylation status of drug-resistant genes in glioblastoma multiforme (GBM). GBM is the most common form of primary brain tumor in adults and is difficult to completely resect by surgery. The chemotherapy drug temozolomide (TMZ) is often used to treat GBM, however, upregulated O6-methylguanine-DNA methyltransferase (MGMT) in some GBM can neutralize the cytotoxic effect of TMZ. We were employed pyrosequencing assay, quantitative RT-PCR and western blotting to check the methylation status and expression level of MGMT in various GBM cell lines. In addition, we knock down MGMT expression with siRNA in GBM cell lines to confirm if TMZ resistance in the cells can be reduced. Moreover, we established the GBM-initiating cells (GICs) from parental GBM cell lines, and check the difference of MGMT methylation status between parental GBM cells and GICs. Then the GICs were determined the effect of TMZ on cell viability. In summary, we found MGMT can influence TMZ efficacy in GBM, and the MGMT expression level might be a therapeutic prediction of response to TMZ.
"In vitro studies on the mechanisms of hyperthermia- and TNF-α-induced apoptosis". 2002. http://library.cuhk.edu.hk/record=b5896015.
Pełny tekst źródłaThesis (M.Phil.)--Chinese University of Hong Kong, 2002.
Includes bibliographical references (leaves 211-232).
Abstracts in English and Chinese.
Acknowledgements --- p.i
List of Publications and Abstracts --- p.ii
Abbreviations --- p.iv
Abstract --- p.xi
Abstract in Chinese --- p.xiv
List of Figures --- p.xvii
List of Tables --- p.xxiii
Contents --- p.xxiv
Chapter Chapter 1. --- General Introduction --- p.1
Chapter 1.1 --- Hyperthermia --- p.2
Chapter 1.1.1 --- History of Hyperthermia --- p.2
Chapter 1.1.2 --- Biological Functions of Hyperthermia --- p.3
Chapter 1.1.3 --- Clinical Application of Hyperthermia --- p.4
Chapter 1.1.3.1 --- Whole-body Hyperthermia --- p.4
Chapter 1.1.3.2 --- Regional Hyperthermia --- p.4
Chapter 1.1.3.3 --- Local Hyperthermia --- p.5
Chapter 1.1.4 --- Combination Therapy --- p.5
Chapter 1.1.4.1 --- Combined treatment with Hyperthermia and Radiotherapy --- p.6
Chapter 1.1.4.2 --- Combined treatment with Hyperthermia and Chemotherapy --- p.6
Chapter 1.2 --- Tumour Necrosis Factor --- p.9
Chapter 1.2.1 --- History of Tumour Necrosis Factor --- p.9
Chapter 1.2.2 --- Sources of TNF-α and TNF-β --- p.9
Chapter 1.2.3 --- Biological Roles of TNF --- p.10
Chapter 1.2.3.1 --- Receptors of TNF-α --- p.11
Chapter 1.2.4 --- Signaling Pathway of TNF --- p.12
Chapter 1.2.4.1 --- Activation of Death Domain --- p.12
Chapter 1.2.4.2 --- Activation of Sphingomyelin Pathway --- p.13
Chapter 1.2.4.3 --- Activation of NF-kB pathway --- p.13
Chapter 1.3 --- Types of Cell Death: Necrosis and Apoptosis --- p.16
Chapter 1.3.1 --- Necrosis --- p.16
Chapter 1.3.2 --- Apoptosis --- p.16
Chapter 1.4 --- Signaling Pathway in Apoptosis --- p.19
Chapter 1.4.1 --- Factors Involved in Apoptotic Pathway --- p.19
Chapter 1.4.1.1 --- Caspases --- p.19
Chapter 1.4.1.2 --- Death Substrates --- p.20
Chapter 1.4.1.3 --- Bcl-2 Protein Family --- p.21
Chapter 1.4.1.4 --- Role of Mitochondria --- p.23
Chapter 1.5 --- Objectives of the Project --- p.26
Chapter Chapter 2. --- Materials and Methods --- p.28
Chapter 2.1 --- Materials --- p.29
Chapter 2.1.1 --- Culture of Cells --- p.34
Chapter 2.1.1.1 --- "TNF-α Sensitive Cell Line, L929" --- p.34
Chapter 2.1.1.2 --- "TNF-α Resistance Cell Line, L929-11E" --- p.34
Chapter 2.1.1.3 --- Preservation of Cells --- p.35
Chapter 2.1.2 --- Culture Media --- p.36
Chapter 2.1.2.1 --- RPMI 1640 (Phenol Red Medium) --- p.36
Chapter 2.1.2.2 --- RPMI 1640 (Phenol Red-Free Medium) --- p.36
Chapter 2.1.3 --- Buffers and Reagents --- p.37
Chapter 2.1.3.1 --- Preparation of Buffers --- p.37
Chapter 2.1.3.2 --- Buffer for Common Use --- p.37
Chapter 2.1.3.3 --- Reagents for Annexin-V-FITC/PI assay --- p.37
Chapter 2.1.3.4 --- Reagents for Cytotoxicity Assay --- p.37
Chapter 2.1.3.5 --- Reagents for Molecular Biology Work --- p.38
Chapter 2.1.3.6 --- Reagents for Western Blotting Analysis --- p.38
Chapter 2.1.4 --- Chemicals --- p.40
Chapter 2.1.4.1 --- Recombinant Murine TNF-α --- p.40
Chapter 2.1.4.2 --- Dye for Cytotoxicity Assay --- p.41
Chapter 2.1.4.3 --- Fluorescence Dyes --- p.41
Chapter 2.1.4.4 --- Chemicals Related to Mitochondrial Studies --- p.41
Chapter 2.1.4.5 --- Inhibitors of Caspases --- p.42
Chapter 2.1.4.6 --- Antibodies for Western Blotting --- p.42
Chapter 2.1.4.7 --- Other Chemicals --- p.43
Chapter 2.2 --- Methods --- p.44
Chapter 2.2.1 --- Treatment with TNF-α --- p.44
Chapter 2.2.2 --- Treatment with Hyperthermia --- p.44
Chapter 2.2.3 --- In vitro Cell Cytotoxicity Assay --- p.45
Chapter 2.2.4 --- Flow Cytometry --- p.46
Chapter 2.2.4.1 --- Introduction --- p.46
Chapter 2.2.4.2 --- Analysis by FCM --- p.48
Chapter 2.2.4.3 --- Determination of Apoptotic and Late Apoptotic/Necrotic Cells with Annexin-V-FITC/PI Cytometric Analysis --- p.50
Chapter 2.2.4.4 --- Determination of Mitochondrial Membrane Potential (ΔΨm) --- p.51
Chapter 2.2.4.5 --- Determination of Hydrogen Peroxide (H202) Release --- p.52
Chapter 2.2.4.6 --- Determination of Intracellular Free Calcium ([Ca2+]i) Level --- p.52
Chapter 2.2.4.7 --- Determination of the Relationship of ΔΨm and [Ca2+]i Level --- p.53
Chapter 2.2.5 --- Western Blotting Analysis --- p.53
Chapter 2.2.5.1 --- Preparation of Proteins from Cells --- p.53
Chapter 2.2.5.2 --- SDS Polyacrylamide Gel Electophoresis (SDS- PAGE) --- p.56
Chapter 2.2.5.3 --- Electroblotting of Proteins --- p.57
Chapter 2.2.5.4 --- Probing Antibodies for Proteins --- p.57
Chapter 2.2.5.5 --- Enhanced Chemiluminescence (ECL) assay --- p.58
Chapter 2.2.6 --- Reverse Transcriptase Polymerase Chain Reaction --- p.58
Chapter 2.2.6.1 --- Extraction of RNA by Trizol Reagent --- p.59
Chapter 2.2.6.2 --- Determination of the Amount of RNA --- p.60
Chapter 2.2.6.3 --- Agarose Gel Electrophoresis --- p.60
Chapter 2.2.6.4 --- Reverse Transcription --- p.63
Chapter 2.2.6.5 --- Polymerase Chain Reaction (PCR) --- p.63
Chapter 2.2.6.6 --- Design of Primers for Different Genes --- p.64
Chapter 2.2.6.7 --- Determination of the Number of Cycles in PCR for Different Genes --- p.67
Chapter 2.2.7 --- Caspase Fluorescent Assay --- p.67
Chapter 2.2.7.1 --- Caspase-3 or ´ؤ8 Assay --- p.67
Chapter Chapter 3. --- Results --- p.59
Chapter 3.1 --- Studies of the Characteristics of L929 and L929-11E cells --- p.70
Chapter 3.1.1 --- Determination of the Growth Curve of L929 and L929-11E Cells --- p.70
Chapter 3.2 --- Studies on the Effect of TNF-α on L929 and L929-11E Cells --- p.73
Chapter 3.2.1 --- TNF-α Induced Cell Death in L929 Cells but not in L929- 11E Cells --- p.73
Chapter 3.2.2 --- TNF-α Induced Apoptosis in a Time-dependent Manner in L929Cells but not in L929-11E Cells --- p.80
Chapter 3.2.3 --- TNF-α Induced Mitochondrial Membrane Depolarization in a Time-dependent Manner in L929 Cells but notin L929-11E Cells --- p.87
Chapter 3.2.4 --- TNF-α Induced Cytochrome c Release in a Time- dependent Manner in L929 Cells but not in L929-11E Cells --- p.92
Chapter 3.3 --- Effect of Hyperthermia on L929 and L929-11E Cells --- p.96
Chapter 3.3.1 --- Introduction --- p.95
Chapter 3.3.2 --- Hyperthermia Induced Apoptosis in L929 and L929-11E Cells --- p.96
Chapter 3.3.3 --- Effect of Hyperthermia on Mitochondrial Membrane Depolarization --- p.100
Chapter 3.3.4 --- Hyperthermia Induced Cyto c Release in a Time-dependent Manner in L929 and L929-11E Cells --- p.105
Chapter 3.4 --- Relationship of Hyperthermia and TNF-α with PTP in L929 Cells --- p.107
Chapter 3.5 --- Effect of TNF-α and Hyperthermia on the Level of Hydrogen Peroxide (H202) in L929 and L929-11E Cells --- p.114
Chapter 3.5.1 --- Introduction --- p.114
Chapter 3.5.2 --- TNF-α Enhanced the Level of H202 in L929 cells but not in L929-11E Cells --- p.115
Chapter 3.5.3 --- Hyperthermia Enhanced the Level of H202 in L929 and L929-11E cells --- p.117
Chapter 3.6 --- Effect of TNF-α and Hyperthermia on the Level of Intracellular Calcium in L929 and L929-11E Cells --- p.122
Chapter 3.6.1 --- Increase in the Intracellular Calcium Level Induced by TNF-α Was Related to the Mitochondrial Membrane Depolarization in L929 Cells but not in L929-11E Cells --- p.122
Chapter 3.6.2 --- Hyperthermia Increased the Level of [Ca2+]i in L929 and L929-11E Cells in a Time-dependent Manner --- p.124
Chapter 3.7 --- Effect of Combined Hyperthermia and TNF-α Treatment on the Induction of Apoptosis in L929 and L929-1 1E Cells --- p.129
Chapter 3.7.1 --- Combined Treatment with Hyperthermia and TNF- α Induced Apoptosis in Both L929 and L929-11E cells --- p.129
Chapter 3.7.2 --- Hyperthermia and Its Combined Treatment with TNF-α Induced Mitochondrial Membrane Depolarization in L929 and L929-11E Cells --- p.135
Chapter 3.8 --- Investigation of the Downstream Apoptotic Pathway in L929 and L929-11E Cells Upon Hyperthermia and TNF-a treatment --- p.142
Chapter 3.8.1 --- Introduction --- p.142
Chapter 3.8.2 --- Effect ofTNF-α and Hyperthermia on p53 Expression --- p.142
Chapter 3.8.3 --- Effect of Hyperthermia and TNF-α on PARP --- p.146
Chapter 3.8.4 --- Effect of Hyperthermia and TNF-α on Caspase-3 Activity --- p.149
Chapter 3.8.5 --- Effect of Hyperthermia and TNF-α on Bid protein --- p.158
Chapter 3.8.6 --- Effect of Hyperthermia and TNF-α on Caspase-8 Activity --- p.165
Chapter 3.8.7 --- Effect ofTNF-α on TNFR1 Expression --- p.169
Chapter Chapter 4. --- Discussion
Chapter 4.1 --- TNF-α Induced Apoptosis and Changed the Mitochondrial Activities in L929 Cells --- p.176
Chapter 4.2 --- L929-11E cells Possessed Resistance Towards TNF-α --- p.187
Chapter 4.3 --- Hyperthermia Triggered Apoptosis and Changed Mitochondrial Activities in L929 and L929-11E cells --- p.190
Chapter 4.4 --- Combined hyperthermia and TNF-α treatment induced cell death and changed mitochondria activities in L929 and L929-11E cells --- p.195
Chapter 4.5 --- Reversal of the TNF-α resistance and Enhancement of Sensitivity Towards Hyperthermia in L929-11E cells --- p.197
Chapter 4.6 --- Proposed Pathway in the TNF-α- and Hyperthermia-mediated Apoptosis --- p.200
Chapter 4.7 --- Application of TNF-α and Hyperthermia on Clinical Cancer Treatment --- p.203
Chapter Chapter 5. --- Future Perspective of the Project --- p.206
References --- p.210
Teesdale-Spittle, P. H., Klaus Pors, R. Brown, Laurence H. Patterson i J. A. Plumb. "Development of nonsymmetrical 1,4-disubstituted anthraquinones that are potently active against cisplatin-resistant ovarian cancer cells". 2005. http://hdl.handle.net/10454/3191.
Pełny tekst źródłaA novel series of 1,4-disubstituted aminoanthraquinones were prepared by ipso-displacement of 1,4-difluoro-5,8-dihydroxyanthraquinones by hydroxylated piperidinyl- or pyrrolidinylalkyl-amino side chains. One aminoanthraquinone (13) was further derivatized to a chloropropyl-amino analogue by treatment with triphenylphosphine-carbon tetrachloride. The compounds were evaluated in the A2780 ovarian cancer cell line and its cisplatin-resistant variants (A2780/ cp70 and A2780/MCP1). The novel anthraquinones were shown to possess up to 5-fold increased potency against the cisplatin-resistant cells compared to the wild-type cells. Growth curve analysis of the hydroxyethylaminoanthraquinone 8 in the osteosarcoma cell line U-2 OS showed that the cell cycle is not frozen, rather there is a late cell cycle arrest consistent with the action of a DNA-damaging topoisomerase II inhibitor. Accumulative apoptotic events, using time lapse photography, indicate that 8 is capable of fully engaging cell cycle arrest pathways in G2 in the absence of early apoptotic commitment. 8 and its chloropropyl analogue 13 retained significant activity against human A2780/cp70 xenografted tumors in mice.
Części książek na temat "Malignancy - Cytotoxicity"
Luciani, M. F., i P. Golstein. "Fas-based d10S-mediated cytotoxicity requires macromolecular synthesis for effector cell activation but not for target cell death". W The Role of Apoptosis in Development, Tissue Homeostasis and Malignancy, 67–73. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0553-8_12.
Pełny tekst źródłaOhnishi, Takanori, Hiromitsu Iwasaki, Norio Arita, Shoju Hiraga i Toru Hayakawa. "Potentiation of VP-16 Cytotoxicity by Dipyridamole in Malignant Glioma Cells". W Biological Aspects of Brain Tumors, 252–59. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68150-2_32.
Pełny tekst źródłaSchackert, G., M. Kirsch, H. Fischer, H. K. Schackert i S. Kunze. "Comparative Study of Monocyte-Mediated Cytotoxicity and Biological Response Modifier-Mediated Cytotoxicity Against Malignant Human Brain Tumor Cells In Vitro". W Advances in Neurosurgery, 312–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77997-8_58.
Pełny tekst źródłaMiyagi, Koichi, Jiro Mukawa, Hisashi Koga, Yasushi Higa, Susumu Nakasone, Susumu Mekaru i Marylou Ingram. "Interferon Effect on Cytotoxicity of Autologous Stimulated Lymphocytes from Patients with Malignant Glioma". W Biological Aspects of Brain Tumors, 207–14. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68150-2_26.
Pełny tekst źródłaPhillips, David H. "Chemical carcinogens". W Oxford Textbook of Cancer Biology, redaktorzy Francesco Pezzella, Mahvash Tavassoli i David J. Kerr, 79–90. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0007.
Pełny tekst źródłaSankar Satpathy, Bhabani, Binapani Barik, Ladi Alik Kumar i Sangram Biswal. "Potential of Lipid Based Nanodrug Carriers for Targeted Treatment of Glioblastoma: Recent Progress and Challenges Ahead". W Glioblastoma - Current Evidences [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108419.
Pełny tekst źródłaTaber, Douglass. "The Roush Synthesis of ( + )-Superstolide A". W Organic Synthesis. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199764549.003.0093.
Pełny tekst źródłaFenchel, K., L. Bergmann, B. Jahn i P. S. Mitrou. "Up-Regulation of Adhesion Molecules by Immunotherapy as a Mechanism of Cytotoxicity in Renal Cell Cancer, Malignant Melanoma, and Acute Myelocytic Leukemia". W Contributions to Oncology, 336–46. S. Karger AG, 1994. http://dx.doi.org/10.1159/000422840.
Pełny tekst źródłaStreszczenia konferencji na temat "Malignancy - Cytotoxicity"
Hussein, Ola, Feras Alali, Ala‐Eddin Al Mustafa i Ashraf Khalil. "Development of Novel Chalcone Analogs as Potential Multi-Targeted Therapies for Castration-Resistant Prostate Cancer". W Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0114.
Pełny tekst źródłaHussein, Ola, Feras Alali, Ala-Eddin Al Moustafa i Ashraf Khalil. "Design, Synthesis and Biological Evaluation of Novel Chalcone Analogs as Potential Therapeutic Agents for Castration-Resistant Prostate Cancer". W Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0179.
Pełny tekst źródłaSong, Michael M., Monish R. Makena, Ashly Hindle, Balakrishna Koneru, Thinh H. Nguyen, Hwangeui Cho, Barry J. Maurer, Min H. Kang i C. Patrick Reynolds. "Abstract 2616: Comparison of the cytotoxicity and increase of reactive oxygen species and dihydroceramides of fenretinide to its major metabolites (4-oxo- and 4-methoxyphenyl fenretinide) in T-cell lymphoid malignancy, neuroblastoma, and ovarian cancer cell lines". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2616.
Pełny tekst źródłaLee, David J., Yeo-Hyun Hwang i In Ah Kim. "Abstract A37: MicroRNA-26b potentiates cytotoxicity of malignant glioma cells by radiation". W Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-a37.
Pełny tekst źródłaKaza, Niroop, i Kevin A. Roth. "Abstract A34: Analysis of gossypol-induced cytotoxicity in malignant peripheral nerve sheath tumor cells." W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a34.
Pełny tekst źródłaTruxova, Iva, Lenka Kasikova, Cyril Salek, Michal Hensler, Daniel Lysak, Peter Holicek, Pavla Bilkova i in. "Abstract B96: Calreticulin exposure on malignant blasts correlates with improved NK cell-mediated cytotoxicity in AML patients". W Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-b96.
Pełny tekst źródłaJane, Esther P., Daniel R. Premkumar, Naomi R. Agostino, Joseph L. Scialabba i Ian F. Pollack. "Abstract 5209: Abrogation of STAT3 activation by JSI-124 enhances dasatinib-induced cytotoxicity in malignant human glioma cell lines". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5209.
Pełny tekst źródłaCooper, Jason P., Charles P. Reynolds, Robert W. Curley i Min H. Kang. "Abstract 1676: Cytotoxicity of fenretinide and its metabolite 4-oxo-4-HPR in malignant lymphoid cells can be dependent and independent of reactive oxygen species (ROS)". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1676.
Pełny tekst źródłaSantos, Javier V., Alex Vara, Craig Thomas, Medhi Wangpaichitr, Min You, Niramol Savaraj i Dao M. Nguyen. "Abstract 3489: Profound cytotoxicity of the histone deacetylase inhibitor SAHA (Suberoylanilide Hydroxamic Acid) and TRAIL (Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand) combination in malignant pleural mesothelioma". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3489.
Pełny tekst źródłaSantos, Javier V., Min You, Medhi Wangpaichitr, Niramol Savaraj i Dao M. Nguyen. "Abstract LB-222: Identifying cFLIP as a marker and also a potentially “druggable” target of SAHA+TRAIL (TNF-Related Apoptosis Inducing Ligand), cytotoxicity in malignant pleural mesothelioma (MPM)". W 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-lb-222.
Pełny tekst źródła