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Relevant bibliographies by topics / Sensitizing Agents

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Academic literature on the topic 'Sensitizing Agents'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 January 2023

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Journal articles on the topic "Sensitizing Agents"

1

Barnett, A. H. "Insulin-Sensitizing Agents –Thiazolidinediones (Glitazones)." Current Medical Research and Opinion 18, sup1 (2002): s31—s39. http://dx.doi.org/10.1185/030079902125000219.

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Nakanishi, Hideyuki, Shinya Shimizu, and Katherine Isbister. "SENSITIZING SOCIAL AGENTS FOR VIRTUAL TRAINING." Applied Artificial Intelligence 19, no. 3-4 (2005): 341–61. http://dx.doi.org/10.1080/08839510590910192.

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Kubo, Spencer H. "Inotropic agents with calcium-sensitizing properties." Coronary Artery Disease 5, no. 2 (1994): 119–26. http://dx.doi.org/10.1097/00019501-199402000-00005.

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Saltiel, Alan R., and Hiroyoshi Horilcoshi. "Thiazolidinediones are novel insulin-sensitizing agents." Current Opinion in Endocrinology and Diabetes 2, no. 4 (1995): 341–47. http://dx.doi.org/10.1097/00060793-199508000-00009.

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Végh, Agnes, Julius Gy Papp, Éva Udvary, and Károly Kaszala. "Hemodynamic Effects of Calcium-Sensitizing Agents." Journal of Cardiovascular Pharmacology 26 (1995): 20–31. http://dx.doi.org/10.1097/00005344-199500001-00004.

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Végh, Agnes, Julius Gy Papp, Éva Udvary, and Károly Kaszala. "Hemodynamic Effects of Calcium-Sensitizing Agents." Journal of Cardiovascular Pharmacology 26 (1995): 20–31. http://dx.doi.org/10.1097/00005344-199506261-00004.

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Kotchen, Theodore A. "Attenuation of Hypertension by Insulin-Sensitizing Agents." Hypertension 28, no. 2 (1996): 219–23. http://dx.doi.org/10.1161/01.hyp.28.2.219.

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SIMONIS, C., and AJ KRENTZ. "INSULIN-SENSITIZING AGENTS FOR POLYCYSTIC OVARY SYNDROME." Reproductive Medicine Review 11, no. 2-3 (2004): 121–46. http://dx.doi.org/10.1017/s0962279904000055.

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Pasquali, Renato, and Alessandra Gambineri. "Insulin-sensitizing agents in polycystic ovary syndrome." European Journal of Endocrinology 154, no. 6 (2006): 763–75. http://dx.doi.org/10.1530/eje.1.02156.

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Insulin-sensitizing agents have been recently proposed as the therapy of choice for polycystic ovary syndrome (PCOS), since insulin resistance and associated hyperinsulinemia are recognized as important pathogenetic factors of the syndrome. Moreover, since almost all obese PCOS women and more than half of those of normal weight are insulin resistant, and therefore present some degree of hyperinsulinemia, the use of insulin sensitizers should be suggested in most patients with PCOS. Insulin sensitizer treatment has been associated with a reduction in serum androgen levels and gonadotropins, and with an improvement in serum lipids and in prothrombotic factor plasminogen-activator inhibitor type 1, whatever the insulin sensitizer used. This therapy has also been associated with a decrease in hirsutism and acne, and with a regulation of menses and an improvement of ovulation and fertility. Notable improvements in all these parameters have also been described after a change in lifestyle approach, particularly in the presence of obesity. Lifestyle interventions should therefore be combined with insulin sensitizers in PCOS when obesity is present.

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Trowbridge, Ryan M., Mario V. Mitkov, Mark R. Pittelkow, and Devendra K. Agrawal. "Immunomodulation of malignant melanoma by contact sensitizing agents." Expert Review of Clinical Immunology 10, no. 1 (2013): 63–76. http://dx.doi.org/10.1586/1744666x.2014.850415.

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Dissertations / Theses on the topic "Sensitizing Agents"

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Manouchehri, Jasmine Marie. "RhTRAIL with Sensitizing Agents for Breast Carcinoma Treatment." Cleveland State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=csu1543316657492919.

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Tvermoes, Nicolai Aage. "A mechanistic investigation of the experimental radiation sensitizer gadolinium(III) texaphyrin /." Full text (PDF) from UMI/Dissertation Abstracts International, 2000. http://wwwlib.umi.com/cr/utexas/fullcit?p9992932.

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Beickelman, Amy C. "The synthesis and biological characterization of a potential hypoxic cell sensitizer /." Connect to full text in OhioLINK ETD Center, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=toledo1197412856.

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Thesis (M.S.)--University of Toledo, 2007.
Typescript. "Submitted as partial fulfillment of the requirements for The Master of Pharmaceutical Sciences." "A thesis entitled"--at head of title. Bibliography: leaves 53-55.

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Chan, Peter Ka-Lin. "Ruthenium nitroimidazole complexes as radiosensitizers." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28639.

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Local control of tumours by radiotherapy may fail due to the presence of regions of hypoxic cells. Radiosensitizers, such as nitroimidazoles, enhance killing of the resistant cells by ionizing radiation. However, dose limiting side-effects have prevented the attainment of maximum sensitization. The successful chemotherapeutic drug, cis-diamminedichloroplatinum(II) (cis-DDP), and analogues show moderate radiosensitizing effects, possibly because of binding to DNA. A rationale is then to use the DNA binding property of a metal to carry a sensitizer to the target of radiation damage, DNA, thereby improving the radiosensitizing effect while reducing the toxic side-effects of nitroimidazoles. The complex cis-RuCI₂(dmso)₄ was used as a precursor for synthesis of Ru(II)-nitroimidazole complexes because of its anti-tumour and DNA binding activities. A series of Ru(II) complexes of formulation RuCI₂(dmso)₂Ln, where dmso is S-bonded dimethyl sulphoxide, L = a nitroimidazole, and n=1 or 2, has been synthesized and characterized, and their toxicities and radiosensitizing abilities examined in vitro. When L = 2-nitroimidazole or a substituted-2-nitroimidazole, n = 2, but the nitroimidazole ligands dissociate in aqueous medium. With L = the 5-nitroimidazole, metronidazole, n=2, the sensitizing ability of the six-coordinate cis complex was disappointing with sensitizer enhancement ratio (SER) of 1.2 in hypoxic Chinese hamster ovary (CHO) cells. A series of 4-nitroimidazoles ligands was then studied. With L = 4-nitroimidazole (4-NO₂-Im), 1-(1' -aziridinyl-2' -propanol)-2-methyl-4-nitroimidazole (RSU-1170), 2-(1,2-dimethyl-4-nitroimidazolyl)-2-aminoethanol (RSU-3083), and 1-methyl-4-nitro-5-phenoxyimidazole (RSU-3100), n=2 and the six coordinate complexes appear to be of all cis geometry. The NMe-4-NO₂-Im ligand (n=1) chelates through the imidazole-N and the oxygen of NO₂ group as evidenced from spectroscopic data. Coordination via the nitrito group is uncommon and other examples involving nitroimidazole ligands have not been reported. For the 1-methyl-5-(2'-thioimidazolyl)-4-nitroimidazole (RSU-3159) ligand (n=1), binding to Ru occurs through the thioether and chelation may occur through the imidazole-NCH₃. In this series of Ru(II)-4-nitroimidazole complexes studied, RuC1₂(dmso)₂-NO₂-Im)₂, 5, was the most effective radiosensitizer (SER = 1.6 at 200 ,μM) and is better than the clinically used misonidazole (SER = 1.3 at 200 μM). In addition, 5 did not sensitize oxic CHO cells. Other Ru-N-substituted-4-nitroimidazole complexes gave SER values of 1.1-1.4 at 100-200 μM. Complex 5 also produced a dose-dependent increase in genotoxic activity (as measured by the in vitro induction of chromosome aberrations in CHO cells), which is similar to that of misonidazole but much less than that of c/s-DDP. Two changes in ancillary ligands and geometry of complexes were also examined: replacement of (i) dmso by tmso (tetramethylene sulphoxide), (ii) C1⁻ by Br⁻. The Ru-nitroimidazole complexes were synthesized from the precursors RuCl₂(tmso)₄ and trans-RuBr₂(dmso)₄. In this series of complexes, only RuCl₂(tmso)₂(4-NO₂-Im)₂, 15, and RuCl₂(tmso)₂(SR-2508), 18, have significantly higher SER values (1.6 and 1.5, respectively) than their corresponding nitroimidazole ligands. The tmso complexes of 2-NO₂-Im derivatives were more stable than the dmso series in aqueous solution with respect to the dissociation of the nitroimidazole ligands, which might be due to the improved lipophilicity of tmso complexes. Complex 18. is suggested to be penta-coordinated from XPS and ir data. The RuBr₂(dmso)₂(4-NO₂-Im)₂ was a less effective sensitizer (SER = 1.3 at 200 μM) than the dichloro analogue which may result from different geometrical structures or different behaviour in aqueous solution chemistry. The enhanced radiosensitizing effect over the corresponding free nitroimidazole ligand observed for complexes 5, 15 and 18 may depend on: (a) the metal's ability to target the sensitizer to DNA; complex 5 does bind to DNA, dissociation of C1⁻ perhaps facilitating the reaction; (b) the increase in reduction potential or (c) an increase in lipophilicity of the nitroimidazole ligand on coordination. However, the enhanced radiosensitization does not result from depletion of non-protein thiols. In the present study, the Ru complexes are less toxic than their corresponding nitroimiazole ligands in vitro. The radiosensitization and toxicity of the complexes 5, 15 and 18 are better than those of the free nitroimidazole ligands and the clinically used radiosensitizer, misonidazole. The data encourage further investigations of the use of transition metal complexes as radiosensitizers to combat the hypoxic tumour cells. [Formula Omitted]
Science, Faculty of
Chemistry, Department of
Graduate

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Tiwana, Gaganpreet Singh. "Discovery and investigation of novel radiosensitising genes." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:ee44297c-9b01-4c31-a4f8-6be3585c3557.

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Radiotherapy is second only to surgery in the curative management of patients with cancer, and yet the molecular mechanisms that determine the sensitivity of tumours to radiation remain largely unclear. A high-throughput radiosensitivity screening method based on clonogenicity was developed and a siRNA library against kinase targets was screened. The gold standard colony formation endpoint was chosen for determining reproductive cell death after radiation treatment, since effects on proliferation often do not reflect survival. Thiamine pyrophosphokinase-1 (TPK1), a key component of Vitamin B1/thiamine metabolism, was identified as a target for radiosensitisation. TPK1 knockdown caused significant radiosensitisation in cancer but not normal tissue cell lines. Other means of blocking this pathway such as knockdown of thiamine transporter-1 (THTR1) or treatment with the thiamine analogue pyrithiamine hydrobromide (PyrH) caused significant tumour specific radiosensitisation. There was persistent DNA damage in cells irradiated after TPK1 and THTR1 knockdown or PyrH treatment. Thus this screen allowed the identification of thiamine metabolism as a novel radiosensitisation target that affects DNA repair. Short-term modulation of thiamine metabolism could be a clinically exploitable strategy to achieve tumour specific radiosensitisation. Three additional genes, signal recognition particle-72 kDa (SRP72), glycogen synthase 3-beta (GSK3β) and MAP/Microtubule Affinity-Regulating Kinase 2 (MARK2) were also investigated. Knockdown of these genes radiosensitised both tumour and normal tissue cell lines and expression of two of them, GSK3β and SRP72 were found to be associated with poor recurrence-free survival in early breast cancer patients.

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Hamid, Mogammad Baahith. "Radiosensitisation of low HER-2 expressing human breast cancer cell lines." Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/96786.

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Thesis (MSc)--Stellenbosch University, 2015.
ENGLISH ABSTRACT: Breast Cancer remains one of the world’s leading causes of cancer related deaths amongst women. Its treatment has evolved from invasive, highly toxic therapies to treatments that possess a higher specificity and a lower toxicity. Despite improvements in overall survival, many patients do not benefit from these agents because of acquired and/or inherent tumour resistance, which could hinder treatment efficacy. Novel treatment strategies are, therefore, warranted to address these challenges and to significantly improve patient responses. Inhibiting components of the HER-2 signalling pathway can significantly sensitise breast cancer cells to low doses of ionising radiation. The objective of this study was to inhibit key molecular targets of the human epidermal growth factor receptor 2 (HER-2) signalling pathway and expose breast cancer cell lines to doses of radiation, so as to establish potential therapeutic targets that may be amenable to combined modality therapy, and formulate a cocktail of inhibitors to evaluate its radiosensitising capability. This study found that pre-treatment of two breast cancer cell lines (MDA-MB-231 and MCF-7) with a HER-2 inhibitor (TAK-165) had little or no effect on radiosensitivity. However, a radiation enhancement was observed when these cells were pre-treated either with BEZ235, a dual inhibitor of phosphoinositide 3-kinase (PI3K) and mammalian target for rapamycin (mTOR), or a cocktail of TAK-165 and BEZ235. These findings suggest that concurrent inhibition of HER-2, PI3K and mTOR during radiotherapy might improve treatment response of breast cancer patients.
AFRIKAANSE OPSOMMING: Borskanker bly steeds een van die leidende oorsake van sterftes aan kanker in vrouens. Behandeling het vanaf ‘n ingrypende, hoogs toksiese terapie verander na ‘n regimen wat hoogs spesifiek met ‘n laer toksisiteit is. Nogtans trek baie pasiënte geen voordeel uit hierdie nuwe benadering nie, omdat inherente en/of verworwe tumorweerstand daarteen suksesvolle uitkomste verhoed. Nuwe behandelingstrategieë is dus nodig om hierdie uitdagings te bekamp en om resultate in pasiënte aansienlik te verbeter. Inhibisie van komponente van die HER-2-seinoordragkaskade kan borskankerselle gevoelig maak vir lae dosisse van geïoniseerde bestraling. Die doelwit van hierdie studie was om sleutelteikens in die HER-2- seinoordragkaskade te inhibeer en om borskankerselle daarna aan bestralings dosisse bloot te stel. Sodoende word potensiële terapeutiese teikens wat vatbaar is vir gekombineerde modaliteitsterapie geïdentifiseer, waarna ‘n kombinasie van inhibitore geformuleer en geëvalueer kan word ten opsigte van hulle kapasiteit om gevoeligheid vir bestraling te verhoog. Die studie bevind dat voorbehandeling met ‘n HER-2-inhibitor (TAK-165) van borskankersellyne (MDA-MB-231 en MCF-7) min of geen invloed gehad het op stralingsensitiwiteit nie. ‘n Stralingsversterking is egter geïdentifiseer toe die selle vooraf behandel is met óf BEZ-235, ‘n tweevoudige inhibitor van fosforinositied 3-kinase (PI3K) en soogdierteiken vir rapamisien (mTOR), óf ‘n mengsel van TAK-165 en BEZ-235. Hierdie bevindinge suggereer dat gelyktydige inhibisie van die HER-2- seinoordragkaskade, PI3K en mTOR gedurende stralingsterapie moontlik die uitkoms in borskankerpasiënte kan verbeter.

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Xin, Yan. "Suramin as a chemo- and radio-sensitizer preclinical translational studies /." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1144958112.

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Farmer, Joseph Peter. "Defining the Radiation Sensitizing Activity of the Tubulin Depolymerizing Agent N-Acetyl Colchicinol (NAC)." Thesis, The University of Arizona, 2010. http://hdl.handle.net/10150/156912.

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The goal of this study was to examine the potential for the drug N-acetyl colchicinol (NAC) to be used to increase the efficacy of radiation therapy in the treatment of rectal cancer. In initial studies we defined the maximum non-cytotoxic dose of NAC and demonstrated the ability of NAC to transiently arrest tumor cells in the radiation sensitive G2/M phase of the cell cycle. Using standard clonogenic assays we examined the impact of NAC pretreatment on the cytotoxic activity of the radiomimetic drug Zeocin. Although the unexpectedly high degree of cell death produced by the NAC dose used in these later studies prevented definitive conclusions from being drawn, the results as a whole were encouraging and support further research on the potential of combination therapies employing transient tubulin depolymerizing agents such as NAC and radiation in the treatment of cancer.

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Kennedy, Mitchell Keith. "Murine IgE antibody responses to diverse contact sensitizing agents." 1986. http://hdl.handle.net/1993/24422.

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Green, Shane Kurtis. "The use of blocking antibodies targeting E-cadherin as sensitizing agents for anti-cancer therapy." 2004. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=80297&T=F.

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Books on the topic "Sensitizing Agents"

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Ciach, Michelle. Novel antimalarials and sensitizing agents. National Library of Canada, 2002.

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Ozdemir, Mehmet Vural. Meta-analysis of the clinical efficacy of alcohol-sensitizing agents in the treatment of alcohol dependance. National Library of Canada, 1993.

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Benjamin, Bonavida, ed. Sensitization of cancer cells for chemo/immuno/radio-therapy. Humana Press, 2008.

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International, Symposium on Radiotherapy in Developing Countries-Present Status and Future Trends (1986 Vienna Austria). Radiotherapy in developing countries: Proceedings of an International Symposium on Radiotherapy in Developing Countries--Present Status and Future Trends. The Agency, 1987.

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Shaheen, Faisal Haq. Pakistan's trade and related interests at the Doha round of WTO negotiations: An agenda for the masses : sensitizing the WTO to a "pro poor agenda'. Sustainable Development Policy Institute, 2001.

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Ketola, Kirsi. Chemotherapy Sensitizing Agents for Prostate Cancer. Elsevier Science & Technology Books, 2019.

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Chen, Zhe-Sheng (Jason), and Dong-Hua Yang. Protein Kinase Inhibitors As Sensitizing Agents for Chemotherapy. Elsevier Science & Technology, 2018.

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Bonavida, Benjamin, Dong-Hua Yang, and Zhe-Sheng Chen. Protein Kinase Inhibitors As Sensitizing Agents for Chemotherapy. Elsevier Science & Technology Books, 2018.

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Protein Kinase Inhibitors as Sensitizing Agents for Chemotherapy. Elsevier, 2019. http://dx.doi.org/10.1016/c2016-0-03564-7.

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Dreicer, Robert, Varinder Kaur, and Al-Ola A. Abdallah. BTK Inhibitors As Sensitizing Agents in Solid Tumors. Elsevier Science & Technology Books, 2022.

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Book chapters on the topic "Sensitizing Agents"

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Gerberick, G. Frank. "Risk Assessment of Sensitizing Agents." In Use of Mechanistic Information in Risk Assessment. Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78640-2_11.

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Maina, Flavio, and Rosanna Dono. "p53 Inhibitors as Cancer Sensitizing Agents." In Sensitization of Cancer Cells for Chemo/Immuno/Radio-therapy. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-474-2_12.

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Dings, Ruud P. M., Mark Klein, and Kevin H. Mayo. "Non-Peptidic Mimetics as Cancer-Sensitizing Agents." In Sensitization of Cancer Cells for Chemo/Immuno/Radio-therapy. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-474-2_18.

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Banerji, Shantanu, Sudharsana Rao Ande, Subbareddy Maddika, et al. "Peptides and Peptidomimetics as Cancer Therapy Sensitizing Agents." In Sensitization of Cancer Cells for Chemo/Immuno/Radio-therapy. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-474-2_17.

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Siddiqui, Mohammad S., and Arun J. Sanyal. "Drug Therapy for NASH: Insulin-Sensitizing Agents (Metformin and Thiazolidinediones)." In Non-Alcoholic Fatty Liver Disease. Wiley-Blackwell, 2013. http://dx.doi.org/10.1002/9781118556153.ch24.

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Zuddas, Alessandro, Alberto Bocchetta, and Giovanni U. Corsini. "Effects of Copper-chelating Agents and Alcohol-sensitizing Drugs on MPTP-induced Neurotoxicity in Mice." In Pharmacology and Functional Regulation of Dopaminergic Neurons. Palgrave Macmillan UK, 1988. http://dx.doi.org/10.1007/978-1-349-10047-7_58.

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Li, Tian, Wenyan Fu, Changhai Lei, and Shi Hu. "Current status of anti-EGFR agents." In Novel Sensitizing Agents for Therapeutic Anti-EGFR Antibodies. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-12-821584-5.00027-4.

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Huang, Maohua, Minfeng Chen, Wencai Ye, and Dongmei Zhang. "VEGFR Inhibitors as Sensitizing Agents for Cancer Chemotherapy." In Protein Kinase Inhibitors as Sensitizing Agents for Chemotherapy. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-816435-8.00003-1.

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Yang, Yang, and Zhi Shi. "STAT3 Inhibitors as Sensitizing Agents for Cancer Chemotherapy." In Protein Kinase Inhibitors as Sensitizing Agents for Chemotherapy. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-816435-8.00005-5.

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Baer, Maria R. "FLT3 Inhibitors as Sensitizing Agents for Cancer Chemotherapy." In Protein Kinase Inhibitors as Sensitizing Agents for Chemotherapy. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-816435-8.00006-7.

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Conference papers on the topic "Sensitizing Agents"

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D'Hallewin, Marie-Ange, Luc Baert, and Herman A. Vanherzeele. "In-vivo detection of human bladder carcinoma without sensitizing agents." In OE/LASE '94, edited by Graham M. Watson, Rudolf W. Steiner, and Douglas E. Johnson. SPIE, 1994. http://dx.doi.org/10.1117/12.175027.

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Smith, Ian, Rachel Bell, Meghan Lambie, Benjamin Haibe-Kains, and Scott Bratman. "Abstract PO-071: Characterizing transcriptomic indicators of radiosensitivity in cancer and identifying sensitizing therapeutic agents." In Abstracts: AACR Virtual Special Conference on Radiation Science and Medicine; March 2-3, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1557-3265.radsci21-po-071.

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Sciegienka, Sebastian, Samuel Rodman, Ann Tomanek-Chalkley, Kelly C. Falls, Douglas R. Spitz, and Melissa A. Fath. "Abstract 3219: Sensitizing hypoxic small cell lung cancer cells to radiation and hydrogen peroxide-producing agents using CuATSM." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3219.

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Soh, Katherine K., Wontak Kim, Ye Sol Lee, et al. "Abstract 235: AXL inhibition leads to a reversal of a mesenchymal phenotype sensitizing cancer cells to targeted agents and immuno-oncology therapies." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-235.

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Zhang, Wenguan, Lian Qin, and Shengmin Zhao. "Efficient solution-processable electrophosphorescence for trifluoromethylpyridinto iridium with sensitizing agent." In 2015 6th International Conference on Manufacturing Science and Engineering. Atlantis Press, 2015. http://dx.doi.org/10.2991/icmse-15.2015.331.

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Senbabaoglu, Filiz, Ahmet Cingöz, Ezgi Kaya, et al. "Abstract B73: Screen among 1200 FDA-approved drug library reveals mitoxantrone as a TRAIL-sensitizing agent for glioblastoma multiforme." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-b73.

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Evans, Ashley L., Jason Carey, Shanora Glymph, Derrick Morton, and Jaideep Chaudhary. "Abstract 63: Id4 acts as a tumor suppressor by inducing apoptosis and sensitizing prostate cancer cells to chemotherapeutic agent doxorubicin." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-63.

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Zanini, E., LS Louis, J. Antony, et al. "Abstract NTOC-116: THE TUMOUR SUPPRESSOR PROTEIN OPCML ACTS AS A SENSITIZING AGENT IN ANTI–EGFR/HER2 THERAPY AND CISPLATIN TREATMENT IN OVARIAN CANCER." In Abstracts: 11th Biennial Ovarian Cancer Research Symposium; September 12-13, 2016; Seattle, WA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3265.ovcasymp16-ntoc-116.

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Reports on the topic "Sensitizing Agents"

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Morrow, Charles S. Turning Chemopreventive Agents Against Breast Cancer: Sensitizing Cancers to Therapeutics While Protecting Normal Tissues from Toxicity. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada589289.

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