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Books on the topic 'Cancer drug resistance, tumor metabolism'

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Author: Grafiati
Published: 14 March 2023

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1

Dr, Mehta Kapil, and Siddik Zahid H, eds. Drug resistance in cancer cells. New York, NY: Springer, 2009.

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2

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

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3

S, El-Deiry Wafik, ed. Tumor progression and therapeutic resistance. New York, NY: New York Academy of Sciences, 2005.

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4

B, Roninson Igor, ed. Molecular and cellular biology of multidrug resistance in tumor cells. New York: Plenum Press, 1991.

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5

Lauricella, Marianna, and Sonia Emanuele. Novel apoptotic drugs in targeting tumor cells. Trivandrum, Kerala, India: Researh Signpost, 2007.

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6

Kim, Kŏn-hong. Yubangam ŭi taje yangmul naesŏng saengchʻe chipʻyo palgul mit kŭ yuyongsŏng kŏmjŭng =: Identification of biomarkers for multidrug resistance and validation of markers in breast cancer tissue. [Seoul]: Sikpʻum Ŭiyakpʻum Anjŏnchʻŏng, 2007.

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7

Bonavida, Benjamin. Chemo-immunosensitization of resistant tumor cells to cell death by apoptosis, 2006. Trivandrum: Transworld Research Network, 2006.

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8

Hiscox, Stephen. Therapeutic Resistance to Anti-Hormonal Drugs in Breast Cancer: New Molecular Aspects and their Potential as Targets. Dordrecht: Springer Netherlands, 2009.

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9

Nikko Brain Tumor Conference (8th 1990 Karatsu-shi, Japan). Biological aspects of brain tumors: Proceedings of the 8th Nikko Brain Tumor Conference, Karatsu (Saga) 1990. Tokyo: Springer-Verlag, 1991.

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10

Gregory, Bock, Goode Jamie, Novartis Foundation, and Symposium on Mechanisms of Drug Resistance in Epilepsy : Lessons from Oncology (2001 : London, England), eds. Mechanisms of drug resistance in epilepsy: Lessons from oncology. Chichester, England: Wiley, 2002.

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11

Bates, Susan E., Kapil Mehta, and Zahid H. Siddik. Drug Resistance in Cancer Cells. Springer, 2010.

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12

Bonavida, Benjamin. Sensitization of Cancer Cells for Chemo/Immuno/Radio-Therapy. Humana Press, 2010.

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13

Molecular Mechanisms Of Tumor Cell Resistance To Chemotherapy Targeted Therapies To Reverse Resistance. Springer-Verlag New York Inc., 2013.

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14

Gonzalez-Perez, Ruben R., and Bo R. Rueda. Tumor Angiogenesis Regulators. Taylor & Francis Group, 2013.

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15

Gonzalez-Perez, Ruben R., and Bo R. Rueda. Tumor Angiogenesis Regulators. Taylor & Francis Group, 2013.

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16

Gonzalez-Perez, Ruben R. Tumor Angiogenesis Regulators. Taylor & Francis Group, 2013.

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17

Gonzalez-Perez, Ruben R., and Bo R. Rueda. Tumor Angiogenesis Regulators. Taylor & Francis Group, 2013.

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18

Pacak, Karel, and INTERNATIONAL SYMPOSIUM ON CATECHOLAMINE. Tumor Progression and Therapeutic Resistance (TPR) (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2006.

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19

Hiscox, Stephen, Julia Gee, and Robert I. Nicholson. Therapeutic Resistance to Anti-hormonal Drugs in Breast Cancer: New Molecular Aspects and their Potential as Targets. Hiscox Stephen Gee Julia Nicholson Robert I, 2010.

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20

Biological aspects of brain tumors: Proceedings of the 8th Nikko Brain Tumor Conference, Karatsu (Saga) 1990. Springer-Verlag, 1991.

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21

Multidrug resistance in cancer cells: Molecular, biochemical, physiological, and biological aspects. Chichester: J. Wiley, 1996.

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22

(Editor), Sudhir Gupta, and Takashi Tsuruo (Editor), eds. Multidrug Resistance in Cancer Cells: Molecular, Biochemical, Physiological and Biological Aspects. Wiley, 1996.

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23

Tsuruo, Takashi, and Sudhir Gupta. Multidrug Resistance in Cancer Cells: Molecular, Biochemical, Physiological and Biological Aspects. Wiley & Sons, Incorporated, John, 2007.

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24

Farghaly, Samir A. Adoptive Cell Immunotherapy for Epithelial Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0005.

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The standard management for epithelial ovarian cancer (EOC) is a combination of aggressive debulking surgery with residual tumor of less than 1 cm and platinum-based chemotherapy. However, a high percentage of patients experience disease recurrence. Extensive efforts to find new therapeutic options have been made, albeit cancer cells develop drug resistance and malignant progression occurs. Novel therapeutic strategies are needed to enhance progression-free survival and overall survival of patients with advanced EOC. Several preclinical and clinical studies investigated feasibility and efficacy of adoptive cell therapy (ACT) in EOC. The aim of this chapter is to present an overview of ACT in EOC, focusing on Human Leukocyte Antigen (HLA)-restricted tumor infiltrating lymphocytes and MHC-independent immune effectors such as natural killer and cytokine-induced killer. The available data suggest that ACT may provide the best outcome in patients with low tumor burden, minimal residual disease, or maintenance therapy. Further preclinical studies and clinical trials are needed.
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25

Josephs, Debra H., Heather J. Bax, Giulia Pellizzari, James F. Spicer, Ana Montes, and Sophia N. Karagiannis. Antibody Therapeutics for Ovarian Carcinoma and Translation to the Clinic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0001.

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Despite improvements over the past decade in the treatment of ovarian cancer, many patients are at risk of recurrent disease and emerging drug resistance. The increased selectivity and reduced toxicity of molecularly targeted anti-cancer agents renders them attractive for development in ovarian cancer, and monoclonal antibodies targeting ovarian cancer-specific tumor antigens represent the largest such group investigated in this clinical setting. This chapter describes examples of monoclonal antibodies clinically evaluated for efficacy in ovarian cancer. These agents recognize molecular targets expressed on tumors or within tumor microenvironments that may be essential for tumor cell survival and proliferation. Recently, antibodies targeting checkpoint molecules on immune cells have shown efficacy in modulating anti-tumor immunity, and applications in ovarian carcinomas are evaluated. The chapter focuses on therapeutic agents’ attributes on targeting key cancer growth and progression pathways, and propensity to engender effector functions by activating immune effector cells in tumors and the circulation.
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