Journal articles on the topic 'Anti-cancer'

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1

Tyagi, Nidhi, Ganesh N. Sharma, Birendra Shrivastava, Prasoon Saxena, and Nitin Kumar. "Medicinal plants: used in Anti-cancer treatment." International Journal of Research and Development in Pharmacy & Life Sciences 6, no. 5 (August 2017): 2732–39. http://dx.doi.org/10.21276/ijrdpl.2278-0238.2017.6(5).2732-2739.

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Dr Anand Kumar, Dr Anand Kumar, and *. Dr RuchikaKhanna * Dr RuchikaKhanna. "Glutathione A Super Anti-Oxidant in Preventing Oral Cancer." International Journal of Scientific Research 3, no. 5 (June 1, 2012): 423–24. http://dx.doi.org/10.15373/22778179/may2014/133.

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3

Hoefnagel, Cornelis A. "Anti-cancer radiopharmaceuticals." Anti-Cancer Drugs 2, no. 2 (April 1991): 107–32. http://dx.doi.org/10.1097/00001813-199104000-00001.

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4

D, Devananda. "Annona Muricata (Linn.) Acetogenins as Potent Anti-Breast Cancer Agents." International Journal of Pharmacognosy & Chinese Medicine 4, no. 2 (2020): 1–8. http://dx.doi.org/10.23880/ipcm-16000202.

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Breast cancer is the most common type of cancer in women, globally. In India, it has been ranked number one with regard to cancer incidence in both men and women. Phytotherapy has been extensively considered against cancer, and Annona muricata is one such plant species that has gained scientific interest for decades. The acetogenins, a class of phytocompounds exclusively to the Annonaceae family of plant kingdom, are known contributors towards this biomedical significance of the A. muricata. In this review, we have identified those A. muricata acetogenins that exhibit anti-breast cancer activity.
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5

Gupta, Tarun, Virendra Kumar Vishwakarma, and Manoj Kumar Maurya Khushdil Khan. "Anti-cancer Activity of Vitamin-C Against Leukemia: A Review." International Journal of Trend in Scientific Research and Development Volume-2, Issue-4 (June 30, 2018): 1264–72. http://dx.doi.org/10.31142/ijtsrd14250.

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6

Moku, Gopikrishna, Suresh Kumar Gulla, Narendra Varma Nimmu, Sara Khalid, and Arabinda Chaudhuri. "Delivering anti-cancer drugs with endosomal pH-sensitive anti-cancer liposomes." Biomaterials Science 4, no. 4 (2016): 627–38. http://dx.doi.org/10.1039/c5bm00479a.

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Numerous prior studies have been reported on the use of pH-sensitive drug carriers such as micelles, liposomes, peptides, polymers, nanoparticles,etc. that are sensitive to the acidic (pH = ∼6.5) microenvironments of tumor tissues.
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7

Tahara, Makoto. "Anti-cancer drugs for thyroid cancer." Annals of Oncology 28 (October 2017): ix63. http://dx.doi.org/10.1093/annonc/mdx612.

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8

D, Dinesh M., Neethu George, and Abdul Bari K. K. Hima K. U. S. Meenatchisundaram. "In vitro anti-cancer activity of Piper betel leaf extract on HA -29 and its anti-oxidant activity." International Journal of Trend in Scientific Research and Development Volume-2, Issue-4 (June 30, 2018): 289–92. http://dx.doi.org/10.31142/ijtsrd12926.

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9

H Tan, Peng, Mingrui Xie, and Eleftherios Sfakianakis. "Complex interaction of adipokines in breast cancer and anti-tumour immunity; a new paradigm for cancer treatment." Cancer Research and Cellular Therapeutics 5, no. 2 (June 9, 2021): 01–16. http://dx.doi.org/10.31579/2640-1053/077.

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Obesity and its related complications have been the pressing disease pandemic affecting the developed world. It is well-established that the direct consequence of obesity in the cardiovascular system resulting in many diseases. However, its implications in carcinogenesis, cancer treatment and one’s anti-tumour immunity are gradually unfolding. To understand how fat cells can affect these, one needs to explore how the fat cell affects epithelial and immune cells. To this end, we explore the way how the adipocytes, via its production of adipokines, influence these cells, resulting in early epithelial cell transformation into cancer cells and influencing anti-tumour immunity once the cancer is established. In order to simplify our discussion, we focus this review on breast cancer. We propose that to have an effective therapy for cancer treatment, we need to intervene at the adipokine interaction with epithelial cells, cancer cells, and immune cells. In this review we also decipher the potential therapeutic targets in controlling carcinogenesis and disease progression.
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10

Galaup, A., C. Magnon, P. Opolon, M. Pérricaudet, and F. Griscelli. "Anti-angiogenèse et cancer." Journal des Maladies Vasculaires 29 (March 2004): 13–14. http://dx.doi.org/10.1016/s0398-0499(04)96803-5.

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11

Shimizu, Kosuke, and Naoto Oku. "Cancer Anti-angiogenic Therapy." Biological & Pharmaceutical Bulletin 27, no. 5 (2004): 599–605. http://dx.doi.org/10.1248/bpb.27.599.

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12

Dixon, Bernard. "“Anti-cancer gene found”." Current Biology 8, no. 12 (June 1998): R402. http://dx.doi.org/10.1016/s0960-9822(98)70259-3.

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13

Moore, Michael. "Anti-Cancer Drug Design." British Journal of Cancer 52, no. 5 (November 1985): i3. http://dx.doi.org/10.1038/bjc.1985.242.

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14

Zhao, Keji, and Yun-Bo Shi. "An anti-cancer Smurf." Cell & Bioscience 2, no. 1 (2012): 10. http://dx.doi.org/10.1186/2045-3701-2-10.

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15

Blagosklonny, Mikhail V. "Selective anti-cancer agents as anti-aging drugs." Cancer Biology & Therapy 14, no. 12 (December 2013): 1092–97. http://dx.doi.org/10.4161/cbt.27350.

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16

Ingrassia, Laurent, Isabelle Camby, Florence Lefranc, Veronique Mathieu, Prosper Nshimyumukiza, Francis Darro, and Robert Kiss. "Anti-Galectin Compounds as Potential Anti-Cancer Drugs." Current Medicinal Chemistry 13, no. 29 (December 1, 2006): 3513–27. http://dx.doi.org/10.2174/092986706779026219.

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17

Torquato, Heron, Marcia Goettert, Giselle Justo, and Edgar Paredes-Gamero. "Anti-Cancer Phytometabolites Targeting Cancer Stem Cells." Current Genomics 18, no. 2 (January 30, 2017): 156–74. http://dx.doi.org/10.2174/1389202917666160803162309.

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18

Amato, Robert J., and Jaroslaw Jac. "Targeted Anti-Cancer Therapies for Renal Cancer." Drugs 66, no. 17 (2006): 2161–71. http://dx.doi.org/10.2165/00003495-200666170-00002.

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19

Epenetos, A. A., G. Bower, M. Deonarain, and L. Bonney. "Anti-lactadherin antibodies in anti-angiogenic cancer therapy of breast cancer stem cells." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 14138. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.14138.

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14138 Background: Angiolix (Hu-Mc3) is a humanized monoclonal antibody that recognizes a migrating adhesion molecule called Lactadherin. This novel antibody has a high affinity for its antigen and recognizes an epitope on Lactadherin which interacts with the the ’RGD’- motif found on integrin receptors on newly formed endothelial cells. Lactadherin binding leads to signalling via a VEGF-independent integrin receptor signalling cascade leading to vascular endothelial cell profileration. Lactadherin binding may also increase the potency of VEGF-VEGF receptor signalling. Methods: We studied the expression of Lactadherin on breast cancer cell lines, the biodistribution of Angiolix in human breast cancer xeografts and its ability to inhibit tumor growth in vivo. Results: Our data show that tumor cells express lactadherin in vivo and that Angiolix could achieve more than 75% growth inhibition of human breast cancer growing as xenografts . Conclusions: In view of the recent finding that cancer stem cells can over-express the pro-angiogenic VEGF and make a major contribution to tumor vasculature proliferation leads to the possibility that Angiolix may be able to act to specifically target breast cancer stem cell and cause tumor regression by blocking the growth of tumor vasculature by its ability to neutralise Lactadherin-integrin receptor binding. [Table: see text]
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20

Kurebayashi, J., N. Kanomata, T. Yamashita, T. Shimo, and T. Moriya. "P083 Anti-tumor and anti-cancer stem cell activities of eribulin and anti-estrogens in breast cancer cells." Breast 24 (March 2015): S53. http://dx.doi.org/10.1016/s0960-9776(15)70128-1.

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21

Podhorecka, Monika, Blanca Ibanez, and Anna Dmoszyńska. "Metformin – its potential anti-cancer and anti-aging effects." Postępy Higieny i Medycyny Doświadczalnej 71, no. 1 (March 2, 2017): 0. http://dx.doi.org/10.5604/01.3001.0010.3801.

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The generally accepted mechanism of metformin’s effect is stimulation of adenosine monophosphate (AMP)-activated protein kinase (AMPK). AMPK is directly activated by an increase in AMP:ATP ratio in metabolic stress conditions including hypoxia and glucose deprivation. Lately, many novel pathways, besides AMPK induction, have been revealed, which can explain some of metformin’s beneficial effects. It may help to identify new targets for treatment of diabetes and metabolic syndrome. Moreover, metformin is now attracting the attention of researchers in fields other than diabetes, as it has been shown to have anti-cancer, immunoregulatory and anti-aging effects. The aim of this review is to describe the potential anti-cancer and anti-aging properties of metformin and discuss the possible underlying mechanisms.
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22

Liu, Jing, Feiyang Liu, David L. Waller, Junfeng Wang, and Qingsong Liu. "Kinase Inhibitors Targeting Anti-angiogenesis as Anti-cancer Therapies." Current Angiogenesis 1, no. 4 (October 29, 2012): 335–46. http://dx.doi.org/10.2174/2211552811201040335.

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23

Kurata, Yasuko, Satoko Fujiwara, Makoto Kajizono, Megumu Aoyagi, Yoshihisa Kitamura, and Toshiaki Sendo. "Drug interaction (27. anti-emetics during anti-cancer chemotherapy)." Okayama Igakkai Zasshi (Journal of Okayama Medical Association) 125, no. 2 (2013): 163–67. http://dx.doi.org/10.4044/joma.125.163.

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24

Jung, Young, Sun Hwang, Gautam Sethi, Lu Fan, Frank Arfuso, and Kwang Ahn. "Potential Anti-Inflammatory and Anti-Cancer Properties of Farnesol." Molecules 23, no. 11 (October 31, 2018): 2827. http://dx.doi.org/10.3390/molecules23112827.

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Farnesol, an acyclic sesquiterpene alcohol, is predominantly found in essential oils of various plants in nature. It has been reported to exhibit anti-cancer and anti-inflammatory effects, and also alleviate allergic asthma, gliosis, and edema. In numerous tumor cell lines, farnesol can modulate various tumorigenic proteins and/or modulates diverse signal transduction cascades. It can also induce apoptosis and downregulate cell proliferation, angiogenesis, and cell survival. To exert its anti-inflammatory/anti-oncogenic effects, farnesol can modulate Ras protein and nuclear factor kappa-light-chain-enhancer of activated B cells activation to downregulate the expression of various inflammatory mediators such as cyclooxygenase-2, inducible nitric oxide synthase, tumor necrosis factor alpha, and interleukin-6. In this review, we describe the potential mechanisms of action underlying the therapeutic effects of farnesol against cancers and inflammatory disorders. Furthermore, these findings support the clinical development of farnesol as a potential pharmacological agent in clinical studies.
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25

Kuo, Shu-Ru, Salahaldin A. Tahir, Sanghee Park, Timothy C. Thompson, Scott Coffield, Arthur E. Frankel, and Jen-Sing Liu. "Anti-caveolin-1 Antibodies As Anti-Prostate Cancer Therapeutics." Hybridoma 31, no. 2 (April 2012): 77–86. http://dx.doi.org/10.1089/hyb.2011.0100.

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26

Bar, Jair, and Amir Onn. "Combined anti-proliferative and anti-angiogenic strategies for cancer." Expert Opinion on Pharmacotherapy 9, no. 5 (March 17, 2008): 701–15. http://dx.doi.org/10.1517/14656566.9.5.701.

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27

J.-M. M. "Un anti-ostéosarcome qui dope les macrophages anti-cancer." Revue Francophone des Laboratoires 2006, no. 387 (December 2006): 12. http://dx.doi.org/10.1016/s1773-035x(06)80474-0.

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28

Johnson, Jeremy J. "Carnosol: A promising anti-cancer and anti-inflammatory agent." Cancer Letters 305, no. 1 (June 2011): 1–7. http://dx.doi.org/10.1016/j.canlet.2011.02.005.

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29

Siavash Hosseinpour Chermahini. "Bromelain as an anti-inflammatory and anti-cancer compound." International Journal of Research in Pharmaceutical Sciences and Technology 1, no. 2 (May 4, 2019): 53–57. http://dx.doi.org/10.33974/ijrpst.v1i2.68.

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Inflammation is a complicated problem for today’s human beings. Large numbers of people have been diagnosed with arthritis along with inflammation. This is beside the others that suffer inflammation caused by an injury. There are alternatives that can be considered as temporary or permanent treatments of chronic inflammatory diseases. Plants, as well as other biological resources, are most welcomed to the therapeutic area. Using the plants’ compounds with high potential as novel techniques are today’s bio-pharmacologist concern. Bromelain has been more attractive due to its characteristics. This review is an overview of anti-inflammatory and anti-cancer effect of bromelain as a confident treatment for all inflammatory disease.
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30

Christine, Wade, Duffy Robert, and Chang Raymond. "Natural-product anti-cancer drug discovery from anti-malarials." European Journal of Integrative Medicine 4 (September 2012): 133–34. http://dx.doi.org/10.1016/j.eujim.2012.07.783.

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31

Fu, Wencheng, and Geng Wu. "Targeting mTOR for Anti-Aging and Anti-Cancer Therapy." Molecules 28, no. 7 (April 1, 2023): 3157. http://dx.doi.org/10.3390/molecules28073157.

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The balance between anabolism and catabolism is disrupted with aging, with the rate of anabolism being faster than that of catabolism. Therefore, mTOR, whose major function is to enhance anabolism and inhibit catabolism, has become a potential target of inhibition for anti-aging therapy. Interestingly, it was found that the downregulation of the mTOR signaling pathway had a lifespan-extending effect resembling calorie restriction. In addition, the mTOR signaling pathway promotes cell proliferation and has been regarded as a potential anti-cancer target. Rapamycin and rapalogs, such as everolimus, have proven to be effective in preventing certain tumor growth. Here, we reviewed the basic knowledge of mTOR signaling, including both mTORC1 and mTORC2. Then, for anti-aging, we cited a lot of evidence to discuss the role of targeting mTOR and its anti-aging mechanism. For cancer therapy, we also discussed the role of mTOR signaling in different types of cancers, including idiopathic pulmonary fibrosis, tumor immunity, etc. In short, we discussed the research progress and both the advantages and disadvantages of targeting mTOR in anti-aging and anti-cancer therapy. Hopefully, this review may promote more ideas to be generated for developing inhibitors of mTOR signaling to fight cancer and extend lifespan.
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32

Jang, Ji-Hoon, and Tae-Jin Lee. "Mechanisms of Phytochemicals in Anti-Inflammatory and Anti-Cancer." International Journal of Molecular Sciences 24, no. 9 (April 26, 2023): 7863. http://dx.doi.org/10.3390/ijms24097863.

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33

Tsuneo, Ishida. "Highly Bactericidal Silver () against Bacteria and Anti-Cancer Activity of Ag+ ions for Regulation of Cancer/Tumor Cell Growth." Cancer Medicine Journal 1, no. 1 (August 31, 2018): 24–36. http://dx.doi.org/10.46619/cmj.2018.1-1004.

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Since highly bactericidal silver (I) ions against bacteria have been obtained, as highly accurate results, prospect effects of silver (I) ions for regulation of cancer and tumor cell growth can be expected to occur even at apoptotic conditions. This mini-review article is reported that as an availability for most highly bactericidal effect of Ag+ ions, the regulation of cancer cell growth may be able to be achieved by Ag+ ions-mediated hydrolyzing and degrading functions. Bactericidal effects of silver (I) ions on bacteriolyses of bacterial cell walls by activation of peptidoglycan (PGN) autolysins and silver ion-mediated cancer cell hydrolyzing and degrading activity by endolysins have been analyzed. Bacteriolysis against Staphylococcus aureus (S. aureus) PGN cell wall by Ag+ ions is caused by the inhibition of PGN elongation due to regulation of PGN synthetic transglycosylase (TG) and transpeptidase (TP), and the enhancement of activation of PGN autolysins of amidases. On the other hand, bacteriolysis and destruction against Escherichia coli (E. coli) cell wall by Ag+ ions are caused by the destruction of outer membrane structure due to degradative enzymes of lipoproteins at N- and Cterminals, and by the inhibition of PGN elongation owing to inactivation of PGN TP synthetic enzyme endopeptidase and enhancement of the activations of PGN hydrolases and autolysins of amidase, peptidase, and carboxypeptidase. Ag+ ions-mediated cancerous cell hydrolyzing enzyme that binds to and degrades intact cancer cells of the producing organism are classified as autolysins or endolysins (phage lysin), resulting that the hydrolase activity is an essential as regulator of cancer and tumor cell growth and hydrolase activation may be promoted the apoptosis and the necrosis of cancer cells, and subsequently lead to cancer cell death by this hydrolase. Thus, highly bactericidal Ag+ ions against bacteria and effect of Ag+ ions for cancer cell growth regulation or cell death can be able to realize at the same time. Silver ions induced ROS generations such as O2 - , H2O2,・OH, OH- producing in bacterial and tumorous cells occur and lead to oxidative stress. DNA damages may be due to linear coordinated Ag+ complex formations by Ag+ substitution within double and triple hydrogen bonds in DNA base pairs.
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34

O’Neill, Eric J., Deborah Termini, Alexandria Albano, and Evangelia Tsiani. "Anti-Cancer Properties of Theaflavins." Molecules 26, no. 4 (February 13, 2021): 987. http://dx.doi.org/10.3390/molecules26040987.

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Cancer is a disease characterized by aberrant proliferative and apoptotic signaling pathways, leading to uncontrolled proliferation of cancer cells combined with enhanced survival and evasion of cell death. Current treatment strategies are sometimes ineffective in eradicating more aggressive, metastatic forms of cancer, indicating the need to develop novel therapeutics targeting signaling pathways which are essential for cancer progression. Historically, plant-derived compounds have been utilized in the production of pharmaceuticals and chemotherapeutic compounds for the treatment of cancer, including paclitaxel and docetaxel. Theaflavins, phenolic components present in black tea, have demonstrated anti-cancer potential in cell cultures in vitro and in animal studies in vivo. Theaflavins have been shown to inhibit proliferation, survival, and migration of many cancer cellswhile promoting apoptosis. Treatment with theaflavins has been associated with increased levels of cleaved poly (ADP-ribose) polymerase (PARP) and cleaved caspases-3, -7, -8, and -9, all markers of apoptosis, and increased expression of the proapoptotic marker Bcl-2-associated X protein (Bax) and concomitant reduction in the antiapoptotic marker B-cell lymphoma 2 (Bcl-2). Additionally, theaflavin treatment reduced phosphorylated Akt, phosphorylated mechanistic target of rapamycin (mTOR), phosphatidylinositol 3-kinase (PI3K), and c-Myc levels with increased expression of the tumour suppressor p53. This review summarizes the current in vitro and in vivo evidence available investigating the anti-cancer effects of theaflavins across various cancer cell lines and animal models.
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35

Crezee, Johannes, Nicolaas A. P. Franken, and Arlene L. Oei. "Hyperthermia-Based Anti-Cancer Treatments." Cancers 13, no. 6 (March 12, 2021): 1240. http://dx.doi.org/10.3390/cancers13061240.

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36

Fukasawa, Hirotaka, Ryuichi Furuya, Hideo Yasuda, Tatsuo Yamamoto, Akira Hishida, and Masatoshi Kitagawa. "Anti-Cancer Agent-Induced Nephrotoxicity." Anti-Cancer Agents in Medicinal Chemistry 14, no. 7 (January 26, 2014): 921–27. http://dx.doi.org/10.2174/1871520614666140127105809.

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37

Ali, A., M. Toi, and T. Ueno. "Anti-Angiogenic Cancer Therapy Updates." Current Molecular Medicine 9, no. 8 (November 1, 2009): 954–66. http://dx.doi.org/10.2174/156652409789712756.

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38

Thangavel, K. "Selenium Properties for Anti-Cancer." Research Journal of Pharmacy and Technology 10, no. 10 (2017): 3595. http://dx.doi.org/10.5958/0974-360x.2017.00651.5.

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39

Kabir, Md Lutful, Feng Wang, and Andrew H. A. Clayton. "Intrinsically Fluorescent Anti-Cancer Drugs." Biology 11, no. 8 (July 28, 2022): 1135. http://dx.doi.org/10.3390/biology11081135.

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At present, about one-third of the total protein targets in the pharmaceutical research sector are kinase-based. While kinases have been attractive targets to combat many diseases, including cancer, selective kinase inhibition has been challenging, because of the high degree of structural homology in the active site where many kinase inhibitors bind. Despite efficacy as cancer drugs, kinase inhibitors can exhibit limited target specificity and rationalizing their target profiles in the context of precise molecular mechanisms or rearrangements is a major challenge for the field. Spectroscopic approaches such as infrared, Raman, NMR and fluorescence have the potential to provide significant insights into drug-target and drug-non-target interactions because of sensitivity to molecular environment. This review places a spotlight on the significance of fluorescence for extracting information related to structural properties, discovery of hidden conformers in solution and in target-bound state, binding properties (e.g., location of binding sites, hydrogen-bonding, hydrophobicity), kinetics as well as dynamics of kinase inhibitors. It is concluded that the information gleaned from an understanding of the intrinsic fluorescence from these classes of drugs may aid in the development of future drugs with improved side-effects and less disease resistance.
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40

Prudhomme, Michelle. "lndolocarbazoles as Anti-Cancer Agents." Current Pharmaceutical Design 3, no. 3 (June 1997): 265–90. http://dx.doi.org/10.2174/138161280303221007123245.

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Abstract: Protein kinase C (PKC) is a family of phospholipid-dependent serine/threonine protein kinases that plays a key role in signal transduction. Consequently, PKC controls a large variety of cellular processes such as proliferation and differentiation as well as smooth muscle contraction and secretions. The disruption of these processes would have severe implications for many physiological functions. The twelve known PKC isoenzymes show great variations in their substrate specificity and their distribution among different tissues, indicating their specialised role in certain tissue functions. Altered expression of PKC isoenzymes has been reported in a wide range of diseases. DNA topoisomerase I is a nuclear enzyme, involved in replication, transcription and recombination, that modifies and regulates the topological state of DNA. Many microbial metabolites and synthetic compounds possessing an indolocarbazole unit are biologically active products with antitumor properties. Antibiotic indolocarbazoles staurosporine, K-252a, UCN-01 and 02 are known protein kinase C inhibitors while structurally related rebeccamycin and ED-110 are topoisomerase I inhibitors without inhibitory effect against PKC. This review will update efforts made toward the discovery of antitumor indolocarbazoles and their possible mode of action via either PKC or topoisomerase I inhibition. Structure-activity relationship studies in a series of maleamide and maleimide indolocarbazoles bearing or not a sugar moiety linked either to both indole nitrogens such as staurosporine, or to one indole nitrogen such as rebeccamycin, will be reported.
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41

Kondo, Shunsuke, and Nagahiro Saijo. "Target-based anti-cancer drugs." Drug Delivery System 19, no. 2 (2004): 103–9. http://dx.doi.org/10.2745/dds.19.103.

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42

Ohyama, Chikara, Tomonori Habuchi, and Tetsuro Kato. "Carbohydrate-based anti- cancer drug." Drug Delivery System 19, no. 1 (2004): 51–55. http://dx.doi.org/10.2745/dds.19.51.

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43

Patočka, Jiří, and Zdeněk Hon. "Epothilones - new anti-cancer medicines." Kontakt 9, no. 2 (December 21, 2007): 403–6. http://dx.doi.org/10.32725/kont.2007.061.

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44

Negrini, Simone, Raffaele De Palma, and Gilberto Filaci. "Anti-Cancer Immunotherapies Targeting Telomerase." Cancers 12, no. 8 (August 12, 2020): 2260. http://dx.doi.org/10.3390/cancers12082260.

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Telomerase is a reverse transcriptase that maintains telomeres length, compensating for the attrition of chromosomal ends that occurs during each replication cycle. Telomerase is expressed in germ cells and stem cells, whereas it is virtually undetectable in adult somatic cells. On the other hand, telomerase is broadly expressed in the majority of human tumors playing a crucial role in the replicative behavior and immortality of cancer cells. Several studies have demonstrated that telomerase-derived peptides are able to bind to HLA (human leukocyte antigen) class I and class II molecules and effectively activate both CD8+ and CD4+ T cells subsets. Due to its broad and selective expression in cancer cells and its significant immunogenicity, telomerase is considered an ideal universal tumor-associated antigen, and consequently, a very attractive target for anti-cancer immunotherapy. To date, different telomerase targeting immunotherapies have been studied in pre-clinical and clinical settings, these approaches include peptide vaccination and cell-based vaccination. The objective of this review paper is to discuss the role of human telomerase in cancer immunotherapy analyzing recent developments and future perspectives in this field.
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45

"Potential New Anti-Cancer Mechanism." International Journal of Cancer Research 7, no. 2 (March 15, 2011): 167. http://dx.doi.org/10.3923/ijcr.2011.167.167.

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46

Lakhtin, M. V., V. M. Lakhtin, V. A. Aleshkin, M. S. Afanasiev, and S. S. Afanasiev. "LECTINS IN ANTI-CANCER STRATEGIES." Acta Biomedica Scientifica 3, no. 4 (July 28, 2018): 69–77. http://dx.doi.org/10.29413/abs.2018-3.4.11.

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The published during last few years data concerning communicative role of lectins (proteins and their complexes which recognize carbohydrates, glycoconjugates and their patterns) in on-duty supporting and increasing anticancer status of human immunity are analyzed. Examples of lectin-(glycoconjugate pattern) strategies, approaches and tactic variants in study and development of anticancer treatments, principle variants of therapy, possible vaccines in 35 cases of blood connected tumors (leukemia, lymphomas, others), solid tumors (carcinomas, sarcoma, cancers of vaginal biotopes, prostate, bladder, colon, other intestinal compartments, pancreas, liver, kidneys, others) and cancer cell lines are described and systemized. The list of mostly used communicative lectins (pattern recognition receptors, their soluble forms, other soluble lectins possessing specificities of importance) involving in key intercellular cascades and pathway co-functioning is presented. The regulation of resulting expression of distinct active lectins (available and hetero/di/oligomeric forms) and their interaction to adequate glycoconjugate patterns as well as influence distribution of co-functioning lectins and antigens CD between populations and subpopulations of antigen-presented cells (dendritic cells cDC, mDC, moDC, pDC; macrophages M2 and M1), mucosal M-cells, NK-cells play key role for choice and development of anticancer complex procedures increasing innate and innate-coupled immune responses. Prospects of (receptor lectin)-dependent intercellular communications and targeting glycoconjugate constructions into innate immunity cells for therapy of cancer and development of anticancer vaccines are evaluated and discussed.
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47

Haykinson, N. M. "Organization of anti-cancer fight." Kazan medical journal 43, no. 6 (October 19, 2021): 78–79. http://dx.doi.org/10.17816/kazmj83372.

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48

Pacholczak, Renata, Jerzy Dropiński, Jerzy Walocha, and Jacek Musiał. "Anti-cancer agents and endothelium." Oncology in Clinical Practice 14, no. 5 (November 25, 2018): 249–56. http://dx.doi.org/10.5603/ocp.2018.0032.

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49

Locker, Gerhson Y. "Progress in Anti-Cancer Chemotherapy." Annals of Internal Medicine 128, no. 3 (February 1, 1998): 252. http://dx.doi.org/10.7326/0003-4819-128-3-199802010-00026.

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50

Chandraratna, Roshantha AS, and Sunil Nagpal. "Retinoids as Anti-Cancer Agents." Current Pharmaceutical Design 2, no. 3 (June 1996): 295–316. http://dx.doi.org/10.2174/1381612802666220921174554.

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Abstract: Retinoids, synthetic and natural analogs of retinoic acid, exhibit potent growth inhibitory and cell differentiation activities which account for their beneficial effects in cancer in ex vivo and in vivo models. These simple molecules with pleiotropic effects have shown potential as therapeutic agents for the treatment of cancer either alone or in combination with other agents. Retinoids regulate the growth of various cell types by directly modulating the expression of responsive genes through nuclear retinoid receptors (RARs and RXRs), which are ligand dependent transcription factors. The translo­ cation of RARCX in acute pro-myelocytic leukemia, decreased expression of RARP and reduced activity of the •RARP promoter in various tumors and cancer cell lines, and restoration of retinoid sensitivity to cancer cells by RAR expression vector transfection, are all indicative of the direct involvement of RAR malfunction in the process of tumorigenesis and also suggest a role for RARs as ligand dependent tumor suppressors. The current use of retinoids in cancer is limited because of their associated toxicities and lack of efficacy at tolerated doses. In order to improve the therapeutic index of retinoids, various strategies are currently being employed, e.g., receptor selective retinoids, anti-AP! selective retinoids and combination therapies. The development of novel retinoids along with an increased understanding of the biological functions and mechanisms of action of retinoid receptors are likely to usher in a new era of retinoid therapy of cancers.
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