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3. Therapeutic targeting of replicative immortality

Author

Yaswen, Paul, MacKenzie, Karen L, Keith, W Nicol, Hentosh, Patricia, Rodier, Francis, Zhu, Jiyue, Firestone, Gary L, Matheu, Ander, Carnero, Amancio, Bilsland, Alan, Sundin, Tabetha, Honoki, Kanya, Fujii, Hiromasa, Georgakilas, Alexandros G, Amedei, Amedeo, Amin, Amr, Helferich, Bill, Boosani, Chandra S, Guha, Gunjan, Ciriolo, Maria Rosa, Chen, Sophie, Mohammed, Sulma I, Azmi, Asfar S, Bhakta, Dipita, Halicka, Dorota, Niccolai, Elena, Aquilano, Katia, Ashraf, S Salman, Nowsheen, Somaira, and Yang, Xujuan

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biological Sciences, Genetics, Cancer, 5.1 Pharmaceuticals, 2.1 Biological and endogenous factors, Antineoplastic Agents, Cell Proliferation, Cell Transformation, Neoplastic, Cellular Senescence, Genomic Instability, Humans, Molecular Targeted Therapy, Neoplasms, Phosphatidylinositol 3-Kinases, Signal Transduction, Telomerase, Tumor Suppressor Protein p53, Senescence, Oncogenic stress, p53, pRB, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

One of the hallmarks of malignant cell populations is the ability to undergo continuous proliferation. This property allows clonal lineages to acquire sequential aberrations that can fuel increasingly autonomous growth, invasiveness, and therapeutic resistance. Innate cellular mechanisms have evolved to regulate replicative potential as a hedge against malignant progression. When activated in the absence of normal terminal differentiation cues, these mechanisms can result in a state of persistent cytostasis. This state, termed "senescence," can be triggered by intrinsic cellular processes such as telomere dysfunction and oncogene expression, and by exogenous factors such as DNA damaging agents or oxidative environments. Despite differences in upstream signaling, senescence often involves convergent interdependent activation of tumor suppressors p53 and p16/pRB, but can be induced, albeit with reduced sensitivity, when these suppressors are compromised. Doses of conventional genotoxic drugs required to achieve cancer cell senescence are often much lower than doses required to achieve outright cell death. Additional therapies, such as those targeting cyclin dependent kinases or components of the PI3K signaling pathway, may induce senescence specifically in cancer cells by circumventing defects in tumor suppressor pathways or exploiting cancer cells' heightened requirements for telomerase. Such treatments sufficient to induce cancer cell senescence could provide increased patient survival with fewer and less severe side effects than conventional cytotoxic regimens. This positive aspect is countered by important caveats regarding senescence reversibility, genomic instability, and paracrine effects that may increase heterogeneity and adaptive resistance of surviving cancer cells. Nevertheless, agents that effectively disrupt replicative immortality will likely be valuable components of new combinatorial approaches to cancer therapy.

Published
2015

4. Designing a broad-spectrum integrative approach for cancer prevention and treatment

Author

Block, Keith I, Gyllenhaal, Charlotte, Lowe, Leroy, Amedei, Amedeo, Amin, ARM Ruhul, Amin, Amr, Aquilano, Katia, Arbiser, Jack, Arreola, Alexandra, Arzumanyan, Alla, Ashraf, S Salman, Azmi, Asfar S, Benencia, Fabian, Bhakta, Dipita, Bilsland, Alan, Bishayee, Anupam, Blain, Stacy W, Block, Penny B, Boosani, Chandra S, Carey, Thomas E, Carnero, Amancio, Carotenuto, Marianeve, Casey, Stephanie C, Chakrabarti, Mrinmay, Chaturvedi, Rupesh, Chen, Georgia Zhuo, Chen, Helen, Chen, Sophie, Chen, Yi Charlie, Choi, Beom K, Ciriolo, Maria Rosa, Coley, Helen M, Collins, Andrew R, Connell, Marisa, Crawford, Sarah, Curran, Colleen S, Dabrosin, Charlotta, Damia, Giovanna, Dasgupta, Santanu, DeBerardinis, Ralph J, Decker, William K, Dhawan, Punita, Diehl, Anna Mae E, Dong, Jin-Tang, Dou, Q Ping, Drew, Janice E, Elkord, Eyad, El-Rayes, Bassel, Feitelson, Mark A, Felsher, Dean W, Ferguson, Lynnette R, Fimognari, Carmela, Firestone, Gary L, Frezza, Christian, Fujii, Hiromasa, Fuster, Mark M, Generali, Daniele, Georgakilas, Alexandros G, Gieseler, Frank, Gilbertson, Michael, Green, Michelle F, Grue, Brendan, Guha, Gunjan, Halicka, Dorota, Helferich, William G, Heneberg, Petr, Hentosh, Patricia, Hirschey, Matthew D, Hofseth, Lorne J, Holcombe, Randall F, Honoki, Kanya, Hsu, Hsue-Yin, Huang, Gloria S, Jensen, Lasse D, Jiang, Wen G, Jones, Lee W, Karpowicz, Phillip A, Keith, W Nicol, Kerkar, Sid P, Khan, Gazala N, Khatami, Mahin, Ko, Young H, Kucuk, Omer, Kulathinal, Rob J, Kumar, Nagi B, Kwon, Byoung S, Le, Anne, Lea, Michael A, Lee, Ho-Young, Lichtor, Terry, Lin, Liang-Tzung, Locasale, Jason W, Lokeshwar, Bal L, Longo, Valter D, Lyssiotis, Costas A, MacKenzie, Karen L, Malhotra, Meenakshi, Marino, Maria, Martinez-Chantar, Maria L, and Matheu, Ander

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Rare Diseases, Precision Medicine, Aetiology, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, Good Health and Well Being, Antineoplastic Agents, Phytogenic, Drug Resistance, Neoplasm, Genetic Heterogeneity, Humans, Molecular Targeted Therapy, Neoplasms, Signal Transduction, Tumor Microenvironment, Multi-targeted, Cancer hallmarks, Phytochemicals, Targeted therapy, Integrative medicine, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Targeted therapies and the consequent adoption of "personalized" oncology have achieved notable successes in some cancers; however, significant problems remain with this approach. Many targeted therapies are highly toxic, costs are extremely high, and most patients experience relapse after a few disease-free months. Relapses arise from genetic heterogeneity in tumors, which harbor therapy-resistant immortalized cells that have adopted alternate and compensatory pathways (i.e., pathways that are not reliant upon the same mechanisms as those which have been targeted). To address these limitations, an international task force of 180 scientists was assembled to explore the concept of a low-toxicity "broad-spectrum" therapeutic approach that could simultaneously target many key pathways and mechanisms. Using cancer hallmark phenotypes and the tumor microenvironment to account for the various aspects of relevant cancer biology, interdisciplinary teams reviewed each hallmark area and nominated a wide range of high-priority targets (74 in total) that could be modified to improve patient outcomes. For these targets, corresponding low-toxicity therapeutic approaches were then suggested, many of which were phytochemicals. Proposed actions on each target and all of the approaches were further reviewed for known effects on other hallmark areas and the tumor microenvironment. Potential contrary or procarcinogenic effects were found for 3.9% of the relationships between targets and hallmarks, and mixed evidence of complementary and contrary relationships was found for 7.1%. Approximately 67% of the relationships revealed potentially complementary effects, and the remainder had no known relationship. Among the approaches, 1.1% had contrary, 2.8% had mixed and 62.1% had complementary relationships. These results suggest that a broad-spectrum approach should be feasible from a safety standpoint. This novel approach has potential to be relatively inexpensive, it should help us address stages and types of cancer that lack conventional treatment, and it may reduce relapse risks. A proposed agenda for future research is offered.

Published
2015

7. An Integrated Professional and Transferable Skills Course for Undergraduate Chemistry Students

Author

Ashraf, S. Salman, Marzouk, Sayed A. M., and Shehadi, Ihsan A.

Abstract

Upon graduation, chemistry majors often find themselves inadequately prepared for the "real world" that awaits them when they join the workplace. Some employers find chemistry graduates lacking written- and oral-communication skills, critical-thinking skills, group-work skills, as well as the ability to efficiently analyze data and retrieve chemical information. To address these deficiencies, we developed an undergraduate chemistry course that focuses on professional and transferable skills and have incorporated it into the chemistry curriculum. Two specific hands-on examples to effectively teach students data acquisition and manipulation from a chemistry perspective are described. This course received positive feedback from students and gave them skills that helped them not only during their chemistry education, but also when they entered the workforce. Universities that do not have a similar course should consider adopting and incorporating it in their curricula. (Contains 2 tables, 1 figure and 2 notes.)

Published
2011
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24. Broad targeting of angiogenesis for cancer prevention and therapy

Author

Wang, Zongwei, Dabrosin, Charlotta, Yin, Xin, Fuster, Mark M., Arreola, Alexandra, Rathmell, W. Kimryn, Generali, Daniele, Nagaraju, Ganji P., El-Rayes, Bassel, Ribatti, Domenico, Chen, Yi Charlie, Honoki, Kanya, Fujii, Hiromasa, Georgakilas, Alexandros G., Nowsheen, Somaira, Amedei, Amedeo, Niccolai, Elena, Amin, Amr, Ashraf, S. Salman, Helferich, Bill, Yang, Xujuan, Guha, Gunjan, Bhakta, Dipita, Ciriolo, Maria Rosa, Aquilano, Katia, Chen, Sophie, Halicka, Dorota, Mohammed, Sulma I., Azmi, Asfar S., Bilsland, Alan, Keith, W. Nicol, Jensen, Lasse D., Wang, Zongwei, Dabrosin, Charlotta, Yin, Xin, Fuster, Mark M., Arreola, Alexandra, Rathmell, W. Kimryn, Generali, Daniele, Nagaraju, Ganji P., El Rayes, Bassel, Ribatti, Domenico, Chen, Yi Charlie, Honoki, Kanya, Fujii, Hiromasa, Georgakilas, Alexandros G., Nowsheen, Somaira, Amedei, Amedeo, Niccolai, Elena, Amin, Amr, Ashraf, S. Salman, Helferich, Bill, Yang, Xujuan, Guha, Gunjan, Bhakta, Dipita, Ciriolo, Maria Rosa, Aquilano, Katia, Chen, Sophie, Halicka, Dorota, Mohammed, Sulma I., Azmi, Asfar S., Bilsland, Alan, Keith, W. Nicol, and Jensen, Lasse D.

Subjects
Cancer och onkologi, Cancer Research, Neovascularization, Pathologic, Anti-angiogenic, Phytochemicals, Angiogenesis Inhibitors, Review, Phytochemical, Antineoplastic Agents, Phytogenic, Angiogenesis Cancer Phytochemicals Treatment Anti-angiogenic, Treatment, Angiogenesi, Angiogenesis, Cancer, Cancer and Oncology, Neoplasms, Blood Vessels, Humans, Immunotherapy, Settore BIO/10, Cell Proliferation
Abstract

Deregulation of angiogenesis - the growth of new blood vessels from an existing vasculature - is a main driving force in many severe human diseases including cancer. As such, tumor angiogenesis is important for delivering oxygen and nutrients to growing tumors, and therefore considered an essential pathologic feature of cancer, while also playing a key role in enabling other aspects of tumor pathology such as metabolic deregulation and tumor dissemination/metastasis. Recently, inhibition of tumor angiogenesis has become a clinical anti-cancer strategy in line with chemotherapy, radiotherapy and surgery, which underscore the critical importance of the angiogenic switch during early tumor development. Unfortunately the clinically approved anti-angiogenic drugs in use today are only effective in a subset of the patients, and many who initially respond develop resistance over time. Also, some of the anti-angiogenic drugs are toxic and it would be of great importance to identify alternative compounds, which could overcome these drawbacks and limitations of the currently available therapy. Finding "the most important target" may, however, prove a very challenging approach as the tumor environment is highly diverse, consisting of many different cell types, all of which may contribute to tumor angiogenesis. Furthermore, the tumor cells themselves are genetically unstable, leading to a progressive increase in the number of different angiogenic factors produced as the cancer progresses to advanced stages. As an alternative approach to targeted therapy, options to broadly interfere with angiogenic signals by a mixture of non-toxic natural compound with pleiotropic actions were viewed by this team as an opportunity to develop a complementary anti-angiogenesis treatment option. As a part of the "Halifax Project" within the "Getting to know cancer" framework, we have here, based on a thorough review of the literature, identified 10 important aspects of tumor angiogenesis and the pathological tumor vasculature which would be well suited as targets for anti-angiogenic therapy: (1) endothelial cell migration/tip cell formation, (2) structural abnormalities of tumor vessels, (3) hypoxia, (4) lymphangiogenesis, (5) elevated interstitial fluid pressure, (6) poor perfusion, (7) disrupted circadian rhythms, (8) tumor promoting inflammation, (9) tumor promoting fibroblasts and (10) tumor cell metabolism/acidosis. Following this analysis, we scrutinized the available literature on broadly acting anti-angiogenic natural products, with a focus on finding qualitative information on phytochemicals which could inhibit these targets and came up with 10 prototypical phytochemical compounds: (1) oleic acid, (2) tripterine, (3) silibinin, (4) curcumin, (5) epigallocatechin-gallate, (6) kaempferol, (7) melatonin, (8) enterolactone, (9) withaferin A and (10) resveratrol. We suggest that these plant-derived compounds could be combined to constitute a broader acting and more effective inhibitory cocktail at doses that would not be likely to cause excessive toxicity. All the targets and phytochemical approaches were further cross-validated against their effects on other essential tumorigenic pathways (based on the "hallmarks" of cancer) in order to discover possible synergies or potentially harmful interactions, and were found to generally also have positive involvement in/effects on these other aspects of tumor biology. The aim is that this discussion could lead to the selection of combinations of such anti-angiogenic compounds which could be used in potent anti-tumor cocktails, for enhanced therapeutic efficacy, reduced toxicity and circumvention of single-agent anti-angiogenic resistance, as well as for possible use in primary or secondary cancer prevention strategies. Funding agencies: Swedish Society for Medical Research; Goesta Fraenkel Foundation; Ake Wibergs Foundation; Ollie och Elof Ericssons Foundation; Karolinska Institute; Linkoping University; University of Glasgow; Beatson Oncology Center Fund; Cancer Research UK grant

Published
2015
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28. Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition

Author

Ferguson, Lynnette R., Chen, Helen, Collins, Andrew R., Connell, Marisa, Damia, Giovanna, Dasgupta, Santanu, Malhotra, Meenakshi, Meeker, Alan K., Amedei, Amedeo, Amin, Amr, Ashraf, S. Salman, Aquilano, Katia, Azmi, Asfar S., Bhakta, Dipita, Bilsland, Alan, Boosani, Chandra S., Chen, Sophie, Ciriolo, Maria Rosa, Fujii, Hiromasa, Guha, Gunjan, Halicka, Dorota, Helferich, William G., Keith, W. Nicol, Mohammed, Sulma I., Niccolai, Elena, Yang, Xujuan, Honoki, Kanya, Parslow, Virginia R., Prakash, Satya, Rezazadeh, Sarallah, Shackelford, Rodney E., Sidransky, David, Tran, Phuoc T., Yang, Eddy S., and Maxwell, Christopher A.

Subjects
Centrosome, Genomic instability, Cancer Research, DNA Repair, Cancer therapy, Review, Prognosis, Diet, Cancer prevention, Neoplasms, Humans, DNA damage, Nutraceutical, Settore BIO/10, Telomerase
Abstract

Genomic instability can initiate cancer, augment progression, and influence the overall prognosis of the affected patient. Genomic instability arises from many different pathways, such as telomere damage, centrosome amplification, epigenetic modifications, and DNA damage from endogenous and exogenous sources, and can be perpetuating, or limiting, through the induction of mutations or aneuploidy, both enabling and catastrophic. Many cancer treatments induce DNA damage to impair cell division on a global scale but it is accepted that personalized treatments, those that are tailored to the particular patient and type of cancer, must also be developed. In this review, we detail the mechanisms from which genomic instability arises and can lead to cancer, as well as treatments and measures that prevent genomic instability or take advantage of the cellular defects caused by genomic instability. In particular, we identify and discuss five priority targets against genomic instability: (1) prevention of DNA damage; (2) enhancement of DNA repair; (3) targeting deficient DNA repair; (4) impairing centrosome clustering; and, (5) inhibition of telomerase activity. Moreover, we highlight vitamin D and B, selenium, carotenoids, PARP inhibitors, resveratrol, and isothiocyanates as priority approaches against genomic instability. The prioritized target sites and approaches were cross validated to identify potential synergistic effects on a number of important areas of cancer biology.

Published
2015
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35. Designing a broad-spectrum integrative approach for cancer prevention and treatment

Author

Bishayee, Anupam, Arbiser, Jack, Casey, Stephanie C., Bhakta, Dipita, Chakrabarti, Mrinmay, Amedei, Amedeo, Chaturvedi, Rupesh, Ashraf, S. Salman, Block, Keith I., Carey, Thomas E., Chen, Yi Charlie, Benencia, Fabian, Arzumanyan, Alla, Amin, A.R.M. Ruhul, Blain, Stacy W., Lowe, Leroy, Choi, Beom K., Chen, Sophie, Arreola, Alexandra, Boosani, Chandra S., Ciriolo, Maria Rosa, Aquilano, Katia, Carotenuto, Marianeve, Chen, Georgia Zhuo, Coley, Helen M., Carnero, Amancio, Amin, Amr, Azmi, Asfar S., Chen, Helen, Bilsland, Alan, Block, Penny B., and Gyllenhaal, Charlotte

Abstract

Targeted therapies and the consequent adoption of “personalized” oncology have achieved notable successes in some cancers; however, significant problems remain with this approach. Many targeted therapies are highly toxic, costs are extremely high, and most patients experience relapse after a few disease-free months. Relapses arise from genetic heterogeneity in tumors, which harbor therapy-resistant immortalized cells that have adopted alternate and compensatory pathways (i.e., pathways that are not reliant upon the same mechanisms as those which have been targeted). To address these limitations, an international task force of 180 scientists was assembled to explore the concept of a low-toxicity “broad-spectrum” therapeutic approach that could simultaneously target many key pathways and mechanisms. Using cancer hallmark phenotypes and the tumor microenvironment to account for the various aspects of relevant cancer biology, interdisciplinary teams reviewed each hallmark area and nominated a wide range of high-priority targets (74 in total) that could be modified to improve patient outcomes. For these targets, corresponding low-toxicity therapeutic approaches were then suggested; many of which were phytochemicals. Proposed actions on each target and all of the approaches were further reviewed for known effects on other hallmark areas and the tumor microenvironment. Potential contrary or procarcinogenic effects were found for 3.9% of the relationships between targets and hallmarks, and mixed evidence of complementary and contrary relationships was found for 7.1%. Approximately 67% of the relationships revealed potentially complementary effects, and the remainder had no known relationship. Among the approaches, 1.1% had contrary, 2.8% had mixed and 62.1% had complementary relationships. These results suggest that a broad-spectrum approach should be feasible from a safety standpoint. This novel approach has potential to help us address disease relapse, which is a substantial and longstanding problem, so a proposed agenda for future research is offered.

Published
2015
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36. Immune evasion in cancer: Mechanistic basis and therapeutic strategies

Author

Vinay, Dass S., primary, Ryan, Elizabeth P., additional, Pawelec, Graham, additional, Talib, Wamidh H., additional, Stagg, John, additional, Elkord, Eyad, additional, Lichtor, Terry, additional, Decker, William K., additional, Whelan, Richard L., additional, Kumara, H.M.C. Shantha, additional, Signori, Emanuela, additional, Honoki, Kanya, additional, Georgakilas, Alexandros G., additional, Amin, Amr, additional, Helferich, William G., additional, Boosani, Chandra S., additional, Guha, Gunjan, additional, Ciriolo, Maria Rosa, additional, Chen, Sophie, additional, Mohammed, Sulma I., additional, Azmi, Asfar S., additional, Keith, W. Nicol, additional, Bilsland, Alan, additional, Bhakta, Dipita, additional, Halicka, Dorota, additional, Fujii, Hiromasa, additional, Aquilano, Katia, additional, Ashraf, S. Salman, additional, Nowsheen, Somaira, additional, Yang, Xujuan, additional, Choi, Beom K., additional, and Kwon, Byoung S., additional

Published
2015
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37. A multi-targeted approach to suppress tumor-promoting inflammation

Author

Samadi, Abbas K., primary, Bilsland, Alan, additional, Georgakilas, Alexandros G., additional, Amedei, Amedeo, additional, Amin, Amr, additional, Bishayee, Anupam, additional, Azmi, Asfar S., additional, Lokeshwar, Bal L., additional, Grue, Brendan, additional, Panis, Carolina, additional, Boosani, Chandra S., additional, Poudyal, Deepak, additional, Stafforini, Diana M., additional, Bhakta, Dipita, additional, Niccolai, Elena, additional, Guha, Gunjan, additional, Vasantha Rupasinghe, H.P., additional, Fujii, Hiromasa, additional, Honoki, Kanya, additional, Mehta, Kapil, additional, Aquilano, Katia, additional, Lowe, Leroy, additional, Hofseth, Lorne J., additional, Ricciardiello, Luigi, additional, Ciriolo, Maria Rosa, additional, Singh, Neetu, additional, Whelan, Richard L., additional, Chaturvedi, Rupesh, additional, Ashraf, S. Salman, additional, Shantha Kumara, H.M.C., additional, Nowsheen, Somaira, additional, Mohammed, Sulma I., additional, Keith, W. Nicol, additional, Helferich, William G., additional, and Yang, Xujuan, additional

Published
2015
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38. Sustained proliferation in cancer: Mechanisms and novel therapeutic targets

Author

Feitelson, Mark A., primary, Arzumanyan, Alla, additional, Kulathinal, Rob J., additional, Blain, Stacy W., additional, Holcombe, Randall F., additional, Mahajna, Jamal, additional, Marino, Maria, additional, Martinez-Chantar, Maria L., additional, Nawroth, Roman, additional, Sanchez-Garcia, Isidro, additional, Sharma, Dipali, additional, Saxena, Neeraj K., additional, Singh, Neetu, additional, Vlachostergios, Panagiotis J., additional, Guo, Shanchun, additional, Honoki, Kanya, additional, Fujii, Hiromasa, additional, Georgakilas, Alexandros G., additional, Bilsland, Alan, additional, Amedei, Amedeo, additional, Niccolai, Elena, additional, Amin, Amr, additional, Ashraf, S. Salman, additional, Boosani, Chandra S., additional, Guha, Gunjan, additional, Ciriolo, Maria Rosa, additional, Aquilano, Katia, additional, Chen, Sophie, additional, Mohammed, Sulma I., additional, Azmi, Asfar S., additional, Bhakta, Dipita, additional, Halicka, Dorota, additional, Keith, W. Nicol, additional, and Nowsheen, Somaira, additional

Published
2015
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39. Broad targeting of resistance to apoptosis in cancer

Author

Mohammad, Ramzi M., primary, Muqbil, Irfana, additional, Lowe, Leroy, additional, Yedjou, Clement, additional, Hsu, Hsue-Yin, additional, Lin, Liang-Tzung, additional, Siegelin, Markus David, additional, Fimognari, Carmela, additional, Kumar, Nagi B., additional, Dou, Q. Ping, additional, Yang, Huanjie, additional, Samadi, Abbas K., additional, Russo, Gian Luigi, additional, Spagnuolo, Carmela, additional, Ray, Swapan K., additional, Chakrabarti, Mrinmay, additional, Morre, James D., additional, Coley, Helen M., additional, Honoki, Kanya, additional, Fujii, Hiromasa, additional, Georgakilas, Alexandros G., additional, Amedei, Amedeo, additional, Niccolai, Elena, additional, Amin, Amr, additional, Ashraf, S. Salman, additional, Helferich, William G., additional, Yang, Xujuan, additional, Boosani, Chandra S., additional, Guha, Gunjan, additional, Bhakta, Dipita, additional, Ciriolo, Maria Rosa, additional, Aquilano, Katia, additional, Chen, Sophie, additional, Mohammed, Sulma I., additional, Keith, W. Nicol, additional, Bilsland, Alan, additional, Halicka, Dorota, additional, Nowsheen, Somaira, additional, and Azmi, Asfar S., additional

Published
2015
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40. Evasion of anti-growth signaling: A key step in tumorigenesis and potential target for treatment and prophylaxis by natural compounds

Author

Amin, A.R.M. Ruhul, primary, Karpowicz, Phillip A., additional, Carey, Thomas E., additional, Arbiser, Jack, additional, Nahta, Rita, additional, Chen, Zhuo G., additional, Dong, Jin-Tang, additional, Kucuk, Omer, additional, Khan, Gazala N., additional, Huang, Gloria S., additional, Mi, Shijun, additional, Lee, Ho-Young, additional, Reichrath, Joerg, additional, Honoki, Kanya, additional, Georgakilas, Alexandros G., additional, Amedei, Amedeo, additional, Amin, Amr, additional, Helferich, Bill, additional, Boosani, Chandra S., additional, Ciriolo, Maria Rosa, additional, Chen, Sophie, additional, Mohammed, Sulma I., additional, Azmi, Asfar S., additional, Keith, W. Nicol, additional, Bhakta, Dipita, additional, Halicka, Dorota, additional, Niccolai, Elena, additional, Fujii, Hiromasa, additional, Aquilano, Katia, additional, Ashraf, S. Salman, additional, Nowsheen, Somaira, additional, Yang, Xujuan, additional, Bilsland, Alan, additional, and Shin, Dong M., additional

Published
2015
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