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Cancer is a major health encumbrance in both developed and underdeveloped countries

involving numerous spatiotemporal changes in cell physiology. According to the World Health
Organization(WHO) report, 8.8 million people died of cancer globally in 2015 [1]. A recent
survey by the American Cancer Society of epidemiologists revealed that approximately one-third
of 595,690 cancer deaths in the USA were due to smoking, the main cause of lung cancer that
accounted for the highest number of cancer deaths (Fig. 1) worldwide [2]. In addition, 20% of all
cancers diagnosed are associated with obesity, physical inactivity, excess alcohol consumption,
and/or poor nutrition while certain cancers are related to infections caused by the human
papilloma virus (HPV), hepatitis B virus (HBV), hepatitis C virus (HCV), human
immunodeficiency virus (HIV), and Helicobacter pylori (H. pylori). These cancers could be
circumvented through behavioural changes, vaccination, or by treating the infection. Most
cancers are recognized by uninhibited growth of cells without demarcation due to the
deregulation of crucial enzymes and proteins controlling cell division and proliferation [3,4]. The
biological process responsible for the transformation of normal cells into malignant cancer cells
has been the focus of research endeavours in the biomedical sciences. Although much progress
has been aspired from the identification to the treatment of cancer, factors like poor patient
compliance, drug resistance and drug induced toxicities has provided a strong impetus for the
discovery and development of novel cancer chemotherapeutic hybrids of clinical significance [5-
7]. Anticancer drugs have been categorized in consonance with their mechanism of action as
molecular targeting hybrids, antimetabolites, antitubulin and DNA-interactive hybrids,
monoclonal antibodies and hormones [8,9]. However, the single target approach also leads to
cytotoxicity, predominantly on normal proliferating tissues such as hematopoietic system
[10,11]. Consequently, in the development of effectual and discerning anticancer drugs having
low incidence of side effects, toxicity and emergence of drug resistance is of high priority [12].

[1] WHO Global Cancer report. http://www.who.int/cancer/en/, 2015. Accessed


May 16, 2017.
[2] WHO Global Cancer report. http://www.who.int/mediacentre/factsheets/
fs297/en/, 2012. Accessed on May 14, 2017.
[3] M. Mareel, A. Leroy, Clinical, cellular, and molecular aspects of cancer invasion,
Physiol. Rev. 83 (2003) 337e376.
[4] J. Wesche, K. Haglund, E.M. Haugsten, Fibroblast growth factors and their
receptors in cancer, Biochem. J. 437 (2011) 199-213.
[5] S.K. Grant, Therapeutic protein kinase inhibitors, Cell. Mol. Life. Sci. 66 (2009)
1163-1177.
[6] G.I. Solyanik, Multifactorial nature of tumor drug resistance, Exp. Oncol. 32
(2011) 181e185.
[7] S. Vijayaraghavalu, C. Peetla, S. Lu, V. Labhasetwar, Epigenetic modulation of
the biophysical properties of drug-resistant cell lipids to restore drug transport
and endocytic functions, Mol. Pharm. 9 (2012) 2730-2742.
[8] M.M. Gottesman, T. Fojo, S.E. Bates, Multidrug resistance in cancer: role of
ATP-dependent transporters, Nat. Rev. Cancer 2 (2002) 48e58.
[9] D.M. Molina, R. Jafari, M. Ignatushchenko, T. Seki, E.A. Larsson, C. Dan,
L. Sreekumar, Y. Cao, P. Nordlund, Monitoring drug target engagement in cells
and tissues using the cellular thermal shift assay, Science 341 (2013) 84e87.
[10] S.W. Fesik, Promoting apoptosis as a strategy for cancer drug discovery, Nat.
Rev. Cancer 5 (2005) 876e885.
[11] D. Sloane, Cancer epidemiology in the United States: racial, social, and economic
factors, Methods Mol. Biol. 471 (2009) 65e83.
[12] G. kibria, H. Hatakeyama, H. Harashima, Cancer multidrug resistance mechanisms
involved and strategies for circumvention using a drug delivery system,
Arch. Pharm. Res. 37 (2014) 4e15.

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