**Part 4**

**Drug Therapeutics/Biological Agents** 

302 Prostate Cancer – From Bench to Bedside

Zhang, Y.X. & Kong, C.Z. (2008). The role of mitogen-activated protein kinase cascades in

Zhao, M.; New, L.; Kravchenko, V.V.; Kato, Y.; Gram, H.; di Padova, F.; Olson, E.N.;

Zheng, B.; Fiumara, P.; Li, Y.V.; Georgakis, G.; Snell, V.; Younes, M.; Vauthey, J.N.; Carbone,

Zhou, G.; Bao, Z.Q.; Dixon, J.E. (1995). Components of a new human protein kinase signal

Zhu, Y.; Culmsee, C.; Klumpp, S.; Krieglstein, J. (2004). Neuroprotection by transforming

Zubelewicz, B.; Muc-Wierzgon, M.; Wierzgon, J.; Romanowski, W.; Mazurek, U.; Wilczok,

by p38. *Molecular and Cellular Biology*, Vol. 19, No. 1 (Jan), pp. 21-30.

*Oncology*, Vol. 136, No. 3 (Mar), pp. 437-445, ISSN: 0171-5216.

271-5, ISSN: 0376-2491.

pp. 12665-12669, ISSN: 0021-9258

No. 4, pp. 897-906, ISSN: 0306-4522.

104, ISSN: 0393-974X.

4971.

human non-small cell lung cancer A549*. Journal of Cancer Research and Clinical* 

inhibition of proliferation in human prostate carcinoma cells by raloxifene: an in vitro experiment. *Zhonghua yi xue yi chuan xue za zhi*, Jan 22;Vol. 88, No. 4 (), pp.

Ulevitch, R.J.; Han, J. (1999). Regulation of the MEF2 family of transcription factors

A., Younes, A. (2003). MEK/ERK pathway is aberrantly active in Hodgkin disease: a signaling pathway shared by CD30, CD40, and RANK that regulates cell proliferation and survival. *Blood*, Vol. 102, No. 3 (Aug 1), pp. 1019-1027, ISSN: 0006-

transduction pathway. *The Journal of Biological Chemistry*, Vol. 270, No. 21 (May 26),

growth factor-beta1 involves activation of nuclear factor-kappaB through phosphatidylinositol-3-OH kinase/Akt and mitogen-activated protein kinaseextracellular-signal regulated kinase1,2 signaling pathways. *Neuroscience,* Vol. 123,

T.; Podwinska, E. (2002). Genetic disregulation of gene coding tumor necrosis factor alpha receptors (TNF alpha Rs) in follicular thyroid cancer-preliminary report. *Journal of Biological Regulators & Homeostatic Agents*, Vol.16, No. 2 (Apr-Jun), pp. 98-

**14** 

*University of Malaya* 

*Malaysia* 

**Evaluation of Phyllanthus,** 

**for Its Anti-Cancer Properties** 

Cancer is a name given to a group of diseases that arise from a single cell when it starts to grow abnormally in an uncontrollable manner to form a group of undifferentiated cells, known as tumour. Tumour can be classified into two categories; benign and malignant. Not all benign tumours are cancerous but all malignant tumours are (Hanahan & Weinberg, 2000). The main difference between these tumours is benign tumour lack the metastatic ability, grows locally and is less harmful. However, some benign tumours can transform into malignant tumours that possess the metastatic ability to invade and spread to other parts of the body via the blood or lymphatic circulation and form secondary tumour and

Cancer develops through a multistep process known as carcinogenesis (Fig 1), which includes initiation, promotion and progression (Pitot, 2006). An initiation stage is a permanent and irreversible event, which involves one or more cellular changes arising upon exposure to carcinogens, which leads to alteration in DNA and may result in a mutated cell to divide rapidly (hyperplasia). These transformed (initiated) cells can remain harmless, unless exposed to a stimulator, which enhances the tumour to grow into a larger mass. This is a reversible process and is known as the promotion stage. The progression stage is an irreversible conversion of a benign tumour to become a malignant tumour. This carcinogenesis process usually takes 10 years or more to develop and usually depends on the internal (life style) and external (environmental) factors of the

A transformed cell has to acquire six hallmarks in order to be developed into cancer (Fig 2) (Hanahan & Weinberg, 2000). Each of these hallmarks is derived upon changes in the normal cell's physiology and interacts with each other to promote malignant growth. The conversion from a normal cell to become a transformed cell usually starts from mutations in DNA which cause the cells no longer depend on growth signals, thus gaining uncontrolled growth and proliferation. The irresponsiveness or insensitivity to anti-growth signals in

**1. Introduction** 

patient (Pitot, 2002).

**1.3 Hallmarks of cancer** 

eventually lead to death (Vincent & Gatenby, 2008).

**1.2 Development of cancer (carcinogenesis)** 

**1.1 Cancer** 

Yin-Quan Tang and Shamala Devi Sekaran
