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Cancer is a disease
caused by abnormal cell division which can lead to tumour formation. Normal
cells will always divide in an ordered way whereas damaged and unwanted cells
will undergo cell death (Knowles & Selby, 2005). Uncontrolled cell division of cancer
cells can eventually cause accumulation and formation lumps which is also known
as tumour. The cells in the tumour always exhibit six hallmarks for malignant
tumour growth and metastasis. These hallmarks include sustained proliferative
signalling, evasion of growth suppressors, cell death resistance, activation of
invasion and metastasis, induction of angiogenesis, and replicative immortality
(Hanahan & Weinberg, 2011). However, the early stage of
tumorigenesis shows no harmful effect to the patient (Thomas et al., 2004; Yeqi et al., 2008). When the tumour is not suppressed
by proper treatments, it may continue to proliferate or even disperse to other
tissues and organ, becoming malignant (Kelvin & Tyson, 2010). In this case, some common symptoms
of cancer such as presence of lump (Jones, 2003) can be diagnosed in patients through
medical tests.

Based on a reported study
(Anand et al., 2008), 90-95% of cancers are caused by the
environmental factors while the rest are caused by genetic inheritance. The
environmental factors that adds to cancer risk include intake of tobacco,
excessive consumption of alcohol, dietary habit, obesity, viral infection,
environmental pollution, and radiation (Anand
et al., 2008). Among these, the main factor known
to induce cancer is tobacco smoking. The chemicals found in cigarettes can
damage and alter gene expression (Jin et al., 2017), thus promoting the onset of cancer (Sasco et al., 2004). Smoking has caused 90% of lung
cancer cases (Biesalski et al., 1998) and is accountable as the main
carcinogen for 20% of all cancers worldwide (Kuper et al., 2002). Excessive consumption of alcohol
has also been tied to higher incidence of various types of cancer, by causing
DNA damage and oxidative stress (Zhao et al., 2017). Consumption of commercial crops
contaminated with toxic molecules such as mycotoxins from fungi Aspergillus flavus, is also known to
cause cancer, as is evident by the increased incidence of oesophageal cancer
within a population in Western Kenya (Kigen et al., 2017). Recent studies has also identified
obesity as a contributor for some cancers such as breast cancer and bowel
cancer (Lauby-Secretan et al., 2016). The thickness of adipose tissues
encourages the proliferation of cancer cells and tumorigenesis (Iyengar et al., 2015). Additionally, infectious agents
include virus and bacteria may lead to cancer as well (Pagano et al., 2004). For instance, the most common
virus, human papillomavirus (HPV) that usually infects women is associated with
many types of cancers including cervical cancer (Ljubojevic
& Skerlev, 2014). Meanwhile, environmental pollution
caused by cigarette smoke (Pope et al., 2011) and smoke from factory chimneys (Hassan et al., 2017) distributes carcinogens to the air
therefore increasing the probability of patients with lung cancer. The last
environmental factor of cancer is radiation of UV ray and ionizing agents (Belpomme et al., 2007). Overexposure  to UV might lead to skin cancer as UV ray can
damage DNA (Bast et al., 2017). In addition to environmental
factors, cancer can also be caused by the inheritable mutation of the gene,
such as BRCA1 and BRCA2 in breast cancer (Ford et al., 1998).According to Malaysian National Cancer Registry Report
2007-2011, around 18000 out of 14 million women are diagnosed with breast
cancer, with their age ranging between 25 to 59 years, (Kirubakaran et al., 2017). Breast cancer are
usually detected when lump is observed in the lymph nodes near the armpits
through mammography (Tabár et al., 1985). The patient may suffer
from breast pain and able to observe swelling bumps when the tumour became more
malignant. In addition, breast cancer might cause metastasis that migrate and
invade other organs (Lacroix, 2006).

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cancer can be classified into two groups by identifying the expression of the
estrogen receptor (ER): ER+ and ER- (McGuire et al., 2015). There are two
sub-groups of ER+ tumours which are luminal A and luminal B. Luminal A and
luminal B breast cancer are responsive to signals from estrogen which promote cancer
cell growth. To treat both luminal A and luminal B breast cancer, estrogen
expression is knocked down to reduce cancer cell growth. There are also two
sub-groups of ER- tumours which are the HER2+ and the basal type. HER2+ breast
cancer can be treated by targeting HER2 protein using trastuzumab, an FDA
approved anticancer drug. HER2+ breast cancer cells grow and proliferate faster
than luminal A and luminal B. Lastly, basal type breast cancer is the most
common among young females and Black Americans women with BRCA1 gene mutations (Desmedt et al., 2008; Eliyatk?n et al., 2015). These classifications are often
used to identify better treatment options for patients with by identifying the
connection between the clinical outcomes of tumours and cDNA microarray (Zepeda-Castilla et al., 2008).Apoptosis
can be mediated through two pathways, which are the intrinsic and extrinsic
pathways (Gilmore, 2005). Intrinsic pathway of apoptosis is
regulated by maintaining the balance between two sets of proteins,
anti-apoptotic proteins and pro-apoptotic proteins (Othman et al., 2013). Interaction
between these proteins in healthy normal cells works to prevent caspase activation
and subsequently apoptosis. When cells are damaged or are no longer needed, the
anti-apoptotic Bcl-2 proteins are blocked to prevent them from binding to BAX
proteins. BAX protein, one of the member of Bcl-2 family, is encoded by BAX
gene and acts as an apoptotic activator to increase the opening of
mitochondrial voltage-dependent anion channel (VADC) that results in the loss
of membrane potential. Clusters of BAX proteins are now free to punch a series
of channels in mitochondria (von Ahsen et al., 2000), allowing
cytochrome c to leak out to the cytosol (Saelens et al., 2004). Leaked
cytochrome c then binds to Apaf-1 proteins to create compound known as
apoptosome that induces the activation of caspase cascade by losing
mitochondria membrane potential (Waterhouse et al., 2001). For instance,
apoptosome cleaves pro-caspase-9 to its active form, which then activates the
effector executioner caspase-3. On the other hand, extrinsic pathway is
initiated when Fas ligand (FasL), a molecule which can be found on the surface
of T lymphocyte, binds to the Fas receptor on the target cell (Wajant, 2002). The binding of both FasL and Fas
receptor together with initiator caspases such as caspase-3 or caspase-10 forms
Death Inducing Signalling Complex (DISC), which is mediated by Fas Associated
Death Domain (FADD). After the initiator caspase is processed, it will then
activate the executioner caspases and trigger apoptosis to take place (Berry, 2007).

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