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HSNS364 Written Assignment 1: Response 2
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Discuss the pathophysiology of Breast cancer disease in relation to
Kathy’s examinations.
Breast cancer is the most common form of cancer in western women (Bullock
& Hales, 2012), and was the third diagnosed cancer in Australia in 2011
(AIHW, 2016). Kathy has been diagnosed with invasive ductal carcinoma,
which is a common form of breast cancer that accounts for up to 70-80% of all
breast cancer cases (Gannon, Cotter & Quinn, 2013)
Brest cancer always begins with a tumour much like the other forms of cancer
(Bullock & Hales, 2012). Women generally discover these tumours during
self-breast exams or sometimes by their partners during sexual activity
(Berman, Kozier & Erb, 2015). Cancer occurs due to an interaction between
an external factor and a genetic suspectible host. There are a number of risk
factors associated with breast cancer such as age, sex, the number of
children a women gives birth to, the duration of reproductive life, giving birth
later in life, cholesterol level, obesity, alcohol intake, urban living, ethnicity,
genetics, family history, radiation exposure and hormone therapy (Bullock &
Hales, 2012). In the case study, Kathy has a number of the risk factors, such
as she was a previous heavy drinker, family history and genetics. In relation to
the genetics risk factor, having specific gene mutations such as BRCA1 and
BRCA2, have a strong link with an increase in breast cancer risk. BRCA1 and
BRCA2 are genes that produce tumour supressing proteins, which assist in
repairing damaged DNA (Bordeleau, Lipscombe, Lubinski, Ghadirian,
Foulkes, Neuhausen, Ainsworth, Pollak, Sun & Narod, 2011).
As normal cells within the body grow and divide as needed, during this
process abnormalities can occur. Cells within the body divide as many times
as required before stopping by a process called apoptosis, which is commonly
known as cell suicide. Cells within the body also attach to other cells and stay
in place within the tissues of the body (Bullock & Hales, 2012).
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To stop the cell suicide, several protein clusters and pathways protect the
cells. The genes along the these protective pathways can become mutated in
a way which turns the cell permanently on, rendering the cell being incapable
to commit suicide, when it is no longer needed (Berman, Kozier & Erb, 2015).
When the cells are permanently on, they lose the inability to attach to other
cells and stay in place within the tissues. This state of being unable to die
when needed and the inability to attach to other cells is one of the first steps
to a cell turning cancerous (Berman, Kozier & Erb, 2015).
Once a cell is cancerous, the cells keep dividing until there is a mass of cells.
This mass of cells then forms a lump or a tumour. Breast cancer tumours,
normally form within the epithelium lining of the milk duct and the lobule,
which is the small part of the breast where milk is formed. As it is generally
formed in these two areas of the breast, breast cancer is normally referred to
ductal or lobular carcinoma, depending on where the cancer has formed
(Grayson, 2012). In the case study of Kathy, the tumour has formed in the
lining of the milk duct; the cancer can remain in situ or become invasive,
infiltrating the surrounding breast tissue, including the lymph nodes, as shown
in Kathy’s pathology report. Breast cancer can metastasise, which means
that it can spread from one organ or another part of the body not directly
connected with it (Locker & Segall, 2011). Cancer cells can acquire the ability
to penetrate the wall of lymphatic and blood vessels and circulate through the
bloodstream stream, before coming to rest at another site, where they enter
the vessel or wall and continue to multiply before forming another tumour
(Sandholm, Kauppila, Pressey, Tuomela, Jukkola-Vuorinen, Vaarala,
Johnson, Harris & Selander, 2011).
The cancerous cells have a number of different receptors that are located on
the surface of the cells, which can be affected by a number of growth factors.
Oestrogen and progesterone are both important growth factors, and when
they fill the receptors on the surface of the cancerous cell, they emit strong
signals for cell growth, which causes the cell to multiply, as in the case of
Kathy who is oestrogen and progesterone positive (Langhorne, Fulton & Otto,
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2007). Another factor that can influence how quickly breast cancer cells divide
in response to growth factors is a protein called HER2. Not all patients
diagnosed with breast cancer have an increase in their HER2 and only about
10-20% of women with breast cancer are shown to be HER2 positive (Cancer
Australia, 2016). The detection of the increased in the HER2 protein as in
Kathy’s case may indicate a more aggressive form of breast cancer.
Discuss the chemotherapeutic treatment available for Kathy
Chemotherapy uses cytotoxic drugs, which kill cancer cells, and is a systemic
treatment given to patients such as Kathy, who has early breast cancer
(Breast Cancer Network Australia, 2015) Chemotherapy is a systemic
treatment, it does not focus on the area or areas where tumour was located
but is used to destroy cancer cells that have left the site of the original tumour,
and is used to reduce the risk of cancer returning positive (Langhorne, Fulton
& Otto, 2007).
Chemotherapy treatment can be used in conjunction with a number of
treatments such as hormonal therapy and, can be used pre or post surgery
(Von Minckwitz & Loibl, 2015). If chemotherapy is given pre- surgery, it is
known as neoadjuvent chemotherapy, which aims to shrink the tumour before
surgery and, if given after surgery, is it known as adjuvant chemotherapy,
which aims to prevent the recurrence of the disease. (Von Minckwitz & Loibl,
2015).
In relation to Kathy’s breast cancer, there are various types of
chemotherapeutic medicines available to treat her specific type of breast
cancer (Cancer Australia, 2016). There are a number of considerations that
need to be taken into account to determine which chemotherapy option is
right for the situation and, whether there are any other related health
conditions (Unitt, Montazeri, Tolaney & Moslehi, 2015). Another factor in
deciding which chemotherapeutic medicine to use is whether the tumour
tested positive for HER2 receptors (Montemurro, Rossi, Cossu Rocca,
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Martinello, Verri, Redana, Adamoli, Valabrega, Sapino, Aglietta, Viale,
Goldhirsch and Nole, 2011).
Cancerous cells have the ability to further divide and multiply at a rapid rate,
so the aim of chemotherapy is to kill the cells, which are in the process of
dividing (Puhulla & Brufsky, 2013). Different types of chemotherapy drugs kill
the cells at different stages of division, and many chemotherapy drugs are
given in combination so there is a higher chance of killing more cells
(Valachis, Nearchou, Lind & Mauri, 2012). This combination chemotherapy
usually consists of drugs from anthracyclines, taxanes and targeted therapies
(Valachis, Nearchou, Lind & Mauri, 2012).
Kathy has tested positive to oestrogen and progesterone which can promote
the growth of breast cancer cells. A way to combat the growth in the hormone
responsive cells is to use hormone therapy, which slows or stops the hormone
sensitive tumours by blocking the body’s ability to produce these hormones
(Howell & Evans, 2013). The blocking of the estrogen is normally through a
selective estrogen receptor modulator (SERM) such as tamoxifen and is used
in conjunction with chemotherapy (Bergmaschi & Katzenellenbogen, 2011).
As Kathy’s tumour has tested positive for HER2 receptors, one of the
chemotherapeutic treatments available to her would be the use of monoclonal
antibodies, otherwise known as targeted therapies (Higgins & Baselga, 2011).
Monoclonal antibodies work by focusing on specific proteins, receptors, on the
surface of the cells (Munagala, Aqil & Gupta, 2011). There are three
commonly used targeted therapy drugs that treat HER2 positive breast
cancer, these being Trastuzumab, Lapatanib and Pertuzumab. Each one of
these drugs works on a different part of the HER2 protein and stop the cells
from growing and dividing (Perez & Spano, 2011).
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Bordeleau, L., Lipscombe, L., Lubinski, J., Ghadirian, P., Foulkes, W., &
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