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Introduction
Cancer results from the cellular disorder that involves a poorly characterized sequence of molecular events that comprise unrestrained cell propagation, morphological and cellular alteration. It may also result from deregulation of apoptosis, angiogenesis, increased invasive cell activity as well as succeeding confined and remote metastases. It has now been approved that tumor microenvironment that increase and modifies in line with the growth load is central in the cancer development process (Menard et al, 2000, p.256). Indeed cancer growth is a series of processes that is driven by alterations of genes that bring about the progressive conversion of usual body cells into extremely malignant imitation. The altered cell explosive phenotype of malignancy involves distinguished progression of molecular events that in most cases lead to the growth of metastasis (Menard et al., 2000, p.256).
According to Gajria and Chandarlapaty (2011), about 5 to 10 percent cases of breast cancer are hereditary, the abnormal genes causing cancer is passed on the child from the parent (p.270). Genes are the unit particles of a cell but they are contained in chromosomes and are made up of deoxyribonucleic acid (DNA). DNA is the part of the gene that contains coded instructions that built up proteins. Proteins are the building blocks of the body structure of a cell and controls the functions of a cell that make up the whole body of an organism. Abnormalities in the gene structure may result in the coding error or instructional error leading to defective growth in cells or its function (Gajria & Chandarlapaty, 2011, p.269).
Breast Cancer gene 1 (BRCA1) and Breast Cancer gene 2 (BRCA2)
Most of the breast cancer cases are related to the BRCA1 and BRCA2 abnormal genes. All people posses the two genes in their breast cells and the major functions are to repair damages in the breast cells and to maintain the normal growth of these cells. Any abnormality in the gene structure will cause a malfunction and uncontrolled growth of the breast cells (Gajria & Chandarlapaty, 2011, p.269). The abnormalities in the genetic coded structure may be caused by mutations that might be inherited or may be caused by other environmental causative agents. However, mutations in the BRCA genes do not necessarily mean that one will be diagnosed with breast cancer. Nevertheless, cases of Breast cancer that result from the BRCA abnormalities accounts for only 10%. In most cases the gene mutations that result in breast cancer are inheritable (Gajria & Chandarlapaty, 2011, p.269).
Several researches have confirmed that other gene mutations called single nucleotide polymorphisms (SNPS) also occur in the peace of chromosomes that contain the BRCA genes. When combined together with the BRCA abnormality, there are high chances that an individual will develop breast cancer particularly those women that do not possess the inheritable BRCA abnormality (Jones & Buzdar, 2009, p.1181). Majority of women that are diagnosed with breast cancer in one way or the other have a family history of other forms of cancer such as the ovarian cancer. But this is not true to all the breast cancer victims.
How Herceptin Works
Herceptin is part of the monoclonal groups of drugs that are used in the treatment of cancer. Monoclonal antibodies distinguish specific proteins and locks onto the surface of cancerous cells. This helps the body immune system to destroy the recognized cancer cells. Monoclonal therapies are known as targeted treatments since their designation are to target specific cancer cells (Spector & Blackwell, 2009, p.5840).
Monoclonal antibodies treatment is relatively a modern type of targeted cancer therapy. Antibodies are element of the larger body immune system. In most cases the body manufacture antibodies in response to any foreign materials entering the body (antigen). The antibody works by attaching to the surface of the antigen and destroying the foreign body or preparing the antigen for further action by other elements of the immune system (Spector & Blackwell, 2009, p.5842). Scientists are capable of analyzing the antigen that can specifically attach to the surfaces of particular cancer cells. Using the antibody antigen key and lock technology scientists has created a particular antibody that attaches itself to the surfaces of the antigenic cancer cells outgrowths. Moreover the technology has allowed the treatment of targeted cancer cells without further destruction or toxicating other healthy cells. Monoclonal therapy is only applied to the cancer cells whose antigens and their receptive antibodies have been identified (Spector & Blackwell, 2009, p.5842).
Herceptin works by aiming at the antigen HER-2 receptors on the surfaces of cancer cells. Basically, HER-2 genes produce a particular receptor protein on the breasts cell surfaces stimulating growth and multiplication. The cancerous breast cells produces too much of the HER-2 protein triggering an abnormal rapid cell division and multiplication (Garrett & Arteaga, 2011, p.795). Herceptin is an artificial antibody that binds to with the extra HER-2 receptors preventing over-multiplication of cells hence reducing the rate of tumor growth and decreasing the cancer progression. Herceptin may also stimulate the immune system to naturally work destroy the tumor cells or slow the growth of tumor cells.
Cancer cells have a tendency of growing uncontrollably. On the surface of these cells herceptin blocks the chemical signal that act as a stimulant to the uncontrolled growth. Various cancer cells are capable of over expressing many copies of a certain gene known as the HER-2 which is responsible for manufacturing HER-2 receptor protein (Garrett & Arteaga, 2011, p.795). The HER -2 are responsible for the growth and multiplication of the cells. However the HER-2 receptors can be over stimulated resulting into haphazard growth and multiplication leading to breast cancer. HER-2 breast cancer positive are the cancer cells that over express the HER-2 genes in their surfaces (Garrett & Arteaga, 2011, p.795).
Herceptin attaches itself to the HER-2 receptors on the breast cancer cells surfaces and stops growth stimulation. Hence herceptin slows down the growth of breast cancer. The drug is an example of immune therapy that targets a particular antibody. Apart from blocking the HER-2 receptors from over expressing itself herceptin can also inform the body immune system to kill cancer cells that it attaches to (Jones & Buzdar, 2009, p.1181). In addition, herceptin can be combined with chemotherapy can synergistically and effectively destroy the tumor cells.
HER-2 is 20-25% is over expressed invasive breast cancer cells that are linked with aggressive tumor phenotype as well as the reduced survival rate (Addeo & Caraglia, 2011, p.140). The status of HER-2 in a tumor is essential in determining the response to the targeted antibody Herceptin. Hence the expression levels of the HER-2 in the tumor cells must be accurately assessed so as to determine the breast cancer patients who can particularly benefit from the HER-2-targeted treatment. Herceptin combine with other therapies such as chemotherapy and hormonal therapy augments the response rate, slows down the tumor growth and increases the chances of survival (Jones & Buzdar, 2009, p.1181). However, majority of cancer patients that originally react to herceptin commence to progress once more a year after the treatment.
The side effects of Herceptin
Individuals react differently to the treatment of cancer more in the use of drugs especially herceptin. While some people may experience minor and few side effects others may experience severe effects of the drug. Herceptin side effects are grouped into two. They include the effects that are experienced in the early stages in the drug infusion and the effects that may occur later after the drug has been used. Early infusion-related effects normally occur within four hours after the diagnosis (Menard et al, 2000, p.257). The side effects are imminent with the first few doses but disappear with subsequent doses. The late side effects normally occur after some days or may extent to some weeks after the therapy.
Early fusion-related side-effects
These include Flu-like symptoms that are characterized with headaches, high temperature or fever. These types of side effects normally come about as a result of immediate body reaction to the drugs. Another immediate body reaction to the drug is allergy though uncommon. The signs for allergy may include wheezing, breathlessness, body rashes and itching. Allergic reactions occur due to the activation of immune system surrounding these cells (Addeo & Caraglia, 2011, p.143). The reaction of the immune system to the surrounding cells may trigger their overproduction or inducing them to produce more antigens to react with the antibody entering the body.
The late side effects
These may include diarrhea which may be mild or severe. Others are headaches, nausea which is very common with many monoclonal drugs. In most cases these normally occur as a result of the interferences with body systems such as the digestive and circulatory systems. These systems normally produce a lot of antibodies and therefore any addition of the antibodies may kill the normal proteins in the system. In the circulatory system is where all the antibodies are produced hence the system must be greatly interfered with by the introduction of the drug. These side effects together with the early infusion- side-effects can be reduced by using the necessary prescribed drugs (Garrett & Arteaga, 2011, p.793).
The greatest and most lethal side effect of the herceptin is associated with the heart failure. The drug may cause heart problem to some people. It is not always recommended for people with heart problem history or with high blood pressure. Herceptin destroys the heart linings thereby causing the slow malfunctioning of the heart. Cells aligning the major tissues of the heart are prone to the herceptin antibodies thus causing their destruction (Garrett & Arteaga, 2011, p.795). Before herceptin diagnosis the victims are recommended for checks to determine the patients chances of developing heart problems. The other side effect is the destruction of fetuses in pregnant women. In some cases the drug may cause the death of the fetus. It is recommended that women who are likely to become pregnant use the appropriate birth control measures while undergoing herceptin treatment (Menard et al, 2000, p.257). Similarly, mothers nursing their babies should also avoid the drug or completely stop nursing.
Conclusion
Herceptin is monoclonal antibody therapy that kills or destroys tumor cells using the natural body immune system. Though cancerous cells may grow beyond the normal level, they similar to the body cells hence are capable of escaping the normal destruction by the natural body immune mechanisms. However there exist some remarkable differences between normal and cancer cells. In case of breast cancer, there are numerous copies of cancer causing gene known as the HER-2. This implies that HER-2 results in the over expression of receptor protein on the surface of the cells responsible for the growth and cell multiplication. Over production of the proteins may result in the increased growth or multiplication of the cells leading to a tumor. Herceptin is made in such a way that it targets the cells that over express HER-2 genes. Herceptin, though not very effective in the treatment of breast cancer, when combined with other therapies it becomes more effective.
References
Addeo, R. & Caraglia, M. 2011. The oral tyrosine kinase inhibitors lapatinib and sunitinib: New opportunities for the treatment of brain metastases from breast cancer? Expert Review of Anticancer Therapy, 11(2), pp. 139-142.
Gajria, D. & Chandarlapaty, S. 2011. HER2-amplified breast cancer: mechanisms of trastuzumab resistance and novel targeted therapies. Expert Review Anticancer Therapy, 11(2), pp.263275.
Garrett, J. T, & Arteaga, C. L. 2011. Resistance to HER2-directed antibodies and tyrosine kinase inhibitors: mechanisms and clinical implications. Cancer Biology Therapy, 11, pp.793800.
Jones, K. L. & Buzdar, A. U. 2009. Evolving novel anti-HER2 strategies. Lancet Oncology, 10, pp.11791187.
Menard, S., Tagliabue E, Campiglio M. & Pupa S. M.2000. Role of HER2 gene over expression in breast carcinoma. Journal of Cell Physiology, 182, pp.150162.
Spector, N. L. & Blackwell, K. L. 2009. Understanding the mechanisms behind trastuzumab therapy for human epidermal growth factor receptor 2-positive breast cancer. Journal of Clinical Oncology, 27, pp.58385847.
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