Molecular Biology of Cancer

Subject: Science
Type: Synthesis Essay
Pages: 6
Word count: 1693
Topics: Biology, Cancer, Genetics, Public Health


Cancer refers to a disease characterized by a group of abnormal cells that grow uncontrollably by ignoring the ordinary rules of cell division. Cancer poses a worldwide threat to human health and it comes second after cardiovascular diseases in leading causes of death in the United States (Martinez et al., 2003). Significant progress in understanding the molecular basis of cancer has been in the recent past to establish that defective genes cause a variety of diseases which in turn cause cancer. Further insights have been made on both the internal factors within the cell and external environmental factors through which cancer develops. These include factors such as inherited mutations, immune conditions chemicals, radiation and infectious organisms, among others.

Molecular Causes of Cancer

All cancers arise from abnormal changes that take place in the DNA sequence of the genomes of cancer cells. There are over 100 distinct diseases that result from these mutations and the abnormal genes present in human cancers. The mutations causing cancer fall into two broad categories; somatic mutations and epigenetic mutations. 

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Somatic Mutations

In somatic mutation, normal cells are transformed into cancer cells through a sequence of minor discrete genetic events. Cancer can thus be viewed as a genetic disease of somatic cells. The rate of somatic mutation in the human body is subject to certain environmental agents such as mutagenic or ionizing radiation, or heredity factors that either increase the rate of somatic mutation or the rate of cell proliferation, or both. Accumulation of DNA mutation in the cell alters the sequence of amino acid resulting in cellular malignant transformation. The resulting mutant protein further leads to the development of cataracts of downstream signaling such as cell proliferation and reserve of apoptosis before transforming the normal cellular phenotype to malignant. The entire somatic process occurs in three phases. First, fast genetic variation caused by the high rate of uncontrolled proliferation and compromised DNA integrity. Second, different proliferation and death rates sequences occur in cells of varying genetic type. Third, the acquired mutant genotypes spread to the surrounding cells through clonal expansion stimulated by harsh environmental pressures such as glucose starvation or physical pressure (Luzzatto, 2011). 

Epigenetic Mutations

Epigenetic changes result in a pattern of altered gene expressions caused by factors that do not change the primary DNA sequence or the DNA based pairing (Baylin & Ohm, 2006). Such mutations include DNA methylation, Chromatin remodeling, and histone modification. The mutations cause the affected genes to behave differently without altering the underlying DNA sequence. Factors such as environmental chemicals, aging, diet, drugs, and pharmaceuticals affect the process of epigenetic mutation. The resulting rate of epigenetic alterations is higher in chromatin of neoplastic cells compared to the normal cells where they were originally derived from. The subsequent growth of gene alterations leads to the development of tumor-suppressor and candidate tumor-suppressor genes, both that causes chromosomal abnormalities in cells and thus cancer. 

Principal Processes Altered in Cancer

Molecular organisms can thrive only when their cells functions take place within the biological rules that control cell growth and reproduction. However, when cells break these rules (for instance cancer cells), they multiply recklessly, usurp resources and invade other tissues altering the normal body process. Although cancer consists of more than 100 different diseases, all cancer cells are abnormal cells which disrupt the processes for governing normal cell division. Therefore, cancer grows from changes that attribute abnormal functions to normal cells. As such, cancer can be seen to affect the process of cell division (Wong, 2011).

In normal cells, the process of cell division is stimulated through signals sent to the nucleus by proto-oncogenes code for the protein. These proteins act through a series of signal transduction cascade that includes a signal receptor, intermediary protein and a transcription factor that activate the genes for cell division in the nucleus. In cancerous cells, however, oncogenes are altered resulting in continuous signaling cascades leading to increased production of factors that stimulate growth (Scott & Athena, 2000). Mutations in the oncogene inhibit its function of switching off the signaling cascade thus the pathway remains active leading to uncontrolled cell growth. Such uncontrolled growth causes tumors in lungs, colon, pancreas, and thyroid, which further affect their functioning.  

Health body tissues are subject to apoptosis, a rapid and irreversible process through which the body eliminate dysfunctional cells. Cancer, however, causes malignant cells to evade apoptosis and at the same time, these cells may obtain various properties that would initiate apoptosis in healthy cells. Such properties allow cancer cells to thrive at the expense of healthy cells. Cancer cells avoid apoptosis through downregulation of suppressor genes that are responsible for the reception of cell death signals (Wong, 2011). The resulting imbalance between cell division and cell death causes enhanced tumor growth and further inactivation of tumor suppressor genes.

Molecular Techniques used to Diagnose Cancer

In the recent years, advanced clinical research in cancer has led to remarkable scientific and technological progress in approaches to cancer diagnosis. Primary cancer prevention treatment methods continue to attract more research because of the poor diagnoses result for cancer at an advanced level. Various molecular alterations consisting of DNA, RNA, microRNAs, and proteins are being used to control development, invasion, and metastasis of cancer. Since the treatment process of cancer begins with mutation detection, sensitive sequencing methods have been established to detect minority of mutant cells among wild-type cells. 

Detection of somatic point substitution is an important step in characterizing the cancer genome. MuTect is a key method for detecting somatic point substitution in low-allelic fraction mutations that occur in a subset of the sequenced cells. In such cells, the mutations may be unidentifiable due to tumor heterogeneity or contamination by normal cells impacting their visibility. The technique entails three different standard processes; analysis of the clonal mutations that may be present in some metastases from a single patient; detection of subclonal mutations by ultra-deep sequencing; and sequencing of small numbers of single cells (Wardle et al., 2015). Somatic mutation detection with MuTect applies input sequence data from tumor and ordinary DNA to produce identical reads, recalibration of base value notches and local realignment. The method is operated in four main steps. These include the elimination of poor quality sequence data, use of Bayesian classifier to detect variant in the tumor, removal of false positives caused by correlated sequencing data, and quantification of gene products as somatic or germline. 

The Recurrent and Mutually Exclusive (RME)35 method is used to detect mutually exclusive and co-occurring mutations. In these mutations, the mutated genes in the tumor cells acquire a selective advantage such as reduced apoptosis, which promotes clonal expansion resulting in robust negative association among mutations in genes of the identical pathways. RME35 method, therefore, provides evidence for detecting positively correlated gene mutations through contrast. This approach is important in detecting mutually exclusive events among rare mutations that are difficult to identify as they happen by chance (Mahdieh & Rabbani, 2013). Similar techniques applied in detection of more advanced co-occurring and mutually exclusive gene mutations are the Dendrix36, MEMo43 and Multi-Dendrix.37.

Ethical Considerations in Cancer Screening

The goal of public health is to provide universal safety to the population through the realization of the optimum health level achieved through prevention and transmission of diseases. Screening is one of the strategies through which public health systems employ to ensure early detection of disease or its antecedents in asymptomatic society thought to be at risk (Martinez et al., 2003). However, the process of screening to identify various diseases intrinsically is troubled by numerous ethical challenges. Analysis of ethical challenges in the screening of patients for mutations associated with the development of cancer is, in particular, taxing to policy makers and service providers since ethics paradigms for considerations in public health practice are varied. Ethical analysis, therefore, is important in clarifying the contextual level of screening cancer patients.

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Early detection and intervention in cancer diagnosis are intuitively attractive for cancer since the impacts of the ailment are serious while early detection is beneficial. This, however, raises the question of who should be screened and the screening programs that should be adopted to ensure early detection and intervention. Introduction of screening processes according to Barratt et al. (2002) should entail the provision of adequate information regarding the probable benefits and harms associated with the exercise for the purpose of making informed decisions. Screening of patients with cancer is a voluntary exercise and should remain that, but people should be sensitized adequately on the life benefits of cancer screening.

Population-based cancer screening is driven by the goal of reducing the disease-specific mortality rate. Given that screening allows early detection and subsequent treatment of cancer in an effort to reduce possible deaths, more people should be encouraged to undertake screening. The ratio of persons seeking screening services to the entire population is significantly small owing to the costs associated. Insurance providers should provide medical covers for cancer screening because early detection and treatment would be less expensive compared to interventions at later stages. Insurance providers, in particular, private firms, may be compelled to charge higher premiums for people with a mutation linked with cancer on the basis of health risk involved. Such a person may not afford to secure a medical cover and this would threaten the objectives of public health systems (Bioeth, 2009). This situation can, however, be addressed through government intervention by providing attractive medical covers that would force the private firms to scale their premiums downwards. 


Cancer consists of a group of genetic diseases caused by unregulated cell growth resulting from gene mutations. The alterations of the DNA function (tumor) can be induced by various environmental factors such as exposure to radiations or chemicals as well as internal factors within the cell such as inherited mutations. Cancer cells often interfere with the natural balance between cell division and apoptosis resulting in abnormal functioning of the cells affected. Early detection of cancer is a key step in achieving positive outcomes for cancer diagnosis. The process of cancer screening, however, subject to numerous ethical considerations regarding individual and population-based screening as well as the cost-effective public health measures. 

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  9. Wong, R. (2011). Apoptosis in Cancer: From Pathogenesis to Treatment. Experimental & Clinical Cancer Research, 30(1), 87-94.
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