Answer

Scientific Article Analysis

            The article titled ‘The long trail of cancer’s clues’ by Johnson (2013) gives new insights about causation, nature, and potential treatment of cancer. The traditional conceptualization cancer development is cancerous cells is a product of mutations that accumulates over time. One cancerous cell known as cell, known as a clone, multiplies uncontrollably, which contributes to development of tumors. Typical cancerous cells have certain characteristics. These characteristics include inability to slow down its multiplication (or uncontrolled division), circumvention of apoptosis, auto-stimulation of own growth, and a mass of cancerous cells tend to initiate the process of angiogenesis (Johnson, 2013). Cancer often commences with a single renegade cell, that expands to form a tumor. In such cells, there is activation of oncogenes and deactivation of tumor suppressor genes. However, the author has made it clear that cancer stem cells are the only cancerous cells with ability to metastasize and seed a different malignancy in another organ, site, or tissue. The author envisions a time in which there will be holistic treatment of cancer. In this knowledge and strategies developed in disciplines such as genetics, immunology, biochemistry, histopathology, cell biology, and pharmacology ought to be integrated in developing new novel therapies for cancer. One such strategy is utilization of stem cells to replace cancerous cells (Johnson, 2013). Apart from accumulation of mutations, cancer may develop from other strategies including collaboration of normal cells and cancerous cells since normal cells participate in synthesis of proteins utilized by cancerous cells. Genetic alterations that contribute to development of cancer need not to be alterations in deoxyribonucleic acid (DNA) but cancer my develop due to faulty binding of molecular tags such as addition of methyl groups. Some alterations in cells can lead to altered cell function without actual alterations in DNA. Disturbances in a cell caused by stress, diet and/or carcinogens may lead to epigenetic tag alterations. One of the major epigenetic tag is the methyl group. Methylation process is regarded as important since it keeps an oncogene from dividing in an uncontrolled manner. An oncogene stimulates cellular division. When regulatory mechanism is lost, then a cell may divide uncontrollably resulting in copying errors (Johnson, 2013).

            The content in Johnson’s (2013) article relates or is relevant to the course content learnt in class. In class, I learnt that cells in tissues that often regenerate also have the capability of transforming into cancerous cells; especially if DNA copying errors occur during regeneration process. Likewise, Johnson (2013) state that cancerous cells may develop from normal dividing cells if copying errors in the genetic material occur. Similarly, exposure of carcinogens was mentioned class as well as in the article as the major aetiologic factors for cancer. Mitosis was mentioned as the process in which cells divide into identical daughter cells. Similarly, a cancerous cell multiplies via the process of mitosis to develop into a tumor. A single cancerous cell is referred to as a clone since it multiplies into numerous similar cells with the same genetic aberrations (Johnson, 2013). In the course content, I learnt that a normal dividing cell usually divides in a regulated and controlled manner but Johnson (2013), describes a cancerous cell as capable of dividing uncontrollably since it has lost regulatory mechanism or simply cannot respond to regulatory mechanism found in a normal functional cell. Cell division process requires growth of the cell in which there is duplication of macromolecules and organelles and replication of DNA followed by division of DNA via the process of mitosis. Finally, both normal and cancerous cells then divide into two daughter cells through the process known as cytokinesis. In a normal cell cycle is regulated and there are times in which the cell division is inhibited; however, Johnson (2013) describes cancerous cells as dividing in a continuous manner. Thus, cancerous cell always have an active cell cycle.

The article is simple to read even to the lay persons. The article captures the attention of the reader and it is structured in a way that there is a systematic train of thought. Building from the body of knowledge the author has openly provided his opinion concerning the topic. Despite having drawn knowledge and information from published sources of evidence it does feel that the depth of knowledge is shallow since the author has only used two sources of evidence. By drawing evidence from broad and multiple sources the author could have increased the level of acceptability, credibility, quality, reliability and generalizability of findings. Besides, use of multiple sources could have helped the author to identify other non-DNA alteration causes of cancer and tumors. On the other hand, important to note that author used latest sources of evidence relative to publication year of Johnson’s (2013) article. I do find it surprising in Johnson’s (2013) article, is that cellular alterations that contribute to cancer development need to be alteration of DNA. In other words, mutations are not the only explanation about the cause and nature of cancer (Johnson, 2013). I used to think that cancer arises only when there are changes in the DNA material of a cell. There are some issues that I differ with the author. For example, Johnson (2013), describes introns placed in genetic codes are errors of evolution but I do personally belief that introns have important function in the genome. In my prediction, they serve to increase the length of DNA strand and thus reduced risk of mutations from occurring on coding genes since mutations may occur on intron portions. Another issue is that cancerous cells can be passed to the next generation, which is not completely true since only mutated DNA strands in gametocytes are actually the only ones that can be passed to the next generation as far as human biology is concerned.  There are some questions that I would like to ask is does alterations in epigenetic tags occur in normal cells? Besides, I should ask on whether deviation in epigenetic tag binding can occur without changes in DNA sequence? Am also eager to know whether new medication or drugs for treatment or prevention of cancer can be developed to target alteration in binding of epigenetic tags?