Cancer is an abnormal signal transduction resulting in uncontrolled cell proliferation, loss of apoptosis or programmed cell death, tissue invasion and metastasis permitting spread of the cancer and angiogenesis leading to enhanced blood supply of tumors. Tumors can be Benign or Malignant. Benign tumors are slow growing whereas cancers are malignant tumors that can spread beyond of the limit of the original organ. Cancers starts from the damage in the DNA of the cell, this damage is called mutation. Mutation happens when the cell duplicates its DNA prior to cell division and makes mistakes. Usually one mutation is not enough to cause cancer, as it makes cell cycle less reliable, many damage of DNA or mutations would go unnoticed. Cancer is usually the result of accumulation of many mutations of genes involved in the cell cycle control and DNA repair. This commonly happens over a long period of time, over many rounds of cell divisions and this explains why cancers are more common in older people, this is because they are born with a mutation that makes them more likely to develop a cancer.
According to (Leitner, 2012) DNA replication is started at separate places called replication origins, where couples of replication forks starts to duplicate DNA bidirectionally outward from the origin places until the merge with another fork. Each daughter cell is produced during cell division, which contains an identical copy of the genetic material. Moreover, The replication is semiconservative and that occurs in an intermittent manner, which work with purified enzymes of the polymerization reaction, which helps to replicate DNA faithfully and promptly. It also helps to lead for the expansion of several in vitro systems and finally to the reconstitution since purified components of complexes is capable of limited replication. As we know, a short length of a DNA double helix has the nucleotide sequence where, the two strands of DNA are untwisted and aparted from each other to form two single chains where each base in the single strands are attached to itself. Furthermore, the complementary deoxyribose nucleotides by the same hydrogen bonding are intact with DNA double helix. Ultimately, when these devoted mononucleotides are polymerized to form a polynucleotide chain it results with configuration of two complete DNA double helices, which are identical with one another and with the prototype molecule. During the replication one strand of each daughter molecule are originated from the unique DNA molecule while the other will result in new synthesis, this method is explained as semiconservative to differentiate it from other achievable mechanisms. Furthermore, in the conservative mechanism the two strands of DNA are not aparted but perform jointly as a template to form totally novel double helical molecule; in this circumstance one daughter molecule would be completely new and the other totally result to the parent. During the process of dispersive mechanism the parental molecule are partly tainted and the fragments are combined into two new daughter double helices. In addition, figure 1.0 shows DNA replication, which occurs over one short section at a time where two parental strands split only at the socket of replication to create a Y, shaped molecule as the replication fork permits lengthways to DNA. Likewise, the two DNA chains are antiparallel, where on runs in 5′ – 3′ direction and other runs in 3′ – 5′ direction, whereas, the sum of four columns shows equivalence of A – T and G – C.
During the process of replication, if the DNA does not merge with another fork while duplicating, then it cause defects in DNA replication sequence which can slow or stop the replication process. Such fork stands can activate native and global barriers, which can interrupt replication. Moreover, in embryonic cells, such intervals may cause cell death, meanwhile, replication may be decoupled from cell division, while in mature (somatic) cells, and DNA damage paly vital role in the development of cancer.( Ghadimi, Ried, & SpringerLink, 2015)
1.3 DIFFERENCES BETWEEN NORMAL CELLS AND CANCER CELLS
Awasthi, K., Moriya, D., Nakabayashi, T., Li, L., & Ohta, N. (2016).
v Normal cells carry characteristics that are essential for normal body function.
v Abnormal or mutant cells are cancer cells.
v Normal cells have uniform shapes and sizes.
v Cancer cells have a large variety of shapes and sizes.
v In a controlled manner normal cells grow and divides.
v It does not stop growing resulting to appear as a tumor (a cluster of mutant cells).
v It under go process of apoptosis (self destruction) if they detect abnormalities and damage in their organelles.
v There is no process of self destruction in cancer cells
v Normal cells start out as immature cells and mature with certain specialized functions.
v Cancer cells do not mature instead become immature over time.
v It recognizes signals and they know when they are enough new cells and stops dividing.
v Cancer cells do not recognize signals; hence these cells erratically reproduce mutated cells.
There is not just one cause but multiple unknown causes which lead to cancer. From the Physiological stand point anything that gets inside the cell that could disrupt the replication cycle, which may cause cancer. Through figure 1.3 and 1.4 we can clearly see that, Age, smoking, Obesity, drinking, poor diet, Physical inactivity and many other common factor causes cancer. Cancer can also replicate through infection where viruses carry their own genetic information and transfers to alternating cells, which initiate genes cell to become active, and result as a tumor. (Woloshin, S., Schwartz, L. M., & Welch, 2008)
The main objectives of cancer diagnosis and treatment are to cure the life of patients and to ensure the possible excellence of life for cancer survivors. The most effective treatment for cancers are: To provide an reasonable and sustainable way, Early detection and accurate staging and diagnosis, To provide an evidence-based on standards of care (WHO, 2017). Some people who are diagnosed with cancer will have only one treatment. However, many people have a combination of various treatments, such as surgery, chemotherapy, radiation therapy, immunotherapy, targeted therapy, or hormone therapy (National cancer Institute,2015).
Part B: Commonly diagnosed cancers in Australia
According to the researched data of Baade, P. D., Fritschi, L., & Eakin, E. G. (2006), the cancer cohort had a considerably high risk of mortality from rather than other various diseases.
The risks of non-cancer mortality are higher in patients with colorectal cancer approximately 40% than the general population. Comparing to the general population, patients with colorectal cancer have over twice the risk of dying from than other diseases.
Overall, the rates of non-cancer mortality among men with prostate cancer are diagnosed 30% higher than other non-cancer male general population.
The rates of non-cancer mortality of women who are diagnosed with breast cancer were not meaningfully different to that of general female population. There were no causes of non-cancer death where, the risk of patients dying with breast cancer is greater than the general population.
Furthermore, non-cancer mortality rate between women diagnosed with cervical cancer is 50% higher than that of the general population. Meanwhile, the diagnosed numbers of cervical cancer were much fewer than other cancers whereas, the ability to detect significant differences between the causes of non-cancer death was limited.
The highest comparable risk of dying from non-cancer causes of death than the other cancers considered in this study were lung cancer.
In a nutshell, mitosis and cancer are related where cancer is caused by DNA mutation also; apoptosis or programmed cell death plays a vital role in understanding of cancer. Cancer cells can spread throughout the body so; it should be prevented or diagnosed early.