Solution:

Hallmarks of Cancer

Introduction

Research indicates that the genotype of the cancer cells is manifested in eight fundamental changes of the cellular physiology. That is; the hallmarks of cancer and the hallmark of the cancer- the next generation (Sitaramayya, 2010). This includes incentives to antigrowth signals, self-sufficiency in growth signals, reduces the replicative potential, and the avading apoptosis, sustained angiogenesis avoiding immune destruction, tissue invasion, and metastasis as well as the reprogramming energy metabolism.

The above physiologic changes have the abilities to acquire the violation of an anti-cancer defense mechanism during the tumor progression that is wired in normal tissue and cells (Tu, s.-m, 2010).

The acquisition of these traits is enabled by two characters which includes the inflammation of malignant lesions and pre-malignant as well as the development of genomic instability cancer cells (Karp, 2010).

Self-Sufficiency in Growth Signals

In order to normal cell to switch from quiescence to a proliferative, a cell requires to have mitogenic growth signals. On the other hand, the cancer cell reduced dependence upon the exogenous growth stimulation (Ibarra, Kari & Kopecki, 2014). Therefore, the cancer cell generates many of their own growth signals that disrupt the homeostatic mechanism needed for operation to ensure there is normal behavior of the various cells types within the tissue. In addition, the cancer cells can switch the extracellular matrix receptors that they express and favor those transmitting pro-growth signals.

Insensitivity to Antigrowth Signals

The normal tissues have multiple anti-proliferative signals that enable in maintaining cellular quiescence as well as maintaining the tissues homeostasis. The two signals can block the proliferation by forcing the cell to change from proliferative stage to the quiescent state (Seyfried, 2012). The signals can also be blocked by being induced and move from permanently to a proliferation potential. Therefore, if these pre-cancerous cells should avoid the signals in order to survive.

Evading Apoptosis

Cellular membrane is damaged during the apoptosis process while the cytosols are extruded, and the chromosomes are degraded and the cytosols extruded. The nearby cells engulf the dead cell, and they all vanish.

The different stages of human carcinogenesis indicate that cancer cells can resist against apoptosis in different ways (Hejmadi, 2010). In returns, this causes the withdrawal of important components of the DNA damage sensor that induces the apoptosis.

Limitless Replicative Potential

When the cells carry an intrinsic program, it is possible for such cells to limit their multiplication (Halperin, Perez & Brady, 2008). Usually, in the process of the different numbers of division, the cell stops growing and enter into a senescence state, and many cancer cell becomes immortalized.

The number of cells generation can be done by counting the end of telomeres or chromosomes. For example, at the end of the cellular cycle, there is usually a loss of fifty to hundred bp of the telomeric DNA. On the other hand, most of the cancers maintain telomeres by regulating the teleomerase enzymes or by inter-chromosomal exchange of cycle information (Sarakāra & Fisher, 2013).

Sustained Angiogenesis

The nutrients and the oxygen produced by the vasculature enable the survival of the cells. This assists in the coordination of both parenchyma and vasculature growth, and thus the angiogenesis can be regulated every minute (Dark, 2013).

Tissue Invasion and Metastasis

In the cancer progression, the primary tumor releases the pioneer cells that fight the nearby tissues. The space and nutrients continue to generate and based on the new settlement, as a result; there develop a metastasis which cause almost eighty percent of the human cancer deaths. The metastasis arises as a mixture of cells, and the normal supporting cells are overthrown by the host tissue (Sitaramayya, 2010).

Reprogramming Energy Metabolism

The normal cell process glucose under erobic conditions by glycolysis in the cytoso, and thereafter to CO2 in the mitochondria. Under anaerobic conditions, the glycolysis is favored, and there is relatively small pyruvate that is distributed to the oxygen-consuming mitochondria. Even during the presence of oxygen, the cancer cells reprogram their glucose metabolism to promote glycosis through up-regulating glucose transporter (Ibarra, Kari & Kopecki, 2014).

Avoiding Immune Destruction

Immunogenic cancers cells and the immune ecompetent subjects can be eliminated and leave the weak variant that can colonize both immune competent host and immune-deficient hosts (Seyfried, 2012). Likewise, these types of cell multiply in immune deficient subjects and ensure that the immune system does not eliminate them.

Tumor-Promoting Inflammation

The inflammatory cells can release chemicals that are active for mutagenic to the nearby cells. The inflammatory cells accelerate genetic evolution towards malignancy (Seyfried, 2012).

Genome Instability and Mutation

The acquisition of the hallmark capability usually depends on how the alterations in cancer cell genomes proceeds. The mutant genotypes have various advantages to the sub-clonal cells and hence leading to their dominance in the local tissue environment (Ibarra, Kari & Kopecki, 2014).

INDUCING ANGIOGENESIS

A good example of extrinsic NOA is by solidifying the tumor in order to recruit new blood vessel by use of secretion of angiogenic factors (Dannenberg, 2003). The tumor angiogenesis enables the cells in the interior of the tumor to get enough nutrients and oxygen that helps them to survive. Therefore, the tumor angiogenesis are blocked and hence reducing tumor growth. Early experiment that used mouse xenografts indicated that the antibody –mediated inhibited the vascular endothelial cells, as well as the sprouting of vessels. This could severely constrain the growth of the tumor and the angiogenesis. The study led to the innovation of the anti-VEGF antibody bevacizumab that was used for therapeutic.  The sorafenib and sunitinib are small molecule inhabitors that target multiple receptor tyrosine kinases and have show great potential or efficiency of treating metastatic renal cell carcinoma (Mousa, 2004).

One of the methods used to inducing angiogenesis is the cryosurgery method.

Cryosurgery

This is a technique that is used to freezing and destroying abnormal cells in our bodies. This is done by producing an extreme cold argon gas or liquid nitrogen. The method is also used to cure cancers that are precancerous or noncancerous conditions (Oldham & Dillman, 2009). The method can be applied in the body or on a skin by use of an instrument known as “cryoprobe” that is guided by ultrasound or MRI. It is then placed on the tumor. After the cryosurgery process, the frozen tissue melts and it either dissolves or forms a scab or it may as well be absorbed by the body (Oldham & Dillman, 2009).

References

Dannenberg, A. J. (2003). Cox-2: a new target for cancer prevention and treatment; 20 tables. Basel, Karger.

Dark, G. G. (2013). Oncology at a Glance. Hoboken, Wiley.

Halperin, E. C., PEREZ, C. A., & BRADY, L. W. (2008). Perez and Brady’s principles and practice of radiation oncology. Philadelphia, Wolters Kluwer Health/Lippincott Williams & Wilkins.

Hejmadi, M. (2010). Introduction to cancer biology. Frederiksberg, Denmark, BoonBooks.com.

Ibarra, O. H., Kari, L., & Kopecki, S. (2014). Unconventional Computation and Natural Computation 13th International Conference, UCNC 2014, London, ON, Canada, July 14-18, 2014, Proceedings. Cham, Springer.

Karp, G. (2010). Cell and molecular biology: concepts and experiments. Hoboken, NJ, John Wiley.

Mousa, S. A. (2004). Anticoagulants, antiplatelets, and thrombolytics. Totowa, N.J., Humana Press.

Oldham, R. K., & dillman, R. O. (2009). Principles of cancer biotherapy. Dordrecht, Springer.

Sarakāra, D., & Fisher, P. B. (2013). AEG-1/MTDH/lyric-implicated in multiple human cancers.

Seyfried, T. N. (2012). Cancer as a metabolic disease on the origin, management, and prevention of cancer. Hoboken, John Wiley & Sons.

Sitaramayya, A (2010). Signal transduction: pathways, mechanisms, and diseases. Heidelberg, Springer

Tu, s.-m. (2010). Origin of cancers: clinical perspectives and implications of a stem-cell theory of cancer. New York, Springer