Neoplastic Diseases: A Genetic Analysis

Cancer is a disease caused by an uncontrolled division of abnormal cells. The DNA sequence in cells can be changed as a result of copying errors during replication. If these changes whatever their cause are left uncorrected, both growing and non-growing somatic cells might gain many mutations that they could no longer function. The relevance of DNA damage and repair to the generation of cancer was obvious when it was recognized that everything that causes cancer also cause a change in the DNA sequence. Tumor suppressor genes are protective genes and normally they limit cell growth by monitoring the speed of cell division, repair mismatched DNA and control when a cell dies. When a tumor suppressor gene is mutated cells grow

Cell replication and division is vital for growth and development. The mechanisms associated with replication of DNA are very precise. However, there can be errors at times and when these errors occur there could be problems in reproduction process. Some of these errors can cause uncontrolled cell growth causing tumor formation. There are genes within the human genome that prevent this uncontrolled growth from occurring. These genes are known as tumor suppression genes. They work in a very specific way and are vital for proper growth. Though they fix errors, the tumor suppression genes can malfunction or be malformed at times as well. When these errors occur, there can be serious consequences.

Cell abnormalities come about through mutations arising in the genomic sequences. The defining abnormalities of cancer cells are organized into eight distinguishing ‘hallmarks,’ as outlined in Hanahan and Weinberg’s paper, “Hallmarks of Cancer: The Next Generation.” The eight general characteristics of cancer cells are: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis (2). These characteristics ascend through mutations in the genetic makeup of a cell. Mutations can arise in various ways as previously discussed, such as environmental factors, heredity, and cell division rate. A single mutation can have a devastating effect on a cell’s function, and can potentially lead to the cell gaining a hallmark of cancer. Tomasettie and Vogelstein’s article, as mentioned above, provides supportive evidence for the hallmarks of cancer. The concept that more rapidly dividing cells leads to an increased rate of cancer risk lends well to the hallmarks of cancer. As cells divide they are at constant risk for potentially making an error in the genetic code, which could lead to a larger, more impactful mistake. As genetic errors accumulate through the process of cell replication, the hallmarks of cancer gain the opportunity to characterize within a tissue. Tissues that

In a typical cell, the progress of organised systems manage the pace and timing of cell development, division and death. Be that as it may, now and again, this cell cycle can go amiss. External components, for example, cancer-causing agents, toxins and UV beams, can harm the cells ' DNA, setting off the loss of the control system that direct when and how quick certain cells partition and die. Heredity can likewise have a part in a few varieties of malignancies, especially when joined with these outer triggers.

Tumor suppressor gene tells the when to die, repair the mistakes made in the DNA, and slow down cell division. If a tumor suppressor gene gets mutated the cells will grow out of control with nothing to stop them. The mutation can be caused when this gene isn’t activated. Two common example of a tumor suppressor are the p53 and NF1. Proto oncogenes codes for protein which helps with the cell cycle, prevents differentiation in cell, and programs cell death. If a proto oncogenes gets mutated there would be change in the protein sequence which would interfere normal cell regulations. The name of the proto oncogene was oncogene. DNA repair identifies incorrections and damages and fixes them. These three genes are mostly used to find cancer because

The overall analysis of this manuscript was indicating how a particular gene is connected to how tumors/cancer are suppressed and how tumors/cancer also grow and multiply. When the codon is manipulated and mutated, the point in which the codon becomes altered, or the point in which the p53 gene is stimulated, forms reactions that may be harmful or can be non-threatening. The reaction that could be harmful could generate destruction to the gene and therefore form cancer. A non-threatening reaction may cause a reconstruction in the mutation, which is beneficial.

A missing or defective p53 protein is usually the culprit in cancer, being that is in over 50% of cancers. The p53 gene codes for a protein that stops the growth as well as the development of tumors, as well as other functions. This is known as a tumor suppressor gene. If the gene is mutated, it allows damaged cells to survive and make tumors. The p53 gene can be mutated by cancer-causing substances in the environment. The p53 is responsible for proteins that fix damaged cells or cause damaged cells to die (apoptosis). It does this so the damaged cells do not pass on. The p53 gene prevents irregular cells from turning into tumors.

The regulation of cell growth and differentiation is critical to the survival of multicellular organisms. Typically cells growth is tightly regulated. Precursor cells will proliferate and differentiate into mature cell types. Upon differentiation to the terminal, mature cell type, cells would then enter into stasis, or quiescence. In quiescence cells stop dividing and perform their cellular function. Quiescent cells no longer grow or proliferate. If cells become damaged, are no longer useful, or for some other reason need to be eliminated cells will undergo a regulated cell death process called apoptosis. Neoplasia is the process of Inheritable changes in cell growth that have lost normal control processes. , at the cellular level, autonomous

Cancer, also known as a malignant tumor, is a disease in which some cells in the body multiply uncontrollably leading to a mass of abnormal cells (“What is Cancer”).This is the result of damage to the DNA (deoxyribonucleic acid) of a normal healthy cell which causes the natural biological function of the cell behavior to become altered (Mandal). Normal cell behavior is directed by the DNA which regulates the growth and death of the cell among other things (Mandal). When a normal cell’s DNA is damaged, the cell tries to repair the DNA and if it is unable to

These subpopulations area unit called sub clones. every of those increasing sub clones undergoes Darwinian evolution and natural action (Figure one.1), which means these clones bear positive choice once advantageous mutations arise and negative choice once hurtful mutations arise. The well positive mutations, called “driver mutations”, area unit the most actuation behind the expan- two Figure one.2: Example showing emergence and progression of cancer. sion of the clones. Alternative sorts of mutations, called “passenger mutations”, ride on the increasing clones however area unit assumed to be not below selective pressure. an easier pictorial read of initiation and progression of cancer is given in Figureone.2. in a very healthy tissue, mutations could arise in sure genes in one among the cells that end in that cell’s effort higher proliferative potential as compared to the healthy cells. This cell (as shown by D1 in Figure one.2) grows, divides quicker and quickly overpopulates the healthy cells within the tissue. As tumour cells generally acquire injury to the deoxyribonucleic acid replication system, that makes them at risk of additional mutations, alternative mutations could arise leading to another cell population (as shown by D2 cell sort within the

Historically cancer research has focused on finding “a cure” for what has been thought of as a single disease with rogue cells dividing madly, but research and technologies have exposed how complex cancers really are with intricate genetic differences demonstrating patients are much less alike than we once thought. Genetic and environmental facts have provided myriad different tumor types with unique biological pathways insights.

According to The National Cancer Institute, cancer is the name given to a collection of related diseases. In all types of cancer, some of the body’s cells begin to divide without stopping

In the view of biological evolution, the history of cancer is even longer than that of the human being, because before the appearance of human, there have been other animals and plants living in this planet, and the malignant tumor may just appear on any kinds of creatures. But the real beginning of cancer research only start

Osteosarcoma is a frequent primary malignant cancerous tumor of the skeleton characterized by the direct formation of immature bone or how it arises in the osteoid tissue in the bone (Picci). This type of bone cancer develops in the osteoblasts cells in normal bone. It begins in the bones but it can sometimes spread to other areas of the body including organs, such as lungs, and bones. Osteosarcoma unfolds in areas where the bone is growing fast because of the uncontrolled growth of the cells in the bone. “In fact Scientist have not discovered the causes of most cases of osteosarcoma” (Ryan). This is a

In cancer cells, the normal control systems that prevent cell overgrowth and invasion such as tumour suppressor and cell cycle check point genes are disabled, therefore; they no longer require special signals to induce cell growth and division. As these cells grow, they develop new acquired characteristics, including changes in cell structure, decreased cell adhesion, amplification or inactivation of specific genes, expression of tumor markers, alternation in tissue architecture, change in extra cellular matrix and production of new enzymes (Kumar and Weaver, 2009). Cancer cells can spread to other parts of the body through the blood and lymph systems