Some countries have more cancer cases and some have less, some have one type of cancer, some have another. There are various types of cancers, each with its own special properties, the race it effects, the age, the sex and the different part of the body.

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Mihajlo (Michael) Najdovski 2107931E

Cancer

Michael Najdovski 2107931E

RMIT University

Department of Applied Biotechnology & Environmental Biology

ONPS 1031 Molecular Biology


Contents

Abstract        

Introduction        

Properties of Cancer        

Diagnosis        

Treatment        

Prevention        

Summary        

References        


Abstract

Cancer is a major contributor to deaths around the world.  Some countries have more cancer cases and some have less, some have one type of cancer, some have another.  There are various types of cancers, each with its own special properties, the race it effects, the age, the sex and the different part of the body.  

Introduction

Cancer is a progressive disease and as such it will be fatal if it is not treated effectively.  Cancer (in most cases) arises from a single cell.  All cancer cells have mutations or changes affecting one or more oncogenes in the cells.  These mutations or changes are usually caused by a foreign source such as cigarette smoke or sunlight.  Because of these mutations some genes may not function properly.  Normal cells replicate and eventually die so space is preserved and life goes on.  With cancer cells, due to mutations somewhere along the genes, after their time of working and replicating, they do not die, they continue replicating and grow over each other and form a tumour.  This continues to grow and eventually interferes with the normal function of vital organs in the body.  This will eventually cause death.  Treatment is usually by surgical removal of the cancer cells and/or different types of drugs.  Complications may also arise here.  Prevention is the best way to go about it but it may be harder than it sounds.

This papers aim is to inform about cancer, diagnosis, treatment and prevention in a short overview.

Properties of Cancer

Normal cells have a routine life.  For example the normal cells of the gut, first divide to form two daughter cells, one like the parent cell (still capable of cell division), and the other cell matures to complete a function, no capability of division and a fixed life span.  When its life span is up, it will die and the other cell will just multiply again and the cycle continues and the gut remains the same size because there is a certain number of cells in the gut.  With cancer cells, more of them have the parental type characteristics and so the cells can divide in greater numbers so the gut grows with the overflow of cells and becomes cancerous and ceases to function properly after a while.

Normal cells also need outside information (growth factors) that tell them to divide.  In almost all cancers, the cells learn how to avoid these growth factors which tell them to divide and to stop so therefore they have nothing to say stop.  One way to avoid these growth factors is to produce your own.

Normal cells do not transform into cancer cells by a single change.  Cancer cells evolve into a tumour as a result of many sequential changes.  These changes take time, usually years to decades from when the patient was first exposed to the carcinogen until the patient starts showing symptoms.

The body can recognise abnormalities and has natural resistance systems against the cancer cells.  There are various types of systems, one being the natural killer (NK) cells.  They kill everything which is not normal.  But this does not work in later stages of cancer as the cancer is too big to control.  Also if the cancer exhibits surface antigens, the immune system will recognise it and try to destroy it.

Although many factors may contribute to cancer development, cancer is a genetic disease and is caused by genetic alterations in certain genes. Cancer development is associated with oncogene over expression and inactivation of tumour suppressor genes.  One of these genes is the p53 tumour suppressor gene.  It plays an important role in preventing cancer development, by killing potential tumour cells. Mutations within the p53 gene, leading to the loss of p53 activity, are found in about half of all human cancers, while many of the tumours that retain wild type p53 carry mutations in the pathways that allow full activation of p53.  In either case, the result is a defect in the ability to bring a p53 response in cells undergoing oncogenic stress. Significant advances have been made recently in our understanding of the molecular pathways through which p53 activity is regulated, bringing with them fresh possibilities for the design of cancer therapies based on reactivation of the p53 response(Vousden, KH. 2002). One of the causes of oncogene over expression is mutation in the regulatory regions or in the genes encoding transacting factors that have regulatory roles on oncogenes. However, the most noticeable genetic alteration causing oncogene over expression is gene amplification (Schwab, M. 1998).  In some cancers, accumulation of oncogene and tumour suppressor gene mutations appear to be critical to tumour development(Fearon ER. 1990)), which is the continued rapid replication of cancerous cells upon each other.  

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Once the mutations occur and replication leads to tumour growth, the cells may spread throughout the body.  The original cancer cell replicates and with the replication it passes on the mutations to every other cell that is a result of the initial replication.  This renders all the cells cancerous and unable to carry out normal functions such as termination.  This means all these cells can become a tumour.  Cancer cells do not adhere to each other very firmly and can penetrate the boundaries of adjacent tissues.  For this reason cancer cells tend to spread beyond their original position to the ...

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