Cancer, carcinogenesis and oncogenes

Running head: CANCER: CARCINOGENESIS AND ONCOGENES 1
Cancer: Carcinogenesis and Oncogenes
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Running head: CANCER: CARCINOGENESIS AND ONCOGENES 2
Cancer: Carcinogenesis and Oncogenes
Introduction
Cancer is the uncontrolled growth of abnormal cells in the body. The cancerous cells can also be
called malignant cells. Normal cells have growth-control genes which regulate their rate of
proliferation. These genes are known as tumor suppressor genes. Malignant cells lack these tumor-
suppressor genes. Subsequently, they multiply endlessly leading to the formation of tumors. There
are several differences between normal and malignant cells as expressed in the table below.
Characteristic
Normal cells
Malignant cells
1.
Appearance
The cells are generally of the
same size, have a moderately
dark nucleus and only
specific number of
chromosomes.
The cells have extremely variable sizes,
have an extremely dark nucleus due to
the excess DNA. They also have an
abnormal number of chromosomes
which are disorganized within the cell.
2.
Growth
These cells stop growing at
some point when the number
of cells required is at
maximum.
These cells never stop growing even
after sufficient number of cells have
been formed. This results in formation
of tumors.
3.
Communication
These cells respond to
signals by neighboring cells
to terminate their
proliferation process.
They do not respond to signals to end
their reproduction. Instead, they
continue proliferating.
Running head: CANCER: CARCINOGENESIS AND ONCOGENES 3
4.
Cell repair and
apoptosis
These cells undergo cell
repair and cell death process
within their lifespan
Malignant cells do not undergo any of
these processes.
5.
Stickiness
Normal cells produce some
secretions to make them stick
to one another hence
facilitating localized growth.
Cancerous cells lack these secretions
hence they do not stick to each other.
Consequently, they can move from one
place to another freely.
6.
Ability to
spread
Owing to their adhesive
character, they do not move
from one body part to
another.
They move from one place to another
through metastasis. This can be through
the lymphatic system, circulation
system or merely floating away to new
locations.
7.
Maturation
They reach maturation at one
point of their growth cycle.
They are undifferentiated cells
(immature). This is because they
proliferate rapidly even before complete
maturation.
8.
Evasion of the
immune system
Normal cells become
destroyed by lymphocytes
once they get damaged.
Cancerous evade the action of white
blood cells by secreting protein
complexes to inactivate the
lymphocytes.
9.
Blood supply
Normal cells undergo
angiogenesis to acquire
Malignant cells undergo angiogenesis
even when it is irrelevant ie when they
ought to stop their proliferation process.
Running head: CANCER: CARCINOGENESIS AND ONCOGENES 4
nutrients for their growth and
proliferation
10.
Energy source
Normal cells obtain their
energy from Kreb’s cycle
and glycolysis. Their
produce their energy in the
presence of oxygen.
Cancerous cells produce most of their
energy in the absence of oxygen.
("Difference between Cancer Cells and Normal Cells | Difference Between," n.d.)
The check points for a normal cell to qualify to be a cancerous cell are:
a) The cell ought to have growth factors that prompt it to continue proliferating even when it
should stop.
b) The cell should have the ability to evade proteins that code for apoptosis to avoid cell death
when the abnormal growth commences.
c) The cell needs to neglect/ avoid the signals of neighboring cells to stop proliferating.
d) The normal cells also need to shed off their adhesive feature so that they can move from
place to place within the body.
Carcinogenesis
Carcinogenesis is the process of the formation of cancerous cells, their development and eventual
spreading out. It occurs in stages which can be studied in two distinct models (Roberts, 2010,
p. 12)
a) TNM staging system
b) Number staging system
Running head: CANCER: CARCINOGENESIS AND ONCOGENES 5
TNM staging system
TNM stands for Tumor, Node, Metastasis staging system. It describes the initial tumor, whether
the cancer cells have spread to the lymph node, and if it has spread to other body parts. The system
also integrates numbers in a specific manner (Tonissen, 2013, p. 38).
T refers to the size of the primary tumor. It can be ranked from T1 to T2.
N refers to whether the cancer has gotten to the lymph nodes. It can be ranked from N0 to
N3.
M refers to whether the cancer has reached other body parts. It can either be M0 or M1.
Examples of these include:
T2N1M0- The cancer has spread to the lymph nodes but not ye to other body parts
T4N3M1- This is symbolic of advanced cancer.
Sometimes letters ‘a’, ‘b’, and ‘c’ can be used to sub divide the categories further. Letter ‘p’ can
also be used before TNM to indicate that these are pathological findings. When letter ‘c’ is used
before TNM, it indicates that those are clinical findings ("Experimental Carcinogenesis," n.d.,
p. 34).
Number Staging System
Conceptually, carcinogenesis can be divided into four stages (Roberts, 2010, p. 16). These are:
a) Initiation
b) Promotion
c) Progression
d) Metastasis
Running head: CANCER: CARCINOGENESIS AND ONCOGENES 6
Initiation
This stage involves the alteration of proto-oncogenes by carcinogens. It can be either spontaneous
or induced. The DNA methylation of promoter gene regions can transcriptionally repress the tumor
suppressor genes. The mutation of the DNA synthesis process due to chemical carcinogens
eventually leads to proliferation of the cells. These cells tend to have a lifespan equal to that of the
organism. Basically, the DNA adduct formation which activates proto-oncogenes and conversely
inactivates tumor suppressor genes is the tumor-initiating event.
Tumor Promotion
This stage is considered to be the longest phase but is reversible. As the rate of proliferation
increases, the probability of the conversion of cells to malignant cells increases. The tumor
promoter can either reduce the rate of malignant conversion or on the other hand speed up the
process Tumor promoters are fundamentally known to be both mutagenic and carcinogenic hence
they can perform both tasks. Carcinogens which display both tumor initiation and promotion
qualities are known to be complete carcinogens. A good example is 4-aminobiphenyl
("Experimental Carcinogenesis," n.d., p. 37).
Malignant conversion and Tumor Progression
This is the stage in which preneoplastic cells are converted to cancerous cells. This only occurs as
a result of further genetic mutation on the cell. It is crucial to note that the level of tumor promoters
must remain constant or increase for this to happen. If not so, the cells form benign lesion (non-
cancerous swellings). The preneoplastic cells are converted to malignant cells which invade the
cellular territories of neighboring cells and tissues.
Running head: CANCER: CARCINOGENESIS AND ONCOGENES 7
Metastasis
In this phase, the cancerous cells move from one point to another point of the body. This can be
through the circulatory system, lymphatic system, and/or simply floating away from one point to
another.
Oncogenes
These are cancer causing genes which result from the mutation in proto-oncogenes. They work
against the tumor suppressor genes by promoting the uncontrollable proliferation of cells. The
form of mutations involved are gain-of-function mutations which increase the expression of the
normal cells(Benz, C.C, Liu, & E.T, 2011, p. 26) . Subsequently, only one copy of the gene needs
to be mutated to initiate cancer.
There are numerous types of oncogenes. These include:
a) HER2/neu
b) Ras
c) Myc
d) Cyclin D
e) hTERT
f) Src
Myc oncogene
This gene is primarily found in the nucleus of a cell. It serves as a signal for cell proliferation after
a series of mechanisms. It acts as a transcriptional factor for the cyclin D gene ("Examples of
Oncogenes and How Mutations Can Lead to the Development of Cancer," n.d.). Excess amounts
of Myc genes can make the cells to multiply uncontrollably. Myc genes can also be activated via
Running head: CANCER: CARCINOGENESIS AND ONCOGENES 8
chromosomal re-arrangement. This is when a strong promoter sequence is located inappropriately
next to the myc protein coding sequence. This in turn leads to production of vast amounts of the
Myc mRNA. Mutant B cells are known to produce excess amounts of Myc proteins. This makes
them proliferate rapidly and form tumors.
Running head: CANCER: CARCINOGENESIS AND ONCOGENES 9
References
Benz, C.C, Liu, & E.T. (2011). Oncogenes. Springer Verlag.
The Difference between Cancer Cells and Normal Cells | Difference Between. (n.d.).
Retrieved August 26, 2017, from http://www.differencebetween.net/science/health/the-
difference-between-cancer-cells-and-normal-cells/
Examples of Oncogenes and How Mutations Can Lead to the Development of Cancer. (n.d.).
Retrieved August 26, 2017, from
http://www.brighthub.com/science/genetics/articles/76140.aspx
Experimental Carcinogenesis. (n.d.). Encyclopedia of Cancer, 1078-1078. doi:10.1007/978-3-
540-47648-1_2061
Roberts, R. (Ed.). (2010). Carcinogenesis. Amsterdam: Elsevier.
Tonissen, K. (2013). Carcinogenesis. Rijeka, Croatia: InTech.

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