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Transcript
FREE
ST U DY
BOOKS
INTRODUCTION TO
CANCER BIOLOGY
MOMNA HEJMADI
FREE STUDY BOOKS
WWW.BOOKBOON.COM
1
Momna Hejmadi
Introduction to Cancer Biology
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Introduction to Cancer Biology
© 2009 Momna Hejmadi & Ventus Publishing ApS
ISBN 978-87-7681-478-6
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Introduction to Cancer Biology
Contents
Contents
How cancer arises
6
1.1
Defining cancer
6
1.2
Cancer is clonal in origin
6
1.3
Insights into cancer
8
1.4
Causes of cancer (Aetiology of cancer)
8
1.4.1
Lifestyle and Environment
8
1.4.2
Age
10
1.5
Identification and histopathology of cancers
11
1.6
The 6 hallmarks of cancer
11
2.
Immortality: Continuous cell division
13
3.
Sustained growth signals (oncogenes*)
17
4.
Bypass anti-growth signals (tumour suppressor genes*)
24
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Introduction to Cancer Biology
Contents
5.
Avoidance of cell death (apoptosis)
28
5.1
When does apoptosis occur?
28
5.2
What triggers apoptosis?
28
5.3
How does apoptosis occur?
29
6.
Ensuring blood vessel growth (angiogenesis)
33
7.
Spread to other sites (metastasis)
36
7.1.
What are the stages of metastasis?
36
7.2.
Key molecules involved in metastasis
38
8.
Summary
40
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Introduction to Cancer Biology
How cancer arises
1. How cancer arises
1.1 Defining cancer
Cancer can be defined as a disease in which a group of abnormal cells grow uncontrollably by
disregarding the normal rules of cell division. Normal cells are constantly subject to signals that dictate
whether the cell should divide, differentiate into another cell or die. Cancer cells develop a degree of
autonomy from these signals, resulting in uncontrolled growth and proliferation. If this proliferation is
allowed to continue and spread, it can be fatal. In fact, almost 90% of cancer-related deaths are due to
tumour spreading – a process called metastasis.
The foundation of modern cancer biology rests on a simple principle - virtually all mammalian cells share
similar molecular networks that control cell proliferation, differentiation and cell death. The prevailing
theory, which underpins research into the genesis and treatment of cancer, is that normal cells are
transformed into cancers as a result of changes in these networks at the molecular, biochemical and
cellular level, and for each cell there is a finite number of ways this disruption can occur.
Phenomenal advances in cancer research in the past 50 years have given us an insight into how cancer
cells develop this autonomy. We now define cancer as a disease that involves changes or mutations in the
cell genome. These changes (DNA mutations) produce proteins that disrupt the delicate cellular balance
between cell division and quiescence, resulting in cells that keep dividing to form cancers.
1.2 Cancer is clonal in origin
Current dogma states that cancer is a multi-gene, multi-step disease originating from a single abnormal
cell (clonal origin) with an altered DNA sequence (mutation). Uncontrolled proliferation of these
abnormal cells is followed by a second mutation leading to the mildly aberrant stage. Successive rounds of
mutation and selective expansion of these cells (natural selection) results in the formation of a tumour
mass (FIG 1.1 a & b).
Figure 1.1 a: Clonal expansion. Cancer is a multi-gene,
multi-step disease originating from single abnormal cell
(clonal origin). Changes in DNA sequences result in the
cell progressing slowly to the mildly aberrant stage.
Successive rounds of mutation & natural selection leads
to a mass of abnormal cells called tumours. Some cells in
the tumour undergo further rounds of mutations leading
to the formation of malignant cells which cause
metastasis.
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6