HUMAN BIOLOGY

428 Chapter 22

Cancer, a Genetic disease

it may be converted into an oncogene—a gene that

does not respond to the control signals that regulate

cell division.

By itself, an oncogene does not cause malignant cancer.

That usually requires mutations in several other genes (Fig-

ure 22.5). At least one of the altered genes is likely to be a

tumor suppressor gene. These are genes that can halt

abnormal cell growth and division, preventing cancers

from developing. They also may prevent oncogenes from

being expressed.

We now understand how

some tumor suppressor genes

operate. For example, the child-

hood eye cancer retinoblastoma

(left) is likely to develop when

a child has only one functional

copy of a tumor suppressor gene

on chromosome 13. The genes

associated with a predisposition to breast cancer, BRCA1 and

BRCA2, also are tumor suppressor genes. People who inherit

mutant forms of these genes are at high risk of developing

breast cancer.

Researchers know a lot about a tumor

suppressor gene called p53. This gene codes

for a regulatory protein that stops cell divi-

sion when cells are stressed or damaged.

When p53 mutates, the controls turn off.

Then an affected cell may begin runaway

division. Even worse, a mutated p53 g e n e’s

faulty protein may turn on an oncogene.

Half or more of cancers involve a mutated

or missing p53 gene.

Various factors can cause

mutations leading to cancer

inherited susceptibility to cancer

Heredity plays a major role in about 5 per-

cent of cancers, including cases of familial

breast cancer, lung cancer, and colorectal

cancer. If a mutation in a germ cell or

a gamete (sperm or egg) alters a proto-

oncogene or tumor suppressor gene, the

defect can be passed on from parent to

child. An affected person may be more

likely to develop cancer if later mutations

occur in other proto-oncogenes, in tumor

suppressor genes, or in genes that control

aspects of cell metabolism and responses

to hormones. Figure 22.6 diagrams the

steps toward a common type of colo -

rectal cancer.

Retinoblastoma

ISM/Phototake

n Cancer is a genetic disease that develops in a predictable

sequence of steps.

n Links to Cell-mediated immunity 9.7, Glucocorticoids 15.7,

Cell cycle 18.2, Radiation 18.5, Gene mutation 21.2

Cancer develops through a series

of steps in which gene mutation

removes normal controls over cell

division. The transformation of a

normal cell into a cancer cell is

called carcinogenesis.

Cancer usually involves several genes

As a rule, the beginning of can-

cer involves two main types of

genes. Proto-oncogenes (proto,

“before,” and onco, “mass”) are

genes in normal cells. They code for proteins that act

in cell division. If a mutation alters a proto-oncogene

or the way its protein-making instructions are read out,

22.2

Figure 22.5 Carcinogenesis occurs in steps as cells acquire mutations. Only two mutation
events may be enough to launch the development of some cancers. Three or more separate
mutations may underlie other malignancies, such as colon cancer (see Figure 22.6).

Cell division over time

Number of cells

First mutation

Second mutation

Uncontrolled

proliferation,

cancer formation

Controlled growth;

potential for cancer

formation with a

second mutation

Controlled growth,

no cancer

© Cengage Learning

carcinogenesis Transfor-

mation of a normal cell into

a cancer cell.

oncogene Gene that

doesn’t respond to control

signals for cell division.

proto-oncogene Normal

gene that codes for a pro-

tein that stimulates cell

division.

tumor suppressor

gene Gene that can halt

cell growth and division.

Copyright 2016 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s).