Biology (Holt)

SECTION 2 The Cell Cycle 127

Cancer

Although all cancers are not curable, great
progress has been made in cancer research over
the last 30 years. We now know that cancer
results from damage to a small set of genes that,
in normal cells, limits the ability of cells to divide.
What causes this damage? Certain environmental
factors appear to be associated with cancer. For
example, the incidence of cancer per thousand
people is not uniform throughout the United
States. Rather, it is higher in cities and in the
Mississippi delta, suggesting that pollution and
pesticide runoff may contribute to cancer. When
pollutants, radiation, and other environmental fac-
tors associated with cancer are analyzed, a clear
pattern emerges. Most cancer-causing agents are
powerful mutagens—that is, they readily damage
DNA. The conclusion that cancer is caused by
mutation of a cell’s DNA is now supported by a
very large body of evidence.
How many mutations are required to produce
cancer? Research in the last several years indicates
that mutation of only a few genes can transform
normal cells into cancerous ones. All of these
cancer-causing genes are involved with regulating
how fast cells grow and divide. How is cell division
regulated? As a crude analogy, imagine a car
parked on the side of a road. To get it going, you
must step on the accelerator and release the brake.

Stepping on the Accelerator
A cell divides when it receives a signal to do so. A
“divide” signal is usually in the form of a chemical
substance released by another cell. The sub-
stance is bound by a protein on the surface of
the receiving cell. This binding activates a second
protein inside the cell—relaying the signal from
the outside of the cell to the inside. Here, a family
of proteins then relay the signal inward to the

nucleus. One protein mol-

ecule passes the signal to

the next like a baton in a

relay race. The genes for

these signal-carrying

proteins are called onco-

genes(oncois Greek for

“mass” or “tumor.”). If

oncogenes are changed

by mutation to become

more active, cancer can

result. Like stepping on

the accelerator of a car,

an increase in the activity

of these proteins amplifies the “divide” signal.

This causes the cell to divide more often.

Releasing the Brakes

At the nucleus, the divide signal overrides a

set of genes that act as “brakes.” These braking

genes—called tumor supressor genes—prevent cell

division from occurring too often. In cancer, these

tumor suppressor genes are damaged. Like remov-

ing pressure from the brakes of a car increases a

car’s speed, decreasing the activity of tumor sup-

pressors speeds up cell division.

Cells have three kinds of tumor suppressors, all of

which must be disabled before cancer can occur.

First, cells have proteins that inhibit DNA replication

for limited periods. In cancer cells they are

permanently inactivated. Second, cells have error-

correcting proteins that detect damage to genes.

In most cancers this error-detection has been

disabled. Third, cancer cells rebuild the tips of

their chromosomes. A little is lost from the ends

of chromosomes at

each replication, lim-

iting the number of

times a normal cell

can divide. Adding

the deleted material

back to the tips

removes this limit to

a cell’s life span.

Exploring FurtherFurther

Section 2 Review

Differentiatebetween the G 1 , G 2 , and S phases

of the eukaryotic cell cycle.

Relatewhat occurs at each of the three principal

checkpoints in the cell cycle.

Critical ThinkingEvaluating Information

Why are individual chromosomes more difficult

to see during interphase than during mitosis?

In the cell cyle of typical

cancer cells, mutations have caused

Aslower growth. Cuncontrolled growth.

Ba failure in mitosis. Da halt in cell division.

TAKS Test PrepTAKS Test Prep

4B 6C

4B 6E

Melanoma cells

http://www.scilinks.org

Topic: Cancer Cells

Keyword: HX4030

4B 6E

4B 6E