14.07.2022 Views

Essential Cell Biology 5th edition

You also want an ePaper? Increase the reach of your titles

YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.

722 CHAPTER 20 Cell Communities: Tissues, Stem Cells, and Cancer

1

2 3 4 5

1

2 3 4 5

6 7 8 9 10 11 12

6 7 8 9 10 11 12

13

14 15 16 17 18

13

14 15 16 17 18

19 20 21 22 X

19 20 21 22 X

(A)

(B)

Figure 20–44 Cancer cells often have highly abnormal chromosomes, reflecting genetic instability. Shown

here are karyotypes displaying the chromosomes of (A) a normal human cell and (B) a breast cancer cell. The

chromosomes are “painted” with a combination of fluorescent stains that give each chromosome a different

color. The breast cancer karyotype shows multiple translocations, including two instances of a translocation

ECB5 n20.102/20.47

of material from chromosome 6 (red) to chromosome 4 (light blue), one of which also includes a piece of

chromosome 1 (yellow). Whereas the normal cell contains 46 chromosomes, the breast cancer cell has 51; several

of its chromosomes are missing, and it has an extra copy of a handful of chromosomes—along with 6 copies of

chromosome 19. Such abnormalities in chromosome number can cause chromosome-segregation errors when the

cell divides, so that the degree of genetic disruption goes from bad to worse over time (see Table 20–1). (Courtesy

of Mira Grigorova and Paul Edwards.)

a mutation gives one

cell an advantage

normal

epithelial cells

growing on

basal lamina

precursor cell in the epithelial lining of the gut, for example, must undergo

changes that permit it to carry on dividing when it would normally stop

(see Figure 20–35). That cell and its progeny must also be able to avoid

cell death, displace their normal neighbors, and attract a blood supply

to nourish continued tumor growth (Movie 20.9). For the tumor cells to

then become invasive, they must be able to detach from the epithelial

sheet and digest their way through the basal lamina into the underlying

connective tissue. To spread to other organs and form metastases, they

must be able to get in, and then out, of blood or lymph vessels and settle,

survive, and proliferate in new sites (see Figure 20–42).

a second mutation increases the advantage

a third mutation

increases the

advantage further

and makes the

cell invasive

CELL SURVIVAL AND

PROLIFERATION

CELL SURVIVAL AND

PROLIFERATION

Different cancers display different combinations of properties.

Nevertheless, we can draw up a general list of characteristics that distinguish

cancer cells from normal cells.

1. Cancer cells have a reduced dependence on signals from other cells

for their survival, growth, and division. Often, this is because they

contain mutations in components of the cell signaling pathways that

normally respond to such stimuli. An activating mutation in a Ras

gene (discussed in Chapter 16), for instance, can cause an intracellular

signal for proliferation even in the absence of the extracellular cue

that would normally be needed to turn Ras on—like a faulty doorbell

that rings even when nobody is pressing the button.

DANGEROUS

CELL SURVIVAL,

PROLIFERATION,

AND INVASION

Figure 20–45 Tumors evolve by repeated rounds of mutation,

proliferation, and natural selection. The final outcome is a fully

malignant tumor. At each step, a single cell undergoes a mutation

that enhances its ability to proliferate, or survive, or both, so that its

progeny become a dominant clone in the tumor. Proliferation of this

clone then hastens occurrence of the next step of tumor progression

by increasing the size of the cell population at risk of undergoing an

additional mutation. Some cancers contain multiple malignant clones,

each with its own collection of mutations, in addition to a common set

of mutations that reflect the tumor’s origin from a founding mutant cell

(not shown).

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!