BIOL 207 Biology of Cancer August 31, 2007
Lecture 2: Normal cells vs. cancer cells
Reading: Chap. 1 Kleinsmith pp. 13-14; INT site “Cells Alive”, Chap. 2 pp. 18-22
Outline:
1.
Cancer Causes
2.
DNA structure/function
3.
Normal cell structure/function
4.
Cancer cells
1. What causes cancer?

Genes

Chemicals

Radiation

Viruses
What roles do genes play?
Genes involved in cancer:
Oncogenes—promote cancer
Tumor suppressor genes—genes normally suppress cancer
2. DNA structure/function
Genes=segments of DNA, deoxyribonucleic acid that code for protein; provide a linear code
Fig. 1-8
DNA is built from chains of nucleotides
Nucleotides made of bases A,C,G,T; sugar=deoxyribose; phosphate
DNA consists of 2 strands
Each strand goes in the opposite direction (antiparallel)
A pairs with T
G pairs with C
Information from DNA is transferred to protein via
DNA

RNA

protein
Fig. 1-9
In our cells, DNA is in the nucleus; mRNA is made in the nucleus, first in a longer form
(pre-mRNA) and processed to give mRNA. mRNA leaves the nucleus for the cytoplasm. mRNA attaches to ribosomes or to rough endoplasmic reticulum to make a protein.
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How are genes involved in cancer? Typically altered or “mutant” forms of normal genes are involved.
Mutation—changes in base sequence to alter the genetic code.
Some genes encode proteins that are involved with growth, cell division, cell adhesion
(how cells stick together); these are often mutated in cancers.
3. Normal cell structure: See Cells Alive Web Site
1.
Plasma membrane—Boundary surrounding cells “security guard”
2.
Nucleus—Central compartment in cell that contains the DNA in chromosomes
“master control center”
3.
Cytoplasm—The compartment between the nucleus and the plasma membrane.
4.
Mitochondrion—Double membrane bound organelle involve in energy metabolism “power plant”
5.
Ribosomes—Site of protein synthesis “protein factory”
6.
Rough or smooth endoplasmic reticulum, Golgi body—Stacks of membranes involved in protein synthesis and packaging “packaging center”
7.
Cytoskeleton—Network of proteins in cytoplasm that give cell its shape
8.
Cell junctions—Connections between cells
9.
Extracellular matrix—Materials outside of cells that help maintain cells in place.
Different parts of cells can be altered in cancer. Some examples

Alterations in plasma membrane receptors can promote cancer. Her-2/neu receptor and breast cancer.

Several different types of hereditary colon cancer are associated with defective DNA repair enzymes.

Loss of a cell adhesion protein E-cadherin occurs in highly invasive cancers.
4. Cancer cells
What are some of the key features of cancer cells?

Uncontrolled proliferation

Selfishly divide without consideration of needs of whole organism, while cells that are undergoing “controlled” division reproduce only when needed.

Produce tumors when injected into laboratory animals o Mouse cancer cells

inject into mouse

mouse gets tumor o Human cancer cells  inject into immune deficient mice (so they don’t recognize human cells)

mouse gets tumor
 Are less “density-dependent” in their cell growth. Can be studied in cell culture
Fig. 2-1.
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
The more the cells can overcrowd, the more likely they will cause tumors when injected into lab animals.

Cancer cells require fewer growth factors than normal cells.

Many cancer cells growing in vitro become anchorage independent (no longer need to attach to dish.

Cancer cells begin to alter the proteins on their surfaces that allow them to attach
(i.e. integrins).

Cancer cells reproduce indefinitely in culture; normal cells in culture typically only divide 50-60x. o HeLa cells: human cervical cancer cells from patient Henrietta Lachs who had a tumor removed in 1951 (she died not long afterwards), cells have been grown in culture since then, having divided more than 18,000 times.
Note: These were the cancer cells that were demonstrated during the histology workshop.

Cancer cells keep replicating the ends of their chromosomes, normal cells lose their chromosome ends. The enzyme telomerase that copies the ends is reactivated in can cells and has lost efficiency in normal cells. Fig. 2-5
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