BIOL 104 Lecture Notes - Lecture 9: Vascular Endothelial Growth Factor, Tumor Suppressor Gene, Uraninite
Cancer cells do not obey checkpoints. Chromosomal abnormalities arise and are potentially harmful to a
cell. Therefore, at these checkpoints, a cell must decide whether it should replicate DNA or produce
more damaged cells. There are specific proteins that find these problems and tell the cell to die
(programmed cell death or apoptosis) or fix itself.
As a result, a cancer cell lives too long, and continues to divide to form a tumor. If the tumor is not
invasive it is considered benign. However, if cells have become invasive and break through the
basement membrane they are considered malignant. In this way, tumor cells can enter the bloodstream
to form a secondary tumor in another location. This is called metastasis.
The tumor expresses molecules (such as Vascular Endothelial Growth Factor) that attract blood
vasculature to it. Indeed, the ord aer as oied Hipporates to desrie the ra leg-like
vessels around the tumor. The tumor grows faster with this increase nutrition and oxygen.
The Causes of Cancer By the 20th century, it was obvious that specific environmental chemicals had a
role in inducing cancer. -higher rate of scrotal cancer in men who had been chimney sweeps -higher
rate of lung cancer in pitchblende miners (uranium) -higher rate of throat and mouth cancer in
snuff/cigar users
At this time, it was also clear that a small % of cancers (5-10%) are inherited.
As you know, disease can result when a DNA mutation causes the protein to be abnormal. We have
looked at many examples of this so far this semester. It becomes easier to use letters to describe this on
paper.
There are multiple versions of a gene (based on changes in the DNA), called alleles. We can use big and
sall letters to rite these alleles o paper. If e assue that G represets the oral allele ad g
represets the utat allele… A perso ho is GG ill ol ake oral protei
A perso ho is Gg ill ake oral protei fro G allele ad a utat protei fro g allele
A perso ho is gg ill ol ake utat protei
**Usually, the amount of normal protein made fro the G allele is eough. That is h soeoe ho
is GG or Gg ill ot hae the disease.
We now know that two classes of genes are responsible for promoting cancer. Tumor Suppressor
Genes -Genes that code for growth suppressive proteins that might also have roles in shutting down a
cell, repairing chromosomal damage, or inducing apoptosis.
-Because of their molecular nature, one normal copy can often compensate for the loss of the other
copy. This is why mutations in both copies of a tumor suppressor gene is necessary to lead to problems.
-A eaple is the p53 protei that plas a ke role i sesig DNA/ell daage ad tells the ell to fi
the problem, arrest the cell cycle, or die. Mutations in p53 have been associated with 50% of all
cancers.
Oncogenes -Genes that code for normal growth promoting proteins.
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Document Summary
Chromosomal abnormalities arise and are potentially harmful to a cell. Therefore, at these checkpoints, a cell must decide whether it should replicate dna or produce more damaged cells. There are specific proteins that find these problems and tell the cell to die (programmed cell death or apoptosis) or fix itself. As a result, a cancer cell lives too long, and continues to divide to form a tumor. If the tumor is not invasive it is considered benign. However, if cells have become invasive and break through the basement membrane they are considered malignant. In this way, tumor cells can enter the bloodstream to form a secondary tumor in another location. The tumor expresses molecules (such as vascular endothelial growth factor) that attract blood vasculature to it. Indeed, the (cid:449)ord (cid:862)(cid:272)a(cid:374)(cid:272)er(cid:863) (cid:449)as (cid:272)oi(cid:374)ed (cid:271)(cid:455) hippo(cid:272)rates to des(cid:272)ri(cid:271)e the (cid:272)ra(cid:271) leg-like vessels around the tumor. The tumor grows faster with this increase nutrition and oxygen.
