Gene and Cancer Assignment

Part I

Your grandmother was recently diagnosed with and is currently undergoing

treatment for colorectal cancer. Fortunately, the cancer was detected very early
and her prognosis is excellent; you have every expectation that she will make a
full recovery. Your cousin, who is still in high school, knows very little about
cancer but has an interest in science and what makes cells work and has many
questions about what the oncologist has told you. How would you answer
questions? You’ll need to address at least the following, and remember, your
audience is your cousin, so explain things clearly adn consider his/her base
knowledge.

1. Your cousin knows cancer has something to do with cells growing out of
control, but what normally is involved in cells growing under normal
control, what mechanisms allow cells to grow normally? Hint: for full
credit, be sure to start with the signal and mention the specific molecular
mechanisms involved in regulating cell growth, including at least one
specific molecule name in each of the mechanistic routes that are involved
in normal cell growth (your cousin is very interested in hearing some detail,
but you should still be able to do so in ~3-4 sentences.)

Answer:

Cell growth normally entails a very regulated process that is instructed by signals that
form pathways and molecular mechanisms. At the center of the regulation is this cell
cycle, which ends in cell division. The initiation of cell growth usually starts with signals
being sent externally, as growth factors bind to cellular surface receptors. A prominent
pathway is the Ras pathway, where activated Ras triggers multiple events, ending in the
activation of factors that promote cell cycle progression.

2. The oncologist said that your grandmother has a mutation in a gene called
K-ras and that the mutation made her cells divide too much and caused
polyps (note: in class we went over this molecule, also called “Ras”). He
also said something about K-ras being a proto-oncogene, or maybe an
oncogene. A. Explain to your cousin what a mutation is and how they arise.
B. Explain how a mutation in proto-oncogene can make cells divide too
much using an example of a specific protein that is not Ras but that we
talked about in class to illustrate your point. C. Explain what proto-
 oncogenes and oncogenes are and how they relate to K-ras and your
grandmother’s cancer.

Answer:

A. Mutations are changes in genetic material of organisms, and occurs in various

ways. DNA serves as the blueprint for not only building, but maintaining
organisms by containing instructions for proteins and important molecules.
B. Proto-oncogenes are normal genes involved in the regulation of cell growth and
division. Mutations in these genes can convert them into oncogenes, however,
contributing to uncontrolled cell division and possibly even lead to cancer.
a. An example is the proto-oncogene MYC, the coding assert for the c-Myc
protein. This protein assists in the regulation of the cell cycle but if a
mutation occurs in the MYC gene, it can lead to the overproduction or
overstabilization of the c-Myc protein.
C. When a mutation occurs in the K-ras gene within the cells, like that of grandma’s
body, it resulted in the production of a mutated K-ras protein that persistently
sends signals for cells to divide. This uncontrolled cell growth led to the formation
of a tumor, and these cells acquired additional mutations, which became
cancerous.

3. Your grandmother has had polyps before. The oncologist said that she
probably had other mutations besides the K-ras one and that something
probably went wrong with her tumor-suppressor genes, especially
something called p53. A. Explain to your cousin what tumor-suppressor
genes are, and what two cellular processes are generally responsible for.
B. Specifically address what p53 is, and why something going wrong with
p53 could make polyps likely to become cancerous. Hint: mention two
different roles of p53 that make it so important in this process.

Answer:

A. Tumor-suppressor genes play an important role in preventing the development of

cancer by putting restrictions on cell growth and division. They police the body,
making sure everything runs smoothly. They handle the regulation of the cell
cycle and DNA repair respectively.
B. p53 is a critical tumor-suppressor protein, it’s primary function is to monitor the
integrity of the cell’s DNA and regulate the cell cycle. Polyps are abnormal
growths in the tissue lining the colon or rectum. In a case with polyps, a
malfunctioning p53 allowed cells with DNA damage to accumulate and progress
toward cancerous transformation.
 4. The oncologist also said that your grandmother’s type of cancer can be
hereditary-that you and your cousin could also have the mutated K-ras
gene. If the mutation is in your grandmother’s intestines. A. explain how
could the two of you could both have the mutated K-ras gene. B. If you do
have it, your cousin wants to know if you both will for sure get cancer -
explain.

A. The gene would have been passed down in the genetic material, or DNA,
of our parents and to us.
B. While it’s possible that we could have it, it’s not a for sure thing.
Exposures to certain things such as tobacco, chemicals, and our lifestyles
will inevitably play a role in whether or not we get cancer.

Part II

For your final portfolio, consider the above questions, and write a 200-250 word
introduction to cancer, focusing on the molecular causes. Your audience is an
educated person who is not a scientist, but who has a keen interest in your ability
to think and write clearly in explaining a complex topic.

Answer:

Cancer is a multifaceted and challenging disease. At its core, cancer represents a

disruption in the complicated process that molecular mechanisms undergo to govern
normal cell behavior. Proto-oncogenes, typically orchestrators of controlled cell growth,
can transform into oncogenes when mutated. These altered genes cultivate
uncontrolled cell proliferation.

Opposite of this, tumor-suppressor genes act as cellular brakes, inhibiting excessive

growth and aiding in DNA repair. When these genes undergo mutations, their ability to
curb abnormal cell growth weakens, contributing to cancer development. The K-ras
gene, a significant player in cell signaling pathways, exemplifies this. Mutations in K-ras
can result in persistent activation, disrupting the delicate balance that governs cell
division.

Another tumor-suppressor gene, p53, plays a pivotal role in overseeing DNA integrity.
Mutations in p53 can compromise the cell’s ability to repair damaged DNA or lead to cell
death, culminating in an environment that is conducive to cancer.
Understanding the molecular intricacies is crucial for unraveling the origins of cancer
and devising targeted therapeutic strategies. This exploration aims to dissect the
molecular underpinnings of cancer without resorting to metaphor, delving into the
intricate language of genes and proteins that shapes cellular behavior and drives the
complexities of this disease.