Background
What an incredible medical discovery we have made together! A contagious cancer is one of the rarest
diseases throughout the galaxy. If left untreated, the cancer will not only spread from the lungs to other
organs but will spread from sick gliders to healthy gliders.
Fortunately, we have collected the data to determine how the tumor cells differ from healthy cells. The
elevated concentration of Growth Factor L in the blood of spotted gliders provides a clue to the mutations
responsible for the cancer. We may be able to use this information to devise a treatment that targets
tumor cells.
Use the following questions to guide your work:
● Which receptors in the cell membrane bind Growth Factor L? (Appendix 1)
● Which proteins in the cytoplasm are activated when a receptor binds Growth Factor L? (Appendix
2)
● Should we treat the cancer of spotted gliders with a drug or a virus? (Appendix 3)
Universally, in your debt,
The AI
You have been asked to identify the cellular component contributing to the spotted gliders’ cancer
and chose a treatment.
Appendix 1
Which receptors in the cell membrane bind to
Growth Factor L?
Cancer—the uncontrolled growth of abnormal cells—results from a malfunction in a signaling pathway.
The figure below shows a signaling pathway that regulates cell division in spotted gliders.
When the signaling pathway is inactive, a protein called CDI2 is active and prevents the cell from dividing.
All other proteins (R1, KR1, KR2, KR3, and CDP1) are inactive form.
When the signaling pathway is in the active state, the following steps occur:
1) A signal (SR1) binds to a receptor (R1), activating this receptor through phosphorylation.
2) The active form of R1 or R2 binds and phosphorylates a kinase (KR1).
3) The active form of KR1 binds and phosphorylates a second kinase (KR2).
4) The active form of KR2 binds and phosphorylates a third kinase (KR3).
5) The active form of KR3 interacts directly with two proteins, CDP1 and CDI2. KR3 activates
CDP1, which enables CDP1 to promote rapid cell division. KR3 inactivates CDI2, preventing
CDI2 from slowing cell division.
When examining the spotted gliders, we discovered an elevated concentration of a second type of signal,
which Phygaran scientists called Growth Factor L (abbreviated as GF-L). According to my database,
GF-L only reaches these concentrations during the embryonic stage, early in the development of spotted
gliders, when cells rapidly divide.
By experimenting with some cells from a spotted glider, you discovered that GF-L binds to receptors in
the membrane of a tumor cell. We might presume that these receptors are the same as R1, which would
explain how GF-L promotes cell division (see Figure 1). However, after you left the Intergalactic Wildlife
Sanctuary, I analyzed the membrane of tumor cells and discovered a second type of receptor, R2, that
has a similar structure to R1. According to research conducted on Phygaris, spotted gliders usually
produce R2 as embryos when rapid cell division creates new tissues and organs. R2 is not usually
expressed in adult gliders.
We need to understand GF-L's role in the cancer of spotted gliders. First, we need to determine
whether GF-L binds to R1 or R2. This knowledge will help us identify the cause of the cancer.
We will follow three steps to answer the question, “Is Growth Factor L binding to Receptor 1 or 2?”
Step 1: Anticipate your analysis. Determine what you should observe if GF-L binds to R1, R2, both
receptors, or neither receptor. This step will help us identify the evidence needed to build an argument in
Step 3.
Step 2: Model the effects of GF-L on the activity of R1 and the activity of R2. Determine how the
presence of GF-L affects the activity of R1 and the activity of R2. This step gives us the evidence needed
to build an argument in Step 3, when we will conclude whether GF-L binds to R1, R2, both receptors, or
neither receptor.
Step 3: Weigh the evidence and conclude if GF-L binds to R1, R2, both receptors, or neither
receptor. Construct an argument to answer the question “Does GF-L bind only to R1, only to R2, both
receptors, or neither receptor?” Your argument should draw on your answers in Steps 1 and 2.