I. What is DNA’s Role in Cancer Biology?
Although the etiology of such a devastating disease, cancer biology is one of the most fascinating topics in molecular and cellular biology, all the more reason to develop more research in this topic! Try and take a cancer biology class if offered by your school!
Although viewed as a disease on the organ or the cellular level, cancer pathology often originates at the DNA level due to mutations, most notably in the forms of oncogenes and tumor suppressor genes which will be covered in this article!
Aside from the review content that’ll be covered, another big takeaway from this article is the development of analytical and critical thinking skills! You’ll see that in the article, there’ll be some topics that will require you to have a neat, concise flow of logic, a skill that’s highly useful when approaching MCAT questions!
II. Content Review
As stated above, the 2 main types of genes that will focus on their role in cancer progression are 1) oncogenes and 2) tumor suppressor genes. Though there are more, these 2 genes are actually 2 main hallmarks of cancer!
Oncogenes
These types of genes are actually mutated forms of proto-oncogenes, which are basically genes that promote normal cell growth and proliferation.
All cells need normal cell growth in order to survive and multiply. However, it’s when these genes become overly active where uncontrolled cell growth and proliferation occurs, leading to cancer.
Specifically, the mutation from a proto-oncogene to an oncogene is called a gain of function mutation. Simply, this type of mutation results in the function being promoted/upregulated.
At this point, the oncogene promotes unregulated cell growth and proliferation. Another way to look at this is that the oncogene promotes further, uncontrolled progression into the cell cycle, a series of cellular events that must occur for cellular proliferation.
Tumor Suppressor Genes
These genes are exactly what they sound like! They work to regulate cell growth and proliferation, notably through inhibition of progression to the cell cycle.
Think of them like checks and balances to the proto-oncogenes! When cell growth/proliferation is not needed, these genes are active and prevent cell cycle entry. However, it’s when these genes lose their function that cell growth is unregulated!
As such, the loss of tumor suppressor gene function is not surprisingly called a loss of function mutation, where the function is inhibited/downregulated!
This is where developing analytical and logical thinking kicks in! What happens if tumor suppressor (TS) function is lost? Think about it first and then take a look at the figure below!
Aside from the main content about understanding oncogenes and tumor suppressor genes, another takeaway as we said before is the development of your critical and logical thinking skills! Developing a good flow of information and logic is crucial when approaching and answering MCAT questions.
Hopefully, this was evident when discussing the difference between gain and loss of function mutations! We’ll summarize the 2 mutations types below one more time:
In the context of cancer cells, think which functions/features cancer cells would want to upregulate (gain of function) and which functions/features cancer cells would want to downregulate (loss of function).
III. Bridge/Overlap
As noted above, the ultimate result of oncogenic gain of function and tumor suppressor loss of function is increased progression into the cell cycle.
Simply, the cell cycle is a series of cellular processes organized into different phases which ultimately results in cell division. We’ll go over the cell cycle in more detail in another article, but here's a basic overview of the cell cycle and its phases below:
IV. Wrap Up/Key Terms
Let’s take this time to wrap up & concisely summarize what we covered above in the article!
There are 2 types of genes that mainly contribute to cancer pathology:
Oncogenes
A gain of function in proto-oncogenes, genes involved in promoting normal cell growth, results in an oncogene.
Tumor Suppressor Genes
The function of these genes is to inhibit cell growth when not necessary, acting similar to a check and balance for proto-oncogenes. A loss of function in these genes results in unregulated cell growth.
The gain of function in proto-oncogenes to oncogenes and the loss of function in tumor suppressors results in increased cell cycle progression!
Cell Cycle:
A regulated series of cellular processes divided into phases which results in the division of a cell into 2 daughter cells. The cell cycle phases include:
G1 Phase: Cellular growth occurs while deciding whether to continue to next phase
S Phase: DNA replication occurs so both daughter cells have equal amount of DNA
G2 Phase: Cell checks for errors during DNA replication
M Phase: Cell undergoes mitosis, creating to daughter cells
V. Practice
Take a look at these practice questions to see and solidify your understanding!
Sample Practice Question 1
Apoptosis is defined as programmed cell death which occurs as a normal part of a cell’s life cycle. In the context of cancer cell pathology, would cancer cells want to have a gain or loss of function in this feature?
Ans. Loss of Function
Apoptosis would be a feature that the cancer cell would like to LOSE because apoptosis would inhibit cancer cell growth and pathology, which is ultimately uncontrolled cell proliferation. A loss of function in apoptosis would increase cell survival and increase cancer cell biology.
Sample Practice Question 2
Immunoevasion is defined as the ability for cells to avoid immune detection and ultimately avoid immune cell mediated cell death. In the context of cancer cell pathology, would cancer cells want to have a gain or loss function in this feature.
Ans. Gain of Function
A gain of function in this feature would mean that the cell can avoid immune mediated cell death. This would prolong the lifespan of the cancer cell, a characteristic that the cancer cell needs in order to continue to grow and proliferate.
To help you achieve your goal MCAT score, we take turns hosting these