Directions: Prepare your answers to ALL prompts below.
• Complete all questions in paragraph form:
§ 11pt or 12pt standard font (times, arial, cambria, calibri etc. Just nothing weird)
§ 0.5 or 1 inch margins, which ever one puts you within the physical page limit
§ Single Spaced
§ Each prompt can be answered in 1-2 pages. Your compiled writing should not exceed 6 pages. This is a hard
cut off. Your reference page(s) is NOT included in the page limit.
§ Citations are mandatory.
• There is not a minimum number of citations. You should be listing a citation anytime you use reference material,
which should be frequently, as none of you are current experts in the field.
• Your references should be formal, peer reviewed scientific publications (reviews, primary literature, or the
textbook.) Use results on PubMed or the reviews provided as examples of the type of literature you should be
using.
• Use super scripted in text citations and include a numbered reference page at the end of your submission.
§ Example: Write an informative sentence about cell biology that tells me you learned something.1
§ Format for the actual citations on your references page (MLA/APA/Nature/etc) doesn’t matter, just be
consistent in your chosen format. I need to be able to find your reference easily if I want to make a check. This
is a common format:
o Author Last Name, Author 1st Initial. Second Author Last Name, 2nd Author 1st Initial. (Year of
Publication). Article Title. Journal. Volume, Page Numbers
§ I would recommend you download a citation manager and figure out how to use it to make your life easier
(Zotero is a decent free one). You won’t need to hand write every citation if you do this and they will be
autoformatted.
• TURNING IT IN:
o Due FRIDAY May 3rd by NOON
o You must type your responses and submit it to TurnItIn on canvas. Similarity and AI contribution reports will
be generated through turn it in. I will also be turning the essays into ChatGPT and asking it to detect it’s own
contributions. You may make as many submissions to canvas as you need until you are satisfied with the analysis
before the due date.
• OTHER RULES:
o Don’t plagarize. Don’t consult your classmates or any other writing service. You may not use generative AI as a
writer. The writing and final product should be YOUR RESEARCH, EFFORT, THOUGHT, AND VOICE. You
may consult notes, textbooks, and the internet to complete this assessment. You may not consult any humans besides
me (Dr. Gifford).
o Be thorough in your responses and use language that demonstrates YOUR ability to understand, synthesize, and
communicate cellular biology. I’m not expecting you to sound like scientists with a decade of research in the field,
but I do want to know that you learned some biology and can discuss it intelligently. Just tell me what you found
and what you think. I’ve read (literally) hundreds of these essays over the years of teaching this class. I know what
kind of responses to expect from students at your level. I also know well what Chat GPT writing reads like and can
tell when you aren’t using your own brain to communicate and that makes me incredibly grumpy. (PROMPT 1) Easy skill developed through our Jigsaws: Can you read information from a review article on your
own, summarize it, and do a little research to tell me more about it? (10 points)
Read over The series of “Hallmarks of Cancer” papers posted on blackboard to get you started, though this is not the only
resource you should use to address this prompt.
• Pick your favorite of the hallmarks
A. Describe this hallmark using the reviews and information you’ve learning throughout the class. Talk about common
cellular defects associated with the hallmark and how it affects overall cell behavior.
B. Describe how this specific hallmark has been targeted in the clinic to manage tumor initiation/progression. If there
are specific drugs that have been developed, how do they work?
C. Discuss how successful targeting this hallmark has been in the clinic. If unsuccessful, why is targeting that hallmark
difficult? Success can be gauged by patient survival, downgrading the tumor, side effects and toleration, completion
of trial phases etc. You may need to go digging on pubmed or clinicaltrials.gov to find information about tested
treatments.
(PROMPT 2) Medium skill developed through lecture content: Can you use specific knowledge you already learned
in class to provide a rationale for a real world application/cellular phenomenon? (15 points)
Erlotinib and gefitinib are first generation inhibitors that were approved to treat Non-Small Cell Lung Cancer (NSCLC) in
the early 2000’s. Afatinib was developed as a second generation inhibitor and demonstrated significantly higher progression
free survival in patients. Osimertinib is a third generation small molecule inhibitor developed by AstraZeneca and approved
in 2017 for the treatment of Non-Small Cell Lung Cancer.
A. Explain the difference between standard chemotherapy and targeted therapies. Are the above listed drugs considered
standard chemotherapies or targeted chemotherapies? Why?
B. Explain the scientific rationale for developing a third generation inhibitor (Osimertinib) when first and second
generation inhibitors already existed for treatment of NSCLC.
o Be sure to include an explanation for how each of these drugs work, what they target, what their ultimate
purpose is in these cells, and overall success in the clinic has been. Be sure to include concepts related to
mutations and protein structure in your rationale where appropriate.
(PROMPT 3): Harder Skill: Can you use your cell biology knowledge to evaluate claims/competing theories in the
field that we haven’t explicitly discussed in great detail? (20 points)
For the last 50+ years of cancer research, scientists have used the somatic mutation theory (SMT) to explain carcinogenesis,
the process by which cancer initiates. In the last twenty years, a growing community of scientists have generated research
to challenge this traditional theory with a new one, the Tissue Organization Field Theory (TOFT). Journals published
discussions and counterpoints from experts (Soto/Vaux discussion provided) and research continues explore the new theory
and determine its relevance to disease initiation.
Use the provided reviews (and any other publications you find interesting or helpful) to answer the following:
A. Summarize what these theories generally state. How are they distinctly different?
B. Read the dialogue between Soto and Vaux. What are the strengths and weaknesses of each theory? What evidence
exists to support or refute the theories. Include specific references as needed and you’re welcome/encouraged to go
digging into the actual research they mention to elaborate on the evidence.
C. Based on what you’ve read, which one is more convincing to you and why?
D. Is there any room for both of these theories to be compatible in sporadic (non-heritable) cancers or are you not
convinced they’re compatible?
