When development goes awry: how cancer co-opts mechanisms of embryogensis
Bachelor's degree
In Maynard (USA)
Description
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Type
Bachelor's degree
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Location
Maynard (USA)
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Start date
Different dates available
During this course, we will study the similarities between cancer and normal development to understand how tumors co-opt normal developmental processes to facilitate cancer initiation, maintenance and progression. We will examine critical signaling pathways that govern these processes and, importantly, how some of these pathways hold promise as therapeutic targets for cancer treatment. We will discuss how future treatments might be personalized to target cancer cells in specific patients. We will also consider examples of newly-approved drugs that have dramatically helped patients combat this devastating disease.
Facilities
Location
Start date
Start date
Reviews
Subjects
- Combat
- Biology
Course programme
Lectures: 1 session / week, 2 hours / session
At least one of the following:
7.03 Genetics
7.05 General Biochemistry
7.06 Cell Biology
7.28 Molecular Biology
Cancer is a leading cause of death worldwide. Few treatment options exist, most of which rely on a single characteristic of cancer cells—their increased proliferation rate. Treatment with traditional therapies, such as radiation or chemotherapy, can be highly toxic, and patients often experience relapse as cancers acquire mutations that confer drug resistance. More effective cancer therapies are very much needed. Such therapies are now being developed based upon an understanding of cancer biology, which in many ways involves dysregulation of the normal biology of development. During human embryonic development, a single cell—the fertilized egg—divides and its descendants grow, differentiate, and assemble to generate a highly complex human being. Throughout these developmental processes, cells communicate with each other via complex signaling networks composed of proteins interacting with other proteins. Signaling pathways that drive development have been identified, and, strikingly, many of them are altered in cancer. Cancer involves uncontrolled cell growth, failure to differentiate into a particular cell type, resistance to cell death, increased cellular motility, and formation of new blood vessels. All of these processes are utilized during development, and all are misused in cancer.
During this course, we will study the similarities between cancer and normal development to understand how tumors co-opt normal developmental processes to facilitate cancer initiation, maintenance and progression. We will examine critical signaling pathways that govern these processes and, importantly, how some of these pathways hold promise as therapeutic targets for cancer treatment. We will discuss how future treatments might be personalized to target cancer cells in specific patients. We will also consider examples of newly-approved drugs that have dramatically helped patients combat this devastating disease.
At the end of this course, you should be able to:
The content of this course will be based on the primary research literature. For each class, students will be assigned to read two papers. Students should formulate two questions per paper and send them by email to the instructors by the night before each class. Questions may pertain to: background, interpretation of results, a technique, follow-up experiments, etc. During class, we will discuss the papers interactively as a group. Students may be asked to present specific figures in each paper, or may be called upon to answer questions about the papers. At the end of each session, the instructors will introduce the papers for the next week.
There will be two assignments: a written assignment (due before Ses #7) and an oral assignment (due before Ses #12).
Grading for this course is pass/fail and will depend on student attendance, preparedness, participation in class discussions, and completion of the required assignments. If you must miss a class, you must complete a make-up assignment based on the papers to be discussed.
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When development goes awry: how cancer co-opts mechanisms of embryogensis
