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BIOL 1051 Lecture Notes - Lecture 9: Genetically Modified Bacterium, Hair Cell, Oncogene

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School
ECU
Department
Biology
Course
BIOL 1051
Professor
Jarrett Whelan

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Document Summary

Metastasis: the spread of cancer cells; occurs when tumor cells leave the primary tumor and enter into the circulation; once the cells are metastasized, they can spread to the rest of the body. A biopsy is a surgical removal of cells or material to determine if they are cancerous; Radiation therapy is site directed therapy aimed at a certain site and disrupts cell division; chemotherapy is systemic and targets the cells that are rapidly dividing (includes hair cells and blood cells) uses multiple drugs to disrupt cell division; Today"s goals: methods for biotechnology, human health uses, agricultural uses. For the exam- all of chapter 5 and chapter 6 (sections 1-9) Biotechnology: organisms, cells, and their molecules are modified to achieve practical benefits; one emphasis is genetic engineering which is a manipulation of organisms" genes (you can add, delete, or move genes from one species to another.

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Related Questions

Question 7

The TERT gene encodes for telomerase and is an example of a(n) ________________.

tumor suppressor gene

oncogene

histone

transcription factor

Question 9

Which of the following is true regarding tumors?

Their environments are ideal for rapid cell growth, providing nutrients and oxygen
They are comprised of proliferating and necrotic cells
They do not recruit their own blood supply
They are homogeneous

Question 10

During surgery to remove a primary tumor, nearby _________ are often additionally removed or biopsied to look for the presence of invasive cancer cells.

lymph nodes
blood vessels
epithelial cells
bone marrow

It was all over the news (March 29, 2018) that a new cancer “vaccine” was about to begin human trials after a 97% success rate in mouse trials against both blood cancers (lymphomas) and solid tumors such as breast and colon cancer. I will excerpt a description compiled from several scientific and news sources. Based on what we talked about in Bio 221, you should be able to understand this. Answer each of the questions about this exciting new “vaccine.” T cells are present in most tumors by infiltration. These include CTLA4-expressing Treg cells, as well as CD4- expressing TH cells and CD8-expressing cytotoxic T-lymphocytes. Once cancer is well established, the balance between these inputs is tipped toward immunosuppression. We found that a Toll-like receptor 9 (TLR9) ligand, CpG, induces the expression of OX40, an alternate costimulatory receptor, on CD4 T cells when it is injected into the tumor microenvironment. This is an indirect induction, in which CpG induces cytokine secretion by myeloid cells which in turn induces OX40 expression on T cells. Then OX40 can be activated using anti-OX40 antibodies, thereby activating TH cells in the tumor.

D. How do antibodies that recognize OX40 help to stimulate TH cells? (Hint: think about autoimmune diseases. There is one we didn’t talk about, called Graves’ disease, that you might want to look up, too.) What else is required for the TH cells to become activated?

E. How does all of this kill the cancer cells? What other cells in the tumor also must become activated? How?

F. How does this differ from the CAR-T cell therapy?

It was all over the news this morning (March 29, 2018) that a new cancer “vaccine” was about to begin human trials after a 97% success rate in mouse trials against both blood cancers (lymphomas) and solid tumors such as breast and colon cancer. I will excerpt a description compiled from several scientific and news sources. Based on what we talked about in Bio 221, you should be able to understand this. Answer each of the questions about this exciting new “vaccine.”

T cells are present in most tumors by infiltration. These include CTLA4-expressing Treg cells, as well as CD4- expressing TH cells and CD8-expressing cytotoxic T-lymphocytes. Once cancer is well established, the balance between these inputs is tipped toward immunosuppression. We found that a Toll-like receptor 9 (TLR9) ligand, CpG, induces the expression of OX40, an alternate costimulatory receptor, on CD4 T cells when it is injected into the tumor microenvironment. This is an indirect induction, in which CpG induces cytokine secretion by myeloid cells which in turn induces OX40 expression on T cells. Then OX40 can be activated using anti-OX40 antibodies, thereby activating TH cells in the tumor.

A. What is CTLA4 and how does it establish immunosuppression?

B. What is a costimulatory receptor, and why is an alternate one required here?

C. How does a TLR ligand such as CpG induce cytokine expression by myeloid cells? What myeloid cells are involved here?

D. How do antibodies that recognize OX40 help to stimulate TH cells? (Hint: think about autoimmune diseases. There is one we didn’t talk about, called Graves’ disease, that you might want to look up, too.) What else is required for the TH cells to become activated? E. How does all of this kill the cancer cells? What other cells in the tumor also must become activated? How? F. How does this differ from the CAR-T cell therapy?