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Homework 2

by: Jacob Decker

Homework 2 ZOL 425

Jacob Decker
GPA 3.71

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This is my completed review paper about the relationship between inflammation and cancer.
Cells and Development (W)
D. Bello-Deocampo
Class Notes
25 ?




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This 2 page Class Notes was uploaded by Jacob Decker on Saturday February 13, 2016. The Class Notes belongs to ZOL 425 at Michigan State University taught by D. Bello-Deocampo in Spring 2016. Since its upload, it has received 25 views. For similar materials see Cells and Development (W) in Microbiology at Michigan State University.


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Date Created: 02/13/16
Decker 1 William Decker ZOL 425 1/26/16 Homework 2: Summary of “Inflammation in prostate carcinogenesis” Recently, great attention has been drawn to the subject of immunity and the role of toll­ like receptors (TLRs). Latest research has acknowledged the importance of TLRs in  “recognizing specific microbial components derived from pathogens including bacteria, fungi,  1  protozoa and viruses” which, in effect, causes a proliferation of effector molecules, chemokines  and assorted pro­inflammatory cytokines. Ten classes of TLR ligands are located in the  membranes of macrophages and dendritic cells, whose role is the phagocytosis and endocytosis  of pathogenic substances. TLRs also upregulate the expression of major histocompatibility  2 complex II (MHC II) molecules.  MHC II molecules are then used by macrophages and dendritic cells which facilitate responses from the adaptive immune system. Along with the adaptive immune system, TLRs also have a significant function in  inflammatory responses. The recognition of pathogens by TLRs promotes their own self­ dimerization, which then results in the activation of signaling pathways from the cytoplasmic  3 TIR (Toll­Interleukin) domain.  Although signaling pathways of TLRs are divergent, a  subsequential TIR­domain adaptor called MyD88 is mutually involved with all TLRs. MyD88  produces cytokines such as TNF­ and IL­12, which are critical in the body’s inflammatory  response.  Inflammation is a protective response of the body to ridden the source of the cellular  damage and mediate reparation. Inflammation can be harmful to the body if not administered in  _____________________________________________________ 1  Kiyoshi Takeda and Shizuo Akira. “Toll­like receptors in innate immunity.” International  Immunology, Vol. 17, No. 1, 2005): 2. 2 Angelo M. De Marzo et al. “Inflammation in prostate carcinogenesis.” Nature Reviews Cancer (2007): 264. 3 Takeda and Akira. “Toll­like receptors,” 5. 4 5 Takeda and Akira. “Toll­like receptors,” 6.  Takeda and Akira. “Toll­like receptors,” 8. Decker 2 the right doses. Too little could allow the source (pathogen) to continue cellular damage, but  excess cytokine production brings a high mortality rate from serious systemic disorders. 5 To prevent this overproduction of cytokines, there are molecules responsible for the  negative regulation of TLR signaling. Single immunoglobulin IL­1 receptor­related molecule  (SIGIRR) and T1/ST2, for example, are membrane proteins that when absent or deficient cause  6 an increased inflammatory response in the body.  There are, however, times when down­ regulation fails and a serious and life­threatening chronic inflammatory state is established. In  fact, a study took place in Sweden that implied strong correlations of chronic inflammation and  the development of cancer.  Carriers of a single nucleotide polymorphism in TLR4 had a 26%  more­likely chance of prostate cancer and were 39% more at risk of early­onset prostate cancer  compared with those without this genetic mutation.  It is safe to assume, then, that because this  lineage of genes is so closely related to adaptive immunity, errors in the mechanisms of  inflammation are significant in the advancement of cancer. _____________________________________________________ 6Takeda and Akira. “Toll­like receptors,” 8. 7 De Marzo. “Inflammation in prostate carcinogenesis,” 256. 8  De Marzo. “Inflammation in prostate carcinogenesis,” 264.


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