Difference between revisions of "User:Cecilia Cisar/Notebook/Mod 3 Research Proposal"

From OpenWetWare
Jump to: navigation, search
(Overview)
(Potential Problems)
 
(12 intermediate revisions by 2 users not shown)
Line 6: Line 6:
  
 
==Overview==
 
==Overview==
* MiRNAs are believed to be important in oncogenesis, as different groups of miRNAs act as either tumor suppressors or oncogenes.  Changes in miRNA expression have been detected in many types of human cancers, in a way that seems to be linked to genomic amplifications, mutations, and deletions. "MiRNA expression fingerprints correlate with clinical and biological characteristics of tumours, including tissue type, differentiation, aggression and response to therapy." [1]
+
* MiRNAs are believed to be important in oncogenesis, as different groups of miRNAs act as either tumor suppressors or oncogenes. For example, miR-145, miR-133a and miR-133b have been found to be tumor-suppressive miRNAs that directly regulate the oncogene FSCN1. [5] Changes in miRNA expression have been detected in many types of human cancers, in a way that seems to be linked to genomic amplifications, mutations, and deletions. "MiRNA expression fingerprints correlate with clinical and biological characteristics of tumours, including tissue type, differentiation, aggression and response to therapy." [1]
  
* Some organisms use miRNA to target and inhibit sections of bacterial DNA.<sup>[2]</sup>
+
* Some bacteria use miRNA to target and post-transcriptionally repress proteins that are involved in innate immune response, [2] and other bacteria release effectors that inhibit miRNA immune response. [3] (Conversely, some miRNA-regulated immune response pathways are activated by bacteria. [4])
 +
 
 +
* Bacteria could be designed to treat various kinds of tumors based on their miRNA expression fingerprint through up/down regulation of oncogene miRNA expression.
 +
 
 +
==Potential Problems==
 +
*Immune response
 +
**Cancer patients may already be immunocompromised through other treatments, so this may not be as big of an issue as it would initially seem, but this leads to...
 +
*Pathogenicity
 +
**If my 20.020 project taught me anything, it's that people are squeamish about introducing bacteria into things even if there isn't anything to point towards it being problematic.
 +
**Would saying that there ''should'' be nothing wrong with the chassis and that it'll have to go through clinical testing be enough?
 +
*Targeting of cancer cells
 +
**Bacteria do not specifically target things based on miRNA signatures
 +
**Could we rely on bacteria to stay localized, depending on treatment method?
 +
**Would regulation of oncogenes in non-target area be an issue? I want to think it would just make cancer-causing mutations even ''less'' likely in affected areas, even if they were not cancerous in the first place...
 +
*Targeting of miRNAs
 +
**This is going to be what we say the focus of the research will be, right?
 +
**Do we know enough to take a stab at this?  It may be worth reading that third paper closer to see if they specify any sort of mechanism...
  
 
==References==
 
==References==
 
# [http://www.gene-quantification.eu/nature-reviews-microrna-3.pdf Calin, George A., and Carlo M. Croce. "MicroRNA signatures in human cancers." Nature Reviews Cancer 6.11 (2006): 857-866.]
 
# [http://www.gene-quantification.eu/nature-reviews-microrna-3.pdf Calin, George A., and Carlo M. Croce. "MicroRNA signatures in human cancers." Nature Reviews Cancer 6.11 (2006): 857-866.]
 
# [http://download.bioon.com.cn/view/upload/201110/19180817_1775.pdf Ma, Feng, et al. "The microRNA miR-29 controls innate and adaptive immune responses to intracellular bacterial infection by targeting interferon-γ."Nature immunology 12.9 (2011): 861-869.]
 
# [http://download.bioon.com.cn/view/upload/201110/19180817_1775.pdf Ma, Feng, et al. "The microRNA miR-29 controls innate and adaptive immune responses to intracellular bacterial infection by targeting interferon-γ."Nature immunology 12.9 (2011): 861-869.]
 
+
# [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570098/ Navarro, Lionel, et al. "Suppression of the microRNA pathway by bacterial effector proteins." Science 321.5891 (2008): 964-967.]
 +
# [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1567904/?report=reader Taganov, Konstantin D., et al. "NF-κB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses." Proceedings of the National Academy of Sciences 103.33 (2006): 12481-12486.]
 +
# [http://onlinelibrary.wiley.com/doi/10.1002/ijc.25284/full Kano, M., Seki, N., Kikkawa, N., Fujimura, L., Hoshino, I., Akutsu, Y., Chiyomaru, T., Enokida, H., Nakagawa, M. and Matsubara, H. (2010), miR-145, miR-133a and miR-133b: Tumor-suppressive miRNAs target FSCN1 in esophageal squamous cell carcinoma. Int. J. Cancer, 127: 2804–2814.]
 
|-
 
|-
 
|colspan="2" style="background-color: #F2F2F2;"|
 
|colspan="2" style="background-color: #F2F2F2;"|
 
{{LnNotebookRecentChanges2}}
 
{{LnNotebookRecentChanges2}}
 
|}
 
|}

Latest revision as of 09:09, 7 May 2014

Project Description

Overview

  • MiRNAs are believed to be important in oncogenesis, as different groups of miRNAs act as either tumor suppressors or oncogenes. For example, miR-145, miR-133a and miR-133b have been found to be tumor-suppressive miRNAs that directly regulate the oncogene FSCN1. [5] Changes in miRNA expression have been detected in many types of human cancers, in a way that seems to be linked to genomic amplifications, mutations, and deletions. "MiRNA expression fingerprints correlate with clinical and biological characteristics of tumours, including tissue type, differentiation, aggression and response to therapy." [1]
  • Some bacteria use miRNA to target and post-transcriptionally repress proteins that are involved in innate immune response, [2] and other bacteria release effectors that inhibit miRNA immune response. [3] (Conversely, some miRNA-regulated immune response pathways are activated by bacteria. [4])
  • Bacteria could be designed to treat various kinds of tumors based on their miRNA expression fingerprint through up/down regulation of oncogene miRNA expression.

Potential Problems

  • Immune response
    • Cancer patients may already be immunocompromised through other treatments, so this may not be as big of an issue as it would initially seem, but this leads to...
  • Pathogenicity
    • If my 20.020 project taught me anything, it's that people are squeamish about introducing bacteria into things even if there isn't anything to point towards it being problematic.
    • Would saying that there should be nothing wrong with the chassis and that it'll have to go through clinical testing be enough?
  • Targeting of cancer cells
    • Bacteria do not specifically target things based on miRNA signatures
    • Could we rely on bacteria to stay localized, depending on treatment method?
    • Would regulation of oncogenes in non-target area be an issue? I want to think it would just make cancer-causing mutations even less likely in affected areas, even if they were not cancerous in the first place...
  • Targeting of miRNAs
    • This is going to be what we say the focus of the research will be, right?
    • Do we know enough to take a stab at this? It may be worth reading that third paper closer to see if they specify any sort of mechanism...

References

  1. Calin, George A., and Carlo M. Croce. "MicroRNA signatures in human cancers." Nature Reviews Cancer 6.11 (2006): 857-866.
  2. Ma, Feng, et al. "The microRNA miR-29 controls innate and adaptive immune responses to intracellular bacterial infection by targeting interferon-γ."Nature immunology 12.9 (2011): 861-869.
  3. Navarro, Lionel, et al. "Suppression of the microRNA pathway by bacterial effector proteins." Science 321.5891 (2008): 964-967.
  4. Taganov, Konstantin D., et al. "NF-κB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses." Proceedings of the National Academy of Sciences 103.33 (2006): 12481-12486.
  5. Kano, M., Seki, N., Kikkawa, N., Fujimura, L., Hoshino, I., Akutsu, Y., Chiyomaru, T., Enokida, H., Nakagawa, M. and Matsubara, H. (2010), miR-145, miR-133a and miR-133b: Tumor-suppressive miRNAs target FSCN1 in esophageal squamous cell carcinoma. Int. J. Cancer, 127: 2804–2814.
Recent changes

20 October 2017

     11:29 

BME100 f2017:Group5 W0800 L4‎‎ (5 changes | history) . . (+62). . [Anna Hoge‎ (5×)]

     

11:29

(cur | prev) . . (+1). . Anna Hoge (talk | contribs) (SNP Information & Primer Design)

     

11:29

(cur | prev) . . (+2). . Anna Hoge (talk | contribs) (SNP Information & Primer Design)

     

11:28

(cur | prev) . . (0). . Anna Hoge (talk | contribs) (SNP Information & Primer Design)

     

11:27

(cur | prev) . . (+62). . Anna Hoge (talk | contribs) (SNP Information & Primer Design)

     

11:26

(cur | prev) . . (-3). . Anna Hoge (talk | contribs) (Protocol)

     11:25 

(Upload log). .

[Anna Hoge‎ (2×)]

     

11:25

. . Anna Hoge (talk | contribs) uploaded File:AHprimers2.png

     

11:23

. . Anna Hoge (talk | contribs) uploaded File:AHprimers1.png

     09:23  Carrico‎ (diff | hist) . . (-305). . Yar (talk | contribs) (use mediawiki markup for images, not raw html)
     09:15 (User creation log) . . User account Msupestka (talk | contribs) was created by Yar (talk | contribs) and password was sent by email ‎

 m   08:27 

Beauchamp:DataSharing‎‎ (2 changes | history) . . (+228). . [John Magnotti‎ (2×)]

 m   

08:27

(cur | prev) . . (-2). . John Magnotti (talk | contribs)

 m   

08:27

(cur | prev) . . (+230). . John Magnotti (talk | contribs)

     08:02  Peyton: Lab Meeting Schedule Fall 2017‎ (diff | hist) . . (0). . Maria F. Gencoglu (talk | contribs)
     07:49  Min-Ho Kim Lab:Lab Members‎ (diff | hist) . . (-89). . Min-Ho Kim (talk | contribs)

19 October 2017

     21:07  BME100 f2017:Group7 W0800 L4‎ (diff | hist) . . (+977). . Miguel R. Almanza Lopez (talk | contribs) (SNP Information & Primer Design)

     18:43 

BME100 f2017:Group6 W1030 L4‎‎ (4 changes | history) . . (+1,447). . [Ray Gerard Regorgo‎ (4×)]

     

18:43

(cur | prev) . . (-196). . Ray Gerard Regorgo (talk | contribs) (OUR TEAM)

     

18:42

(cur | prev) . . (-3). . Ray Gerard Regorgo (talk | contribs) (OUR TEAM)

     

17:59

(cur | prev) . . (-3). . Ray Gerard Regorgo (talk | contribs) (Research and Development)

     

16:46

(cur | prev) . . (+1,649). . Ray Gerard Regorgo (talk | contribs) (Research and Development)

     15:43  User:Julie A. Fogarty‎ (diff | hist) . . (+46). . Julie A. Fogarty (talk | contribs) (Julie A. Fogarty)

     15:33 

Rich Lab:Funding‎‎ (2 changes | history) . . (-12). . [Isabel C. Morales‎ (2×)]

     

15:33

(cur | prev) . . (+12). . Isabel C. Morales (talk | contribs)

     

14:06

(cur | prev) . . (-24). . Isabel C. Morales (talk | contribs)

     14:58  CONJ606:Materials‎ (diff | hist) . . (+685). . Peteral (talk | contribs) (Week 2: Me Myself and I-dentifiers, The Key To Immortality (Persistence))

     14:52 

User:Peteral‎‎ (2 changes | history) . . (+536). . [Peteral‎ (2×)]

     

14:52

(cur | prev) . . (+185). . Peteral (talk | contribs) (Alec's Discussion Questions)

     

13:52

(cur | prev) . . (+351). . Peteral (talk | contribs) (Alec's Discussion Questions)

     14:13 

BME100 f2017:Group14 W0800 L4‎‎ (9 changes | history) . . (+9). . [Shae M. Diaz‎ (9×)]

     

14:13

(cur | prev) . . (+8). . Shae M. Diaz (talk | contribs) (Protocol)

     

14:12

(cur | prev) . . (-31). . Shae M. Diaz (talk | contribs) (TEAM MEMBERS)

     

14:10

(cur | prev) . . (+31). . Shae M. Diaz (talk | contribs) (TEAM MEMBERS)

     

14:09

(cur | prev) . . (+4). . Shae M. Diaz (talk | contribs) (TEAM MEMBERS)

     

14:05

(cur | prev) . . (-1). . Shae M. Diaz (talk | contribs) (TEAM MEMBERS)

     

14:05

(cur | prev) . . (+1). . Shae M. Diaz (talk | contribs) (TEAM MEMBERS)

     

14:04

(cur | prev) . . (-1). . Shae M. Diaz (talk | contribs) (TEAM MEMBERS)

     

13:55

(cur | prev) . . (+1). . Shae M. Diaz (talk | contribs) (TEAM MEMBERS)

     

13:55

(cur | prev) . . (-3). . Shae M. Diaz (talk | contribs) (TEAM MEMBERS)

 m   14:12  Swartz‎ (diff | hist) . . (+61). . Marcus Rohovie (talk | contribs)
     14:10 (Move log) . . Marcus Rohovie (talk | contribs) moved page Swartz to Swartz:Main

     14:08 

(Upload log). .

[Thorntca‎; Shae M. Diaz‎ (3×)]

     

14:08

. . Shae M. Diaz (talk | contribs) uploaded File:100profileshae.JPG

     

14:01

. . Shae M. Diaz (talk | contribs) uploaded File:Shaediaz100.JPG

     

13:51

. . Shae M. Diaz (talk | contribs) uploaded File:BME100ShaeD.JPG

     

13:17

. . Thorntca (talk | contribs) uploaded File:2Dgel.png.jpg

     13:52 

Klenow Assembly Method: Seamless cloning‎‎ (3 changes | history) . . (+101). . [David M.D. Bailey‎ (3×)]

     

13:52

(cur | prev) . . (-5). . David M.D. Bailey (talk | contribs) (The Klenow Assembly Method (KAM) for the seamless cloning of overlapping double stranded DNA fragments: Very cheap alternative to the Gibson Assembly)

     

13:51

(cur | prev) . . (+1). . David M.D. Bailey (talk | contribs) (The Klenow Assembly Method (KAM) for the seamless cloning of overlapping double stranded DNA fragments: Very cheap alternative to the Gibson Assembly)

     

13:50

(cur | prev) . . (+105). . David M.D. Bailey (talk | contribs) (The Klenow Assembly Method (KAM) for the seamless cloning of overlapping double stranded DNA fragments: Very cheap alternative to the Gibson Assembly)

     13:22 

User:Thorntca‎‎ (8 changes | history) . . (+529). . [Thorntca‎ (8×)]

     

13:22

(cur | prev) . . (+145). . Thorntca (talk | contribs)

     

13:19

(cur | prev) . . (+17). . Thorntca (talk | contribs)

     

13:19

(cur | prev) . . (+4). . Thorntca (talk | contribs)

     

13:18

(cur | prev) . . (+30). . Thorntca (talk | contribs)

     

13:16

(cur | prev) . . (+417). . Thorntca (talk | contribs)

     

12:52

(cur | prev) . . (+12). . Thorntca (talk | contribs)

     

12:51

(cur | prev) . . (-5). . Thorntca (talk | contribs)

     

12:51

(cur | prev) . . (-91). . Thorntca (talk | contribs)