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How do cancer cells migrate? Investigating the mechanisms of migration (MUELLERAU19SF)

  • Full or part time
  • Application Deadline
    Friday, May 31, 2019
  • Self-Funded PhD Students Only
    Self-Funded PhD Students Only

Project Description

The migration of cancerous cells is controlled by a number of pro-inflammatory macromolecules such as chemokines and their receptors. When chemokine receptors become activated, a diverse signalling network is stimulated inside the cell, which will ultimately lead to cell migration. If this happens in cancer cells, then this process can lead to the development of secondary tumours. Several members of the signalling networks are kinases, enzymes which can phosphorylate other proteins. In this PhD project we will investigate which kinases are activated by chemokine receptors during the migratory response. Understanding how these receptors lead to cell migration and how kinases are involved in this will provide us with novel therapeutic targets which can eventually lead to medicine which can reduce or even prevent cancer metastasis.

For more information on the supervisor for this project, please go here: http://www.uea.ac.uk/pharmacy/people/profile/anja-mueller

Type of programme: PhD

Project start date: October 2019

Mode of study: Full time

Entry requirements: Acceptable first degree - MPharm, Biological Sciences, Biomedicine, Pharmacology.
The standard minimum entry requirement is 2:1.

Deadline for applications: 31 May 2019

Funding Notes

This PhD project is offered on a self-funding basis. It is open to applicants with funding or those applying to funding sources. Details of tuition fees can be found at View Website.

A bench fee is also payable on top of the tuition fee to cover specialist equipment or laboratory costs required for the research. The amount charged annually will vary considerably depending on the nature of the project and applicants should contact the primary supervisor for further information about the fee associated with the project.

References

i) Mills SC, Goh PH, Kudatsih J, Ncube S, Gurung R, Maxwell W and Mueller A (2016) Cell migration towards CXCL12 in leukemic cells compared to breast cancer cells. Cell Signal. 2016 Jan 21;28(4):316-324. doi: 10.1016/j.cellsig.2016.01.006.

ii) Jacques RO, Mills SC, Cazzonatto Zerwes P, Fagade FO, Green JE, Downham S, Sexton DW and Mueller A (2015) Dynamin function is important for CC-chemokine receptor induced cell migration, Cell Biochemistry and Function, Cell Biochem Funct. 2015 Aug;33(6):407-14. doi: 10.1002/cbf.3131

iii) Kerr JS, Jacques RO, Moyano Cardaba C, Tse T, Sexton D, Mueller A (2013) Differential regulation of chemotaxis: Role of Gβγ in chemokine receptor-induced cell migration. Cell Signal. Volume 25, Issue 4, April 2013, Pages 729–735, doi:pii: S0898-6568(12)00352-X. 10.1016/j.cellsig.2012.12.015.

iv) Khabbazi S, Jacques RO, Moyano Cardaba C, Mueller A (2012) Jak2 and Stat3 activation is not essential for CCL3, CCL5 or CCL8 induced chemotaxis. Cell Biochemistry and Function, Volume 31, Issue 4, June 2013, Pages: 312–318

v) Moyano Cardaba, C., Jacques, R.O., Barrett, J.E., Hassell, K.M., Kavanagh, A., Remington, F.C., Tse, T., Mueller, A. (2012) CCL3 induced migration occurs independently of intracellular calcium release, Biochem Biophys Res Commun. 2012 418(1):17-21. Epub 2011 Dec 22, http://dx.doi.org/10.1016/j.bbrc.2011.12.081

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