Targeting FPR1 and CXCR4 in cancer and the contribution of the tumor microenvironment

Boer, J., 2015, [Groningen]: University of Groningen. 213 p.

Research output: ThesisThesis fully internal (DIV)

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  • Chapter 1

    Final publisher's version, 127 KB, PDF document

  • Title and contents

    Final publisher's version, 192 KB, PDF document

  • Chapter 2

    Final publisher's version, 280 KB, PDF document

  • Chapter 3

    Final publisher's version, 316 KB, PDF document

  • Chapter 4

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  • Chapter 5

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  • Chapter 6

    Final publisher's version, 1.05 MB, PDF document

  • Chapter 7

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  • Chapter 8

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  • Chapter 9

    Final publisher's version, 128 KB, PDF document

  • Chapter 10

    Final publisher's version, 181 KB, PDF document

  • Complete thesis

    Final publisher's version, 2.77 MB, PDF document

  • Propositions

    Final publisher's version, 547 KB, PDF document

  • Jennifer Boer
Solid tumors can be primarily resistant or could become resistant to therapy, due to the protective effect of their direct tumor environment, which is called the microenvironment. UMCG-researcher Jennifer Boer studied the interaction of glioblastoma (GBM) and prostate cancer cells with their tumor microenvironment. In this context she investigated the role of two membrane bound proteins (receptors) called formyl peptide receptor-1 (FPR1) and chemokine receptor-4 (CXCR4).
From laboratory research it became evident that both receptors are involved in the migration and possible dissemination of tumor cells, which migrate towards their ligands present in the microenvironment. The ligands for FPR1 are formyl-methionil-leucine-lysine-isoleucine-valine (fMLKLIV) and formyl-methionil-methionil-tyrosine-alanine-leucine-phenylalanine (fMMYALF), which are released when unregulated cell death occurs. Jennifer Boer used the chemotaxis inhibitory protein of S. aureus (CHIPS), in order to inhibit the migration of FPR1-positive tumor cells. In a preclinical setting the use of this bacterial derived protein led to a slight survival improvement. When CXCR4 is activated by its ligand CXCL12, the receptor contributes to tumor cell mobility but also to therapy resistance mediated by the tumor microenvironment. The CXCR4 inhibitor AMD3100 transiently sensitizes prostate cancer cells to radiation therapy but eventually leads to an increase of circulating tumor cells. According to Jennifer Boer this is an important aspect that should be taken in consideration when designing future clinical trials that involve the use of CXCR4 inhibitors. She concludes that therapies targeting FPR1 and CXCR4 may contribute to the development of new cancer treatments.
Original languageEnglish
QualificationDoctor of Philosophy
Awarding Institution
Award date15-Jun-2015
Place of Publication[Groningen]
Print ISBNs978-90-367-7914-2
Electronic ISBNs978-90-367-7919-7
Publication statusPublished - 2015

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