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You searched for +publisher:"University of Adelaide" +contributor:("White, Deborah Lee"). Showing records 1 – 9 of 9 total matches.

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University of Adelaide

1. Tang, Carine. TKI resistance in CML cell lines : investigating resistance pathways.

Degree: 2012, University of Adelaide

 Chronic myeloid leukaemia (CML) is characterised by the presence of the Philadelphia chromosome which harbours the Bcr-Abl oncogene. BCR-ABL is a constitutively active tyrosine kinase… (more)

Subjects/Keywords: CML; imatinib; nilotinib; dasatinib; TKI; resistance

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Tang, C. (2012). TKI resistance in CML cell lines : investigating resistance pathways. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/82443

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Tang, Carine. “TKI resistance in CML cell lines : investigating resistance pathways.” 2012. Thesis, University of Adelaide. Accessed August 25, 2019. http://hdl.handle.net/2440/82443.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Tang, Carine. “TKI resistance in CML cell lines : investigating resistance pathways.” 2012. Web. 25 Aug 2019.

Vancouver:

Tang C. TKI resistance in CML cell lines : investigating resistance pathways. [Internet] [Thesis]. University of Adelaide; 2012. [cited 2019 Aug 25]. Available from: http://hdl.handle.net/2440/82443.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tang C. TKI resistance in CML cell lines : investigating resistance pathways. [Thesis]. University of Adelaide; 2012. Available from: http://hdl.handle.net/2440/82443

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Adelaide

2. Wang, Jueqiong. Investigating drugs that enhance imatinib uptake and factors which contribute to the functional activity of OCT-1 CML Cells.

Degree: 2013, University of Adelaide

 In CML cells, the functional OCT-1 activity (OA) in mononuclear cells (MNC) from de novo chronic myeloid leukaemia patients in chronic phrase (CP-CML) is significantly… (more)

Subjects/Keywords: chronic myeloid leukaemia; functional OCT-1 activity; diclofenac; drug-drug interaction; peroxisome proliferator-activated receptor γ

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APA (6th Edition):

Wang, J. (2013). Investigating drugs that enhance imatinib uptake and factors which contribute to the functional activity of OCT-1 CML Cells. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/88837

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Wang, Jueqiong. “Investigating drugs that enhance imatinib uptake and factors which contribute to the functional activity of OCT-1 CML Cells.” 2013. Thesis, University of Adelaide. Accessed August 25, 2019. http://hdl.handle.net/2440/88837.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Wang, Jueqiong. “Investigating drugs that enhance imatinib uptake and factors which contribute to the functional activity of OCT-1 CML Cells.” 2013. Web. 25 Aug 2019.

Vancouver:

Wang J. Investigating drugs that enhance imatinib uptake and factors which contribute to the functional activity of OCT-1 CML Cells. [Internet] [Thesis]. University of Adelaide; 2013. [cited 2019 Aug 25]. Available from: http://hdl.handle.net/2440/88837.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wang J. Investigating drugs that enhance imatinib uptake and factors which contribute to the functional activity of OCT-1 CML Cells. [Thesis]. University of Adelaide; 2013. Available from: http://hdl.handle.net/2440/88837

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Adelaide

3. Schafranek, Lisa Rhiannon. Assessment of critical survival mechanisms exploited by BCR-ABL1+ cells to evade tyrosine kinase inhibitor-induced death: determination of novel therapeutic targets in chronic myeloid leukaemia.

Degree: 2014, University of Adelaide

 Chronic myeloid leukaemia (CML) is a clonal myeloid proliferative disease that results from constitutive activation of the Bcr-Abl oncoprotein, which disrupts normal cellular signalling potentiating… (more)

Subjects/Keywords: Chronic Myeloid Leukaemia; BCR-ABL; Tyrosine Kinase Inhibitor; Dasatinib; Resistance; Autophagy; STAT5; JAK; Cytokine

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Schafranek, L. R. (2014). Assessment of critical survival mechanisms exploited by BCR-ABL1+ cells to evade tyrosine kinase inhibitor-induced death: determination of novel therapeutic targets in chronic myeloid leukaemia. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/92213

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Schafranek, Lisa Rhiannon. “Assessment of critical survival mechanisms exploited by BCR-ABL1+ cells to evade tyrosine kinase inhibitor-induced death: determination of novel therapeutic targets in chronic myeloid leukaemia.” 2014. Thesis, University of Adelaide. Accessed August 25, 2019. http://hdl.handle.net/2440/92213.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Schafranek, Lisa Rhiannon. “Assessment of critical survival mechanisms exploited by BCR-ABL1+ cells to evade tyrosine kinase inhibitor-induced death: determination of novel therapeutic targets in chronic myeloid leukaemia.” 2014. Web. 25 Aug 2019.

Vancouver:

Schafranek LR. Assessment of critical survival mechanisms exploited by BCR-ABL1+ cells to evade tyrosine kinase inhibitor-induced death: determination of novel therapeutic targets in chronic myeloid leukaemia. [Internet] [Thesis]. University of Adelaide; 2014. [cited 2019 Aug 25]. Available from: http://hdl.handle.net/2440/92213.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Schafranek LR. Assessment of critical survival mechanisms exploited by BCR-ABL1+ cells to evade tyrosine kinase inhibitor-induced death: determination of novel therapeutic targets in chronic myeloid leukaemia. [Thesis]. University of Adelaide; 2014. Available from: http://hdl.handle.net/2440/92213

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Adelaide

4. Lee, Oi-Lin. The role of cytokines in governing the expansion of the T315I mutation in chronic myeloid leukaemia.

Degree: 2014, University of Adelaide

 Since the introduction of imatinib, the outlook for patients with chronic myeloid leukaemia (CML) has dramatically improved. However, approximately 30-40% of patients develop intolerance or… (more)

Subjects/Keywords: cytokines; T315I mutation; chronic myeloid leukaemia

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APA (6th Edition):

Lee, O. (2014). The role of cytokines in governing the expansion of the T315I mutation in chronic myeloid leukaemia. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/95313

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Lee, Oi-Lin. “The role of cytokines in governing the expansion of the T315I mutation in chronic myeloid leukaemia.” 2014. Thesis, University of Adelaide. Accessed August 25, 2019. http://hdl.handle.net/2440/95313.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Lee, Oi-Lin. “The role of cytokines in governing the expansion of the T315I mutation in chronic myeloid leukaemia.” 2014. Web. 25 Aug 2019.

Vancouver:

Lee O. The role of cytokines in governing the expansion of the T315I mutation in chronic myeloid leukaemia. [Internet] [Thesis]. University of Adelaide; 2014. [cited 2019 Aug 25]. Available from: http://hdl.handle.net/2440/95313.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lee O. The role of cytokines in governing the expansion of the T315I mutation in chronic myeloid leukaemia. [Thesis]. University of Adelaide; 2014. Available from: http://hdl.handle.net/2440/95313

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Adelaide

5. Eadie, Laura Nicole. Nilotinib efflux and resistance development: the effects of combination and concomitant therapies on the transport and efficacy of Nilotinib.

Degree: 2013, University of Adelaide

 Chronic myeloid leukaemia (CML) is characterised by the presence of Bcr-Abl tyrosine kinase. Tyrosine kinase inhibitors (TKIs), such as imatinib, and more recently nilotinib and… (more)

Subjects/Keywords: Nilotinib; ABC transporters; chronic myeloid leukaemia; nilotinib resistance

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APA (6th Edition):

Eadie, L. N. (2013). Nilotinib efflux and resistance development: the effects of combination and concomitant therapies on the transport and efficacy of Nilotinib. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/96160

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Eadie, Laura Nicole. “Nilotinib efflux and resistance development: the effects of combination and concomitant therapies on the transport and efficacy of Nilotinib.” 2013. Thesis, University of Adelaide. Accessed August 25, 2019. http://hdl.handle.net/2440/96160.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Eadie, Laura Nicole. “Nilotinib efflux and resistance development: the effects of combination and concomitant therapies on the transport and efficacy of Nilotinib.” 2013. Web. 25 Aug 2019.

Vancouver:

Eadie LN. Nilotinib efflux and resistance development: the effects of combination and concomitant therapies on the transport and efficacy of Nilotinib. [Internet] [Thesis]. University of Adelaide; 2013. [cited 2019 Aug 25]. Available from: http://hdl.handle.net/2440/96160.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Eadie LN. Nilotinib efflux and resistance development: the effects of combination and concomitant therapies on the transport and efficacy of Nilotinib. [Thesis]. University of Adelaide; 2013. Available from: http://hdl.handle.net/2440/96160

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Adelaide

6. Asari, Kartini. In vitro modelling of high-risk ALL fusions uncovers genomic alterations and non-canonical signalling pathways as a mode of TKI-resistance – implications for targeted therapy.

Degree: 2018, University of Adelaide

 Treatment-resistant acute lymphoblastic leukaemia (ALL) remains a significant clinical issue. Genomic profiling has identified a subtype of high-risk ALL termed Philadelphia-chromosome-like (Ph-like) ALL that is… (more)

Subjects/Keywords: acute lymphoblastic leukaemia; Ph-like and Ph+; tyrosine kinase; inhibitor resistance; genomic alterations

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APA (6th Edition):

Asari, K. (2018). In vitro modelling of high-risk ALL fusions uncovers genomic alterations and non-canonical signalling pathways as a mode of TKI-resistance – implications for targeted therapy. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/115698

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Asari, Kartini. “In vitro modelling of high-risk ALL fusions uncovers genomic alterations and non-canonical signalling pathways as a mode of TKI-resistance – implications for targeted therapy.” 2018. Thesis, University of Adelaide. Accessed August 25, 2019. http://hdl.handle.net/2440/115698.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Asari, Kartini. “In vitro modelling of high-risk ALL fusions uncovers genomic alterations and non-canonical signalling pathways as a mode of TKI-resistance – implications for targeted therapy.” 2018. Web. 25 Aug 2019.

Vancouver:

Asari K. In vitro modelling of high-risk ALL fusions uncovers genomic alterations and non-canonical signalling pathways as a mode of TKI-resistance – implications for targeted therapy. [Internet] [Thesis]. University of Adelaide; 2018. [cited 2019 Aug 25]. Available from: http://hdl.handle.net/2440/115698.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Asari K. In vitro modelling of high-risk ALL fusions uncovers genomic alterations and non-canonical signalling pathways as a mode of TKI-resistance – implications for targeted therapy. [Thesis]. University of Adelaide; 2018. Available from: http://hdl.handle.net/2440/115698

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Adelaide

7. Lu, Liu. In vitro investigation of intracellular ponatinib transport and modelling ponatinib resistance in BCR-ABL1+cell lines: implications for therapeutic strategies.

Degree: 2016, University of Adelaide

 The use of tyrosine kinase inhibitors (TKIs), which target Bcr-Abl, has become the first-line treatment for chronic myeloid leukemia (CML). However, TKI resistance remains a… (more)

Subjects/Keywords: CML; TKI resistance; ponatinib; Research by Publication

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APA (6th Edition):

Lu, L. (2016). In vitro investigation of intracellular ponatinib transport and modelling ponatinib resistance in BCR-ABL1+cell lines: implications for therapeutic strategies. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/114583

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Lu, Liu. “In vitro investigation of intracellular ponatinib transport and modelling ponatinib resistance in BCR-ABL1+cell lines: implications for therapeutic strategies.” 2016. Thesis, University of Adelaide. Accessed August 25, 2019. http://hdl.handle.net/2440/114583.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Lu, Liu. “In vitro investigation of intracellular ponatinib transport and modelling ponatinib resistance in BCR-ABL1+cell lines: implications for therapeutic strategies.” 2016. Web. 25 Aug 2019.

Vancouver:

Lu L. In vitro investigation of intracellular ponatinib transport and modelling ponatinib resistance in BCR-ABL1+cell lines: implications for therapeutic strategies. [Internet] [Thesis]. University of Adelaide; 2016. [cited 2019 Aug 25]. Available from: http://hdl.handle.net/2440/114583.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lu L. In vitro investigation of intracellular ponatinib transport and modelling ponatinib resistance in BCR-ABL1+cell lines: implications for therapeutic strategies. [Thesis]. University of Adelaide; 2016. Available from: http://hdl.handle.net/2440/114583

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Adelaide

8. Engler, Jane. Cell lineage, cell maturity and BCR-ABL: factors which influence imatinib uptake in chronic myeloid leukaemia.

Degree: 2011, University of Adelaide

 Despite the excellent responses observed in patients with chronic phase (CP) chronic myeloid leukaemia (CML) on imatinib therapy, approximately 25% display primary resistance or suboptimal… (more)

Subjects/Keywords: chronic myeloid leukaemia; imatinib; CD34; organic cation transporter 1; BCR-ABL

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APA (6th Edition):

Engler, J. (2011). Cell lineage, cell maturity and BCR-ABL: factors which influence imatinib uptake in chronic myeloid leukaemia. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/70451

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Engler, Jane. “Cell lineage, cell maturity and BCR-ABL: factors which influence imatinib uptake in chronic myeloid leukaemia.” 2011. Thesis, University of Adelaide. Accessed August 25, 2019. http://hdl.handle.net/2440/70451.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Engler, Jane. “Cell lineage, cell maturity and BCR-ABL: factors which influence imatinib uptake in chronic myeloid leukaemia.” 2011. Web. 25 Aug 2019.

Vancouver:

Engler J. Cell lineage, cell maturity and BCR-ABL: factors which influence imatinib uptake in chronic myeloid leukaemia. [Internet] [Thesis]. University of Adelaide; 2011. [cited 2019 Aug 25]. Available from: http://hdl.handle.net/2440/70451.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Engler J. Cell lineage, cell maturity and BCR-ABL: factors which influence imatinib uptake in chronic myeloid leukaemia. [Thesis]. University of Adelaide; 2011. Available from: http://hdl.handle.net/2440/70451

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

9. Watkins, Dale Benjamin. Defining CP-CML patient subsets associated with poor imatinib uptake and response.

Degree: 2014, University of Adelaide

 The introduction of tyrosine kinase inhibitor (TKI) therapy, specifically imatinib, has dramatically improved the treatment outcome for the majority of chronic phase chronic myeloid leukaemia… (more)

Subjects/Keywords: chronic myeloid leukaemia; OCT-1; response; DNA methylation; gene expression; immunophenotyping

…prior approval of the University of Adelaide and where applicable, any partner institution… …research proposal. SAHMRI (Poster) Prize; The University of Adelaide, Faculty of… …Victoria. xiv School of Medicine Poster Prize; The University of Adelaide, Faculty of Health… 

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Watkins, D. B. (2014). Defining CP-CML patient subsets associated with poor imatinib uptake and response. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/91306

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Watkins, Dale Benjamin. “Defining CP-CML patient subsets associated with poor imatinib uptake and response.” 2014. Thesis, University of Adelaide. Accessed August 25, 2019. http://hdl.handle.net/2440/91306.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Watkins, Dale Benjamin. “Defining CP-CML patient subsets associated with poor imatinib uptake and response.” 2014. Web. 25 Aug 2019.

Vancouver:

Watkins DB. Defining CP-CML patient subsets associated with poor imatinib uptake and response. [Internet] [Thesis]. University of Adelaide; 2014. [cited 2019 Aug 25]. Available from: http://hdl.handle.net/2440/91306.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Watkins DB. Defining CP-CML patient subsets associated with poor imatinib uptake and response. [Thesis]. University of Adelaide; 2014. Available from: http://hdl.handle.net/2440/91306

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

.