Marie McIlroy (0000-0002-0827-8096)

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My research is focused on understanding how tumours utilise bioavailable steriods and the implications this may have on the development of resistance to endocrine therapy. An unsustained response to therapy is a major problem in the treatment of breast cancer, impacting around a third of hormone receptor positive patients. Although there have been advances in the past few decades with regards newer drugs including aromatase inhibitor (AI) therapy, a complete understanding of the mechanisms of resistance to these drugs and how it may be circumvented still evades us. How breast cancer cells adapt to an altered steroid state is unclear and we aim to address this using a combination of proteo-genomic analysis in the translational setting.

We have a number of areas of active research:
Investigation into the role of SGK3 in mediating resistance in endocrine driven breast cancer.
Investigation into the role of the androgen receptor and unique protein interactions in AI resistant breast cancer.

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Royal College of Surgeons in Ireland: Dublin, Dublin, IE

2014-10-01 to present | Lecturer (Surgery)

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Marie McIlroy

https://orcid.org/0000-0002-0827-8096

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Biography

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Employment (3)

Royal College of Surgeons in Ireland: Dublin, Dublin, IE

University College Dublin: Dublin, IE

University of Ulster: Coleraine, Coleraine, GB

Education and qualifications (3)

University of Ulster: Belfast, GB

University of Ulster: Belfast, GB

University of Ulster: Belfast , GB

Professional activities (4)

Society for Endocrinology: Bristol, GB

American Association for Cancer Research: PA, PA, US

Irish Association for Cancer Research: Dublin, IE

European Association for Cancer Research: EU, EU, GB

Funding (4)

An Investigation into the utility of prosaposin as a marker of PI3K inhibitor responsiveness.

S100beta a marker of poor outcome in breast cancer.

Transcription factor HOXC11, a novel SRC-1 binding partner; new pathways in endocrine resistance.

Mechanisms of aromatase resistance in breast cancer patients.

Works (50 of 73)

<i>Mechanisms in endocrinology</i>: hypogonadism and metabolic health in men - novel insights into pathophysiology

Impaired 11β-hydroxysteroid dehydrogenase type 2 activity in kidney disease disrupts 11-oxygenated androgen biosynthesis.

Extra-nuclear and cytoplasmic steroid receptor signalling in hormone dependent cancers

Data from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Data from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplemental Figure 6 from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplemental Figure 6 from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplemental Tables from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplemental Tables from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplementary Figure 1 from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplementary Figure 1 from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplementary Figure 2 from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplementary Figure 2 from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplementary Figure 3 from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplementary Figure 3 from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplementary Figure 4 from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplementary Figure 4 from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplementary Figure 5 from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplementary Figure 5 from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplementary Methods from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Supplementary Methods from Altered Steroid Milieu in AI-Resistant Breast Cancer Facilitates AR Mediated Gene-Expression Associated with Poor Response to Therapy

Characterizing skeletal muscle dysfunction in women with polycystic ovary syndrome

Growth Hormone/Insulin Growth Factor Axis in Sex Steroid Associated Disorders and Related Cancers

Steroid Ligands, the Forgotten Triggers of Nuclear Receptor Action; Implications for Acquired Resistance to Endocrine Therapy

ANDROGEN RECEPTOR AS A MEDIATOR OF RESISTANCE TO AROMATASE INHIBITOR THERAPY

Altered steroid milieu in AI-resistant breast cancer facilitates AR mediated gene-expression associated with poor response to therapy

The divergent function of androgen receptor in breast cancer; analysis of steroid mediators and tumor intracrinology

S100β as a serum marker in endocrine resistant breast cancer.

Transcriptomic Profiling of Sequential Tumors from Breast Cancer Patients Provides a Global View of Metastatic Expression Changes Following Endocrine Therapy.

Prosaposin activates the androgen receptor and potentiates resistance to endocrine treatment in breast cancer.

Abstract P2-05-13: Transcriptomic profiling of patient sequential tumours provides cutting edge view of global metastatic expression changes following endocrine therapy

Abstract P3-05-02: Global characterisation of the SRC-1 transcriptome and rational drug design results in the identification of a novel peptide targeting ADAM22 in endocrine resistance

Abstract P3-05-21: Investigation into the oncogenic potential of the androgen receptor in aromatase inhibitor resistant breast cancer

Abstract P3-05-22: PI3K pathway as a novel target in androgen-driven aromatase inhibitor resistant breast cancer

Erratum: Tamoxifen-induced ER-α-SRC3 interaction in HER2 positive human breast cancer; a possible mechanism for ER isoform specific recurrence (Endocr Relat Cancer 21:5 (X1-X3) 10.1677/erc.1.01222e)

Survival benefit conferred by the androgen receptor is lost in aromatase inhibitor treated breast cancer

Epigenetic reprogramming of HOXC10 in endocrine-resistant breast cancer

Global gene repression by the steroid receptor coactivator SRC-1 promotes oncogenesis

Abstract PD3-5: Survival benefit conferred by the androgen receptor is lost in aromatase inhibitor treated breast cancer

Survival Benefit Conferred by the Androgen Receptor is Lost in Aromatase Inhibitor Treated Breast Cancer

A Novel Mechanism for SRC-1 in Suppressing the Luminal a Phenotype in Endocrine Resistant Breast Cancer

PAR-4: A Novel Marker of Luminal A Breast Cancer is Down-Regulated by SRC-1 and HOXC11

AIB1:ERα Transcriptional activity is selectively enhanced in aromatase inhibitor-resistant breast cancer cells

Global characterisation of the SRC-1 transciptome identifies disintegrin C as an ER-independent mediator of endocrine resistant breast cancer

Cross-talk between steroid and developmental pathways mediates recurrence in endocrine resistant breast cancer

Global characterization of the SRC-1 transcriptome identifies ADAM22 as an ER-independent mediator of endocrine resistant breast cancer

Global characterization of the SRC-1 transcriptome identifies ADAM22 as an ER-independent mediator of endocrine-resistant breast cancer

Identifying new transcriptional targets for SRC-1 in breast cancer

The functional role of metalloproteinaseC as an ER independent mediator of endocrine resistant metastatic breast cancer

RuvBl2 cooperates with Ets2 to transcriptionally regulate hTERT in colon cancer