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1. Tumor Biomechanics Alters Metastatic Dissemination of Triple Negative Breast Cancer via Rewiring Fatty Acid Metabolism

Author

Filipe, Elysse C., primary, Velayuthar, Sipiththa, additional, Philp, Ashleigh, additional, Nobis, Max, additional, Latham, Sharissa L., additional, Parker, Amelia L., additional, Murphy, Kendelle J., additional, Wyllie, Kaitlin, additional, Major, Gretel S., additional, Contreras, Osvaldo, additional, Mok, Ellie T. Y., additional, Enriquez, Ronaldo F., additional, McGowan, Suzanne, additional, Feher, Kristen, additional, Quek, Lake‐Ee, additional, Hancock, Sarah E., additional, Yam, Michelle, additional, Tran, Emmi, additional, Setargew, Yordanos F. I., additional, Skhinas, Joanna N., additional, Chitty, Jessica L., additional, Phimmachanh, Monica, additional, Han, Jeremy Z. R., additional, Cadell, Antonia L., additional, Papanicolaou, Michael, additional, Mahmodi, Hadi, additional, Kiedik, Beata, additional, Junankar, Simon, additional, Ross, Samuel E., additional, Lam, Natasha, additional, Coulson, Rhiannon, additional, Yang, Jessica, additional, Zaratzian, Anaiis, additional, Da Silva, Andrew M., additional, Tayao, Michael, additional, Chin, Ian L., additional, Cazet, Aurélie, additional, Kansara, Maya, additional, Segara, Davendra, additional, Parker, Andrew, additional, Hoy, Andrew J., additional, Harvey, Richard P., additional, Bogdanovic, Ozren, additional, Timpson, Paul, additional, Croucher, David R., additional, Lim, Elgene, additional, Swarbrick, Alexander, additional, Holst, Jeff, additional, Turner, Nigel, additional, Choi, Yu Suk, additional, Kabakova, Irina V., additional, Philp, Andrew, additional, and Cox, Thomas R., additional

Published
2024
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2. The International Academy of Cytology Yokohama System for Reporting Breast Fine Needle Aspiration Biopsy Cytopathology: Introduction and Overview

Author

Field, Andrew S., Raymond, Wendy A., Rickard, Mary T., Arnold, Lauren, Brachtel, Elena F., Chaiwun, Benjaporn, Chen, Lan, Chong, P. Y., Di Bonito, Luigi, Hoda, Rana S., Kurtycz, Daniel F. I., Lee, Andrew H. S., Lim, Elgene, Ljung, Britt-Marie, Michelow, Pamela, Osamura, Robert Y., Pinamonti, Maurizio, Sauer, Torill, Segara, Davendra, Tse, Gary M., Vielh, Philippe, Schmitt, Fernando, Field, Andrew S., editor, Raymond, Wendy A., editor, and Schmitt, Fernando, editor

Published
2020
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3. Clinical Management

Author

Cohen-Hallaleh, Ruben, Rickard, Mary T., Lim, Elgene, Raymond, Wendy A., Segara, Davendra, Arnold, Lauren, Lee, Andrew H. S., Schmitt, Fernando, Field, Andrew S., Field, Andrew S., editor, Raymond, Wendy A., editor, and Schmitt, Fernando, editor

Published
2020
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4. A single-cell and spatially resolved atlas of human breast cancers

Author

Wu, Sunny Z., Al-Eryani, Ghamdan, Roden, Daniel Lee, Junankar, Simon, Harvey, Kate, Andersson, Alma, Thennavan, Aatish, Wang, Chenfei, Torpy, James R., Bartonicek, Nenad, Wang, Taopeng, Larsson, Ludvig, Kaczorowski, Dominik, Weisenfeld, Neil I., Uytingco, Cedric R., Chew, Jennifer G., Bent, Zachary W., Chan, Chia-Ling, Gnanasambandapillai, Vikkitharan, Dutertre, Charles-Antoine, Gluch, Laurence, Hui, Mun N., Beith, Jane, Parker, Andrew, Robbins, Elizabeth, Segara, Davendra, Cooper, Caroline, Mak, Cindy, Chan, Belinda, Warrier, Sanjay, Ginhoux, Florent, Millar, Ewan, Powell, Joseph E., Williams, Stephen R., Liu, X. Shirley, O’Toole, Sandra, Lim, Elgene, Lundeberg, Joakim, Perou, Charles M., and Swarbrick, Alexander

Published
2021
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6. Cryopreservation of human cancers conserves tumour heterogeneity for single-cell multi-omics analysis

Author

Wu, Sunny Z., Roden, Daniel L., Al-Eryani, Ghamdan, Bartonicek, Nenad, Harvey, Kate, Cazet, Aurélie S., Chan, Chia-Ling, Junankar, Simon, Hui, Mun N., Millar, Ewan A., Beretov, Julia, Horvath, Lisa, Joshua, Anthony M., Stricker, Phillip, Wilmott, James S., Quek, Camelia, Long, Georgina V., Scolyer, Richard A., Yeung, Bertrand Z., Segara, Davendra, Mak, Cindy, Warrier, Sanjay, Powell, Joseph E., O’Toole, Sandra, Lim, Elgene, and Swarbrick, Alexander

Published
2021
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8. Stromal cell diversity associated with immune evasion in human triple‐negative breast cancer

Author

Wu, Sunny Z, Roden, Daniel L, Wang, Chenfei, Holliday, Holly, Harvey, Kate, Cazet, Aurélie S, Murphy, Kendelle J, Pereira, Brooke, Al‐Eryani, Ghamdan, Bartonicek, Nenad, Hou, Rui, Torpy, James R, Junankar, Simon, Chan, Chia‐Ling, Lam, Chuan En, Hui, Mun N, Gluch, Laurence, Beith, Jane, Parker, Andrew, Robbins, Elizabeth, Segara, Davendra, Mak, Cindy, Cooper, Caroline, Warrier, Sanjay, Forrest, Alistair, Powell, Joseph, O'Toole, Sandra, Cox, Thomas R, Timpson, Paul, Lim, Elgene, Liu, X Shirley, and Swarbrick, Alexander

Published
2020
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10. Common activation of canonical Wnt signaling in pancreatic adenocarcinoma.

Author

Pasca di Magliano, Marina, Biankin, Andrew V, Heiser, Patrick W, Cano, David A, Gutierrez, Pedro JA, Deramaudt, Therese, Segara, Davendra, Dawson, Amanda C, Kench, James G, Henshall, Susan M, Sutherland, Robert L, Dlugosz, Andrzej, Rustgi, Anil K, and Hebrok, Matthias

Subjects
Animals, Humans, Mice, Adenocarcinoma, Pancreatic Neoplasms, Disease Models, Animal, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Wnt Proteins, Hedgehog Proteins, Disease Models, Animal, General Science & Technology
Abstract

Pancreatic ductal adenocarcinoma (PDA) is an extremely aggressive malignancy, which carries a dismal prognosis. Activating mutations of the Kras gene are common to the vast majority of human PDA. In addition, recent studies have demonstrated that embryonic signaling pathway such as Hedgehog and Notch are inappropriately upregulated in this disease. The role of another embryonic signaling pathway, namely the canonical Wnt cascade, is still controversial. Here, we use gene array analysis as a platform to demonstrate general activation of the canonical arm of the Wnt pathway in human PDA. Furthermore, we provide evidence for Wnt activation in mouse models of pancreatic cancer. Our results also indicate that Wnt signaling might be activated downstream of Hedgehog signaling, which is an early event in PDA evolution. Wnt inhibition blocked proliferation and induced apoptosis of cultured adenocarcinoma cells, thereby providing evidence to support the development of novel therapeutical strategies for Wnt inhibition in pancreatic adenocarcinoma.

Published
2007

11. Common Activation of Canonical Wnt Signaling in Pancreatic Adenocarcinoma

Author

di Magliano, Marina Pasca, Biankin, Andrew V, Heiser, Patrick W, Cano, David A, Gutierrez, Pedro JA, Deramaudt, Therese, Segara, Davendra, Dawson, Amanda C, Kench, James G, Henshall, Susan M, Sutherland, Robert L, Dlugosz, Andrzej, Rustgi, Anil K, and Hebrok, Matthias

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Rare Diseases, Digestive Diseases, Pancreatic Cancer, Cancer, Aetiology, 2.1 Biological and endogenous factors, Adenocarcinoma, Animals, Disease Models, Animal, Hedgehog Proteins, Humans, Mice, Pancreatic Neoplasms, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Wnt Proteins, General Science & Technology
Abstract

Pancreatic ductal adenocarcinoma (PDA) is an extremely aggressive malignancy, which carries a dismal prognosis. Activating mutations of the Kras gene are common to the vast majority of human PDA. In addition, recent studies have demonstrated that embryonic signaling pathway such as Hedgehog and Notch are inappropriately upregulated in this disease. The role of another embryonic signaling pathway, namely the canonical Wnt cascade, is still controversial. Here, we use gene array analysis as a platform to demonstrate general activation of the canonical arm of the Wnt pathway in human PDA. Furthermore, we provide evidence for Wnt activation in mouse models of pancreatic cancer. Our results also indicate that Wnt signaling might be activated downstream of Hedgehog signaling, which is an early event in PDA evolution. Wnt inhibition blocked proliferation and induced apoptosis of cultured adenocarcinoma cells, thereby providing evidence to support the development of novel therapeutical strategies for Wnt inhibition in pancreatic adenocarcinoma.

Published
2007

12. Data from Androgen Receptor Inhibits Estrogen Receptor-α Activity and Is Prognostic in Breast Cancer

Author

Peters, Amelia A., primary, Buchanan, Grant, primary, Ricciardelli, Carmela, primary, Bianco-Miotto, Tina, primary, Centenera, Margaret M., primary, Harris, Jonathan M., primary, Jindal, Shalini, primary, Segara, Davendra, primary, Jia, Li, primary, Moore, Nicole L., primary, Henshall, Susan M., primary, Birrell, Stephen N., primary, Coetzee, Gerhard A., primary, Sutherland, Robert L., primary, Butler, Lisa M., primary, and Tilley, Wayne D., primary

Published
2023
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13. Supplementary Tables 1-3 from Androgen Receptor Inhibits Estrogen Receptor-α Activity and Is Prognostic in Breast Cancer

Author

Peters, Amelia A., primary, Buchanan, Grant, primary, Ricciardelli, Carmela, primary, Bianco-Miotto, Tina, primary, Centenera, Margaret M., primary, Harris, Jonathan M., primary, Jindal, Shalini, primary, Segara, Davendra, primary, Jia, Li, primary, Moore, Nicole L., primary, Henshall, Susan M., primary, Birrell, Stephen N., primary, Coetzee, Gerhard A., primary, Sutherland, Robert L., primary, Butler, Lisa M., primary, and Tilley, Wayne D., primary

Published
2023
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14. Abstract OT2-01-10: WinPro: A window of opportunity study of endocrine therapy with and without prometrium in postmenopausal women with early-stage hormone receptor-positive breast cancer

Author

Downton, Teesha, primary, Segara, Davendra, additional, Ong, Andrew, additional, Bingham, Janne, additional, Carson, Emma-Kate, additional, Chen, Julia, additional, Middleton, Kate, additional, Lindeman, Geoffrey, additional, Parker, Andrew, additional, and Lim, Elgene, additional

Published
2023
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15. Oral Selective Estrogen Receptor Degraders (SERDs) in Breast Cancer: Advances, Challenges, and Current Status

Author

Downton,Teesha, Zhou,Fiona, Segara,Davendra, Jeselsohn,Rinath, and Lim,Elgene

Subjects
Drug Design, Development and Therapy
Abstract

Teesha Downton,1,2 Fiona Zhou,1,2 Davendra Segara,1 Rinath Jeselsohn,3,* Elgene Lim1,2,* 1Garvan Institute of Medical Research, Sydney, NSW, Australia; 2School of Clinical Medicine, St Vincent’s Healthcare Clinical Campus, Faculty of Medicine and Health, University of New South Wales, Sydney, NSW, Australia; 3Dana-Farber Cancer Institute, Boston, MA, USA*These authors contributed equally to this workCorrespondence: Elgene Lim, Tel +61 2 9355 5600, Fax +61 2 9355 5602, Email e.lim@garvan.org.auAbstract: Several endocrine therapies are currently available for the treatment of estrogen receptor (ER) positive breast cancer, but the clinical benefit of these agents is limited by endocrine therapy drug resistance. A common mechanism of endocrine therapy resistance is ESR1 mutations. The first-generation selective estrogen receptor degrader (SERD) fulvestrant has activity against ESR1 mutant tumors but requires intramuscular injection and has poor bioavailability that precludes optimal drug dosing. This led to the development of second-generation SERDs which are potent and have improved oral bioavailability and pharmacokinetics. Several of these oral SERDs are now in phase III trials in both the early and advanced ER positive breast cancer settings. This review summarizes the background of oral SERD development, the current status and future perspectives.Keywords: selective estrogen receptor degraders, breast cancer, estrogen receptor

Published
2022

19. Abstract PS18-17: Mdm2 inhibition synergises with endocrine therapy or cdk4/6 inhibition for the treatment of estrogen receptor-positive breast cancer

Author

Portman, Neil, primary, Milioli, Heloisa, additional, Alexandrou, Sarah, additional, Coulson, Rhiannon, additional, Yong, Aliza, additional, Fernandez, Kristine, additional, Chia, KeeMing, additional, Halilovic, Ensar, additional, Segara, Davendra, additional, Parker, Andrew, additional, Haupt, Sue, additional, Haupt, Ygal, additional, Tilley, Wayne, additional, Swarbrick, Alex, additional, Caldon, Liz, additional, and Lim, Elgene, additional

Published
2021
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20. Abstract OT-09-07: Winpro: A window of opportunity study of endocrine therapy with and without prometrium in postmenopausal women with early stage hormone receptor-positive breast cancer

Author

Lau, Brandon, primary, Segara, Davendra, additional, Ong, Andrew, additional, Bingham, Janne, additional, Kiely, Belinda, additional, Carson, Emma-Kate, additional, Chen, Julia, additional, Mak, Cindy, additional, Warrier, Sanjay, additional, Hui, Mun, additional, Middleton, Kate, additional, Parker, Andrew, additional, Mann, Bruce, additional, Lindeman, Geoffrey, additional, Tilley, Wayne, additional, and Lim, Elgene, additional

Published
2021
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21. Overexpression of LMO4 induces mammary hyperplasia, promotes cell invasion, and is a predictor of poor outcome in breast cancer

Author

Sum, Eleanor Y.M., Segara, Davendra, Duscio, Belinda, Bath, Mary L., Field, Andrew S., Sutherland, Robert L., Lindeman, Geoffrey J., and Visvader, Jane E.

Subjects
Oncology, Experimental -- Forecasts and trends, Breast cancer -- Causes of, Cancer -- Research, Cancer -- Forecasts and trends, Market trend/market analysis, Science and technology
Abstract

The zinc finger protein LMO4 is overexpressed in a high proportion of breast carcinomas. Here, we report that overexpression of a mouse mammary tumor virus (MMTV)-Lmo4 transgene in the mouse mammary gland elicits hyperplasia and mammary intraepithelial neoplasia or adenosquamous carcinoma in two transgenic strains with a tumor latency of 13-18 months. To investigate cellular processes controlled by LMO4 and those that may be deregulated during oncogenesis, we used RNA interference. Down-regulation of LMO4 expression reduced proliferation of human breast cancer cells and increased differentiation of mouse mammary epithelial cells. Furthermore, small-interfering-RNA-transfected breast cancer cells (MDA-MB-231) had a reduced capacity to migrate and invade an extracellular matrix. Conversely, overexpression of LMO4 in noninvasive, immortalized human MCF10A cells promoted cell motility and invasion. Significantly, in a cohort of 159 primary breast cancers, high nuclear levels of LMO4 were an independent predictor of death from breast cancer. Together, these findings suggest that deregulation of LMO4 in breast epithelium contributes directly to breast neoplasia by altering the rate of cellular proliferation and promoting cell invasion. LIM domain | oncogene | proliferation

Published
2005

22. EDD, the human orthologue of the hyperplastic discs tumour suppressor gene, is amplified and overexpressed in cancer

Author

Clancy, Jennifer L, Henderson, Michelle J, Russell, Amanda J, Anderson, David W, Bova, Ronaldo J, Campbell, Ian G, Choong, David YH, Macdonald, Graeme A, Mann, Graham J, Nolan, Tania, Brady, Ged, Olopade, Olufunmilayo I, Woollatt, Erica, Davies, Michael J, Segara, Davendra, Hacker, Neville F, Henshall, Susan M, Sutherland, Robert L, and Watts, Colin KW

Published
2003
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27. MDM2 Inhibition in Combination with Endocrine Therapy and CDK4/6 Inhibition for the Treatment of ER-Positive Breast Cancer

Author

Portman, Neil, primary, Milioli, Heloisa H., additional, Alexandrou, Sarah, additional, Coulson, Rhiannon, additional, Yong, Aliza, additional, Fernandez, Kristine J., additional, Chia, Kee Ming, additional, Segara, Davendra, additional, Parker, Andrew, additional, Haupt, Sue, additional, Haupt, Ygal, additional, Tilley, Wayne D., additional, Swarbrick, Alex, additional, Caldon, C. Elizabeth, additional, and Lim, Elgene, additional

Published
2020
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28. Cryopreservation of human cancers conserves tumour heterogeneity for single-cell multi-omics analysis

Author

Wu, Sunny Z., primary, Roden, Daniel L., additional, Al-Eryani, Ghamdan, additional, Bartonicek, Nenad, additional, Harvey, Kate, additional, Cazet, Aurelie S., additional, Chan, Chia-Ling, additional, Junankar, Simon, additional, Hui, Mun N., additional, Millar, Ewan, additional, Beretov, Julia, additional, Horvath, Lisa, additional, Joshua, Anthony M., additional, Stricker, Phillip, additional, Wilmott, James S., additional, Quek, Camelia, additional, Long, Georgina V., additional, Scolyer, Richard A., additional, Yeung, Bertrand Z., additional, Segara, Davendra, additional, Mak, Cindy, additional, Warrier, Sanjay, additional, Powell, Joseph, additional, O'Toole, Sandra, additional, Lim, Elgene, additional, and Swarbrick, Alexander, additional

Published
2020
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29. Single-cell analysis reveals diverse stromal subsets associated with immune evasion in triple-negative breast cancer

Author

Wu, Sunny Z., primary, Roden, Daniel L., additional, Wang, Chenfei, additional, Holliday, Holly, additional, Harvey, Kate, additional, Cazet, Aurélie S., additional, Murphy, Kendelle J., additional, Pereira, Brooke, additional, Al-Eryani, Ghamdan, additional, Bartonicek, Nenad, additional, Hou, Rui, additional, Torpy, James R., additional, Junankar, Simon, additional, Chan, Chia-Ling, additional, Lam, Eric, additional, Hui, Mun N., additional, Gluch, Laurence, additional, Beith, Jane, additional, Parker, Andrew, additional, Robbins, Elizabeth, additional, Segara, Davendra, additional, Mak, Cindy, additional, Cooper, Caroline, additional, Warrier, Sanjay, additional, Forrest, Alistair, additional, Powell, Joseph, additional, O’Toole, Sandra, additional, Cox, Thomas R., additional, Timpson, Paul, additional, Lim, Elgene, additional, Liu, X. Shirley, additional, and Swarbrick, Alexander, additional

Published
2020
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30. Loss of STARD10 expression identifies a group of poor prognosis breast cancers independent of HER2/Neu and triple negative status

Author

Murphy, Niamh C., Biankin, Andrew V., Millar, Ewan K.A., McNeil, Catriona M., OʼToole, Sandra A., Segara, Davendra, Crea, Paul, Olayioye, Monilola A., Lee, Soon C., Fox, Stephen B., Morey, Adrienne L., Christie, Michael, Musgrove, Elizabeth A., Daly, Roger J., Lindeman, Geoffrey J., Henshall, Susan M., Visvader, Jane E., and Sutherland, Robert L.

Published
2010
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32. Window of opportunity treatment in breast cancer

Author

Chen, Julia, primary, Easwaralingam, Neshanth, additional, Warrier, Sanjay, additional, Ong, Andrew, additional, Carson, Emma‐Kate, additional, Mak, Cindy, additional, Snook, Kylie, additional, Middleton, Kate, additional, Parker, Andrew, additional, Palmieri, Carlo, additional, Spillane, Andrew, additional, Mann, G. Bruce, additional, Lim, Elgene, additional, and Segara, Davendra, additional

Published
2019
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33. Targeting AR in endocrine-resistant breast cancer

Author

Chia, KeeMing, primary, Milioli, Heloisa, additional, Portman, Neil, additional, Laven-Law, Geraldine, additional, Coulson, Rhiannon, additional, Yong, Aliza, additional, Segara, Davendra, additional, Parker, Andrew, additional, Caldon, Catherine E, additional, Deng, Niantao, additional, Swarbrick, Alexander, additional, Tilley, Wayne D, additional, Hickey, Theresa E, additional, and Lim, Elgene, additional

Published
2019
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34. The WinPro study: A window of opportunity study of endocrine therapy with and without prometrium in postmenopausal women with early stage hormone receptor-positive breast cancer

Author

Chen, Julia, primary, Carson, Emma, additional, Segara, Davendra, additional, Parker, Andrew, additional, O'Toole, Sandra, additional, Coates, Alan, additional, Mann, Bruce, additional, Lindeman, Geoffrey, additional, Tilley, Wayne, additional, and Lim, Elgene, additional

Published
2019
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35. Non-canonical AR activity facilitates endocrine resistance in breast cancer

Author

Chia, KeeMing, primary, Milioli, Heloisa, additional, Portman, Neil, additional, Laven-Law, Geraldine, additional, Coulson, Rhiannon, additional, Yong, Aliza, additional, Segara, Davendra, additional, Parker, Andrew, additional, Caldon, Catherine E, additional, Deng, Niantao, additional, Swarbrick, Alexander, additional, Tilley, Wayne D, additional, Hickey, Theresa E, additional, and Lim, Elgene, additional

Published
2019
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36. The International Academy of Cytology Yokohama System for Reporting Breast Fine-Needle Aspiration Biopsy Cytopathology

Author

Field, Andrew S., primary, Raymond, Wendy A., additional, Rickard, Mary, additional, Arnold, Lauren, additional, Brachtel, Elena F., additional, Chaiwun, Benjaporn, additional, Chen, Lan, additional, Di Bonito, Luigi, additional, Kurtycz, Daniel F.I., additional, Lee, Andrew H.S., additional, Lim, Elgene, additional, Ljung, Britt-Marie, additional, Michelow, Pamela M., additional, Osamura, Robert Y., additional, Pinamonti, Maurizio , additional, Sauer, Torill, additional, Segara, Davendra, additional, Tse, Gary, additional, Vielh, Philippe, additional, Chong, Phek Y., additional, and Schmitt, Fernando, additional

Published
2019
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37. Window of opportunity treatment in breast cancer.

Author

Chen, Julia, Easwaralingam, Neshanth, Warrier, Sanjay, Ong, Andrew, Carson, Emma‐Kate, Mak, Cindy, Snook, Kylie, Middleton, Kate, Parker, Andrew, Palmieri, Carlo, Spillane, Andrew, Mann, G. Bruce, Lim, Elgene, and Segara, Davendra

Subjects
HORMONE receptor positive breast cancer, BREAST cancer, CANCER treatment, CANCER hormone therapy, BIOMARKERS, PREOPERATIVE period
Abstract

Window of opportunity therapies, which involve short‐term administration of systemic therapy between cancer diagnosis and surgery, have raised significant interest in recent years as a mean of assessing the sensitivity of a patient's cancer to therapy prior to surgery. There is now compelling evidence that in patients with early stage hormone‐receptor positive breast cancer, a 2‐week preoperative treatment with standard hormone therapies in a preoperative window period provides important prognostic information, which in turn helps to aid decision‐making regarding treatment options. Changes in short‐term biomarker endpoints such as cell proliferation measured by Ki‐67 can act as surrogate markers of long‐term outcomes. Paired tissues obtained pre‐ and post‐investigational treatment, without having to subject the patient to additional biopsies, can then be used to conduct translational research to investigate predictive biomarkers and pharmacodynamics. In this review, we will examine the utility and challenges of window of opportunities therapies in breast cancer in the current literature, and the current Australian and international trial landscape in this clinical space. [ABSTRACT FROM AUTHOR]

Published
2020
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39. Non-canonical AR activity facilitates endocrine resistance in breast cancer.

Author

KeeMing Chia, Milioli, Heloisa, Portman, Neil, Laven-Law, Geraldine, Coulson, Rhiannon, Yong, Aliza, Segara, Davendra, Parker, Andrew, Caldon, Catherine E., Niantao Deng, Swarbrick, Alexander, Tilley, Wayne D., Hickey, Theresa E., and Lim, Elgene

Subjects
ANDROGEN receptors, BREAST cancer, GENE expression profiling, CELL lines
Abstract

The role of androgen receptor (AR) in endocrine-resistant breast cancer is controversial and clinical trials targeting AR with an AR antagonist (e.g., e nzalutamide) have been initiated. Here, we investigated the consequence of AR antagonism using in vitro and in vivo models of endocrine resistance. AR antagonism in MCF7-derived tamoxifen-resistant (TamR) and long-term estrogen-deprived breast cancer cell lines were achieved using siRNA-mediated knockdown or pharmacological inhibition with enzalutamide. The efficacy of enzalutamide was further assessed in vivo in an estrogen-independent endocrineresistant patient-derived xenograft (PDX) model. Knockdown of AR inhibited the growth of the endocrine-resistant cell line models. Microarray gene expression profiling of the TamR cells following AR knockdown revealed perturbations in proliferative signaling pathways upregulated in endocrine resistance. AR loss also increased some canonical ER signaling events and restored sensitivity of TamR cells to tamoxifen. In contrast, enzalutamide did not recapitulate the effect of AR knockdown in vitro, even though it inhibited canonical AR signaling, which suggests that it is the non-canonical AR activity that facilitated endocrine resistance. Enzalutamide had demonstrable efficacy in inhibiting AR activity in vivo but did not affect the growth of the endocrine-resistant PDX model. Our findings implicate non-canonical AR activity in facilitating an endocrine-resistant phenotype in breast cancer. Unlike canonical AR signaling which is inhibited by enzalutamide, non-canonical AR activity is not effectively antagonized by enzalutamide, and this has important implications in the design of future AR-targeted clinical trials in endocrine-resistant breast cancer. [ABSTRACT FROM AUTHOR]

Published
2019
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41. Studies of retinoic acid signalling in pancreatic cancer

Author

Segara, Davendra

Subjects
Gastrointestinal system -- Cancer, Digestive organs -- Diseases, Pancreas -- Cancer
Abstract

Pancreatic cancer (PC) is the fourth leading cause of cancer death in Western societies. Despite significant progress in understanding the molecular pathology of PC and its precursor lesion: pancreatic intraepithelial neoplasia (PanIN), there remain no molecules with proven clinical utility. Affymetrix Genechipfi oligonucleotide microarrays were used to interrogate mRNA expression of PC and normal pancreas to identify molecular pathways dysregulated in PC. Analysis of these data identified altered expression of numerous components of the S100 Calcium Binding Protein Family, Retinoic Acid signalling pathway and the HOX transcriptional network in PC compared to normal pancreas. These pathways were assessed using immunohistochemistry (IHC) and in-situ hybridisation (ISH) in a cohort of patients with PC. Increased protein expression, of S100A2, S100A6 and S100P was observed in 43%, 60% and 48% of PC respectively. Expression of S100A2 was associated with a poor outcome (p = 0.009), whilst increased expression of S100A6 (p = 0.0008) and S100P (p = 0.0005) were associated with an improved outcome. Additionally, S100A2 expression was identified as an independent marker of outcome in resected tumours. Aberrant expression of retinoic acid signalling components was demonstrated in PC cell lines using semi-quantitative RT-PCR. ISH demonstrated expression of Retinoic Acid Induced 3 (RAI3), an orphan G protein coupled receptor normally expressed in the fetal lung, in 68% of PC, and this co-segregated with an improved overall survival (p = 0.026).Ectopic protein expression of HOXB2, a transcription factor normally expressed in the developing hindbrain and modulated by retinoic acid, was observed in 15% of early PanIN lesions and 38% of PC specimens. Expression of HOXB2 was associated with non-resectable tumours and was an independent predictor of poor survival in resected tumours. Suppression of HOXB2 protein expression using small interfering RNA, resulted in epithelioid trans-differentiation in the Panc-1 PC cell line, however no alteration in proliferation rates were observed compared to controls. This thesis has shown that transcript profiling and tissue validation has identified potential markers of early diagnosis and outcome in PC. Furthermore, pathways and molecules previously thought to be associated with normal human development have been implicated to play a role in the development and progression of PC. Further analyses of these markers will determine any potential role in future diagnostic and therapeutic strategies.

Published
2006
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42. Appendicitis diagnosed on positron emission tomography scan: an 'incidentalitis'.

Author

Pennington, Thomas E., Enoch, Jade F., and Segara, Davendra

Subjects
POSITRON emission tomography, APPENDICITIS
Abstract

The article presents a case study of a 28-year-old female presented with mast cell sarcoma of the right ilium and local nodal involvement. It discussed the laparoscopic appendicectomy of patient results of Histopathological examination that focused acute perforated appendicitis of submucosal mast cells in absence of tumorous aggregation.

Published
2019
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45. Studies of retinoic acid signalling in pancreatic cancer

Author

Segara, Davendra, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW and Segara, Davendra, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW

Abstract

Pancreatic cancer (PC) is the fourth leading cause of cancer death in Western societies. Despite significant progress in understanding the molecular pathology of PC and its precursor lesion: pancreatic intraepithelial neoplasia (PanIN), there remain no molecules with proven clinical utility.Affymetrix Genechipfi oligonucleotide microarrays were used to interrogate mRNA expression of PC and normal pancreas to identify molecular pathways dysregulated in PC. Analysis of these data identified altered expression ofnumerous components of the S100 Calcium Binding Protein Family, Retinoic Acid signalling pathway and the HOX transcriptional network in PC compared to normal pancreas. These pathways were assessed using immunohistochemistry (IHC) and in-situ hybridisation (ISH) in a cohort of patients with PC. Increased protein expression, of S100A2, S100A6 and S100P was observed in 43%, 60% and 48% of PC respectively.Expression of S100A2 was associated with a poor outcome (p = 0.009), whilst increased expression of S100A6 (p = 0.0008) and S100P (p = 0.0005) were associated with an improved outcome. Additionally, S100A2 expression wasidentified as an independent marker of outcome in resected tumours. Aberrant expression of retinoic acid signalling components was demonstrated in PC cell lines using semi-quantitative RT-PCR. ISH demonstrated expression ofRetinoic Acid Induced 3 (RAI3), an orphan G protein coupled receptor normally expressed in the fetal lung, in 68% of PC, and this co-segregated with an improved overall survival (p = 0.026).Ectopic protein expression of HOXB2, atranscription factor normally expressed in the developing hindbrain and modulated by retinoic acid, was observed in 15% of early PanIN lesions and 38% of PC specimens. Expression of HOXB2 was associated with non-resectabletumours and was an independent predictor of poor survival in resected tumours. Suppression of HOXB2 protein expression using small interfering RNA, resulted in epithelioid trans-different

Published
2006

46. Retinoid Signaling in Pancreatic Cancer, Injury and Regeneration

Author

Colvin, Emily K., primary, Susanto, Johana M., additional, Kench, James G., additional, Ong, Vivienna N., additional, Mawson, Amanda, additional, Pinese, Mark, additional, Chang, David K., additional, Rooman, Ilse, additional, O'Toole, Sandra A., additional, Segara, Davendra, additional, Musgrove, Elizabeth A., additional, Sutherland, Robert L., additional, Apte, Minoti V., additional, Scarlett, Christopher J., additional, and Biankin, Andrew V., additional

Published
2011
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47. 41. Differences in cell cycle and apoptotic biomarker expression between molecular subtypes of invasive ductal breast carcinoma

Author

McNeil, Catriona M., primary, O’Toole, Sandra A., additional, Millar, Ewan K.A., additional, Kench, James G., additional, Segara, Davendra, additional, Morey, Adrienne L., additional, Lopez-Knowles, Elena, additional, Crea, Paul, additional, Henshall, Susan M., additional, Musgrove, Elizabeth A., additional, and Sutherland, Robert L., additional

Published
2011
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48. Expression of S100A2 Calcium-Binding Protein Predicts Response to Pancreatectomy for Pancreatic Cancer

Author

Biankin, Andrew V., primary, Kench, James G., additional, Colvin, Emily K., additional, Segara, Davendra, additional, Scarlett, Christopher J., additional, Nguyen, Nam Q., additional, Chang, David K., additional, Morey, Adrienne L., additional, Lee, C.–Soon, additional, Pinese, Mark, additional, Kuo, Samuel C.L., additional, Susanto, Johana M., additional, Cosman, Peter H., additional, Lindeman, Geoffrey J., additional, Visvader, Jane E., additional, Nguyen, Tuan V., additional, Merrett, Neil D., additional, Warusavitarne, Janindra, additional, Musgrove, Elizabeth A., additional, Henshall, Susan M., additional, and Sutherland, Robert L., additional

Published
2009
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49. Androgen Receptor Inhibits Estrogen Receptor-α Activity and Is Prognostic in Breast Cancer

Author

Peters, Amelia A., primary, Buchanan, Grant, additional, Ricciardelli, Carmela, additional, Bianco-Miotto, Tina, additional, Centenera, Margaret M., additional, Harris, Jonathan M., additional, Jindal, Shalini, additional, Segara, Davendra, additional, Jia, Li, additional, Moore, Nicole L., additional, Henshall, Susan M., additional, Birrell, Stephen N., additional, Coetzee, Gerhard A., additional, Sutherland, Robert L., additional, Butler, Lisa M., additional, and Tilley, Wayne D., additional

Published
2009
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