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2. Molecular characterization of low-grade serous ovarian carcinoma identifies genomic aberrations according to hormone receptor expression

Author

Cheasley, Dane, Fernandez, Marta Llaurado, Köbel, Martin, Kim, Hannah, Dawson, Amy, Hoenisch, Joshua, Bittner, Madison, Chiu, Derek S., Talhouk, Aline, Gilks, C. Blake, Jayawardana, Madawa W., Pishas, Kathleen I., Mes-Masson, Anne-Marie, Provencher, Diane, Nigam, Abhimanyu, Hacker, Neville F., Gorringe, Kylie L., Campbell, Ian G., and Carey, Mark S.

Published
2022
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3. Conservative Management of Vulvar Cancer—Where Should We Draw the Line?

Author

Hacker, Neville F. and Barlow, Ellen L.

Subjects
*CONSERVATIVE treatment, *LYMPH nodes, *POSTOPERATIVE care, *SURVIVAL rate, *EARLY detection of cancer, *VULVAR tumors, *GROIN, *SURGICAL margin, *LENGTH of stay in hospitals, *VULVECTOMY, *SURGICAL site, *OVERALL survival
Abstract

Simple Summary: Vulvar cancer is a rare cancer but has a high cure rate if diagnosed early and treated appropriately. In the early 20th century, 5-year survival rates were only 15–20% because of inadequate treatment of both the primary cancer and the groin lymph nodes. By the mid-20th century, 5-year survival rates rose to 60–70% with the introduction of the radical resection of the vulva, together with the radical resection of the groin and usually pelvic lymph nodes. Although cure rates were good, physical and psychological morbidity were high with this extensive surgery. Hence, various modifications have been proposed over the past 50 years to decrease this morbidity without compromising survival, including modifications to the extent of both the vulvectomy and lymph node dissection. This paper looks at the results these modifications have on both survival and morbidity. Vulvar cancer is a rare disease, and cure rates were low until the mid-20th century. The introduction of an en bloc radical vulvectomy and bilateral groin and pelvic lymph node dissection saw them rise from 15–20% to 60–70%. However, this very radical surgery was associated with high physical and psychological morbidity. Wounds were usually left open to granulate, and the average post-operative hospital stay was about 90 days. Many attempts have been made to decrease morbidity without compromising survival. Modifications that have proven to be successful are as follows: (i) the elimination of routine pelvic node dissection, (ii) the use of separate incisions for groin dissection, (iii) the use of unilateral groin dissection for lateral, unifocal lesions, (iv) and radical local excision with 1 cm surgical margins for unifocal lesions. Sentinel node biopsy with ultrasonic groin surveillance for patients with node-negative disease has been the most recent modification and is advocated for patients whose primary cancer is <4 cm in diameter. Controversy currently exists around the need for 1 cm surgical margins around all primary lesions and on the appropriate ultrasonic surveillance for patients with negative sentinel nodes. [ABSTRACT FROM AUTHOR]

Published
2024
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4. Refined cut-off for TP53 immunohistochemistry improves prediction of TP53 mutation status in ovarian mucinous tumors: implications for outcome analyses

Author

Kang, Eun Young, Cheasley, Dane, LePage, Cecile, Wakefield, Matthew J., da Cunha Torres, Michelle, Rowley, Simone, Salazar, Carolina, Xing, Zhongyue, Allan, Prue, Bowtell, David D.L., Mes-Masson, Anne-Marie, Provencher, Diane M., Rahimi, Kurosh, Kelemen, Linda E., Fasching, Peter A., Doherty, Jennifer A., Goodman, Marc T., Goode, Ellen L., Deen, Suha, Pharoah, Paul D.P., Brenton, James D., Sieh, Weiva, Mateoiu, Constantina, Sundfeldt, Karin, Cook, Linda S., Le, Nhu D., Anglesio, Michael S., Gilks, C. Blake, Huntsman, David G., Kennedy, Catherine J., Traficante, Nadia, Bowtell, D., Chenevix-Trench, G., Green, A., Webb, P., DeFazio, A., Gertig, D., Traficante, N., Fereday, S., Moore, S., Hung, J., Harrap, K., Sadkowsky, T., Pandeya, N., Malt, M., Mellon, A., Robertson, R., Bergh, T. Vanden, Jones, M., Mackenzie, P., Maidens, J., Nattress, K., Chiew, Y.E., Stenlake, A., Sullivan, H., Alexander, B., Ashover, P., Brown, S., Corrish, T., Green, L., Jackman, L., Ferguson, K., Martin, K., Martyn, A., Ranieri, B., White, J., Jayde, V., Mamers, P., Bowes, L., Galletta, L., Giles, D., Hendley, J., Alsop, K., Schmidt, T., Shirley, H., Ball, C., Young, C., Viduka, S., Tran, Hoa, Bilic, Sanela, Glavinas, Lydia, Brooks, Julia, Stuart-Harris, R., Kirsten, F., Rutovitz, J., Clingan, P., Glasgow, A., Proietto, A., Braye, S., Otton, G., Shannon, J., Bonaventura, T., Stewart, J., Begbie, S., Friedlander, M., Bell, D., Baron-Hay, S., Ferrier, A., Gard, G., Nevell, D., Pavlakis, N., Valmadre, S., Young, B., Camaris, C., Crouch, R., Edwards, L., Hacker, N., Marsden, D., Robertson, G., Beale, P., Beith, J., Carter, J., Dalrymple, C., Houghton, R., Russell, P., Links, M., Grygiel, J., Hill, J., Brand, A., Byth, K., Jaworski, R., Harnett, P., Sharma, R., Wain, G., Ward, B., Papadimos, D., Crandon, A., Cummings, M., Horwood, K., Obermair, A., Perrin, L., Wyld, D., Nicklin, J., Davy, M., Oehler, M.K., Hall, C., Dodd, T., Healy, T., Pittman, K., Henderson, D., Miller, J., Pierdes, J., Blomfield, P., Challis, D., McIntosh, R., Parker, A., Brown, B., Rome, R., Allen, D., Grant, P., Hyde, S., Laurie, R., Robbie, M., Healy, D., Jobling, T., Manolitsas, T., McNealage, J., Rogers, P., Susil, B., Sumithran, E., Simpson, I., Phillips, K., Rischin, D., Fox, S., Johnson, D., Lade, S., Loughrey, M., O'Callaghan, N., Murray, W., Waring, P., Billson, V., Pyman, J., Neesham, D., Quinn, M., Underhill, C., Bell, R., Ng, L.F., Blum, R., Ganju, V., Hammond, I., Leung, Y., McCartney, A., Buck, M., Haviv, I., Purdie, D., Whiteman, D., Zeps, N., DeFazio, Anna, Kaufmann, Scott, Churchman, Michael, Gourley, Charlie, Stephens, Andrew N., Meagher, Nicola S., Ramus, Susan J., Antill, Yoland C., Campbell, Ian, Scott, Clare L., Köbel, Martin, Gorringe, Kylie L., Ryland, Georgina L., Allan, Prue E., Alsop, Kathryn, Ananda, Sumitra, Au-Yeung, George, Böhm, Maret, Brand, Alison, Chenevix-Trench, Georgia, Christie, Michael, Chiew, Yoke-Eng, Dudley, Rhiannon, Fairweather, Nicole, Fereday, Sian, Fox, Stephen B., Hacker, Neville F., Hadley, Alison M., Hendley, Joy, Ho, Gwo-Yaw, Hunter, Sally M., Jobling, Tom W., Kalli, Kimberly R., Kaufmann, Scott H., Le Page, Cecile, McNally, Orla M., McAlpine, Jessica N., Mileshkin, Linda, Pyman, Jan, Samimi, Goli, Sharma, Ragwha, and Campbell, Ian G.

Published
2021
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9. Proteogenomic analysis of Inhibitor of Differentiation 4 (ID4) in basal-like breast cancer

Author

Baker, Laura A., Holliday, Holly, Roden, Daniel, Krisp, Christoph, Wu, Sunny Z., Junankar, Simon, Serandour, Aurelien A., Mohammed, Hisham, Nair, Radhika, Sankaranarayanan, Geetha, Law, Andrew M. K., McFarland, Andrea, Simpson, Peter T., Lakhani, Sunil, Dodson, Eoin, Selinger, Christina, Anderson, Lyndal, Samimi, Goli, Hacker, Neville F., Lim, Elgene, Ormandy, Christopher J., Naylor, Matthew J., Simpson, Kaylene, Nikolic, Iva, O’Toole, Sandra, Kaplan, Warren, Cowley, Mark J., Carroll, Jason S., Molloy, Mark, and Swarbrick, Alexander

Published
2020
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10. Exploring international differences in ovarian cancer treatment: a comparison of clinical practice guidelines and patterns of care

Author

Norell, Charles H, Butler, John, Farrell, Rhonda, Altman, Alon, Bentley, James, Cabasag, Citadel J, Cohen, Paul A, Fegan, Scott, Fung-Kee-Fung, Michael, Gourley, Charlie, Hacker, Neville F, Hanna, Louise, Høgdall, Claus Kim, Kristensen, Gunnar, Kwon, Janice, McNally, Orla, Nelson, Gregg, Nordin, Andy, OʼDonnell, Dearbhaile, Schnack, Tine, Sykes, Peter H, Zotow, Ewa, and Harrison, Samantha

Published
2020
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13. Supplementary Table 1 from Simultaneous Suppression of Epidermal Growth Factor Receptor and c-erbB-2 Reverses Aneuploidy and Malignant Phenotype of a Human Ovarian Carcinoma Cell Line

Author

Pack, Svetlana D., primary, Alper, Özgül M., primary, Stromberg, Kurt, primary, Augustus, Meena, primary, Özdemirli, Metin, primary, Miermont, Anne M., primary, Klus, Greg, primary, Rusin, Marek, primary, Slack, Rebecca, primary, Hacker, Neville F., primary, Ried, Thomas, primary, Szallasi, Zoltan, primary, and Alper, Özge, primary

Published
2023
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14. Supplementary Table 2 from Simultaneous Suppression of Epidermal Growth Factor Receptor and c-erbB-2 Reverses Aneuploidy and Malignant Phenotype of a Human Ovarian Carcinoma Cell Line

Author

Pack, Svetlana D., primary, Alper, Özgül M., primary, Stromberg, Kurt, primary, Augustus, Meena, primary, Özdemirli, Metin, primary, Miermont, Anne M., primary, Klus, Greg, primary, Rusin, Marek, primary, Slack, Rebecca, primary, Hacker, Neville F., primary, Ried, Thomas, primary, Szallasi, Zoltan, primary, and Alper, Özge, primary

Published
2023
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16. The molecular origin and taxonomy of mucinous ovarian carcinoma

Author

Cheasley, Dane, Wakefield, Matthew J., Ryland, Georgina L., Allan, Prue E., Alsop, Kathryn, Amarasinghe, Kaushalya C., Ananda, Sumitra, Anglesio, Michael S., Au-Yeung, George, Böhm, Maret, Bowtell, David D. L., Brand, Alison, Chenevix-Trench, Georgia, Christie, Michael, Chiew, Yoke-Eng, Churchman, Michael, DeFazio, Anna, Demeo, Renee, Dudley, Rhiannon, Fairweather, Nicole, Fedele, Clare G., Fereday, Sian, Fox, Stephen B., Gilks, C Blake, Gourley, Charlie, Hacker, Neville F., Hadley, Alison M., Hendley, Joy, Ho, Gwo-Yaw, Hughes, Siobhan, Hunstman, David G., Hunter, Sally M., Jobling, Tom W., Kalli, Kimberly R., Kaufmann, Scott H., Kennedy, Catherine J., Köbel, Martin, Le Page, Cecile, Li, Jason, Lupat, Richard, McNally, Orla M., McAlpine, Jessica N., Mes-Masson, Anne-Marie, Mileshkin, Linda, Provencher, Diane M., Pyman, Jan, Rahimi, Kurosh, Rowley, Simone M., Salazar, Carolina, Samimi, Goli, Saunders, Hugo, Semple, Timothy, Sharma, Ragwha, Sharpe, Alice J., Stephens, Andrew N., Thio, Niko, Torres, Michelle C., Traficante, Nadia, Xing, Zhongyue, Zethoven, Magnus, Antill, Yoland C., Scott, Clare L., Campbell, Ian G., and Gorringe, Kylie L.

Published
2019
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31. Additional file 1 of Proteogenomic analysis of Inhibitor of Differentiation 4 (ID4) in basal-like breast cancer

Author

Baker, Laura A., Holliday, Holly, Roden, Daniel, Krisp, Christoph, Wu, Sunny Z., Junankar, Simon, Serandour, Aurelien A., Mohammed, Hisham, Nair, Radhika, Sankaranarayanan, Geetha, Law, Andrew M. K., McFarland, Andrea, Simpson, Peter T., Lakhani, Sunil, Dodson, Eoin, Selinger, Christina, Lyndal Anderson, Goli Samimi, Hacker, Neville F., Elgene Lim, Ormandy, Christopher J., Naylor, Matthew J., Simpson, Kaylene, Nikolic, Iva, O’Toole, Sandra, Kaplan, Warren, Cowley, Mark J., Carroll, Jason S., Molloy, Mark, and Swarbrick, Alexander

Abstract

Additional file 1: Figure S1. Analysis of ID4 protein expression across a panel of breast and ovarian cell lines. (A) Western blotting analysis of ID4 protein expression across a panel of breast (top) and ovarian (bottom) normal and cancer cell lines. A rabbit monoclonal antibody specific to ID4 (Biocheck, BCH-9/82–12) was used for detection [11]. Two isoforms of ID4 are detectable across the panel. β-Actin is shown as a loading control. Modifications to images indicated with vertical black line. Cell lines selected for further analysis are indicated with a black square. Breast cancer subtypes and ovarian cancer histotypes indicated [82, 83]. (B) Western blot validation of RIME protocol. MDA-MB-468 cells were processed using the RIME protocol. Antibodies targeting ID4 (pooled polyclonal antibodies) and IgG (rabbit species matched control) control were used for immunoprecipitation. Western blot analysis for ID4 protein expression, using an independent ID4 monoclonal antibody, following immunoprecipitation. Figure S2. ID4 ChIP-sequencing analysis of HCC70 cell line identifies reproducible ID4-chromatin binding sites. (A) Table summarising three biological replicates of ID4 ChIP-seq analysis in HCC70 cell line. (B) 10,000 bp resolution image of ID4 ChIP-seq technical replicate #1 binding to MALAT1 gene. Red sequencing reads are aligned to the positive strand (5′ - 3′), and blue to the negative strand of DNA (3′ - 5′). ID4 binding to (C) left to right: GBA, FAIM, MIRLET7BHG, NEAT1 and ZFP36L1. The chromosomal location, size of the gene and Refseq, human reference genome, are displayed at the top of the image. Reads have been aligned to the human reference genome Hg19 and peaks called using MACs peak calling algorithm (v2.0.9) [38]. Images contain ChIP-seq coverage data and the peaks called for each ID4 technical replicate and the consensus peaks called for all three ID4 ChIP-seq biological replicate for selected gene regions. ID4 binding is shown in comparison to IgG and Input data for the same region. Data visualised using IGV [56, 57]. Transcription Start Site (TSS) indicated with black arrow. Figure S3. ID4 ChIP-exonuclease sequencing analysis of HCC70 and HCC1954 cell lines reproduces ChIP-seq analysis. (A) Table summarising ChIP-exonuclease sequencing analysis of ID4 and IgG binding events in HCC70 and HCC1954 breast cancer cell lines. ID4 binding normalised as for ChIP-seq analysis. ChIP-exo analysis of the HCC70 and HCC1954 breast cancer cell lines showing ID4 binding to NEAT1, MALAT1 and GBA (B), ZFP36L1 and ELF3 (C), and KDM4C and ERRFI1 (D). Reads have been aligned to the human reference genome Hg19 and peaks called using MACs peak calling algorithm (v2.0.9) [38]. Images contain ChIP-exo coverage data and the peaks called for each ID4 technical replicate and the consensus peaks called for both ID4 ChIP-exo technical replicate for selected gene regions. ID4 binding is shown in comparison to IgG and input data for the same region. Data visualised using IGV [56, 57]. The chromosomal location and size of the gene are displayed at the top of the image. Below this, Refseq, human reference genome, displays the gene corresponding to particular genomic loci. Transcription Start Site (TSS) indicated with black arrow. Figure S4. Validation of ID4 binding to specific loci in HCC70, MDA-MB-468 and HCC1954 cell lines. (A) Schematic of primer binding across ELF3 gene region. Primers 1–5 are scattered along the length of the ELF3 gene ID4. ChIP-qPCR analysis in (B) HCC70 (n = 2–8), (C) MDA-MB-468 (n = 2) and (D) HCC1954 (n = 2) cells. Multiple primers were designed to tile across the large ID4 binding sites. ID4 binding normalised to input DNA and to a region not bound by ID4 (negative region) and represented as fold-change over IgG control. 1-Way-ANOVA of ID4 binding across all primers compared to negative region: HCC70 p = 0.0001, MDA-MB-468 p = 0.549, HCC1954 p = 0.519. Figure S5. ID4 knockdown using SMARTChoice inducible lentiviral knockdown system. Representative western blot showing ID4 and β-Actin protein expression in wild-type HCC70 cell line and HCC70 cells stably transfected with SMARTChoice vectors containing doxycycline-inducible shRNAs targeting ID4 (shID4 #1, #2 and #3) or non-targeting control region (shNTC). Cells treated with and without DOX for 72 h. (B) Western blotting densitometry quantification of ID4 protein expression across six biological replicates of ID4 knockdown following treatment with and without DOX for 72 h. ID4 expression normalised to β-ACTIN and no DOX control. Error bars measure standard error, n = 4–6. (C) qRT-PCR analysis of ID4 RNA expression matched to cells in (B). Data normalised to B2M housekeeping gene and no DOX control. Error bars measure standard error, n = 4–6. Student’s t-test compares shNTC with the other modified cell lines. ** p

Published
2020
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32. Hereditary gynaecologic cancers in Nepal: a proposed model of care to serve high risk populations in developing countries

Author

Pokharel, Hanoon P., Hacker, Neville F., and Andrews, Lesley

Subjects
Cancer research, Female genital cancer -- Diagnosis -- Care and treatment, Health care disparities -- Forecasts and trends, Market trend/market analysis, Health
Abstract

Background Endometrial, ovarian and breast cancers are paradigms for global health disparity. Women living in the developing world continue to present in later stages of disease and have fewer options for treatment than those in developed countries. Risk reducing surgery is of proven benefit for women at high risk of gynaecological cancer. There is no specific model for identification and management of such women in the developing world. Methods We have integrated data from our published audit of a major gynaecological oncology centre at Royal Hospital for Women in Australia, with data from our survey and a focus group discussion of Nepalese gynaecological health care professionals regarding genetic testing, and findings from the literature. These data have been used to identify current barriers to multidisciplinary gynaecological oncology care in developing nations, and to develop a model to integrate hereditary cancer services into cancer care in Nepal, as a paradigm for other developing nations. Results The ability to identify women with hereditary gynaecological cancer in developing nations is influenced by their late presentation (if active management is declined or not appropriate), limited access to specialised services and cultural and financial barriers. In order to include genetic assessment in multidisciplinary gynaecological cancer care, education needs to be provided to all levels of health care providers to enable reporting of family history, and appropriate ordering of investigations. Training of genetic counsellors is needed to assist in the interpretation of results and extending care to unaffected at-risk relatives. Novel approaches will be required to overcome geographic and financial barriers, including mainstreaming of genetic testing, telephone counselling, use of mouth swabs and utilisation of international laboratories. Conclusion Women in Nepal have yet to receive benefits from the advances in early cancer diagnosis and management. There is a potential of extending the benefits of hereditary cancer diagnosis in Nepal due to the rapid fall in the cost of genetic testing and the ability to collect DNA from a buccal swab through appropriate training of the gynaecological carers. Keywords: Nepal, Hereditary cancer, BRCA, Lynch syndrome, Author(s): Hanoon P. Pokharel[sup.1,2,4] , Neville F. Hacker[sup.1,2] and Lesley Andrews[sup.3,5] Background Poor health within countries and inequities between countries are largely caused by the unequal distribution of power, income, [...]

Published
2017
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33. Low meprin (alpha) expression differentiates primary ovarian mucinous carcinoma from gastrointestinal cancers that commonly metastasise to the ovaries

Author

Heinzelmann-Schwarz, Viola A., Scolyer, Richard A., Scurry, James P., Smith, Alison N., Gardiner-Garden, Margaret, Biankin, Andrew V., Baron-Hay, Sally, Scott, Carolyn, Ward, Robyn L., Fink, Daniel, Hacker, Neville F., Sutherland, Robert L., and O'Brien, Philippa M.

Subjects
Metalloproteins -- Genetic aspects, Metalloproteins -- Research, Gene expression -- Research, Gastrointestinal cancer -- Complications and side effects, Metastasis -- Diagnosis, Ovarian cancer -- Diagnosis, Health
Published
2007

34. Exploring international differences in ovarian cancer treatment:A comparison of clinical practice guidelines and patterns of care

Author

Norell, Charles H., Butler, John, Farrell, Rhonda, Altman, Alon, Bentley, James, Cabasag, Citadel J., Cohen, Paul A., Fegan, Scott, Fung-Kee-Fung, Michael, Gourley, Charlie, Hacker, Neville F., Hanna, Louise, Høgdall, Claus Kim, Kristensen, Gunnar, Kwon, Janice, McNally, Orla, Nelson, Gregg, Nordin, Andy, O'Donnell, Dearbhaile, Schnack, Tine, Sykes, Peter H., Zotow, Ewa, Harrison, Samantha, Norell, Charles H., Butler, John, Farrell, Rhonda, Altman, Alon, Bentley, James, Cabasag, Citadel J., Cohen, Paul A., Fegan, Scott, Fung-Kee-Fung, Michael, Gourley, Charlie, Hacker, Neville F., Hanna, Louise, Høgdall, Claus Kim, Kristensen, Gunnar, Kwon, Janice, McNally, Orla, Nelson, Gregg, Nordin, Andy, O'Donnell, Dearbhaile, Schnack, Tine, Sykes, Peter H., Zotow, Ewa, and Harrison, Samantha

Abstract

Introduction The International Cancer Benchmarking Partnership demonstrated international differences in ovarian cancer survival, particularly for women aged 65-74 with advanced disease. These findings suggest differences in treatment could be contributing to survival disparities. Objective To compare clinical practice guidelines and patterns of care across seven high-income countries. Methods A comparison of guidelines was performed and validated by a clinical working group. To explore clinical practice, a patterns of care survey was developed. A questionnaire regarding management and potential health system-related barriers to providing treatment was emailed to gynecological specialists. Guideline and survey results were crudely compared with 3-year survival by 'distant' stage using Spearman's rho. Results Twenty-seven guidelines were compared, and 119 clinicians completed the survey. Guideline-related measures varied between countries but did not correlate with survival internationally. Guidelines were consistent for surgical recommendations of either primary debulking surgery or neoadjuvant chemotherapy followed by interval debulking surgery with the aim of complete cytoreduction. Reported patterns of surgical care varied internationally, including for rates of primary versus interval debulking, extensive/' ultra-radical' surgery, and perceived barriers to optimal cytoreduction. Comparison showed that willingness to undertake extensive surgery correlated with survival across countries (r s =0.94, p=0.017). For systemic/radiation therapies, guideline differences were more pronounced, particularly for bevacizumab and PARP (poly (ADP-ribose) polymerase) inhibitors. Reported health system-related barriers also varied internationally and included a lack of adequate hospital staffing and treatment monitoring via local and national audits. Discussion Findings suggest international variations in ovarian cancer treatment. Characteristics relating to countries with hig

Published
2020

36. 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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48. Proteogenomic analysis of Inhibitor of Differentiation 4 (ID4) in basal-like breast cancer

Author

Baker, Laura A., primary, Holliday, Holly, additional, Roden, Daniel, additional, Krisp, Christoph, additional, Wu, Sunny Z., additional, Junankar, Simon, additional, Serandour, Aurelien A., additional, Mohammed, Hisham, additional, Nair, Radhika, additional, Sankaranarayanan, Geetha, additional, Law, Andrew M.K., additional, McFarland, Andrea, additional, Simpson, Peter T., additional, Lakhani, Sunil, additional, Dodson, Eoin, additional, Selinger, Christina, additional, Anderson, Lyndal, additional, Samimi, Goli, additional, Hacker, Neville F., additional, Lim, Elgene, additional, Ormandy, Christopher J., additional, Naylor, Matthew J., additional, Simpson, Kaylene, additional, Nikolic, Iva, additional, O’Toole, Sandra, additional, Kaplan, Warren, additional, Cowley, Mark J., additional, Carroll, Jason S., additional, Molloy, Mark, additional, and Swarbrick, Alexander, additional

Published
2020
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50. Triage of ovarian masses

Author

CHIA, Yin Nin, MARSDEN, Donald E., ROBERTSON, Greg, and HACKER, Neville F.

Published
2008

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