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1. Multiomic neuropathology improves diagnostic accuracy in pediatric neuro-oncology

Author

Sturm, Dominik, Capper, David, Andreiuolo, Felipe, Gessi, Marco, Kölsche, Christian, Reinhardt, Annekathrin, Sievers, Philipp, Wefers, Annika K., Ebrahimi, Azadeh, Suwala, Abigail K., Gielen, Gerrit H., Sill, Martin, Schrimpf, Daniel, Stichel, Damian, Hovestadt, Volker, Daenekas, Bjarne, Rode, Agata, Hamelmann, Stefan, Previti, Christopher, Jäger, Natalie, Buchhalter, Ivo, Blattner-Johnson, Mirjam, Jones, Barbara C., Warmuth-Metz, Monika, Bison, Brigitte, Grund, Kerstin, Sutter, Christian, Hirsch, Steffen, Dikow, Nicola, Hasselblatt, Martin, Schüller, Ulrich, Koch, Arend, Gerber, Nicolas U., White, Christine L., Buntine, Molly K., Kinross, Kathryn, Algar, Elizabeth M., Hansford, Jordan R., Gottardo, Nicholas G., Schuhmann, Martin U., Thomale, Ulrich W., Hernáiz Driever, Pablo, Gnekow, Astrid, Witt, Olaf, Müller, Hermann L., Calaminus, Gabriele, Fleischhack, Gudrun, Kordes, Uwe, Mynarek, Martin, Rutkowski, Stefan, Frühwald, Michael C., Kramm, Christof M., von Deimling, Andreas, Pietsch, Torsten, Sahm, Felix, Pfister, Stefan M., and Jones, David. T. W.

Published
2023
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2. Author Correction: Multiomic neuropathology improves diagnostic accuracy in pediatric neuro-oncology

Author

Sturm, Dominik, Capper, David, Andreiuolo, Felipe, Gessi, Marco, Kölsche, Christian, Reinhardt, Annekathrin, Sievers, Philipp, Wefers, Annika K., Ebrahimi, Azadeh, Suwala, Abigail K., Gielen, Gerrit H., Sill, Martin, Schrimpf, Daniel, Stichel, Damian, Hovestadt, Volker, Daenekas, Bjarne, Rode, Agata, Hamelmann, Stefan, Previti, Christopher, Jäger, Natalie, Buchhalter, Ivo, Blattner-Johnson, Mirjam, Jones, Barbara C., Warmuth-Metz, Monika, Bison, Brigitte, Grund, Kerstin, Sutter, Christian, Hirsch, Steffen, Dikow, Nicola, Hasselblatt, Martin, Schüller, Ulrich, Koch, Arend, Gerber, Nicolas U., White, Christine L., Buntine, Molly K., Kinross, Kathryn, Algar, Elizabeth M., Hansford, Jordan R., Gottardo, Nicholas G., Schuhmann, Martin U., Thomale, Ulrich W., Hernáiz Driever, Pablo, Gnekow, Astrid, Witt, Olaf, Müller, Hermann L., Calaminus, Gabriele, Fleischhack, Gudrun, Kordes, Uwe, Mynarek, Martin, Rutkowski, Stefan, Frühwald, Michael C., Kramm, Christof M., von Deimling, Andreas, Pietsch, Torsten, Sahm, Felix, Pfister, Stefan M., and Jones, David. T. W.

Published
2024
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3. Implementation of DNA Methylation Array Profiling in Pediatric Central Nervous System Tumors: The AIM BRAIN Project: An Australian and New Zealand Children's Hematology and Oncology Group Study

Author

White, Christine L., Kinross, Kathryn M., Buntine, Molly K., Rasouli, Elnaz, Strong, Robyn, Jones, Janelle M., Cain, Jason E., Sturm, Dominik, Sahm, Felix, Jones, David T.W., Pfister, Stefan M., Robertson, Thomas, D'Arcy, Colleen, Rodriguez, Michael L., Dyke, Jason M., Junckerstorff, Reimar, Bhuva, Dharmesh D., Davis, Melissa J., Wood, Paul, Hassall, Tim, Ziegler, David S., Kellie, Stewart, McCowage, Geoffrey, Alvaro, Frank, Kirby, Maria, Heath, John A., Tsui, Karen, Dodgshun, Andrew, Eisenstat, David D., Khuong-Quang, Dong-Anh, Wall, Meaghan, Algar, Elizabeth M., Gottardo, Nicholas G., and Hansford, Jordan R.

Published
2023
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4. Response of BRAF-Mutant Melanoma to BRAF Inhibition Is Mediated by a Network of Transcriptional Regulators of Glycolysis

Author

Parmenter, Tiffany J, Kleinschmidt, Margarete, Kinross, Kathryn M, Bond, Simon T, Li, Jason, Kaadige, Mohan R, Rao, Aparna, Sheppard, Karen E, Hugo, Willy, Pupo, Gulietta M, Pearson, Richard B, McGee, Sean L, Long, Georgina V, Scolyer, Richard A, Rizos, Helen, Lo, Roger S, Cullinane, Carleen, Ayer, Donald E, Ribas, Antoni, Johnstone, Ricky W, Hicks, Rodney J, and McArthur, Grant A

Subjects
Clinical Research, Genetics, Cancer, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Cell Line, Tumor, Drug Resistance, Neoplasm, Glycolysis, HEK293 Cells, Humans, Indoles, MAP Kinase Signaling System, Melanoma, Piperazines, Protein Kinase Inhibitors, Proto-Oncogene Proteins B-raf, Pyridines, Sulfonamides, Transcription Factors, Vemurafenib, Oncology and Carcinogenesis
Abstract

UnlabelledDeregulated glucose metabolism fulfills the energetic and biosynthetic requirements for tumor growth driven by oncogenes. Because inhibition of oncogenic BRAF causes profound reductions in glucose uptake and a strong clinical benefit in BRAF-mutant melanoma, we examined the role of energy metabolism in responses to BRAF inhibition. We observed pronounced and consistent decreases in glycolytic activity in BRAF-mutant melanoma cells. Moreover, we identified a network of BRAF-regulated transcription factors that control glycolysis in melanoma cells. Remarkably, this network of transcription factors, including hypoxia-inducible factor-1α, MYC, and MONDOA (MLXIP), drives glycolysis downstream of BRAF(V600), is critical for responses to BRAF inhibition, and is modulated by BRAF inhibition in clinical melanoma specimens. Furthermore, we show that concurrent inhibition of BRAF and glycolysis induces cell death in BRAF inhibitor (BRAFi)-resistant melanoma cells. Thus, we provide a proof-of-principle for treatment of melanoma with combinations of BRAFis and glycolysis inhibitors.SignificanceBRAF is suppress glycolysis and provide strong clinical benefi t in BRAF V600 melanoma. We show that BRAF inhibition suppresses glycolysis via a network of transcription factors that are critical for complete BRAFi responses. Furthermore, we provide evidence for the clinical potential of therapies that combine BRAFis with glycolysis inhibitors.

Published
2014

5. Author Correction: Multiomic neuropathology improves diagnostic accuracy in pediatric neuro-oncology

Author

Sturm, Dominik, primary, Capper, David, additional, Andreiuolo, Felipe, additional, Gessi, Marco, additional, Kölsche, Christian, additional, Reinhardt, Annekathrin, additional, Sievers, Philipp, additional, Wefers, Annika K., additional, Ebrahimi, Azadeh, additional, Suwala, Abigail K., additional, Gielen, Gerrit H., additional, Sill, Martin, additional, Schrimpf, Daniel, additional, Stichel, Damian, additional, Hovestadt, Volker, additional, Daenekas, Bjarne, additional, Rode, Agata, additional, Hamelmann, Stefan, additional, Previti, Christopher, additional, Jäger, Natalie, additional, Buchhalter, Ivo, additional, Blattner-Johnson, Mirjam, additional, Jones, Barbara C., additional, Warmuth-Metz, Monika, additional, Bison, Brigitte, additional, Grund, Kerstin, additional, Sutter, Christian, additional, Hirsch, Steffen, additional, Dikow, Nicola, additional, Hasselblatt, Martin, additional, Schüller, Ulrich, additional, Koch, Arend, additional, Gerber, Nicolas U., additional, White, Christine L., additional, Buntine, Molly K., additional, Kinross, Kathryn, additional, Algar, Elizabeth M., additional, Hansford, Jordan R., additional, Gottardo, Nicholas G., additional, Schuhmann, Martin U., additional, Thomale, Ulrich W., additional, Hernáiz Driever, Pablo, additional, Gnekow, Astrid, additional, Witt, Olaf, additional, Müller, Hermann L., additional, Calaminus, Gabriele, additional, Fleischhack, Gudrun, additional, Kordes, Uwe, additional, Mynarek, Martin, additional, Rutkowski, Stefan, additional, Frühwald, Michael C., additional, Kramm, Christof M., additional, von Deimling, Andreas, additional, Pietsch, Torsten, additional, Sahm, Felix, additional, Pfister, Stefan M., additional, and Jones, David. T. W., additional

Published
2023
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6. A multi-institutional retrospective pooled outcome analysis of molecularly annotated pediatric supratentorial ZFTA-fused ependymoma

Author

Ng, Chia Huan, primary, Obrecht, Denise, additional, Wells, Olivia, additional, Zapotocky, Michal, additional, Sumerauer, David, additional, Coltin, Hallie, additional, Khuong-Quang, Dong-Anh, additional, Eisenstat, David D, additional, Kinross, Kathryn M, additional, White, Christine L, additional, Algar, Elizabeth M, additional, Luck, Amanda, additional, Witt, Hendrik, additional, Schüller, Ulrich, additional, Mynarek, Martin, additional, Pietsch, Torsten, additional, Gerber, Nicolas U, additional, Benesch, Martin, additional, Warmuth-Metz, Monika, additional, Kortmann, Rolf, additional, Bison, Brigitte, additional, Taylor, Michael D, additional, Rutkowski, Stefan, additional, Pfister, Stefan M, additional, Jones, David T W, additional, Gottardo, Nicholas G, additional, von Hoff, Katja, additional, Pajtler, Kristian W, additional, Ramaswamy, Vijay, additional, and Hansford, Jordan R, additional

Published
2023
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7. Supplementary Figures 4-6 from The mTORC1 Inhibitor Everolimus Prevents and Treats Eμ-Myc Lymphoma by Restoring Oncogene-Induced Senescence

Author

Wall, Meaghan, primary, Poortinga, Gretchen, primary, Stanley, Kym L., primary, Lindemann, Ralph K., primary, Bots, Michael, primary, Chan, Christopher J., primary, Bywater, Megan J., primary, Kinross, Kathryn M., primary, Astle, Megan V., primary, Waldeck, Kelly, primary, Hannan, Katherine M., primary, Shortt, Jake, primary, Smyth, Mark J., primary, Lowe, Scott W., primary, Hannan, Ross D., primary, Pearson, Richard B., primary, Johnstone, Ricky W., primary, and McArthur, Grant A., primary

Published
2023
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8. Supplementary Data 2 from Response of BRAF-Mutant Melanoma to BRAF Inhibition Is Mediated by a Network of Transcriptional Regulators of Glycolysis

Author

Parmenter, Tiffany J., primary, Kleinschmidt, Margarete, primary, Kinross, Kathryn M., primary, Bond, Simon T., primary, Li, Jason, primary, Kaadige, Mohan R., primary, Rao, Aparna, primary, Sheppard, Karen E., primary, Hugo, Willy, primary, Pupo, Gulietta M., primary, Pearson, Richard B., primary, McGee, Sean L., primary, Long, Georgina V., primary, Scolyer, Richard A., primary, Rizos, Helen, primary, Lo, Roger S., primary, Cullinane, Carleen, primary, Ayer, Donald E., primary, Ribas, Antoni, primary, Johnstone, Ricky W., primary, Hicks, Rodney J., primary, and McArthur, Grant A., primary

Published
2023
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9. Data from Response of BRAF-Mutant Melanoma to BRAF Inhibition Is Mediated by a Network of Transcriptional Regulators of Glycolysis

Author

Parmenter, Tiffany J., primary, Kleinschmidt, Margarete, primary, Kinross, Kathryn M., primary, Bond, Simon T., primary, Li, Jason, primary, Kaadige, Mohan R., primary, Rao, Aparna, primary, Sheppard, Karen E., primary, Hugo, Willy, primary, Pupo, Gulietta M., primary, Pearson, Richard B., primary, McGee, Sean L., primary, Long, Georgina V., primary, Scolyer, Richard A., primary, Rizos, Helen, primary, Lo, Roger S., primary, Cullinane, Carleen, primary, Ayer, Donald E., primary, Ribas, Antoni, primary, Johnstone, Ricky W., primary, Hicks, Rodney J., primary, and McArthur, Grant A., primary

Published
2023
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10. Supplementary Figures 9-11 from The mTORC1 Inhibitor Everolimus Prevents and Treats Eμ-Myc Lymphoma by Restoring Oncogene-Induced Senescence

Author

Wall, Meaghan, primary, Poortinga, Gretchen, primary, Stanley, Kym L., primary, Lindemann, Ralph K., primary, Bots, Michael, primary, Chan, Christopher J., primary, Bywater, Megan J., primary, Kinross, Kathryn M., primary, Astle, Megan V., primary, Waldeck, Kelly, primary, Hannan, Katherine M., primary, Shortt, Jake, primary, Smyth, Mark J., primary, Lowe, Scott W., primary, Hannan, Ross D., primary, Pearson, Richard B., primary, Johnstone, Ricky W., primary, and McArthur, Grant A., primary

Published
2023
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11. Supplementary Data 1 from Response of BRAF-Mutant Melanoma to BRAF Inhibition Is Mediated by a Network of Transcriptional Regulators of Glycolysis

Author

Parmenter, Tiffany J., primary, Kleinschmidt, Margarete, primary, Kinross, Kathryn M., primary, Bond, Simon T., primary, Li, Jason, primary, Kaadige, Mohan R., primary, Rao, Aparna, primary, Sheppard, Karen E., primary, Hugo, Willy, primary, Pupo, Gulietta M., primary, Pearson, Richard B., primary, McGee, Sean L., primary, Long, Georgina V., primary, Scolyer, Richard A., primary, Rizos, Helen, primary, Lo, Roger S., primary, Cullinane, Carleen, primary, Ayer, Donald E., primary, Ribas, Antoni, primary, Johnstone, Ricky W., primary, Hicks, Rodney J., primary, and McArthur, Grant A., primary

Published
2023
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12. Supplementary Figures 7-8 from The mTORC1 Inhibitor Everolimus Prevents and Treats Eμ-Myc Lymphoma by Restoring Oncogene-Induced Senescence

Author

Wall, Meaghan, primary, Poortinga, Gretchen, primary, Stanley, Kym L., primary, Lindemann, Ralph K., primary, Bots, Michael, primary, Chan, Christopher J., primary, Bywater, Megan J., primary, Kinross, Kathryn M., primary, Astle, Megan V., primary, Waldeck, Kelly, primary, Hannan, Katherine M., primary, Shortt, Jake, primary, Smyth, Mark J., primary, Lowe, Scott W., primary, Hannan, Ross D., primary, Pearson, Richard B., primary, Johnstone, Ricky W., primary, and McArthur, Grant A., primary

Published
2023
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13. Supplementary Tables 1-2 from The mTORC1 Inhibitor Everolimus Prevents and Treats Eμ-Myc Lymphoma by Restoring Oncogene-Induced Senescence

Author

Wall, Meaghan, primary, Poortinga, Gretchen, primary, Stanley, Kym L., primary, Lindemann, Ralph K., primary, Bots, Michael, primary, Chan, Christopher J., primary, Bywater, Megan J., primary, Kinross, Kathryn M., primary, Astle, Megan V., primary, Waldeck, Kelly, primary, Hannan, Katherine M., primary, Shortt, Jake, primary, Smyth, Mark J., primary, Lowe, Scott W., primary, Hannan, Ross D., primary, Pearson, Richard B., primary, Johnstone, Ricky W., primary, and McArthur, Grant A., primary

Published
2023
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14. Supplementary Methods from Response of BRAF-Mutant Melanoma to BRAF Inhibition Is Mediated by a Network of Transcriptional Regulators of Glycolysis

Author

Parmenter, Tiffany J., primary, Kleinschmidt, Margarete, primary, Kinross, Kathryn M., primary, Bond, Simon T., primary, Li, Jason, primary, Kaadige, Mohan R., primary, Rao, Aparna, primary, Sheppard, Karen E., primary, Hugo, Willy, primary, Pupo, Gulietta M., primary, Pearson, Richard B., primary, McGee, Sean L., primary, Long, Georgina V., primary, Scolyer, Richard A., primary, Rizos, Helen, primary, Lo, Roger S., primary, Cullinane, Carleen, primary, Ayer, Donald E., primary, Ribas, Antoni, primary, Johnstone, Ricky W., primary, Hicks, Rodney J., primary, and McArthur, Grant A., primary

Published
2023
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15. Data from The mTORC1 Inhibitor Everolimus Prevents and Treats Eμ-Myc Lymphoma by Restoring Oncogene-Induced Senescence

Author

Wall, Meaghan, primary, Poortinga, Gretchen, primary, Stanley, Kym L., primary, Lindemann, Ralph K., primary, Bots, Michael, primary, Chan, Christopher J., primary, Bywater, Megan J., primary, Kinross, Kathryn M., primary, Astle, Megan V., primary, Waldeck, Kelly, primary, Hannan, Katherine M., primary, Shortt, Jake, primary, Smyth, Mark J., primary, Lowe, Scott W., primary, Hannan, Ross D., primary, Pearson, Richard B., primary, Johnstone, Ricky W., primary, and McArthur, Grant A., primary

Published
2023
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17. Supplementary Figure 12 from The mTORC1 Inhibitor Everolimus Prevents and Treats Eμ-Myc Lymphoma by Restoring Oncogene-Induced Senescence

Author

Wall, Meaghan, primary, Poortinga, Gretchen, primary, Stanley, Kym L., primary, Lindemann, Ralph K., primary, Bots, Michael, primary, Chan, Christopher J., primary, Bywater, Megan J., primary, Kinross, Kathryn M., primary, Astle, Megan V., primary, Waldeck, Kelly, primary, Hannan, Katherine M., primary, Shortt, Jake, primary, Smyth, Mark J., primary, Lowe, Scott W., primary, Hannan, Ross D., primary, Pearson, Richard B., primary, Johnstone, Ricky W., primary, and McArthur, Grant A., primary

Published
2023
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18. Supplementary Figures and Tables from Response of BRAF-Mutant Melanoma to BRAF Inhibition Is Mediated by a Network of Transcriptional Regulators of Glycolysis

Author

Parmenter, Tiffany J., primary, Kleinschmidt, Margarete, primary, Kinross, Kathryn M., primary, Bond, Simon T., primary, Li, Jason, primary, Kaadige, Mohan R., primary, Rao, Aparna, primary, Sheppard, Karen E., primary, Hugo, Willy, primary, Pupo, Gulietta M., primary, Pearson, Richard B., primary, McGee, Sean L., primary, Long, Georgina V., primary, Scolyer, Richard A., primary, Rizos, Helen, primary, Lo, Roger S., primary, Cullinane, Carleen, primary, Ayer, Donald E., primary, Ribas, Antoni, primary, Johnstone, Ricky W., primary, Hicks, Rodney J., primary, and McArthur, Grant A., primary

Published
2023
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19. Supplementary Figures 1-3 from The mTORC1 Inhibitor Everolimus Prevents and Treats Eμ-Myc Lymphoma by Restoring Oncogene-Induced Senescence

Author

Wall, Meaghan, primary, Poortinga, Gretchen, primary, Stanley, Kym L., primary, Lindemann, Ralph K., primary, Bots, Michael, primary, Chan, Christopher J., primary, Bywater, Megan J., primary, Kinross, Kathryn M., primary, Astle, Megan V., primary, Waldeck, Kelly, primary, Hannan, Katherine M., primary, Shortt, Jake, primary, Smyth, Mark J., primary, Lowe, Scott W., primary, Hannan, Ross D., primary, Pearson, Richard B., primary, Johnstone, Ricky W., primary, and McArthur, Grant A., primary

Published
2023
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20. A multi-institutional retrospective pooled outcome analysis of molecularly annotated pediatric supratentorial ZFTA-fused ependymoma

Author

Ng, Chia Huan, Obrecht, Denise, Wells, Olivia, Zapotocky, Michal, Sumerauer, David, Coltin, Hallie, Khuong-Quang, Dong-Anh, Eisenstat, David D; https://orcid.org/0000-0002-5976-0798, Kinross, Kathryn M, White, Christine L, Algar, Elizabeth M, Luck, Amanda, Witt, Hendrik, Schüller, Ulrich; https://orcid.org/0000-0002-8731-1121, Mynarek, Martin; https://orcid.org/0000-0003-3302-2719, Pietsch, Torsten, Gerber, Nicolas U, Benesch, Martin, Warmuth-Metz, Monika; https://orcid.org/0000-0002-3544-319X, Kortmann, Rolf, Bison, Brigitte, Taylor, Michael D, Rutkowski, Stefan, Pfister, Stefan M, Jones, David T W; https://orcid.org/0000-0002-2036-5141, Gottardo, Nicholas G; https://orcid.org/0000-0002-1082-6776, von Hoff, Katja; https://orcid.org/0000-0002-5669-8546, Pajtler, Kristian W; https://orcid.org/0000-0002-3562-6121, Ramaswamy, Vijay; https://orcid.org/0000-0002-6557-895X, Hansford, Jordan R; https://orcid.org/0000-0001-7733-383X, Ng, Chia Huan, Obrecht, Denise, Wells, Olivia, Zapotocky, Michal, Sumerauer, David, Coltin, Hallie, Khuong-Quang, Dong-Anh, Eisenstat, David D; https://orcid.org/0000-0002-5976-0798, Kinross, Kathryn M, White, Christine L, Algar, Elizabeth M, Luck, Amanda, Witt, Hendrik, Schüller, Ulrich; https://orcid.org/0000-0002-8731-1121, Mynarek, Martin; https://orcid.org/0000-0003-3302-2719, Pietsch, Torsten, Gerber, Nicolas U, Benesch, Martin, Warmuth-Metz, Monika; https://orcid.org/0000-0002-3544-319X, Kortmann, Rolf, Bison, Brigitte, Taylor, Michael D, Rutkowski, Stefan, Pfister, Stefan M, Jones, David T W; https://orcid.org/0000-0002-2036-5141, Gottardo, Nicholas G; https://orcid.org/0000-0002-1082-6776, von Hoff, Katja; https://orcid.org/0000-0002-5669-8546, Pajtler, Kristian W; https://orcid.org/0000-0002-3562-6121, Ramaswamy, Vijay; https://orcid.org/0000-0002-6557-895X, and Hansford, Jordan R; https://orcid.org/0000-0001-7733-383X

Abstract

BACKGROUND ZFTA-RELA (formerly known as c11orf-RELA) fused supratentorial ependymoma (ZFTAfus ST-EPN) has been recognized as a novel entity in the 2016 WHO classification of CNS tumors and further defined in the recent 2021 edition. ZFTAfus ST-EPN was reported to portend poorer prognosis when compared to its counterpart, YAP1 ST-EPN in some previously published series. The aim of this study was to determine the treatment outcome of molecularly confirmed and conventionally treated ZFTAfus ST-EPN patients treated in multiple institutions. METHODS We conducted a retrospective analysis of all pediatric patients with molecularly confirmed ZFTAfus ST-EPN patients treated in multiple institutions in 5 different countries (Australia, Canada, Germany, Switzerland, and Czechia). Survival outcomes were analyzed and correlated with clinical characteristics and treatment approaches. RESULTS A total of 108 patients were collated from multiple institutions in 5 different countries across three continents. We found across the entire cohort that the 5- and 10-year PFS were 65% and 63%, respectively. The 5- and 10-year OS of this cohort of patients were 87% and 73%. The rates of gross total resection (GTR) were high with 84 out of 108 (77.8%) patients achieving GTR. The vast majority of patients also received post-operative radiotherapy, 98 out of 108 (90.7%). Chemotherapy did not appear to provide any survival benefit in our patient cohort. CONCLUSION This is the largest study to date of contemporaneously treated molecularly confirmed ZFTAfus ST-EPN patients which identified markedly improved survival outcomes compared to previously published series. This study also re-emphasizes the importance of maximal surgical resection in achieving optimal outcomes in pediatric patients with supratentorial ependymoma.

Published
2023

21. ATRT-17. A phase II study of continuous low dose panobinostat in paediatric patients with malignant rhabdoid tumours and atypical teratoid rhabdoid tumours.

Author

Wood, Paul, primary, Desai, Jayesh, additional, Waldeck, Kelly, additional, Cain, Jason, additional, Gottardo, Nicholas, additional, Strong, Robyn, additional, Kinross, Kathryn, additional, Carr, Michelle, additional, Jones, Janelle, additional, Wong, Lily, additional, Ziegler, David, additional, Hansford, Jordan, additional, Michael, Michael, additional, and Ashley, David, additional

Published
2022
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22. Host immunity contributes to the anti-melanoma activity of BRAF inhibitors

Author

Knight, Deborah A., Ngiow, Shin Foong, Li, Ming, Parmenter, Tiffany, Mok, Stephen, Cass, Ashley, Haynes, Nicole M., Kinross, Kathryn, Yagita, Hideo, Koya, Richard C., Graeber, Thomas G., Ribas, Antoni, McArthur, Grant A., and Smyth, Mark J.

Subjects
Chemokine receptors -- Physiological aspects -- Genetic aspects -- Research, Immunotherapy -- Physiological aspects -- Genetic aspects -- Research, Melanoma -- Genetic aspects -- Care and treatment -- Research, Health care industry
Abstract

The BRAF mutant, [BRAF.sup.V600E], is expressed in nearly half of melanomas, and oral BRAF inhibitors induce substantial tumor regression in patients with [BRAF.sup.V600E] metastatic melanoma. The inhibitors are believed to [...]

Published
2013
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23. An activating Pik3ca mutation coupled with Pten loss is sufficient to initiate ovarian tumorigenesis in mice

Author

Kinross, Kathryn M., Montgomery, Karen G., Kleinschmidt, Margarete, Waring, Paul, Ivetac, Ivan, Tikoo, Anjali, Saad, Mirette, Hare, Lauren, Roh, Vincent, Mantamadiotis, Theo, Sheppard, Karen E., Ryland, Georgina L., Campbell, Ian G., Gorringe, Kylie L., Christensen, James G., Cullinane, Carleen, Hicks, Rodney J., Pearson, Richard B., Johnstone, Ricky W., McArthur, Grant A., and Phillips, Wayne A.

Subjects
Gene mutations -- Health aspects, Carcinogenesis -- Risk factors -- Genetic aspects -- Research, Ovarian cancer -- Genetic aspects -- Risk factors -- Development and progression -- Research, Health care industry
Abstract

Mutations in the gene encoding the p110αsubunit of PI3K (PIK3CA) that result in enhanced PI3K activity are frequently observed in human cancers. To better understand the role of mutant PIK3CA in the initiation or progression of tumorigenesis, we generated mice in which a PIK3CA mutation commonly detected in human cancers (the H1047R mutation) could be conditionally knocked into the endogenous Pik3ca locus. Activation of this mutation in the mouse ovary revealed that alone, [Pik3ca.sup.h1047R] induced premalignant hyperplasia of the ovarian surface epithelium but no tumors. Concomitantly, we analyzed several human ovarian cancers and found PIK3CA mutations coexistent with KRAS and/or PTEN mutations, raising the possibility that a secondary defect in a co-regulator of PI3K activity may be required for mutant PIK3CA to promote transformation. Consistent with this notion, we found that [Pik3ca.sup.h1047R] mutation plus Pten deletion in the mouse ovary led to the development of ovarian serous adenocarcinomas and granulosa cell tumors. Both mutational events were required for early, robust Akt activation. Pharmacological inhibition of PI3K/mTOR in these mice delayed tumor growth and prolonged survival. These results demonstrate that the [Pik3ca.sup.h1047R] mutation with loss of Pten is enough to promote ovarian cell transformation and that we have developed a model system for studying possible therapies., Introduction In human cancers, somatic mutations in PIK3CA commonly target specific hot spots in the helical (E542 and E545) and kinase (H1047) domains (1), (2), resulting in enhanced lipid kinase [...]

Published
2012
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26. EPEN-36. THE TREATMENT OUTCOME OF PAEDIATRIC SUPRATENTORIAL C11ORF95-RELA FUSED EPENDYMOMA: A COMBINED REPORT FROM E-HIT SERIES AND AUSTRALIAN NEW ZEALAND CHILDREN’S HAEMATOLOGY/ONCOLOGY GROUP

Author

Ng, Chia Huan, primary, Obrecht, Denise, additional, Buntine, Molly, additional, Wells, Olivia, additional, Campbell, Martin A, additional, Bhatia, Kanika, additional, Sullivan, Michael, additional, Williams, Molly, additional, Quang, Dong Anh Khuong, additional, Kinross, Kathryn, additional, White, Christine, additional, Algar, Elizabeth, additional, Witt, Hendrik, additional, Schuller, Ulrich, additional, Mynarek, Martin, additional, Pietsch, Torsten, additional, Gerber, Nicolas U, additional, Benesch, Martin, additional, Warmuth-Metz, Monika, additional, Kortmann, Rolf, additional, Bison, Brigitte, additional, Taylor, Michael D, additional, Ramaswamy, Vijay, additional, Rutkowski, Stefan, additional, Pfister, Stefan M, additional, Jones, David T W, additional, Gottardo, Nicholas G, additional, Von Hoff, Katja, additional, Pajtler, Kristian W, additional, and Hansford, Jordan R, additional

Published
2020
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27. ATRT-08. A PHASE II STUDY OF CONTINUOUS LOW DOSE PANOBINOSTAT IN PAEDIATRIC PATIENTS WITH MALIGNANT RHABDOID TUMORS/ATYPICAL TERATOID RHABDOID TUMORS

Author

Wood, Paul, primary, Desai, Jayesh, additional, Waldeck, Kelly, additional, Cain, Jason, additional, Gottardo, Nick, additional, Strong, Robyn, additional, Kinross, Kathryn, additional, Carr, Michelle, additional, Jones, Janelle, additional, Wong, Lily, additional, Ziegler, David, additional, Hansford, Jordan, additional, Michael, Michael, additional, and Ashley, David, additional

Published
2020
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29. GENE-04. ESTABLISHING A MOLECULAR PROFILING SERVICE FOR CHILDREN’S CENTRAL NERVOUS SYSTEM TUMORS IN AUSTRALASIA – THE AUSTRALIAN AND NEW ZEALAND CHILDREN’S HAEMATOLOGY AND ONCOLOGY GROUP (ANZCHOG) AIM BRAIN PROJECT

Author

White, Christine, primary, Kinross, Kathryn, additional, Strong, Robyn, additional, Jones, David, additional, Pfister, Stefan, additional, Hansford, Jordan, additional, Gottardo, Nicholas, additional, and Algar, Elizabeth, additional

Published
2019
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30. Host immunity contributes to the anti-melanoma activity of BRAF inhibitors

Author

Knight, Deborah A., primary, Ngiow, Shin Foong, additional, Li, Ming, additional, Parmenter, Tiffany, additional, Mok, Stephen, additional, Cass, Ashley, additional, Haynes, Nicole M., additional, Kinross, Kathryn, additional, Yagita, Hideo, additional, Koya, Richard C., additional, Graeber, Thomas G., additional, Ribas, Antoni, additional, McArthur, Grant A., additional, and Smyth, Mark J., additional

Published
2015
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31. Ubiquitous expression of thePik3ca H1047Rmutation promotes hypoglycemia, hypoinsulinemia, and organomegaly

Author

Kinross, Kathryn M., primary, Montgomery, Karen G., additional, Mangiafico, Salvatore P., additional, Hare, Lauren M., additional, Kleinschmidt, Margarete, additional, Bywater, Megan J., additional, Poulton, Ingrid J., additional, Vrahnas, Christina, additional, Henneicke, Holger, additional, Malaterre, Jordane, additional, Waring, Paul M., additional, Cullinane, Carleen, additional, Sims, Natalie A., additional, McArthur, Grant A., additional, Andrikopoulos, Sofianos, additional, and Phillips, Wayne A., additional

Published
2014
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32. Physiological expression of the PI3K-activating mutation Pik3caH1047R combines with Apc loss to promote development of invasive intestinal adenocarcinomas in mice

Author

Hare, Lauren M., primary, Phesse, Toby J., additional, Waring, Paul M., additional, Montgomery, Karen G., additional, Kinross, Kathryn M., additional, Mills, Kevin, additional, Roh, Vincent, additional, Heath, Joan K., additional, Ramsay, Robert G., additional, Ernst, Matthias, additional, and Phillips, Wayne A., additional

Published
2014
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33. Synergistic inhibition of ovarian cancer cell growth by combining selective PI3K/mTOR and RAS/ERK pathway inhibitors

Author

Sheppard, Karen E, Cullinane, C, Hannan, Katherine, Wall, Meaghan, Chan, Joanna, Barber, Francis, Foo, Jung, Cameron, Donald, Neilsen, Amelia, Ng, Pui Y., Ellul, Jason, Kleinschmidt, Margarete, Kinross, Kathryn M., Bowtell, David D., Christensen, James G., Hicks, Rodney J., Johnstone, Ricky, McArthur, Grant, Hannan, Ross, Phillips, Wayne A., Pearson, Richard B, Sheppard, Karen E, Cullinane, C, Hannan, Katherine, Wall, Meaghan, Chan, Joanna, Barber, Francis, Foo, Jung, Cameron, Donald, Neilsen, Amelia, Ng, Pui Y., Ellul, Jason, Kleinschmidt, Margarete, Kinross, Kathryn M., Bowtell, David D., Christensen, James G., Hicks, Rodney J., Johnstone, Ricky, McArthur, Grant, Hannan, Ross, Phillips, Wayne A., and Pearson, Richard B

Abstract

Background: Ovarian cancer is the major cause of death from gynaecological malignancy with a 5 year survival of only ∼30% due to resistance to platinum and paclitaxel-based first line therapy. Dysregulation of the phosphoinositide 3-kinase/mammalian target of rapamycin (PI3K/mTOR) and RAS/extracellular signal-regulated kinase (ERK) pathways is common in ovarian cancer, providing potential new targets for 2nd line therapy. Methods:We determined the inhibition of proliferation of an extensive panel of ovarian cancer cell lines, encompassing all the major histotypes, by the dual PI3K/mTOR inhibitor PF-04691502 and a MEK inhibitor, PD-0325901. In addition, we analysed global gene expression, mutation status of key PI3K/mTOR and RAS/ERK pathway members and pathway activation to identify predictors of drug response. Results: PF-04691502 inhibits proliferation of the majority of cell lines with potencies that correlate with the extent of pathway inhibition. Resistant cell lines were characterised by activation of the RAS/ERK pathway as indicated by differential gene expression profiles and pathway activity analysis. PD-0325901 suppressed growth of a subset of cell lines that were characterised by high basal RAS/ERK signalling. Strikingly, using PF-04691502 and PD-0325901 in combination resulted in synergistic growth inhibition in 5/6 of PF-04691502 resistant cell lines and two cell lines resistant to both single agents showed robust synergistic growth arrest. Xenograft studies confirm the utility of combination therapy to synergistically inhibit tumour growth of PF-04691502-resistant tumours in vivo. Conclusions: These studies identify dual targeted inhibitors of PI3K/mTOR in combination with inhibitors of RAS/ERK signalling as a potentially effective new approach to treating ovarian cancer.

Published
2013

34. Synergistic inhibition of ovarian cancer cell growth by combining selective PI3K/mTOR and RAS/ERK pathway inhibitors

Author

Sheppard, Karen E., primary, Cullinane, Carleen, additional, Hannan, Katherine M., additional, Wall, Meaghan, additional, Chan, Joanna, additional, Barber, Frances, additional, Foo, Jung, additional, Cameron, Donald, additional, Neilsen, Amelia, additional, Ng, Pui, additional, Ellul, Jason, additional, Kleinschmidt, Margarete, additional, Kinross, Kathryn M., additional, Bowtell, David D., additional, Christensen, James G., additional, Hicks, Rodney J., additional, Johnstone, Ricky W., additional, McArthur, Grant A., additional, Hannan, Ross D., additional, Phillips, Wayne A., additional, and Pearson, Richard B., additional

Published
2013
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35. The mTORC1 Inhibitor Everolimus Prevents and Treats Eμ-Myc Lymphoma by Restoring Oncogene-Induced Senescence

Author

Wall, Meaghan, primary, Poortinga, Gretchen, additional, Stanley, Kym L., additional, Lindemann, Ralph K., additional, Bots, Michael, additional, Chan, Christopher J., additional, Bywater, Megan J., additional, Kinross, Kathryn M., additional, Astle, Megan V., additional, Waldeck, Kelly, additional, Hannan, Katherine M., additional, Shortt, Jake, additional, Smyth, Mark J., additional, Lowe, Scott W., additional, Hannan, Ross D., additional, Pearson, Richard B., additional, Johnstone, Ricky W., additional, and McArthur, Grant A., additional

Published
2013
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42. Ubiquitous expression of the Pik3caH1047R mutation promotes hypoglycemia, hypoinsulinemia, and organomegaly.

Author

Kinross, Kathryn M., Montgomery, Karen G., Mangiafico, Salvatore P., Hare, Lauren M., Kleinschmidt, Margarete, Bywater, Megan J., Poulton, Ingrid J., Vrahnas, Christina, Henneicke, Holger, Malaterre, Jordane, Waring, Paul M., Cullinane, Carleen, Sims, Natalie A., McArthur, Grant A., Andrikopoulos, Sofianos, and Phillips, Wayne A.

Subjects
*MOLECULAR genetics, *GENE expression, *HYPOGLYCEMIA, *GLUCOSE metabolism, *CARBOHYDRATE metabolism
Abstract

Mutations in PIK3CA, the gene encoding the p1 10a catalytic subunit of PI3K, are among the most common mutations found in human cancer and have also recently been implicated in a range of overgrowth syndromes in humans. We have used a novel inducible "exon-switch" approach to knock in the constitutively active Pik3caH1047R mutation into the endogenous Pik3ca gene of the mouse. Ubiquitous expression of the Pik3caH1047R mutation throughout the body resulted in a dramatic increase in body weight within 3 weeks of induction (mutant 150 ± 5%; wild-type 117 ± 3%, mean ± SEM), which was associated with increased organ size rather than adiposity. Severe metabolic effects, including a reduction in blood glucose levels to 59 ± 4% of baseline (11 days postinduction) and undetectable insulin levels, were also observed. Pik3caH1047R mutant mice died earlier (median survival 46.5 d post-mutation induction) than wild-type control mice (100% survival > 250 days). Although deletion of Akt2 increased median survival by 44%, neither organ overgrowth, nor hypoglycemia were rescued, indicating that both the growth and metabolic functions of constitutive PI3K activity can be Akt2 independent This mouse model demonstrates the critical role of PI3K in the regulation of both organ size and glucose metabolism at the whole animal level. [ABSTRACT FROM AUTHOR]

Published
2015
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44. Physiological expression of the PI3K-activating mutation Pik3caH1047R combines with Apc loss to promote development of invasive intestinal adenocarcinomas in mice.

Author

HARE, Lauren M., PHESSE, Toby J., WARING, Paul M., MONTGOMERY, Karen G., KINROSS, Kathryn M., MILLS, Kevin, ROH, Vincent, HEATH, Joan K., RAMSAY, Robert G., ERNST, Matthias, and PHILLIPS, Wayne A.

Subjects
ADENOCARCINOMA, GENE expression, PHOSPHOINOSITIDES, GENETIC mutation, ADENOMATOUS polyposis coli, LABORATORY mice
Abstract

PIK3CA, the gene encoding the p110a catalytic subunit of PI3K (phosphoinositide 3-kinase), is mutated in approximately 20% of sporadic CRCs (colorectal cancers), but the role of these mutations in the pathogenesis of CRC remains unclear. In the present study we used a novel mouse model to investigate the role of the Pik3caH1047R mutation, the most common PIK3CA mutation in CRC, during the development and progression of intestinal cancer. Our results demonstrate that Pik3caH1047R, when expressed at physiological levels, is insufficient to initiate intestinal tumorigenesis; however, in the context of Apc (adenomatous polyposis coli) loss, which is observed in 80% of CRCs and by itself results in benign intestinal adenomas, the Pik3caH1047R mutation promotes the development of highly aggressive and invasive adenocarcinomas in both the small and large intestines. The results of the present study show that an activating Pik3ca mutation can act in tandem with Apc loss to drive the progression of gastrointestinal cancer and thus this disease may be susceptible to therapeutic targeting using PI3K pathway inhibitors. [ABSTRACT FROM AUTHOR]

Published
2014
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48. Host immunity contributes to the anti-melanoma activity of BRAF inhibitors.

Author

Knight, Deborah A, Ngiow, Shin Foong, Li, Ming, Parmenter, Tiffany, Mok, Stephen, Cass, Ashley, Haynes, Nicole M, Kinross, Kathryn, Yagita, Hideo, Koya, Richard C, Graeber, Thomas G, Ribas, Antoni, McArthur, Grant A, and Smyth, Mark J

Subjects
*MELANOMA, *BRAF genes, *KINASE inhibitors, *IMMUNOLOGY
Abstract

A correction to the article "Host Immunity Contributes to the Anti-Melanoma Activity of BRAF Inhibitors" that was published in a 2013 issue is presented.

Published
2016
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50. Ubiquitous expression of the Pik3caH1047R mutation promotes hypoglycemia, hypoinsulinemia, and organomegaly.

Author

Kinross KM, Montgomery KG, Mangiafico SP, Hare LM, Kleinschmidt M, Bywater MJ, Poulton IJ, Vrahnas C, Henneicke H, Malaterre J, Waring PM, Cullinane C, Sims NA, McArthur GA, Andrikopoulos S, and Phillips WA

Subjects
Amino Acid Substitution, Animals, Class I Phosphatidylinositol 3-Kinases, Female, Gene Expression, Gene Knock-In Techniques, Glucose metabolism, Humans, Hypoglycemia metabolism, Mice, Mice, Knockout, Mice, Mutant Strains, Mice, Transgenic, Mutant Proteins genetics, Mutant Proteins metabolism, Organ Size genetics, Organ Size physiology, Proto-Oncogene Proteins c-akt deficiency, Proto-Oncogene Proteins c-akt genetics, Proto-Oncogene Proteins c-akt metabolism, Weight Gain, Hypoglycemia enzymology, Hypoglycemia genetics, Insulin blood, Mutation, Phosphatidylinositol 3-Kinases genetics, Phosphatidylinositol 3-Kinases metabolism
Abstract

Mutations in PIK3CA, the gene encoding the p110α catalytic subunit of PI3K, are among the most common mutations found in human cancer and have also recently been implicated in a range of overgrowth syndromes in humans. We have used a novel inducible "exon-switch" approach to knock in the constitutively active Pik3ca(H1047R) mutation into the endogenous Pik3ca gene of the mouse. Ubiquitous expression of the Pik3ca(H1047R) mutation throughout the body resulted in a dramatic increase in body weight within 3 weeks of induction (mutant 150 ± 5%; wild-type 117 ± 3%, mean ± sem), which was associated with increased organ size rather than adiposity. Severe metabolic effects, including a reduction in blood glucose levels to 59 ± 4% of baseline (11 days postinduction) and undetectable insulin levels, were also observed. Pik3ca(H1047R) mutant mice died earlier (median survival 46.5 d post-mutation induction) than wild-type control mice (100% survival > 250 days). Although deletion of Akt2 increased median survival by 44%, neither organ overgrowth, nor hypoglycemia were rescued, indicating that both the growth and metabolic functions of constitutive PI3K activity can be Akt2 independent. This mouse model demonstrates the critical role of PI3K in the regulation of both organ size and glucose metabolism at the whole animal level., (© FASEB.)

Published
2015
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