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4. Ex vivo culture of intact human patient derived pancreatic tumour tissue

Author

Kokkinos, John, Sharbeen, George, Haghighi, Koroush S., Ignacio, Rosa Mistica C., Kopecky, Chantal, Gonzales-Aloy, Estrella, Youkhana, Janet, Timpson, Paul, Pereira, Brooke A., Ritchie, Shona, Pandzic, Elvis, Boyer, Cyrille, Davis, Thomas P., Butler, Lisa M., Goldstein, David, McCarroll, Joshua A., and Phillips, Phoebe A.

Published
2021
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6. A novel small molecule that kills a subset of MLL-rearranged leukemia cells by inducing mitochondrial dysfunction

Author

Somers, Klaartje, Wen, Victoria W., Middlemiss, Shiloh M. C., Osborne, Brenna, Forgham, Helen, Jung, MoonSun, Karsa, Mawar, Clifton, Molly, Bongers, Angelika, Gao, Jixuan, Mayoh, Chelsea, Raoufi-Rad, Newsha, Kusnadi, Eric P., Hannan, Kate M., Scott, David A., Kwek, Alan, Liu, Bing, Flemming, Claudia, Chudakova, Daria A., Pandher, Ruby, Failes, Tim W., Lim, James, Angeli, Andrea, Osterman, Andrei L., Imamura, Toshihiko, Kees, Ursula R., Supuran, Claudiu T., Pearson, Richard B., Hannan, Ross D., Davis, Thomas P., McCarroll, Joshua, Kavallaris, Maria, Turner, Nigel, Gudkov, Andrei V., Haber, Michelle, Norris, Murray D., and Henderson, Michelle J.

Published
2019
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10. Supplementary Figure S4 A-E from Drugging MYCN Oncogenic Signaling through the MYCN-PA2G4 Binding Interface

Author

Koach, Jessica, primary, Holien, Jessica K., primary, Massudi, Hassina, primary, Carter, Daniel R., primary, Ciampa, Olivia C., primary, Herath, Mika, primary, Lim, Taylor, primary, Seneviratne, Janith A., primary, Milazzo, Giorgio, primary, Murray, Jayne E., primary, McCarroll, Joshua A., primary, Liu, Bing, primary, Mayoh, Chelsea, primary, Keenan, Bryce, primary, Stevenson, Brendan W., primary, Gorman, Michael A., primary, Bell, Jessica L., primary, Doughty, Larissa, primary, Hüttelmaier, Stefan, primary, Oberthuer, Andre, primary, Fischer, Matthias, primary, Gifford, Andrew J., primary, Liu, Tao, primary, Zhang, Xiaoling, primary, Zhu, Shizhen, primary, Gustafson, W. Clay, primary, Haber, Michelle, primary, Norris, Murray D., primary, Fletcher, Jamie I., primary, Perini, Giovanni, primary, Parker, Michael W., primary, Cheung, Belamy B., primary, and Marshall, Glenn M., primary

Published
2023
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11. Data from Cancer-Associated Fibroblasts in Pancreatic Ductal Adenocarcinoma Determine Response to SLC7A11 Inhibition

Author

Sharbeen, George, primary, McCarroll, Joshua A., primary, Akerman, Anouschka, primary, Kopecky, Chantal, primary, Youkhana, Janet, primary, Kokkinos, John, primary, Holst, Jeff, primary, Boyer, Cyrille, primary, Erkan, Mert, primary, Goldstein, David, primary, Timpson, Paul, primary, Cox, Thomas R., primary, Pereira, Brooke A., primary, Chitty, Jessica L., primary, Fey, Sigrid K., primary, Najumudeen, Arafath K., primary, Campbell, Andrew D., primary, Sansom, Owen J., primary, Ignacio, Rosa Mistica C., primary, Naim, Stephanie, primary, Liu, Jie, primary, Russia, Nelson, primary, Lee, Julia, primary, Chou, Angela, primary, Johns, Amber, primary, Gill, Anthony J., primary, Gonzales-Aloy, Estrella, primary, Gebski, Val, primary, Guan, Yi Fang, primary, Pajic, Marina, primary, Turner, Nigel, primary, Apte, Minoti V., primary, Davis, Thomas P., primary, Morton, Jennifer P., primary, Haghighi, Koroush S., primary, Kasparian, Jorjina, primary, McLean, Benjamin J., primary, Setargew, Yordanos F., primary, and Phillips, Phoebe A., primary

Published
2023
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12. Supplementary Information from Drugging MYCN Oncogenic Signaling through the MYCN-PA2G4 Binding Interface

Author

Koach, Jessica, primary, Holien, Jessica K., primary, Massudi, Hassina, primary, Carter, Daniel R., primary, Ciampa, Olivia C., primary, Herath, Mika, primary, Lim, Taylor, primary, Seneviratne, Janith A., primary, Milazzo, Giorgio, primary, Murray, Jayne E., primary, McCarroll, Joshua A., primary, Liu, Bing, primary, Mayoh, Chelsea, primary, Keenan, Bryce, primary, Stevenson, Brendan W., primary, Gorman, Michael A., primary, Bell, Jessica L., primary, Doughty, Larissa, primary, Hüttelmaier, Stefan, primary, Oberthuer, Andre, primary, Fischer, Matthias, primary, Gifford, Andrew J., primary, Liu, Tao, primary, Zhang, Xiaoling, primary, Zhu, Shizhen, primary, Gustafson, W. Clay, primary, Haber, Michelle, primary, Norris, Murray D., primary, Fletcher, Jamie I., primary, Perini, Giovanni, primary, Parker, Michael W., primary, Cheung, Belamy B., primary, and Marshall, Glenn M., primary

Published
2023
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14. Figure S2 from Cancer-Associated Fibroblasts in Pancreatic Ductal Adenocarcinoma Determine Response to SLC7A11 Inhibition

Author

Sharbeen, George, primary, McCarroll, Joshua A., primary, Akerman, Anouschka, primary, Kopecky, Chantal, primary, Youkhana, Janet, primary, Kokkinos, John, primary, Holst, Jeff, primary, Boyer, Cyrille, primary, Erkan, Mert, primary, Goldstein, David, primary, Timpson, Paul, primary, Cox, Thomas R., primary, Pereira, Brooke A., primary, Chitty, Jessica L., primary, Fey, Sigrid K., primary, Najumudeen, Arafath K., primary, Campbell, Andrew D., primary, Sansom, Owen J., primary, Ignacio, Rosa Mistica C., primary, Naim, Stephanie, primary, Liu, Jie, primary, Russia, Nelson, primary, Lee, Julia, primary, Chou, Angela, primary, Johns, Amber, primary, Gill, Anthony J., primary, Gonzales-Aloy, Estrella, primary, Gebski, Val, primary, Guan, Yi Fang, primary, Pajic, Marina, primary, Turner, Nigel, primary, Apte, Minoti V., primary, Davis, Thomas P., primary, Morton, Jennifer P., primary, Haghighi, Koroush S., primary, Kasparian, Jorjina, primary, McLean, Benjamin J., primary, Setargew, Yordanos F., primary, and Phillips, Phoebe A., primary

Published
2023
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15. Supplementary Table 2 from Cancer-Associated Fibroblasts in Pancreatic Ductal Adenocarcinoma Determine Response to SLC7A11 Inhibition

Author

Sharbeen, George, primary, McCarroll, Joshua A., primary, Akerman, Anouschka, primary, Kopecky, Chantal, primary, Youkhana, Janet, primary, Kokkinos, John, primary, Holst, Jeff, primary, Boyer, Cyrille, primary, Erkan, Mert, primary, Goldstein, David, primary, Timpson, Paul, primary, Cox, Thomas R., primary, Pereira, Brooke A., primary, Chitty, Jessica L., primary, Fey, Sigrid K., primary, Najumudeen, Arafath K., primary, Campbell, Andrew D., primary, Sansom, Owen J., primary, Ignacio, Rosa Mistica C., primary, Naim, Stephanie, primary, Liu, Jie, primary, Russia, Nelson, primary, Lee, Julia, primary, Chou, Angela, primary, Johns, Amber, primary, Gill, Anthony J., primary, Gonzales-Aloy, Estrella, primary, Gebski, Val, primary, Guan, Yi Fang, primary, Pajic, Marina, primary, Turner, Nigel, primary, Apte, Minoti V., primary, Davis, Thomas P., primary, Morton, Jennifer P., primary, Haghighi, Koroush S., primary, Kasparian, Jorjina, primary, McLean, Benjamin J., primary, Setargew, Yordanos F., primary, and Phillips, Phoebe A., primary

Published
2023
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16. Supplementary Figure S1 F-I from Drugging MYCN Oncogenic Signaling through the MYCN-PA2G4 Binding Interface

Author

Koach, Jessica, primary, Holien, Jessica K., primary, Massudi, Hassina, primary, Carter, Daniel R., primary, Ciampa, Olivia C., primary, Herath, Mika, primary, Lim, Taylor, primary, Seneviratne, Janith A., primary, Milazzo, Giorgio, primary, Murray, Jayne E., primary, McCarroll, Joshua A., primary, Liu, Bing, primary, Mayoh, Chelsea, primary, Keenan, Bryce, primary, Stevenson, Brendan W., primary, Gorman, Michael A., primary, Bell, Jessica L., primary, Doughty, Larissa, primary, Hüttelmaier, Stefan, primary, Oberthuer, Andre, primary, Fischer, Matthias, primary, Gifford, Andrew J., primary, Liu, Tao, primary, Zhang, Xiaoling, primary, Zhu, Shizhen, primary, Gustafson, W. Clay, primary, Haber, Michelle, primary, Norris, Murray D., primary, Fletcher, Jamie I., primary, Perini, Giovanni, primary, Parker, Michael W., primary, Cheung, Belamy B., primary, and Marshall, Glenn M., primary

Published
2023
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17. Supplementary Figure S5 F-H from Drugging MYCN Oncogenic Signaling through the MYCN-PA2G4 Binding Interface

Author

Koach, Jessica, primary, Holien, Jessica K., primary, Massudi, Hassina, primary, Carter, Daniel R., primary, Ciampa, Olivia C., primary, Herath, Mika, primary, Lim, Taylor, primary, Seneviratne, Janith A., primary, Milazzo, Giorgio, primary, Murray, Jayne E., primary, McCarroll, Joshua A., primary, Liu, Bing, primary, Mayoh, Chelsea, primary, Keenan, Bryce, primary, Stevenson, Brendan W., primary, Gorman, Michael A., primary, Bell, Jessica L., primary, Doughty, Larissa, primary, Hüttelmaier, Stefan, primary, Oberthuer, Andre, primary, Fischer, Matthias, primary, Gifford, Andrew J., primary, Liu, Tao, primary, Zhang, Xiaoling, primary, Zhu, Shizhen, primary, Gustafson, W. Clay, primary, Haber, Michelle, primary, Norris, Murray D., primary, Fletcher, Jamie I., primary, Perini, Giovanni, primary, Parker, Michael W., primary, Cheung, Belamy B., primary, and Marshall, Glenn M., primary

Published
2023
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18. Supplementary Figure S3 F-G from Drugging MYCN Oncogenic Signaling through the MYCN-PA2G4 Binding Interface

Author

Koach, Jessica, primary, Holien, Jessica K., primary, Massudi, Hassina, primary, Carter, Daniel R., primary, Ciampa, Olivia C., primary, Herath, Mika, primary, Lim, Taylor, primary, Seneviratne, Janith A., primary, Milazzo, Giorgio, primary, Murray, Jayne E., primary, McCarroll, Joshua A., primary, Liu, Bing, primary, Mayoh, Chelsea, primary, Keenan, Bryce, primary, Stevenson, Brendan W., primary, Gorman, Michael A., primary, Bell, Jessica L., primary, Doughty, Larissa, primary, Hüttelmaier, Stefan, primary, Oberthuer, Andre, primary, Fischer, Matthias, primary, Gifford, Andrew J., primary, Liu, Tao, primary, Zhang, Xiaoling, primary, Zhu, Shizhen, primary, Gustafson, W. Clay, primary, Haber, Michelle, primary, Norris, Murray D., primary, Fletcher, Jamie I., primary, Perini, Giovanni, primary, Parker, Michael W., primary, Cheung, Belamy B., primary, and Marshall, Glenn M., primary

Published
2023
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19. Supplementary Table 4 from Cancer-Associated Fibroblasts in Pancreatic Ductal Adenocarcinoma Determine Response to SLC7A11 Inhibition

Author

Sharbeen, George, primary, McCarroll, Joshua A., primary, Akerman, Anouschka, primary, Kopecky, Chantal, primary, Youkhana, Janet, primary, Kokkinos, John, primary, Holst, Jeff, primary, Boyer, Cyrille, primary, Erkan, Mert, primary, Goldstein, David, primary, Timpson, Paul, primary, Cox, Thomas R., primary, Pereira, Brooke A., primary, Chitty, Jessica L., primary, Fey, Sigrid K., primary, Najumudeen, Arafath K., primary, Campbell, Andrew D., primary, Sansom, Owen J., primary, Ignacio, Rosa Mistica C., primary, Naim, Stephanie, primary, Liu, Jie, primary, Russia, Nelson, primary, Lee, Julia, primary, Chou, Angela, primary, Johns, Amber, primary, Gill, Anthony J., primary, Gonzales-Aloy, Estrella, primary, Gebski, Val, primary, Guan, Yi Fang, primary, Pajic, Marina, primary, Turner, Nigel, primary, Apte, Minoti V., primary, Davis, Thomas P., primary, Morton, Jennifer P., primary, Haghighi, Koroush S., primary, Kasparian, Jorjina, primary, McLean, Benjamin J., primary, Setargew, Yordanos F., primary, and Phillips, Phoebe A., primary

Published
2023
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20. Supplementary Figure S6 A-F from Drugging MYCN Oncogenic Signaling through the MYCN-PA2G4 Binding Interface

Author

Koach, Jessica, primary, Holien, Jessica K., primary, Massudi, Hassina, primary, Carter, Daniel R., primary, Ciampa, Olivia C., primary, Herath, Mika, primary, Lim, Taylor, primary, Seneviratne, Janith A., primary, Milazzo, Giorgio, primary, Murray, Jayne E., primary, McCarroll, Joshua A., primary, Liu, Bing, primary, Mayoh, Chelsea, primary, Keenan, Bryce, primary, Stevenson, Brendan W., primary, Gorman, Michael A., primary, Bell, Jessica L., primary, Doughty, Larissa, primary, Hüttelmaier, Stefan, primary, Oberthuer, Andre, primary, Fischer, Matthias, primary, Gifford, Andrew J., primary, Liu, Tao, primary, Zhang, Xiaoling, primary, Zhu, Shizhen, primary, Gustafson, W. Clay, primary, Haber, Michelle, primary, Norris, Murray D., primary, Fletcher, Jamie I., primary, Perini, Giovanni, primary, Parker, Michael W., primary, Cheung, Belamy B., primary, and Marshall, Glenn M., primary

Published
2023
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21. Supplementary Figure S2A-C from Drugging MYCN Oncogenic Signaling through the MYCN-PA2G4 Binding Interface

Author

Koach, Jessica, primary, Holien, Jessica K., primary, Massudi, Hassina, primary, Carter, Daniel R., primary, Ciampa, Olivia C., primary, Herath, Mika, primary, Lim, Taylor, primary, Seneviratne, Janith A., primary, Milazzo, Giorgio, primary, Murray, Jayne E., primary, McCarroll, Joshua A., primary, Liu, Bing, primary, Mayoh, Chelsea, primary, Keenan, Bryce, primary, Stevenson, Brendan W., primary, Gorman, Michael A., primary, Bell, Jessica L., primary, Doughty, Larissa, primary, Hüttelmaier, Stefan, primary, Oberthuer, Andre, primary, Fischer, Matthias, primary, Gifford, Andrew J., primary, Liu, Tao, primary, Zhang, Xiaoling, primary, Zhu, Shizhen, primary, Gustafson, W. Clay, primary, Haber, Michelle, primary, Norris, Murray D., primary, Fletcher, Jamie I., primary, Perini, Giovanni, primary, Parker, Michael W., primary, Cheung, Belamy B., primary, and Marshall, Glenn M., primary

Published
2023
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22. Supplementary Figure S6 G-K from Drugging MYCN Oncogenic Signaling through the MYCN-PA2G4 Binding Interface

Author

Koach, Jessica, primary, Holien, Jessica K., primary, Massudi, Hassina, primary, Carter, Daniel R., primary, Ciampa, Olivia C., primary, Herath, Mika, primary, Lim, Taylor, primary, Seneviratne, Janith A., primary, Milazzo, Giorgio, primary, Murray, Jayne E., primary, McCarroll, Joshua A., primary, Liu, Bing, primary, Mayoh, Chelsea, primary, Keenan, Bryce, primary, Stevenson, Brendan W., primary, Gorman, Michael A., primary, Bell, Jessica L., primary, Doughty, Larissa, primary, Hüttelmaier, Stefan, primary, Oberthuer, Andre, primary, Fischer, Matthias, primary, Gifford, Andrew J., primary, Liu, Tao, primary, Zhang, Xiaoling, primary, Zhu, Shizhen, primary, Gustafson, W. Clay, primary, Haber, Michelle, primary, Norris, Murray D., primary, Fletcher, Jamie I., primary, Perini, Giovanni, primary, Parker, Michael W., primary, Cheung, Belamy B., primary, and Marshall, Glenn M., primary

Published
2023
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23. Supplementary Figure 7 from TUBB3/βIII-Tubulin Acts through the PTEN/AKT Signaling Axis to Promote Tumorigenesis and Anoikis Resistance in Non–Small Cell Lung Cancer

Author

McCarroll, Joshua A., primary, Gan, Pei Pei, primary, Erlich, Rafael B., primary, Liu, Marjorie, primary, Dwarte, Tanya, primary, Sagnella, Sharon S., primary, Akerfeldt, Mia C., primary, Yang, Lu, primary, Parker, Amelia L., primary, Chang, Melissa H., primary, Shum, Michael S., primary, Byrne, Frances L., primary, and Kavallaris, Maria, primary

Published
2023
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24. Data from TUBB3/βIII-Tubulin Acts through the PTEN/AKT Signaling Axis to Promote Tumorigenesis and Anoikis Resistance in Non–Small Cell Lung Cancer

Author

McCarroll, Joshua A., primary, Gan, Pei Pei, primary, Erlich, Rafael B., primary, Liu, Marjorie, primary, Dwarte, Tanya, primary, Sagnella, Sharon S., primary, Akerfeldt, Mia C., primary, Yang, Lu, primary, Parker, Amelia L., primary, Chang, Melissa H., primary, Shum, Michael S., primary, Byrne, Frances L., primary, and Kavallaris, Maria, primary

Published
2023
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25. Supplementary Figure 3 from TUBB3/βIII-Tubulin Acts through the PTEN/AKT Signaling Axis to Promote Tumorigenesis and Anoikis Resistance in Non–Small Cell Lung Cancer

Author

McCarroll, Joshua A., primary, Gan, Pei Pei, primary, Erlich, Rafael B., primary, Liu, Marjorie, primary, Dwarte, Tanya, primary, Sagnella, Sharon S., primary, Akerfeldt, Mia C., primary, Yang, Lu, primary, Parker, Amelia L., primary, Chang, Melissa H., primary, Shum, Michael S., primary, Byrne, Frances L., primary, and Kavallaris, Maria, primary

Published
2023
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26. Supplementary Figure 1 from TUBB3/βIII-Tubulin Acts through the PTEN/AKT Signaling Axis to Promote Tumorigenesis and Anoikis Resistance in Non–Small Cell Lung Cancer

Author

McCarroll, Joshua A., primary, Gan, Pei Pei, primary, Erlich, Rafael B., primary, Liu, Marjorie, primary, Dwarte, Tanya, primary, Sagnella, Sharon S., primary, Akerfeldt, Mia C., primary, Yang, Lu, primary, Parker, Amelia L., primary, Chang, Melissa H., primary, Shum, Michael S., primary, Byrne, Frances L., primary, and Kavallaris, Maria, primary

Published
2023
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27. Supplementary Methods, Figure Legends, Tables 1 - 2 from TUBB3/βIII-Tubulin Acts through the PTEN/AKT Signaling Axis to Promote Tumorigenesis and Anoikis Resistance in Non–Small Cell Lung Cancer

Author

McCarroll, Joshua A., primary, Gan, Pei Pei, primary, Erlich, Rafael B., primary, Liu, Marjorie, primary, Dwarte, Tanya, primary, Sagnella, Sharon S., primary, Akerfeldt, Mia C., primary, Yang, Lu, primary, Parker, Amelia L., primary, Chang, Melissa H., primary, Shum, Michael S., primary, Byrne, Frances L., primary, and Kavallaris, Maria, primary

Published
2023
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29. Supplementary Figure 5 from TUBB3/βIII-Tubulin Acts through the PTEN/AKT Signaling Axis to Promote Tumorigenesis and Anoikis Resistance in Non–Small Cell Lung Cancer

Author

McCarroll, Joshua A., primary, Gan, Pei Pei, primary, Erlich, Rafael B., primary, Liu, Marjorie, primary, Dwarte, Tanya, primary, Sagnella, Sharon S., primary, Akerfeldt, Mia C., primary, Yang, Lu, primary, Parker, Amelia L., primary, Chang, Melissa H., primary, Shum, Michael S., primary, Byrne, Frances L., primary, and Kavallaris, Maria, primary

Published
2023
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31. Supplementary Figure 6 from TUBB3/βIII-Tubulin Acts through the PTEN/AKT Signaling Axis to Promote Tumorigenesis and Anoikis Resistance in Non–Small Cell Lung Cancer

Author

McCarroll, Joshua A., primary, Gan, Pei Pei, primary, Erlich, Rafael B., primary, Liu, Marjorie, primary, Dwarte, Tanya, primary, Sagnella, Sharon S., primary, Akerfeldt, Mia C., primary, Yang, Lu, primary, Parker, Amelia L., primary, Chang, Melissa H., primary, Shum, Michael S., primary, Byrne, Frances L., primary, and Kavallaris, Maria, primary

Published
2023
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32. Supplementary Figure 4 from TUBB3/βIII-Tubulin Acts through the PTEN/AKT Signaling Axis to Promote Tumorigenesis and Anoikis Resistance in Non–Small Cell Lung Cancer

Author

McCarroll, Joshua A., primary, Gan, Pei Pei, primary, Erlich, Rafael B., primary, Liu, Marjorie, primary, Dwarte, Tanya, primary, Sagnella, Sharon S., primary, Akerfeldt, Mia C., primary, Yang, Lu, primary, Parker, Amelia L., primary, Chang, Melissa H., primary, Shum, Michael S., primary, Byrne, Frances L., primary, and Kavallaris, Maria, primary

Published
2023
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33. Supplementary Figure 2 from TUBB3/βIII-Tubulin Acts through the PTEN/AKT Signaling Axis to Promote Tumorigenesis and Anoikis Resistance in Non–Small Cell Lung Cancer

Author

McCarroll, Joshua A., primary, Gan, Pei Pei, primary, Erlich, Rafael B., primary, Liu, Marjorie, primary, Dwarte, Tanya, primary, Sagnella, Sharon S., primary, Akerfeldt, Mia C., primary, Yang, Lu, primary, Parker, Amelia L., primary, Chang, Melissa H., primary, Shum, Michael S., primary, Byrne, Frances L., primary, and Kavallaris, Maria, primary

Published
2023
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36. βIII‐tubulin suppression enhances the activity of Amuvatinib to inhibit cell proliferation in c‐Met positive non‐small cell lung cancer cells

Author

Brayford, Simon, primary, Duly, Alastair, additional, Teo, Wee Siang, additional, Dwarte, Tanya, additional, Gonzales‐Aloy, Estrella, additional, Ma, Zerong, additional, McVeigh, Laura, additional, Failes, Timothy W., additional, Arndt, Greg M., additional, McCarroll, Joshua A., additional, and Kavallaris, Maria, additional

Published
2022
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40. βIII‐tubulin suppression enhances the activity of Amuvatinib to inhibit cell proliferation in c‐Met positive non‐small cell lung cancer cells.

Author

Brayford, Simon, Duly, Alastair, Teo, Wee Siang, Dwarte, Tanya, Gonzales‐Aloy, Estrella, Ma, Zerong, McVeigh, Laura, Failes, Timothy W., Arndt, Greg M., McCarroll, Joshua A., and Kavallaris, Maria

Subjects
NON-small-cell lung carcinoma, TUBULINS, INHIBITION of cellular proliferation, CANCER cells, PROTEIN-tyrosine kinases, THERAPEUTICS
Abstract

Non‐Small Cell Lung Carcinoma (NSCLC) remains a leading cause of cancer death. Resistance to therapy is a significant problem, highlighting the need to find new ways of sensitising tumour cells to therapeutic agents. βIII‐tubulin is associated with aggressive tumours and chemotherapy resistance in a range of cancers including NSCLC. βIII‐tubulin expression has been shown to impact kinase signalling in NSCLC cells. Here, we sought to exploit this interaction by identifying co‐activity between βIII‐tubulin suppression and small‐molecule kinase inhibitors. To achieve this, a forced‐genetics approach combined with a high‐throughput drug screen was used. We show that activity of the multi‐kinase inhibitor Amuvatinib (MP‐470) is enhanced by βIII‐tubulin suppression in independent NSCLC cell lines. We also show that this compound significantly inhibits cell proliferation among βIII‐tubulin knockdown cells expressing the receptor tyrosine kinase c‐Met. Together, our results highlight that βIII‐tubulin suppression combined with targeting specific receptor tyrosine kinases may represent a novel therapeutic approach for otherwise difficult‐to‐treat lung carcinomas. [ABSTRACT FROM AUTHOR]

Published
2023
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43. Intranasal Delivery of Recombinant S100A8 Protein Delays Lung Cancer Growth by Remodeling the Lung Immune Microenvironment

Author

Wong, Sze Wing, McCarroll, Joshua, Hsu, Kenneth, Geczy, Carolyn L., and Tedla, Nicodemus

Subjects
Mice, Lung Neoplasms, Immunology, Tumor Microenvironment, Immunology and Allergy, Animals, Proteins, Calgranulin A, Thorax, Lung
Abstract

Lung cancer is the leading cause of cancer-related death worldwide. Increasing evidence indicates a critical role for chronic inflammation in lung carcinogenesis. S100A8 is a protein with reported pro- and anti-inflammatory functions. It is highly expressed in myeloid-derived suppressor cells (MDSC) that accumulate in the tumor microenvironment and abrogate effective anti-cancer immune responses. Mechanisms of MDSC-mediated immunosuppression include production of reactive oxygen species and nitric oxide, and depletion of L-arginine required for T cell function. Although S100A8 is expressed in MDSC, its role in the lung tumor microenvironment is largely unknown. To address this, mouse recombinant S100A8 was repeatedly administered intranasally to mice bearing orthotopic lung cancers. S100A8 treatment prolonged survival from 19 days to 28 days (p < 0.001). At midpoint of survival, whole lungs and bronchoalveolar lavage fluid (BALF) were collected and relevant genes/proteins measured. We found that S100A8 significantly lowered expression of cytokine genes and proteins that promote expansion and activation of MDSC in lungs and BALF from cancer-bearing mice. Moreover, S100A8 enhanced activities of antioxidant enzymes and suppressed production of nitrite to create a lung microenvironment conducive to cytotoxic lymphocyte expansion and function. In support of this, we found decreased MDSC numbers, and increased numbers of CD4+T cells and natural killer T (NK-T) cells in lungs from cancer-bearing mice treated with S100A8.Ex-vivotreatment of splenocytes with S100A8 protein activated NK cells. Our results indicate that treatment with S100A8 may favourably modify the lung microenvironment to promote an effective immune response in lungs, thereby representing a new strategy that could complement current immunotherapies in lung cancer.

Published
2021

45. Cancer-Associated Fibroblasts in Pancreatic Ductal Adenocarcinoma Determine Response to SLC7A11 Inhibition

Author

Sharbeen, George, primary, McCarroll, Joshua A., additional, Akerman, Anouschka, additional, Kopecky, Chantal, additional, Youkhana, Janet, additional, Kokkinos, John, additional, Holst, Jeff, additional, Boyer, Cyrille, additional, Erkan, Mert, additional, Goldstein, David, additional, Timpson, Paul, additional, Cox, Thomas R., additional, Pereira, Brooke A., additional, Chitty, Jessica L., additional, Fey, Sigrid K., additional, Najumudeen, Arafath K., additional, Campbell, Andrew D., additional, Sansom, Owen J., additional, Ignacio, Rosa Mistica C., additional, Naim, Stephanie, additional, Liu, Jie, additional, Russia, Nelson, additional, Lee, Julia, additional, Chou, Angela, additional, Johns, Amber, additional, Gill, Anthony J., additional, Gonzales-Aloy, Estrella, additional, Gebski, Val, additional, Guan, Yi Fang, additional, Pajic, Marina, additional, Turner, Nigel, additional, Apte, Minoti V., additional, Davis, Thomas P., additional, Morton, Jennifer P., additional, Haghighi, Koroush S., additional, Kasparian, Jorjina, additional, McLean, Benjamin J., additional, Setargew, Yordanos F., additional, and Phillips, Phoebe A., additional

Published
2021
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46. Development of siRNA-based nanomedicines for the treatment of lung cancer

Author

McCarroll, Joshua, Women's & Children's Health, Faculty of Medicine, UNSW, Kavallaris, Maria, Women's & Children's Health, Faculty of Medicine, UNSW, Ma, Zerong, Women's & Children's Health, Faculty of Medicine, UNSW, McCarroll, Joshua, Women's & Children's Health, Faculty of Medicine, UNSW, Kavallaris, Maria, Women's & Children's Health, Faculty of Medicine, UNSW, and Ma, Zerong, Women's & Children's Health, Faculty of Medicine, UNSW

Abstract

Lung cancer is a major cause of cancer-related death. A lack of response to treatment and development of chemoresistance are common for this disease. Novel therapeutic strategies to treat lung cancer are needed. βIII-tubulin and Polo-like kinase 1 (PLK1) are highly expressed in lung cancer cells and play major roles in promoting tumour growth and chemoresistance. Unfortunately, both βIII-tubulin and PLK1 are difficult to selectively inhibit using chemical agents due to their high structural homology with other proteins. Gene silencing drugs (siRNA) offer a solution to this problem but require a delivery vehicle to enter cells.The aims of this study were to: 1) examine the biological properties of non-viral star nanoparticles (star) for the delivery of siRNA to lung cancer cells in vitro; 2) to examine the biodistribution of star-siRNA using systemic and local delivery to mouse lung tumours; and 3) to determine the effect of silencing βIII-tubulin or PLK1 expression using star-siRNA on lung tumour growth in vivo.Star complexed siRNA with high efficiency to form monodisperse nanoparticles (size 14.2nm ± 0.8, zeta potential 8.7mV ± 2.7). At different star-siRNA weight/weight (4:1, 8:1 and 16:1 w/w) ratios, star-siRNA were internalised into lung cancer cells as early as 30 minutes post-treatment. At 16:1 w/w, star-siRNA was able to escape from the endo-lysosomal degradation pathway, which led to potent inhibition of target gene and protein expression in lung cancer cells. Star-siRNA when administered systemically or locally to the lungs were non-toxic to mice. Star-siRNA delivered systemically were localised to the liver, spleen, lungs and kidneys. While star-siRNA delivered using a nebuliser were exclusively localised to the lungs. Finally, silencing PLK1 or βIII-tubulin expression in mouse lung tumours inhibited tumour growth.In conclusion, this study demonstrates for the first time that star nanoparticles can deliver siRNA to lung cancer cells and silence target prot

Published
2021

47. The RNA‐helicase DDX21 upregulates CEP55 expression and promotes neuroblastoma

Author

Putra, Vina, primary, Hulme, Amy J., additional, Tee, Andrew E., additional, Sun, Jane Q.J., additional, Atmadibrata, Bernard, additional, Ho, Nicholas, additional, Chen, Jingwei, additional, Gao, Jixuan, additional, Norris, Murray D., additional, Haber, Michelle, additional, Kavallaris, Maria, additional, Henderson, Michelle J., additional, McCarroll, Joshua, additional, Trahair, Toby, additional, Liu, Tao, additional, and Liu, Pei Y., additional

Published
2021
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48. Phenotypic screen for oxygen consumption rate identifies an anti-cancer naphthoquinone that induces mitochondrial oxidative stress

Author

Byrne, Frances L., Olzomer, Ellen M., Marriott, Gabriella R., Quek, Lake-Ee, Katen, Alice, Su, Jacky, Nelson, Marin E., Hart-Smith, Gene, Larance, Mark, Sebesfi, Veronica F., Cuff, Jeff, Martyn, Gabriella E., Childress, Elizabeth, Alexopoulos, Stephanie J., Poon, Ivan K., Faux, Maree C., Burgess, Antony W., Reid, Glen, McCarroll, Joshua A., Santos, Webster L., Quinlan, Kate G. R., Turner, Nigel, Fazakerley, Daniel J., Kumar, Naresh, Hoehn, Kyle L., Byrne, Frances L., Olzomer, Ellen M., Marriott, Gabriella R., Quek, Lake-Ee, Katen, Alice, Su, Jacky, Nelson, Marin E., Hart-Smith, Gene, Larance, Mark, Sebesfi, Veronica F., Cuff, Jeff, Martyn, Gabriella E., Childress, Elizabeth, Alexopoulos, Stephanie J., Poon, Ivan K., Faux, Maree C., Burgess, Antony W., Reid, Glen, McCarroll, Joshua A., Santos, Webster L., Quinlan, Kate G. R., Turner, Nigel, Fazakerley, Daniel J., Kumar, Naresh, and Hoehn, Kyle L.

Abstract

A hallmark of cancer cells is their ability to reprogram nutrient metabolism. Thus, disruption to this phenotype is a potential avenue for anti-cancer therapy. Herein we used a phenotypic chemical library screening approach to identify molecules that disrupted nutrient metabolism (by increasing cellular oxygen consumption rate) and were toxic to cancer cells. From this screen we discovered a 1,4-Naphthoquinone (referred to as BH10) that is toxic to a broad range of cancer cell types. BH10 has improved cancer-selective toxicity compared to doxorubicin, 17-AAG, vitamin K3, and other known anti-cancer quinones. BH10 increases glucose oxidation via both mitochondrial and pentose phosphate pathways, decreases glycolysis, lowers GSH:GSSG and NAPDH/NAPD(+) ratios exclusively in cancer cells, and induces necrosis. BH10 targets mitochondrial redox defence as evidenced by increased mitochondrial peroxiredoxin 3 oxidation and decreased mitochondrial aconitase activity, without changes in markers of cytosolic or nuclear damage. Over-expression of mitochondria-targeted catalase protects cells from BH10-mediated toxicity, while the thioredoxin reductase inhibitor auranofin synergistically enhances BH10-induced peroxiredoxin 3 oxidation and cytotoxicity. Overall, BH10 represents a 1,4-Naphthoquinone with an improved cancer-selective cytotoxicity profile via its mitochondrial specificity.

Published
2020
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49. Phenotypic screen for oxygen consumption rate identifies an anti-cancer naphthoquinone that induces mitochondrial oxidative stress

Author

Chemistry, Center for Drug Discovery, Byrne, Frances L., Olzomer, Ellen M., Marriott, Gabriella R., Quek, Lake-Ee, Katen, Alice, Su, Jacky, Nelson, Marin E., Hart-Smith, Gene, Larance, Mark, Sebesfi, Veronica F., Cuff, Jeff, Martyn, Gabriella E., Childress, Elizabeth, Alexopoulos, Stephanie J., Poon, Ivan K., Faux, Maree C., Burgess, Antony W., Reid, Glen, McCarroll, Joshua A., Santos, Webster L., Quinlan, Kate G. R., Turner, Nigel, Fazakerley, Daniel J., Kumar, Naresh, Hoehn, Kyle L., Chemistry, Center for Drug Discovery, Byrne, Frances L., Olzomer, Ellen M., Marriott, Gabriella R., Quek, Lake-Ee, Katen, Alice, Su, Jacky, Nelson, Marin E., Hart-Smith, Gene, Larance, Mark, Sebesfi, Veronica F., Cuff, Jeff, Martyn, Gabriella E., Childress, Elizabeth, Alexopoulos, Stephanie J., Poon, Ivan K., Faux, Maree C., Burgess, Antony W., Reid, Glen, McCarroll, Joshua A., Santos, Webster L., Quinlan, Kate G. R., Turner, Nigel, Fazakerley, Daniel J., Kumar, Naresh, and Hoehn, Kyle L.

Abstract

A hallmark of cancer cells is their ability to reprogram nutrient metabolism. Thus, disruption to this phenotype is a potential avenue for anti-cancer therapy. Herein we used a phenotypic chemical library screening approach to identify molecules that disrupted nutrient metabolism (by increasing cellular oxygen consumption rate) and were toxic to cancer cells. From this screen we discovered a 1,4-Naphthoquinone (referred to as BH10) that is toxic to a broad range of cancer cell types. BH10 has improved cancer-selective toxicity compared to doxorubicin, 17-AAG, vitamin K3, and other known anti-cancer quinones. BH10 increases glucose oxidation via both mitochondrial and pentose phosphate pathways, decreases glycolysis, lowers GSH:GSSG and NAPDH/NAPD(+) ratios exclusively in cancer cells, and induces necrosis. BH10 targets mitochondrial redox defence as evidenced by increased mitochondrial peroxiredoxin 3 oxidation and decreased mitochondrial aconitase activity, without changes in markers of cytosolic or nuclear damage. Over-expression of mitochondria-targeted catalase protects cells from BH10-mediated toxicity, while the thioredoxin reductase inhibitor auranofin synergistically enhances BH10-induced peroxiredoxin 3 oxidation and cytotoxicity. Overall, BH10 represents a 1,4-Naphthoquinone with an improved cancer-selective cytotoxicity profile via its mitochondrial specificity.

Published
2020

50. Facile synthesis of lactoferrin conjugated ultra small large pore silica nanoparticles for the treatment of glioblastoma

Author

Janjua, Taskeen Iqbal, primary, Ahmed-Cox, Aria, additional, Meka, Anand Kumar, additional, Mansfeld, Friederike M., additional, Forgham, Helen, additional, Ignacio, Rosa Mistica C., additional, Cao, Yuxue, additional, McCarroll, Joshua A., additional, Mazzieri, Roberta, additional, Kavallaris, Maria, additional, and Popat, Amirali, additional

Published
2021
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