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2. Absolute lymphocyte count is associated with survival in ovarian cancer independent of tumor-infiltrating lymphocytes

Author

Milne Katy, Alexander Cheryl, Webb John R, Sun Winnie, Dillon Kristy, Kalloger Steve E, Gilks C Blake, Clarke Blaise, Köbel Martin, and Nelson Brad H

Subjects
Ovarian cancer, Tumor infiltrating lymphocytes, Prognosis, Tumor immunology, Medicine
Abstract

Abstract Background The immune system strongly influences outcome in patients with ovarian cancer. In particular, the absolute lymphocyte count in peripheral blood (ALC) and the presence of tumor-infiltrating lymphocytes (TIL) have each been associated with favourable prognosis. However, the mechanistic relationships between ALC, TIL and prognosis are poorly understood. We hypothesized that high ALC values might be associated with stronger tumor immunity as manifested by increased TIL, decreased tumor burden and longer survival. Methods ALC values were collected from patient records ≥ 2 years before, during or after primary treatment for high-grade serous ovarian cancer (HGSC). Lymphocyte subsets were assessed in peripheral blood by flow cytometry. CD8+ and CD20+ TIL were assessed by immunohistochemistry. Results Overall, patients had normal ALC values two or more years prior to diagnosis of HGSC. These values were not predictive of disease severity or survival upon subsequent development of HGSC. Rather, ALC declined upon development of HGSC in proportion to disease burden. This decline involved all lymphocyte subsets. ALC increased following surgery, remained stable during chemotherapy, but rarely recovered to pre-diagnostic levels. ALC values recorded at diagnosis did not correlate with CD8+ or CD20+ TIL but were associated with progression-free survival. Conclusions Patients with high intrinsic ALC values show no clinical or survival advantage upon subsequent development of HGSC. ALC values at diagnosis are prognostic due to an association with disease burden rather than TIL. Therapeutic enhancement of ALC may be necessary but not sufficient to improve survival in HGSC.

Published
2012
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3. HER2 overexpression and amplification is present in a subset of ovarian mucinous carcinomas and can be targeted with trastuzumab therapy

Author

Swenerton Kenneth D, Kalloger Steve E, Köbel Martin, Adamiak Anna, Ronnett Bridgett M, Vang Russell, Wiegand Kimberly C, McAlpine Jessica N, Huntsman David G, Gilks C, and Miller Dianne M

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background The response rate of ovarian mucinous carcinomas to paclitaxel/carboplatin is low, prompting interest in targeted molecular therapies. We investigated HER2 expression and amplification, and the potential for trastuzumab therapy in this histologic subtype of ovarian cancer. Methods HER2 status was tested in 33 mucinous carcinomas and 16 mucinous borderline ovarian tumors (BOT)). Five cases with documented recurrence and with tissue from the recurrence available for testing were analyzed to determine whether HER2 amplification status changed over time. Three prospectively identified recurrent mucinous ovarian carcinomas were assessed for HER2 amplification and patients received trastuzumab therapy with conventional chemotherapy. Results Amplification of HER2 was observed in 6/33 (18.2%) mucinous carcinomas and 3/16 (18.8%) BOT. HER2 amplification in primary mucinous carcinomas was not associated with an increased likelihood of recurrence. The prospectively identified recurrent mucinous carcinomas showed overexpression and amplification of HER2; one patient's tumor responded dramatically to trastuzumab in combination with conventional chemotherapy, while another patient experienced an isolated central nervous system recurrence after trastuzumab therapy. Conclusion HER2 amplification is relatively common in ovarian mucinous carcinomas (6/33, 18.2%), although not of prognostic significance. Trastuzumab therapy is a treatment option for patients with mucinous carcinoma when the tumor has HER2 amplification and overexpression.

Published
2009
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4. Ovarian carcinomas with genetic and epigenetic BRCA1 loss have distinct molecular abnormalities

Author

Miller Dianne M, Wang Yuker, Spellman Paul T, Smith Margaret, Blood Katherine A, Kalloger Steve E, Kaurah Pardeep, Ridge Yolanda, Troussard Armelle, Young Sean, Boyd Niki, De Luca Alessandro, Press Joshua Z, Horsman Doug, Faham Malek, Gilks C Blake, Gray Joe, and Huntsman David G

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Background Subclassification of ovarian carcinomas can be used to guide treatment and determine prognosis. Germline and somatic mutations, loss of heterozygosity (LOH), and epigenetic events such as promoter hypermethylation can lead to decreased expression of BRCA1/2 in ovarian cancers. The mechanism of BRCA1/2 loss is a potential method of subclassifying high grade serous carcinomas. Methods A consecutive series of 49 ovarian cancers was assessed for mutations status of BRCA1 and BRCA2, LOH at the BRCA1 and BRCA2 loci, methylation of the BRCA1 promoter, BRCA1, BRCA2, PTEN, and PIK3CA transcript levels, PIK3CA gene copy number, and BRCA1, p21, p53, and WT-1 immunohistochemistry. Results Eighteen (37%) of the ovarian carcinomas had germline or somatic BRCA1 mutations, or epigenetic loss of BRCA1. All of these tumours were high-grade serous or undifferentiated type. None of the endometrioid (n = 5), clear cell (n = 4), or low grade serous (n = 2) carcinomas showed loss of BRCA1, whereas 47% of the 38 high-grade serous or undifferentiated carcinomas had loss of BRCA1. It was possible to distinguish high grade serous carcinomas with BRCA1 mutations from those with epigenetic BRCA1 loss: tumours with BRCA1 mutations typically had decreased PTEN mRNA levels while those with epigenetic loss of BRCA1 had copy number gain of PIK3CA. Overexpression of p53 with loss of p21 expression occurred significantly more frequently in high grade serous carcinomas with epigenetic loss of BRCA1, compared to high grade serous tumors without loss of BRCA1. Conclusion High grade serous carcinomas can be subclassified into three groups: BRCA1 loss (genetic), BRCA1 loss (epigenetic), and no BRCA1 loss. Tumors in these groups show distinct molecular alterations involving the PI3K/AKT and p53 pathways.

Published
2008
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5. Integrative analysis of KRAS wildtype metastatic pancreatic ductal adenocarcinoma reveals mutation and expression-based similarities to cholangiocarcinoma

Author

Topham, James T., Tsang, Erica S., Karasinska, Joanna M., Metcalfe, Andrew, Ali, Hassan, Kalloger, Steve E., Csizmok, Veronika, Williamson, Laura M., Titmuss, Emma, Nielsen, Karina, Negri, Gian Luca, Spencer Miko, Sandra E., Jang, Gun Ho, Denroche, Robert E., Wong, Hui-li, O’Kane, Grainne M., Moore, Richard A., Mungall, Andrew J., Loree, Jonathan M., Notta, Faiyaz, Wilson, Julie M., Bathe, Oliver F., Tang, Patricia A., Goodwin, Rachel, Morin, Gregg B., Knox, Jennifer J., Gallinger, Steven, Laskin, Janessa, Marra, Marco A., Jones, Steven J. M., Schaeffer, David F., and Renouf, Daniel J.

Published
2022
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7. Proteotranscriptomic classification and characterization of pancreatic neuroendocrine neoplasms

Author

Yang, Kevin C., Kalloger, Steve E., Aird, John J., Lee, Michael K.C., Rushton, Christopher, Mungall, Karen L., Mungall, Andrew J., Gao, Dongxia, Chow, Christine, Xu, Jing, Karasinska, Joanna M., Colborne, Shane, Jones, Steven J.M., Schrader, Jörg, Morin, Ryan D., Loree, Jonathan M., Marra, Marco A., Renouf, Daniel J., Morin, Gregg B., Schaeffer, David F., and Gorski, Sharon M.

Published
2021
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8. Regulation of pH by Carbonic Anhydrase 9 Mediates Survival of Pancreatic Cancer Cells With Activated KRAS in Response to Hypoxia

Author

McDonald, Paul C., Chafe, Shawn C., Brown, Wells S., Saberi, Saeed, Swayampakula, Mridula, Venkateswaran, Geetha, Nemirovsky, Oksana, Gillespie, Jordan A., Karasinska, Joanna M., Kalloger, Steve E., Supuran, Claudiu T., Schaeffer, David F., Bashashati, Ali, Shah, Sohrab P., Topham, James T., Yapp, Donald T., Li, Jinyang, Renouf, Daniel J., Stanger, Ben Z., and Dedhar, Shoukat

Published
2019
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10. ATG4B and ATG4A loss result in two-stage cell cycle defects in pancreatic ductal adenocarcinoma cells

Author

Sathiyaseelan, Paalini, primary, Chittaranjan, Suganthi, additional, Kalloger, Steve E., additional, Chan, Jennifer, additional, Go, Nancy E., additional, Jardon, Mario A., additional, Ho, Cally J., additional, Hui, Theodore, additional, Xu, Jing, additional, Chow, Christine, additional, Gao, Dongxia, additional, Johnson, Fraser D., additional, Lockwood, William W., additional, Morin, Gregg B., additional, Renouf, Daniel J., additional, Schaeffer, David F., additional, and Gorski, Sharon M., additional

Published
2023
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15. Data from Endogenous Retrovirus Transcript Levels Are Associated with Immunogenic Signatures in Multiple Metastatic Cancer Types

Author

Topham, James T., primary, Titmuss, Emma, primary, Pleasance, Erin D., primary, Williamson, Laura M., primary, Karasinska, Joanna M., primary, Culibrk, Luka, primary, Lee, Michael K.C., primary, Mendis, Shehara, primary, Denroche, Robert E., primary, Jang, Gun-Ho, primary, Kalloger, Steve E., primary, Wong, Hui-Li, primary, Moore, Richard A., primary, Mungall, Andrew J., primary, O'Kane, Grainne M., primary, Knox, Jennifer J., primary, Gallinger, Steven, primary, Loree, Jonathan M., primary, Mager, Dixie L., primary, Laskin, Janessa, primary, Marra, Marco A., primary, Jones, Steven J.M., primary, Schaeffer, David F., primary, and Renouf, Daniel J., primary

Published
2023
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16. Supplementary table 2 from Endogenous Retrovirus Transcript Levels Are Associated with Immunogenic Signatures in Multiple Metastatic Cancer Types

Author

Topham, James T., primary, Titmuss, Emma, primary, Pleasance, Erin D., primary, Williamson, Laura M., primary, Karasinska, Joanna M., primary, Culibrk, Luka, primary, Lee, Michael K.C., primary, Mendis, Shehara, primary, Denroche, Robert E., primary, Jang, Gun-Ho, primary, Kalloger, Steve E., primary, Wong, Hui-Li, primary, Moore, Richard A., primary, Mungall, Andrew J., primary, O'Kane, Grainne M., primary, Knox, Jennifer J., primary, Gallinger, Steven, primary, Loree, Jonathan M., primary, Mager, Dixie L., primary, Laskin, Janessa, primary, Marra, Marco A., primary, Jones, Steven J.M., primary, Schaeffer, David F., primary, and Renouf, Daniel J., primary

Published
2023
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17. Supplementary Table 5 from Endogenous Retrovirus Transcript Levels Are Associated with Immunogenic Signatures in Multiple Metastatic Cancer Types

Author

Topham, James T., primary, Titmuss, Emma, primary, Pleasance, Erin D., primary, Williamson, Laura M., primary, Karasinska, Joanna M., primary, Culibrk, Luka, primary, Lee, Michael K.C., primary, Mendis, Shehara, primary, Denroche, Robert E., primary, Jang, Gun-Ho, primary, Kalloger, Steve E., primary, Wong, Hui-Li, primary, Moore, Richard A., primary, Mungall, Andrew J., primary, O'Kane, Grainne M., primary, Knox, Jennifer J., primary, Gallinger, Steven, primary, Loree, Jonathan M., primary, Mager, Dixie L., primary, Laskin, Janessa, primary, Marra, Marco A., primary, Jones, Steven J.M., primary, Schaeffer, David F., primary, and Renouf, Daniel J., primary

Published
2023
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18. Supplementary table 1 and figures 1-4 from Endogenous Retrovirus Transcript Levels Are Associated with Immunogenic Signatures in Multiple Metastatic Cancer Types

Author

Topham, James T., primary, Titmuss, Emma, primary, Pleasance, Erin D., primary, Williamson, Laura M., primary, Karasinska, Joanna M., primary, Culibrk, Luka, primary, Lee, Michael K.C., primary, Mendis, Shehara, primary, Denroche, Robert E., primary, Jang, Gun-Ho, primary, Kalloger, Steve E., primary, Wong, Hui-Li, primary, Moore, Richard A., primary, Mungall, Andrew J., primary, O'Kane, Grainne M., primary, Knox, Jennifer J., primary, Gallinger, Steven, primary, Loree, Jonathan M., primary, Mager, Dixie L., primary, Laskin, Janessa, primary, Marra, Marco A., primary, Jones, Steven J.M., primary, Schaeffer, David F., primary, and Renouf, Daniel J., primary

Published
2023
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19. Supplementary Table 4 from Endogenous Retrovirus Transcript Levels Are Associated with Immunogenic Signatures in Multiple Metastatic Cancer Types

Author

Topham, James T., primary, Titmuss, Emma, primary, Pleasance, Erin D., primary, Williamson, Laura M., primary, Karasinska, Joanna M., primary, Culibrk, Luka, primary, Lee, Michael K.C., primary, Mendis, Shehara, primary, Denroche, Robert E., primary, Jang, Gun-Ho, primary, Kalloger, Steve E., primary, Wong, Hui-Li, primary, Moore, Richard A., primary, Mungall, Andrew J., primary, O'Kane, Grainne M., primary, Knox, Jennifer J., primary, Gallinger, Steven, primary, Loree, Jonathan M., primary, Mager, Dixie L., primary, Laskin, Janessa, primary, Marra, Marco A., primary, Jones, Steven J.M., primary, Schaeffer, David F., primary, and Renouf, Daniel J., primary

Published
2023
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20. Supplementary Table 3 from Endogenous Retrovirus Transcript Levels Are Associated with Immunogenic Signatures in Multiple Metastatic Cancer Types

Author

Topham, James T., primary, Titmuss, Emma, primary, Pleasance, Erin D., primary, Williamson, Laura M., primary, Karasinska, Joanna M., primary, Culibrk, Luka, primary, Lee, Michael K.C., primary, Mendis, Shehara, primary, Denroche, Robert E., primary, Jang, Gun-Ho, primary, Kalloger, Steve E., primary, Wong, Hui-Li, primary, Moore, Richard A., primary, Mungall, Andrew J., primary, O'Kane, Grainne M., primary, Knox, Jennifer J., primary, Gallinger, Steven, primary, Loree, Jonathan M., primary, Mager, Dixie L., primary, Laskin, Janessa, primary, Marra, Marco A., primary, Jones, Steven J.M., primary, Schaeffer, David F., primary, and Renouf, Daniel J., primary

Published
2023
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21. Supplementary Table S5 from IL6-STAT3-HIF Signaling and Therapeutic Response to the Angiogenesis Inhibitor Sunitinib in Ovarian Clear Cell Cancer

Author

Anglesio, Michael S., primary, George, Joshy, primary, Kulbe, Hagen, primary, Friedlander, Michael, primary, Rischin, Danny, primary, Lemech, Charlotte, primary, Power, Jeremy, primary, Coward, Jermaine, primary, Cowin, Prue A., primary, House, Colin M., primary, Chakravarty, Probir, primary, Gorringe, Kylie L., primary, Campbell, Ian G., primary, Okamoto, Aikou, primary, Birrer, Michael J., primary, Huntsman, David G., primary, de Fazio, Anna, primary, Kalloger, Steve E., primary, Balkwill, Frances, primary, Gilks, C. Blake, primary, and Bowtell, David D., primary

Published
2023
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22. Figure S6 from Altered Gene Expression along the Glycolysis–Cholesterol Synthesis Axis Is Associated with Outcome in Pancreatic Cancer

Author

Karasinska, Joanna M., primary, Topham, James T., primary, Kalloger, Steve E., primary, Jang, Gun Ho, primary, Denroche, Robert E., primary, Culibrk, Luka, primary, Williamson, Laura M., primary, Wong, Hui-Li, primary, Lee, Michael K.C., primary, O'Kane, Grainne M., primary, Moore, Richard A., primary, Mungall, Andrew J., primary, Moore, Malcolm J., primary, Warren, Cassia, primary, Metcalfe, Andrew, primary, Notta, Faiyaz, primary, Knox, Jennifer J., primary, Gallinger, Steven, primary, Laskin, Janessa, primary, Marra, Marco A., primary, Jones, Steven J.M., primary, Renouf, Daniel J., primary, and Schaeffer, David F., primary

Published
2023
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23. Supplementary Materials from Subtype-Discordant Pancreatic Ductal Adenocarcinoma Tumors Show Intermediate Clinical and Molecular Characteristics

Author

Topham, James T., primary, Karasinska, Joanna M., primary, Lee, Michael K.C., primary, Csizmok, Veronika, primary, Williamson, Laura M., primary, Jang, Gun Ho, primary, Denroche, Robert E., primary, Tsang, Erica S., primary, Kalloger, Steve E., primary, Wong, Hui-li, primary, O'Kane, Grainne M., primary, Moore, Richard A., primary, Mungall, Andrew J., primary, Notta, Faiyaz, primary, Loree, Jonathan M., primary, Wilson, Julie M., primary, Bathe, Oliver, primary, Tang, Patricia A., primary, Goodwin, Rachel, primary, Knox, Jennifer J., primary, Gallinger, Steven, primary, Laskin, Janessa, primary, Marra, Marco A., primary, Jones, Steven J.M., primary, Renouf, Daniel J., primary, and Schaeffer, David F., primary

Published
2023
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24. Supplementary Tables S1-S4 from Amplification of PVT1 Contributes to the Pathophysiology of Ovarian and Breast Cancer

Author

Guan, Yinghui, primary, Kuo, Wen-Lin, primary, Stilwell, Jackie L., primary, Takano, Hirokuni, primary, Lapuk, Anna V., primary, Fridlyand, Jane, primary, Mao, Jian-Hua, primary, Yu, Mamie, primary, Miller, Melinda A., primary, Santos, Jennifer L., primary, Kalloger, Steve E., primary, Carlson, Joseph W., primary, Ginzinger, David G., primary, Celniker, Susan E., primary, Mills, Gordon B., primary, Huntsman, David G., primary, and Gray, Joe W., primary

Published
2023
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25. Supplementary Figures S1-S5 from IL6-STAT3-HIF Signaling and Therapeutic Response to the Angiogenesis Inhibitor Sunitinib in Ovarian Clear Cell Cancer

Author

Anglesio, Michael S., primary, George, Joshy, primary, Kulbe, Hagen, primary, Friedlander, Michael, primary, Rischin, Danny, primary, Lemech, Charlotte, primary, Power, Jeremy, primary, Coward, Jermaine, primary, Cowin, Prue A., primary, House, Colin M., primary, Chakravarty, Probir, primary, Gorringe, Kylie L., primary, Campbell, Ian G., primary, Okamoto, Aikou, primary, Birrer, Michael J., primary, Huntsman, David G., primary, de Fazio, Anna, primary, Kalloger, Steve E., primary, Balkwill, Frances, primary, Gilks, C. Blake, primary, and Bowtell, David D., primary

Published
2023
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26. Supplementary Data from Delving into Early-onset Pancreatic Ductal Adenocarcinoma: How Does Age Fit In?

Author

Tsang, Erica S., primary, Topham, James T., primary, Karasinska, Joanna M., primary, Lee, Michael K.C., primary, Williamson, Laura M., primary, Mendis, Shehara, primary, Denroche, Robert E., primary, Jang, Gun Ho, primary, Kalloger, Steve E., primary, Moore, Richard A., primary, Mungall, Andrew J., primary, Bathe, Oliver F., primary, Tang, Patricia A., primary, Notta, Faiyaz, primary, Wilson, Julie M., primary, Laskin, Janessa, primary, O'Kane, Grainne M., primary, Knox, Jennifer J., primary, Goodwin, Rachel A., primary, Loree, Jonathan M., primary, Jones, Steven J.M., primary, Marra, Marco A., primary, Gallinger, Steven, primary, Schaeffer, David F., primary, and Renouf, Daniel J., primary

Published
2023
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27. Supplementary Tables 1-9 from Biomarker-Based Ovarian Carcinoma Typing: A Histologic Investigation in the Ovarian Tumor Tissue Analysis Consortium

Author

Köbel, Martin, primary, Kalloger, Steve E., primary, Lee, Sandra, primary, Duggan, Máire A., primary, Kelemen, Linda E., primary, Prentice, Leah, primary, Kalli, Kimberly R., primary, Fridley, Brooke L., primary, Visscher, Daniel W., primary, Keeney, Gary L., primary, Vierkant, Robert A., primary, Cunningham, Julie M., primary, Chow, Christine, primary, Ness, Roberta B., primary, Moysich, Kirsten, primary, Edwards, Robert, primary, Modugno, Francesmary, primary, Bunker, Clareann, primary, Wozniak, Eva L., primary, Benjamin, Elizabeth, primary, Gayther, Simon A., primary, Gentry-Maharaj, Aleksandra, primary, Menon, Usha, primary, Gilks, C. Blake, primary, Huntsman, David G., primary, Ramus, Susan J., primary, and Goode, Ellen L., primary

Published
2023
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28. Supplementary Methods from IL6-STAT3-HIF Signaling and Therapeutic Response to the Angiogenesis Inhibitor Sunitinib in Ovarian Clear Cell Cancer

Author

Anglesio, Michael S., primary, George, Joshy, primary, Kulbe, Hagen, primary, Friedlander, Michael, primary, Rischin, Danny, primary, Lemech, Charlotte, primary, Power, Jeremy, primary, Coward, Jermaine, primary, Cowin, Prue A., primary, House, Colin M., primary, Chakravarty, Probir, primary, Gorringe, Kylie L., primary, Campbell, Ian G., primary, Okamoto, Aikou, primary, Birrer, Michael J., primary, Huntsman, David G., primary, de Fazio, Anna, primary, Kalloger, Steve E., primary, Balkwill, Frances, primary, Gilks, C. Blake, primary, and Bowtell, David D., primary

Published
2023
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29. Supplementary Figure Legend from Biomarker-Based Ovarian Carcinoma Typing: A Histologic Investigation in the Ovarian Tumor Tissue Analysis Consortium

Author

Köbel, Martin, primary, Kalloger, Steve E., primary, Lee, Sandra, primary, Duggan, Máire A., primary, Kelemen, Linda E., primary, Prentice, Leah, primary, Kalli, Kimberly R., primary, Fridley, Brooke L., primary, Visscher, Daniel W., primary, Keeney, Gary L., primary, Vierkant, Robert A., primary, Cunningham, Julie M., primary, Chow, Christine, primary, Ness, Roberta B., primary, Moysich, Kirsten, primary, Edwards, Robert, primary, Modugno, Francesmary, primary, Bunker, Clareann, primary, Wozniak, Eva L., primary, Benjamin, Elizabeth, primary, Gayther, Simon A., primary, Gentry-Maharaj, Aleksandra, primary, Menon, Usha, primary, Gilks, C. Blake, primary, Huntsman, David G., primary, Ramus, Susan J., primary, and Goode, Ellen L., primary

Published
2023
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30. Supplementary Figure 1 from Biomarker-Based Ovarian Carcinoma Typing: A Histologic Investigation in the Ovarian Tumor Tissue Analysis Consortium

Author

Köbel, Martin, primary, Kalloger, Steve E., primary, Lee, Sandra, primary, Duggan, Máire A., primary, Kelemen, Linda E., primary, Prentice, Leah, primary, Kalli, Kimberly R., primary, Fridley, Brooke L., primary, Visscher, Daniel W., primary, Keeney, Gary L., primary, Vierkant, Robert A., primary, Cunningham, Julie M., primary, Chow, Christine, primary, Ness, Roberta B., primary, Moysich, Kirsten, primary, Edwards, Robert, primary, Modugno, Francesmary, primary, Bunker, Clareann, primary, Wozniak, Eva L., primary, Benjamin, Elizabeth, primary, Gayther, Simon A., primary, Gentry-Maharaj, Aleksandra, primary, Menon, Usha, primary, Gilks, C. Blake, primary, Huntsman, David G., primary, Ramus, Susan J., primary, and Goode, Ellen L., primary

Published
2023
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31. Data from Biomarker-Based Ovarian Carcinoma Typing: A Histologic Investigation in the Ovarian Tumor Tissue Analysis Consortium

Author

Köbel, Martin, primary, Kalloger, Steve E., primary, Lee, Sandra, primary, Duggan, Máire A., primary, Kelemen, Linda E., primary, Prentice, Leah, primary, Kalli, Kimberly R., primary, Fridley, Brooke L., primary, Visscher, Daniel W., primary, Keeney, Gary L., primary, Vierkant, Robert A., primary, Cunningham, Julie M., primary, Chow, Christine, primary, Ness, Roberta B., primary, Moysich, Kirsten, primary, Edwards, Robert, primary, Modugno, Francesmary, primary, Bunker, Clareann, primary, Wozniak, Eva L., primary, Benjamin, Elizabeth, primary, Gayther, Simon A., primary, Gentry-Maharaj, Aleksandra, primary, Menon, Usha, primary, Gilks, C. Blake, primary, Huntsman, David G., primary, Ramus, Susan J., primary, and Goode, Ellen L., primary

Published
2023
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32. Supplementary Figures S1-S2 from Amplification of PVT1 Contributes to the Pathophysiology of Ovarian and Breast Cancer

Author

Guan, Yinghui, primary, Kuo, Wen-Lin, primary, Stilwell, Jackie L., primary, Takano, Hirokuni, primary, Lapuk, Anna V., primary, Fridlyand, Jane, primary, Mao, Jian-Hua, primary, Yu, Mamie, primary, Miller, Melinda A., primary, Santos, Jennifer L., primary, Kalloger, Steve E., primary, Carlson, Joseph W., primary, Ginzinger, David G., primary, Celniker, Susan E., primary, Mills, Gordon B., primary, Huntsman, David G., primary, and Gray, Joe W., primary

Published
2023
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36. Loss of ATG4B and ATG4A results in two-stage cell cycle defects in pancreatic ductal adenocarcinoma cells.

Author

Sathiyaseelan, Paalini, Chittaranjan, Suganthi, Kalloger, Steve E., Chan, Jennifer, Go, Nancy E., Jardon, Mario A., Ho, Cally J., Hui Hui, Theodore, Jing Xu, Chow, Christine, Dongxia Gao, Johnson, Fraser D., Lockwood, William W., Morin, Gregg B., Renouf, Daniel J., Schaeffer, David F., and Gorski, Sharon M.

Subjects
PANCREATIC duct, CELL cycle, PHASE transitions, ADENOCARCINOMA, GENE expression
Abstract

Pancreatic ductal adenocarcinoma (PDAC) exhibits elevated levels of autophagy, which promote tumor progression and treatment resistance. ATG4B is an autophagy-related cysteine protease under consideration as a potential therapeutic target, but it is largely unexplored in PDAC. Here, we investigated the clinical and functional relevance of ATG4B expression in PDAC. Using two PDAC patient cohorts, we found that low ATG4B mRNA or protein expression is associated with worse patient survival outcomes, poorly differentiated PDAC tumors and a lack of survival benefit from adjuvant chemotherapy. In PDAC cell lines, ATG4B knockout reduced proliferation, abolished processing of LC3B (also known as MAP1LC3B), and reduced GABARAP and GABARAPL1 levels, but increased ATG4A levels. ATG4B and ATG4A double knockout lines displayed a further reduction in proliferation, characterized by delays in G1-S phase transition and mitosis. Pro-LC3B accumulated aberrantly at the centrosome with a concomitant increase in centrosomal proteins PCM1 and CEP131, which was rescued by exogenous ATG4B. The two-stage cell cycle defects following ATG4B and ATG4A loss have important therapeutic implications for PDAC. [ABSTRACT FROM AUTHOR]

Published
2023
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37. Abstract B053: Targeting SMURF1 with low-dose proteasome inhibitors in pancreatic cancer organoids

Author

Metcalfe, Andrew, primary, Karasinska, Joanna M., additional, Topham, James T., additional, Kalloger, Steve E., additional, Ali, Hassan, additional, Ashforth, Dawn, additional, Marra, Marco A., additional, Laskin, Janessa, additional, Tang, Patricia A., additional, Goodwin, Rachel, additional, Bathe, Oliver F., additional, Renouf, Daniel J., additional, and Schaeffer, David F., additional

Published
2022
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42. Ductal pancreatic cancer modeling and drug screening using human pluripotent stem cell- and patient-derived tumor organoids

Author

Huang, Ling, Holtzinger, Audrey, Jagan, Ishaan, BeGora, Michael, Lohse, Ines, Ngai, Nicholas, Nostro, Cristina, Wang, Rennian, Muthuswamy, Lakshmi B, Crawford, Howard C, Arrowsmith, Cheryl, Kalloger, Steve E, Renouf, Daniel J, Connor, Ashton A, Cleary, Sean, Schaeffer, David F, Roehrl, Michael, Tsao, Ming-Sound, Gallinger, Steven, Keller, Gordon, and Muthuswamy, Senthil K

Subjects
Diagnosis, Care and treatment, Usage, Analysis, Research, Mortality -- Analysis, Precision medicine -- Usage, Cancer screening -- Usage, Pancreatic cancer -- Care and treatment -- Diagnosis, Stem cells -- Research
Abstract

Author(s): Ling Huang [1]; Audrey Holtzinger [1, 2]; Ishaan Jagan [1]; Michael BeGora [1]; Ines Lohse [1]; Nicholas Ngai [1]; Cristina Nostro [1, 2]; Rennian Wang [3, 4]; Lakshmi B [...], There are few in vitro models of exocrine pancreas development and primary human pancreatic adenocarcinoma (PDAC). We establish three-dimensional culture conditions to induce the differentiation of human pluripotent stem cells into exocrine progenitor organoids that form ductal and acinar structures in culture and in vivo. Expression of mutant KRAS or TP53 in progenitor organoids induces mutation-specific phenotypes in culture and in vivo. Expression of TP53[sup.R175H] induces cytosolic SOX9 localization. In patient tumors bearing TP53 mutations, SOX9 was cytoplasmic and associated with mortality. We also define culture conditions for clonal generation of tumor organoids from freshly resected PDAC. Tumor organoids maintain the differentiation status, histoarchitecture and phenotypic heterogeneity of the primary tumor and retain patient-specific physiological changes, including hypoxia, oxygen consumption, epigenetic marks and differences in sensitivity to inhibition of the histone methyltransferase EZH2. Thus, pancreatic progenitor organoids and tumor organoids can be used to model PDAC and for drug screening to identify precision therapy strategies.

Published
2015
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