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101. Data from De-Repression of PDGFRβ Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients

Author

Akhavan, David, primary, Pourzia, Alexandra L., primary, Nourian, Alex A., primary, Williams, Kevin J., primary, Nathanson, David, primary, Babic, Ivan, primary, Villa, Genaro R., primary, Tanaka, Kazuhiro, primary, Nael, Ali, primary, Yang, Huijun, primary, Dang, Julie, primary, Vinters, Harry V., primary, Yong, William H., primary, Flagg, Mitchell, primary, Tamanoi, Fuyuhiko, primary, Sasayama, Takashi, primary, James, C. David, primary, Kornblum, Harley I., primary, Cloughesy, Tim F., primary, Cavenee, Webster K., primary, Bensinger, Steven J., primary, and Mischel, Paul S., primary

Published
2023
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102. Supplementary Material from Oncogenic EGFR Signaling Activates an mTORC2–NF-κB Pathway That Promotes Chemotherapy Resistance

Author

Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Nathanson, David, primary, Akhavan, David, primary, Guo, Deliang, primary, Gini, Beatrice, primary, Dang, Julie, primary, Zhu, Shaojun, primary, Yang, Huijun, primary, De Jesus, Jason, primary, Amzajerdi, Ali Nael, primary, Zhang, Yinan, primary, Dibble, Christian C., primary, Dan, Hancai, primary, Rinkenbaugh, Amanda, primary, Yong, William H., primary, Vinters, Harry V., primary, Gera, Joseph F., primary, Cavenee, Webster K., primary, Cloughesy, Timothy F., primary, Manning, Brendan D., primary, Baldwin, Albert S., primary, and Mischel, Paul S., primary

Published
2023
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103. Supplementary Figure Legends 1-10, Methods from Metabolomics Strategy Reveals Subpopulation of Liposarcomas Sensitive to Gemcitabine Treatment

Author

Braas, Daniel, primary, Ahler, Ethan, primary, Tam, Brenna, primary, Nathanson, David, primary, Riedinger, Mirielle, primary, Benz, Matthias R., primary, Smith, Kathleen B., primary, Eilber, Fritz C., primary, Witte, Owen N., primary, Tap, William D., primary, Wu, Hong, primary, and Christofk, Heather R., primary

Published
2023
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106. Supplementary Figure 1 from De-Repression of PDGFRβ Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients

Author

Akhavan, David, primary, Pourzia, Alexandra L., primary, Nourian, Alex A., primary, Williams, Kevin J., primary, Nathanson, David, primary, Babic, Ivan, primary, Villa, Genaro R., primary, Tanaka, Kazuhiro, primary, Nael, Ali, primary, Yang, Huijun, primary, Dang, Julie, primary, Vinters, Harry V., primary, Yong, William H., primary, Flagg, Mitchell, primary, Tamanoi, Fuyuhiko, primary, Sasayama, Takashi, primary, James, C. David, primary, Kornblum, Harley I., primary, Cloughesy, Tim F., primary, Cavenee, Webster K., primary, Bensinger, Steven J., primary, and Mischel, Paul S., primary

Published
2023
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108. Supplementary Figure 2 from De-Repression of PDGFRβ Transcription Promotes Acquired Resistance to EGFR Tyrosine Kinase Inhibitors in Glioblastoma Patients

Author

Akhavan, David, primary, Pourzia, Alexandra L., primary, Nourian, Alex A., primary, Williams, Kevin J., primary, Nathanson, David, primary, Babic, Ivan, primary, Villa, Genaro R., primary, Tanaka, Kazuhiro, primary, Nael, Ali, primary, Yang, Huijun, primary, Dang, Julie, primary, Vinters, Harry V., primary, Yong, William H., primary, Flagg, Mitchell, primary, Tamanoi, Fuyuhiko, primary, Sasayama, Takashi, primary, James, C. David, primary, Kornblum, Harley I., primary, Cloughesy, Tim F., primary, Cavenee, Webster K., primary, Bensinger, Steven J., primary, and Mischel, Paul S., primary

Published
2023
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109. Interview with Dr. Mischel from Oncogenic EGFR Signaling Activates an mTORC2–NF-κB Pathway That Promotes Chemotherapy Resistance

Author

Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Nathanson, David, primary, Akhavan, David, primary, Guo, Deliang, primary, Gini, Beatrice, primary, Dang, Julie, primary, Zhu, Shaojun, primary, Yang, Huijun, primary, De Jesus, Jason, primary, Amzajerdi, Ali Nael, primary, Zhang, Yinan, primary, Dibble, Christian C., primary, Dan, Hancai, primary, Rinkenbaugh, Amanda, primary, Yong, William H., primary, Vinters, Harry V., primary, Gera, Joseph F., primary, Cavenee, Webster K., primary, Cloughesy, Timothy F., primary, Manning, Brendan D., primary, Baldwin, Albert S., primary, and Mischel, Paul S., primary

Published
2023
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111. Supplementary Methods, Figures 1-9 from An LXR Agonist Promotes Glioblastoma Cell Death through Inhibition of an EGFR/AKT/SREBP-1/LDLR–Dependent Pathway

Author

Guo, Deliang, primary, Reinitz, Felicia, primary, Youssef, Mary, primary, Hong, Cynthia, primary, Nathanson, David, primary, Akhavan, David, primary, Kuga, Daisuke, primary, Amzajerdi, Ali Nael, primary, Soto, Horacio, primary, Zhu, Shaojun, primary, Babic, Ivan, primary, Tanaka, Kazuhiro, primary, Dang, Julie, primary, Iwanami, Akio, primary, Gini, Beatrice, primary, DeJesus, Jason, primary, Lisiero, Dominique D., primary, Huang, Tiffany T., primary, Prins, Robert M., primary, Wen, Patrick Y., primary, Robins, H. Ian, primary, Prados, Michael D., primary, DeAngelis, Lisa M., primary, Mellinghoff, Ingo K., primary, Mehta, Minesh P., primary, James, C. David, primary, Chakravarti, Arnab, primary, Cloughesy, Timothy F., primary, Tontonoz, Peter, primary, and Mischel, Paul S., primary

Published
2023
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112. Supplementary Figures 1-13, Tables 1-2 from Oncogenic EGFR Signaling Activates an mTORC2–NF-κB Pathway That Promotes Chemotherapy Resistance

Author

Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Nathanson, David, primary, Akhavan, David, primary, Guo, Deliang, primary, Gini, Beatrice, primary, Dang, Julie, primary, Zhu, Shaojun, primary, Yang, Huijun, primary, De Jesus, Jason, primary, Amzajerdi, Ali Nael, primary, Zhang, Yinan, primary, Dibble, Christian C., primary, Dan, Hancai, primary, Rinkenbaugh, Amanda, primary, Yong, William H., primary, Vinters, Harry V., primary, Gera, Joseph F., primary, Cavenee, Webster K., primary, Cloughesy, Timothy F., primary, Manning, Brendan D., primary, Baldwin, Albert S., primary, and Mischel, Paul S., primary

Published
2023
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113. History of heart failure and chronic kidney disease and risk of all-cause death after COVID-19 during the first three waves of the pandemic in comparison with influenza outbreaks in Sweden: a registry-based, retrospective, case–control study

Author

Ritsinger, Viveca, primary, Bodegård, Johan, additional, Kristofi, Robin, additional, Thuresson, Marcus, additional, Nathanson, David, additional, Nyström, Thomas, additional, Eriksson, Jan, additional, and Norhammar, Anna, additional

Published
2023
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114. Supplementary Figure 5 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

Author

Gini, Beatrice, primary, Zanca, Ciro, primary, Guo, Deliang, primary, Matsutani, Tomoo, primary, Masui, Kenta, primary, Ikegami, Shiro, primary, Yang, Huijun, primary, Nathanson, David, primary, Villa, Genaro R., primary, Shackelford, David, primary, Zhu, Shaojun, primary, Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Akhavan, David, primary, Lin, Kelly, primary, Assuncao, Alvaro, primary, Gu, Yuchao, primary, Bonetti, Bruno, primary, Mortensen, Deborah S., primary, Xu, Shuichan, primary, Raymon, Heather K., primary, Cavenee, Webster K., primary, Furnari, Frank B., primary, James, C. David, primary, Kroemer, Guido, primary, Heath, James R., primary, Hege, Kristen, primary, Chopra, Rajesh, primary, Cloughesy, Timothy F., primary, and Mischel, Paul S., primary

Published
2023
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115. Supplemental Figure 1 from Multiparametric MR-PET Imaging Predicts Pharmacokinetics and Clinical Response to GDC-0084 in Patients with Recurrent High-Grade Glioma

Author

Ellingson, Benjamin M., primary, Yao, Jingwen, primary, Raymond, Catalina, primary, Nathanson, David A., primary, Chakhoyan, Ararat, primary, Simpson, Jeremy, primary, Garner, James S., primary, Olivero, Alan G., primary, Mueller, Lars U., primary, Rodon, Jordi, primary, Gerstner, Elizabeth, primary, Cloughesy, Timothy F., primary, and Wen, Patrick Y., primary

Published
2023
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116. Supplementary Figure 4 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

Author

Gini, Beatrice, primary, Zanca, Ciro, primary, Guo, Deliang, primary, Matsutani, Tomoo, primary, Masui, Kenta, primary, Ikegami, Shiro, primary, Yang, Huijun, primary, Nathanson, David, primary, Villa, Genaro R., primary, Shackelford, David, primary, Zhu, Shaojun, primary, Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Akhavan, David, primary, Lin, Kelly, primary, Assuncao, Alvaro, primary, Gu, Yuchao, primary, Bonetti, Bruno, primary, Mortensen, Deborah S., primary, Xu, Shuichan, primary, Raymon, Heather K., primary, Cavenee, Webster K., primary, Furnari, Frank B., primary, James, C. David, primary, Kroemer, Guido, primary, Heath, James R., primary, Hege, Kristen, primary, Chopra, Rajesh, primary, Cloughesy, Timothy F., primary, and Mischel, Paul S., primary

Published
2023
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117. Supp. Figure 2 from Expression of PD-1 by T Cells in Malignant Glioma Patients Reflects Exhaustion and Activation

Author

Davidson, Tom B., primary, Lee, Alexander, primary, Hsu, Melody, primary, Sedighim, Shaina, primary, Orpilla, Joey, primary, Treger, Janet, primary, Mastall, Max, primary, Roesch, Saskia, primary, Rapp, Carmen, primary, Galvez, Mildred, primary, Mochizuki, Aaron, primary, Antonios, Joseph, primary, Garcia, Alejandro, primary, Kotecha, Nikesh, primary, Bayless, Nicholas, primary, Nathanson, David, primary, Wang, Anthony, primary, Everson, Richard, primary, Yong, William H., primary, Cloughesy, Timothy F., primary, Liau, Linda M., primary, Herold-Mende, Christel, primary, and Prins, Robert M., primary

Published
2023
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118. Supplementary Figure 1 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

Author

Gini, Beatrice, primary, Zanca, Ciro, primary, Guo, Deliang, primary, Matsutani, Tomoo, primary, Masui, Kenta, primary, Ikegami, Shiro, primary, Yang, Huijun, primary, Nathanson, David, primary, Villa, Genaro R., primary, Shackelford, David, primary, Zhu, Shaojun, primary, Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Akhavan, David, primary, Lin, Kelly, primary, Assuncao, Alvaro, primary, Gu, Yuchao, primary, Bonetti, Bruno, primary, Mortensen, Deborah S., primary, Xu, Shuichan, primary, Raymon, Heather K., primary, Cavenee, Webster K., primary, Furnari, Frank B., primary, James, C. David, primary, Kroemer, Guido, primary, Heath, James R., primary, Hege, Kristen, primary, Chopra, Rajesh, primary, Cloughesy, Timothy F., primary, and Mischel, Paul S., primary

Published
2023
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119. Supplementary Figure Legend from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

Author

Gini, Beatrice, primary, Zanca, Ciro, primary, Guo, Deliang, primary, Matsutani, Tomoo, primary, Masui, Kenta, primary, Ikegami, Shiro, primary, Yang, Huijun, primary, Nathanson, David, primary, Villa, Genaro R., primary, Shackelford, David, primary, Zhu, Shaojun, primary, Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Akhavan, David, primary, Lin, Kelly, primary, Assuncao, Alvaro, primary, Gu, Yuchao, primary, Bonetti, Bruno, primary, Mortensen, Deborah S., primary, Xu, Shuichan, primary, Raymon, Heather K., primary, Cavenee, Webster K., primary, Furnari, Frank B., primary, James, C. David, primary, Kroemer, Guido, primary, Heath, James R., primary, Hege, Kristen, primary, Chopra, Rajesh, primary, Cloughesy, Timothy F., primary, and Mischel, Paul S., primary

Published
2023
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120. Supplementary Figure 3 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

Author

Gini, Beatrice, primary, Zanca, Ciro, primary, Guo, Deliang, primary, Matsutani, Tomoo, primary, Masui, Kenta, primary, Ikegami, Shiro, primary, Yang, Huijun, primary, Nathanson, David, primary, Villa, Genaro R., primary, Shackelford, David, primary, Zhu, Shaojun, primary, Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Akhavan, David, primary, Lin, Kelly, primary, Assuncao, Alvaro, primary, Gu, Yuchao, primary, Bonetti, Bruno, primary, Mortensen, Deborah S., primary, Xu, Shuichan, primary, Raymon, Heather K., primary, Cavenee, Webster K., primary, Furnari, Frank B., primary, James, C. David, primary, Kroemer, Guido, primary, Heath, James R., primary, Hege, Kristen, primary, Chopra, Rajesh, primary, Cloughesy, Timothy F., primary, and Mischel, Paul S., primary

Published
2023
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121. Supp Figure 1 from Expression of PD-1 by T Cells in Malignant Glioma Patients Reflects Exhaustion and Activation

Author

Davidson, Tom B., primary, Lee, Alexander, primary, Hsu, Melody, primary, Sedighim, Shaina, primary, Orpilla, Joey, primary, Treger, Janet, primary, Mastall, Max, primary, Roesch, Saskia, primary, Rapp, Carmen, primary, Galvez, Mildred, primary, Mochizuki, Aaron, primary, Antonios, Joseph, primary, Garcia, Alejandro, primary, Kotecha, Nikesh, primary, Bayless, Nicholas, primary, Nathanson, David, primary, Wang, Anthony, primary, Everson, Richard, primary, Yong, William H., primary, Cloughesy, Timothy F., primary, Liau, Linda M., primary, Herold-Mende, Christel, primary, and Prins, Robert M., primary

Published
2023
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122. Supplemental Figure 4 from Multiparametric MR-PET Imaging Predicts Pharmacokinetics and Clinical Response to GDC-0084 in Patients with Recurrent High-Grade Glioma

Author

Ellingson, Benjamin M., primary, Yao, Jingwen, primary, Raymond, Catalina, primary, Nathanson, David A., primary, Chakhoyan, Ararat, primary, Simpson, Jeremy, primary, Garner, James S., primary, Olivero, Alan G., primary, Mueller, Lars U., primary, Rodon, Jordi, primary, Gerstner, Elizabeth, primary, Cloughesy, Timothy F., primary, and Wen, Patrick Y., primary

Published
2023
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123. Supplementary Data from Development of a Real-time RT-PCR Assay for Detecting EGFRvIII in Glioblastoma Samples

Author

Yoshimoto, Koji, primary, Dang, Julie, primary, Zhu, Shaojun, primary, Nathanson, David, primary, Huang, Tiffany, primary, Dumont, Rebecca, primary, Seligson, David B., primary, Yong, William H., primary, Xiong, Zhenggang, primary, Rao, Nagesh, primary, Winther, Henrik, primary, Chakravarti, Arnab, primary, Bigner, Darell D., primary, Mellinghoff, Ingo K., primary, Horvath, Steve, primary, Cavenee, Webster K., primary, Cloughesy, Timothy F., primary, and Mischel, Paul S., primary

Published
2023
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124. Data from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

Author

Gini, Beatrice, primary, Zanca, Ciro, primary, Guo, Deliang, primary, Matsutani, Tomoo, primary, Masui, Kenta, primary, Ikegami, Shiro, primary, Yang, Huijun, primary, Nathanson, David, primary, Villa, Genaro R., primary, Shackelford, David, primary, Zhu, Shaojun, primary, Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Akhavan, David, primary, Lin, Kelly, primary, Assuncao, Alvaro, primary, Gu, Yuchao, primary, Bonetti, Bruno, primary, Mortensen, Deborah S., primary, Xu, Shuichan, primary, Raymon, Heather K., primary, Cavenee, Webster K., primary, Furnari, Frank B., primary, James, C. David, primary, Kroemer, Guido, primary, Heath, James R., primary, Hege, Kristen, primary, Chopra, Rajesh, primary, Cloughesy, Timothy F., primary, and Mischel, Paul S., primary

Published
2023
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125. Supplemental Figure 2 from Multiparametric MR-PET Imaging Predicts Pharmacokinetics and Clinical Response to GDC-0084 in Patients with Recurrent High-Grade Glioma

Author

Ellingson, Benjamin M., primary, Yao, Jingwen, primary, Raymond, Catalina, primary, Nathanson, David A., primary, Chakhoyan, Ararat, primary, Simpson, Jeremy, primary, Garner, James S., primary, Olivero, Alan G., primary, Mueller, Lars U., primary, Rodon, Jordi, primary, Gerstner, Elizabeth, primary, Cloughesy, Timothy F., primary, and Wen, Patrick Y., primary

Published
2023
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126. Supplementary Figure 2 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

Author

Gini, Beatrice, primary, Zanca, Ciro, primary, Guo, Deliang, primary, Matsutani, Tomoo, primary, Masui, Kenta, primary, Ikegami, Shiro, primary, Yang, Huijun, primary, Nathanson, David, primary, Villa, Genaro R., primary, Shackelford, David, primary, Zhu, Shaojun, primary, Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Akhavan, David, primary, Lin, Kelly, primary, Assuncao, Alvaro, primary, Gu, Yuchao, primary, Bonetti, Bruno, primary, Mortensen, Deborah S., primary, Xu, Shuichan, primary, Raymon, Heather K., primary, Cavenee, Webster K., primary, Furnari, Frank B., primary, James, C. David, primary, Kroemer, Guido, primary, Heath, James R., primary, Hege, Kristen, primary, Chopra, Rajesh, primary, Cloughesy, Timothy F., primary, and Mischel, Paul S., primary

Published
2023
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128. Supplemental Figure 3 from Multiparametric MR-PET Imaging Predicts Pharmacokinetics and Clinical Response to GDC-0084 in Patients with Recurrent High-Grade Glioma

Author

Ellingson, Benjamin M., primary, Yao, Jingwen, primary, Raymond, Catalina, primary, Nathanson, David A., primary, Chakhoyan, Ararat, primary, Simpson, Jeremy, primary, Garner, James S., primary, Olivero, Alan G., primary, Mueller, Lars U., primary, Rodon, Jordi, primary, Gerstner, Elizabeth, primary, Cloughesy, Timothy F., primary, and Wen, Patrick Y., primary

Published
2023
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130. Supplementary Methods from Brain-Mimetic 3D Culture Platforms Allow Investigation of Cooperative Effects of Extracellular Matrix Features on Therapeutic Resistance in Glioblastoma

Author

Xiao, Weikun, primary, Zhang, Rongyu, primary, Sohrabi, Alireza, primary, Ehsanipour, Arshia, primary, Sun, Songping, primary, Liang, Jesse, primary, Walthers, Christopher M., primary, Ta, Lisa, primary, Nathanson, David A., primary, and Seidlits, Stephanie K., primary

Published
2023
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131. Supp. Figure 3 from Expression of PD-1 by T Cells in Malignant Glioma Patients Reflects Exhaustion and Activation

Author

Davidson, Tom B., primary, Lee, Alexander, primary, Hsu, Melody, primary, Sedighim, Shaina, primary, Orpilla, Joey, primary, Treger, Janet, primary, Mastall, Max, primary, Roesch, Saskia, primary, Rapp, Carmen, primary, Galvez, Mildred, primary, Mochizuki, Aaron, primary, Antonios, Joseph, primary, Garcia, Alejandro, primary, Kotecha, Nikesh, primary, Bayless, Nicholas, primary, Nathanson, David, primary, Wang, Anthony, primary, Everson, Richard, primary, Yong, William H., primary, Cloughesy, Timothy F., primary, Liau, Linda M., primary, Herold-Mende, Christel, primary, and Prins, Robert M., primary

Published
2023
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132. Supplementary Figure 6 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

Author

Gini, Beatrice, primary, Zanca, Ciro, primary, Guo, Deliang, primary, Matsutani, Tomoo, primary, Masui, Kenta, primary, Ikegami, Shiro, primary, Yang, Huijun, primary, Nathanson, David, primary, Villa, Genaro R., primary, Shackelford, David, primary, Zhu, Shaojun, primary, Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Akhavan, David, primary, Lin, Kelly, primary, Assuncao, Alvaro, primary, Gu, Yuchao, primary, Bonetti, Bruno, primary, Mortensen, Deborah S., primary, Xu, Shuichan, primary, Raymon, Heather K., primary, Cavenee, Webster K., primary, Furnari, Frank B., primary, James, C. David, primary, Kroemer, Guido, primary, Heath, James R., primary, Hege, Kristen, primary, Chopra, Rajesh, primary, Cloughesy, Timothy F., primary, and Mischel, Paul S., primary

Published
2023
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133. Supplementary Figure 7 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

Author

Gini, Beatrice, primary, Zanca, Ciro, primary, Guo, Deliang, primary, Matsutani, Tomoo, primary, Masui, Kenta, primary, Ikegami, Shiro, primary, Yang, Huijun, primary, Nathanson, David, primary, Villa, Genaro R., primary, Shackelford, David, primary, Zhu, Shaojun, primary, Tanaka, Kazuhiro, primary, Babic, Ivan, primary, Akhavan, David, primary, Lin, Kelly, primary, Assuncao, Alvaro, primary, Gu, Yuchao, primary, Bonetti, Bruno, primary, Mortensen, Deborah S., primary, Xu, Shuichan, primary, Raymon, Heather K., primary, Cavenee, Webster K., primary, Furnari, Frank B., primary, James, C. David, primary, Kroemer, Guido, primary, Heath, James R., primary, Hege, Kristen, primary, Chopra, Rajesh, primary, Cloughesy, Timothy F., primary, and Mischel, Paul S., primary

Published
2023
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134. Supp. Table 1 from Expression of PD-1 by T Cells in Malignant Glioma Patients Reflects Exhaustion and Activation

Author

Davidson, Tom B., primary, Lee, Alexander, primary, Hsu, Melody, primary, Sedighim, Shaina, primary, Orpilla, Joey, primary, Treger, Janet, primary, Mastall, Max, primary, Roesch, Saskia, primary, Rapp, Carmen, primary, Galvez, Mildred, primary, Mochizuki, Aaron, primary, Antonios, Joseph, primary, Garcia, Alejandro, primary, Kotecha, Nikesh, primary, Bayless, Nicholas, primary, Nathanson, David, primary, Wang, Anthony, primary, Everson, Richard, primary, Yong, William H., primary, Cloughesy, Timothy F., primary, Liau, Linda M., primary, Herold-Mende, Christel, primary, and Prins, Robert M., primary

Published
2023
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135. Supplementary Methods, Figures 1-14 from A Microfluidic Platform for Systems Pathology: Multiparameter Single-Cell Signaling Measurements of Clinical Brain Tumor Specimens

Author

Sun, Jing, primary, Masterman-Smith, Michael D., primary, Graham, Nicholas A., primary, Jiao, Jing, primary, Mottahedeh, Jack, primary, Laks, Dan R., primary, Ohashi, Minori, primary, DeJesus, Jason, primary, Kamei, Ken-ichiro, primary, Lee, Ki-Bum, primary, Wang, Hao, primary, Yu, Zeta T.F., primary, Lu, Yi-Tsung, primary, Hou, Shuang, primary, Li, Keyu, primary, Liu, Max, primary, Zhang, Nangang, primary, Wang, Shutao, primary, Angenieux, Brigitte, primary, Panosyan, Eduard, primary, Samuels, Eric R., primary, Park, Jun, primary, Williams, Dirk, primary, Konkankit, Vera, primary, Nathanson, David, primary, van Dam, R. Michael, primary, Phelps, Michael E., primary, Wu, Hong, primary, Liau, Linda M., primary, Mischel, Paul S., primary, Lazareff, Jorge A., primary, Kornblum, Harley I., primary, Yong, William H., primary, Graeber, Thomas G., primary, and Tseng, Hsian-Rong, primary

Published
2023
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136. Data from A Microfluidic Platform for Systems Pathology: Multiparameter Single-Cell Signaling Measurements of Clinical Brain Tumor Specimens

Author

Sun, Jing, primary, Masterman-Smith, Michael D., primary, Graham, Nicholas A., primary, Jiao, Jing, primary, Mottahedeh, Jack, primary, Laks, Dan R., primary, Ohashi, Minori, primary, DeJesus, Jason, primary, Kamei, Ken-ichiro, primary, Lee, Ki-Bum, primary, Wang, Hao, primary, Yu, Zeta T.F., primary, Lu, Yi-Tsung, primary, Hou, Shuang, primary, Li, Keyu, primary, Liu, Max, primary, Zhang, Nangang, primary, Wang, Shutao, primary, Angenieux, Brigitte, primary, Panosyan, Eduard, primary, Samuels, Eric R., primary, Park, Jun, primary, Williams, Dirk, primary, Konkankit, Vera, primary, Nathanson, David, primary, van Dam, R. Michael, primary, Phelps, Michael E., primary, Wu, Hong, primary, Liau, Linda M., primary, Mischel, Paul S., primary, Lazareff, Jorge A., primary, Kornblum, Harley I., primary, Yong, William H., primary, Graeber, Thomas G., primary, and Tseng, Hsian-Rong, primary

Published
2023
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137. History of heart failure and chronic kidney disease and risk of all-cause death after COVID-19 during the first three waves of the pandemic in comparison with influenza outbreaks in Sweden : a registry-based, retrospective, case-control study

Author

Ritsinger, Viveca, Bodegard, Johan, Kristófi, Robin, Thuresson, Marcus, Nathanson, David, Nystrom, Thomas, Eriksson, Jan, Norhammar, Anna, Ritsinger, Viveca, Bodegard, Johan, Kristófi, Robin, Thuresson, Marcus, Nathanson, David, Nystrom, Thomas, Eriksson, Jan, and Norhammar, Anna

Abstract

Objectives To explore how cardiorenal disease (CRD; heart failure and/or chronic kidney disease) impacted mortality in men and women hospitalised for COVID-19 during the first three waves of the pandemic in Sweden in comparison to previous influenza outbreaks. Design A registry-based, retrospective, case-control study.SettingHospital care in Sweden. Participants All patients in Sweden with a main hospital diagnosis of COVID-19 (January 2020-September 2021) or influenza (January 2015-December 2019) with previous CRD were identified in registries and compared with a reference group free from CRD but with COVID-19 or influenza. Primary outcome measure Associated risk of all-cause death during the first year was analysed using adjusted Cox proportional hazards models. Results In COVID-19 patients with and without prior history of CRD (n=44 866), mean age was 79.8 years (SD 11.8) and 43% were women. In influenza patients (n=8897), mean age was 80.6 years (SD 11.5) and 45% were women. COVID-19 versus influenza was associated with higher mortality risk during the first two COVID-19 waves (HR 1.53; 95% CI 1.45 to 1.62, p<0.001 and HR 1.52; 95% CI 1.44 to 1.61, p<0.001), but not in the third wave (HR 1.07; 95% CI 0.99 to 1.14, p=0.072). CRD was an independent risk factor for all-cause death after COVID-19 in men and women (men: 1.37; 95% CI 1.31 to 1.44, p<0.001; women: 1.46; 95% CI 1.38 to 1.54, p<0.001). At ages <70 years, women with CRD had a similar mortality rate to men with CRD, while at ages >= 70 years, the mortality rate was higher in men. Conclusions Outcome after COVID-19 is worse if CRD is present. In women at ages <70 years, the presence of CRD attenuates the protective effect of female sex. COVID-19 was associated with higher mortality risk than influenza during the first two pandemic waves.

Published
2023
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138. Depth of Radiographic Response and Time to Tumor Regrowth Predicts Overall Survival Following Anti-VEGF Therapy in Recurrent Glioblastoma.

Author

Ellingson, Benjamin M, Ellingson, Benjamin M, Hagiwara, Akifumi, Morris, Connor J, Cho, Nicholas S, Oshima, Sonoko, Sanvito, Francesco, Oughourlian, Talia C, Telesca, Donatello, Raymond, Catalina, Abrey, Lauren E, Garcia, Josep, Aftab, Dana T, Hessel, Colin, Rachmilewitz Minei, Tamar, Harats, Dror, Nathanson, David A, Wen, Patrick Y, Cloughesy, Timothy F, Ellingson, Benjamin M, Ellingson, Benjamin M, Hagiwara, Akifumi, Morris, Connor J, Cho, Nicholas S, Oshima, Sonoko, Sanvito, Francesco, Oughourlian, Talia C, Telesca, Donatello, Raymond, Catalina, Abrey, Lauren E, Garcia, Josep, Aftab, Dana T, Hessel, Colin, Rachmilewitz Minei, Tamar, Harats, Dror, Nathanson, David A, Wen, Patrick Y, and Cloughesy, Timothy F

Abstract

PurposeAntiangiogenic therapies are known to cause high radiographic response rates due to reduction in vascular permeability resulting in a lower degree of contrast extravasation. In this study, we investigate the prognostic ability for model-derived parameters describing enhancing tumor volumetric dynamics to predict survival in recurrent glioblastoma treated with antiangiogenic therapy.Experimental designN = 276 patients in two phase II trials were used as training data, including bevacizumab ± irinotecan (NCT00345163) and cabozantinib (NCT00704288), and N = 74 patients in the bevacizumab arm of a phase III trial (NCT02511405) were used for validation. Enhancing volumes were estimated using T1 subtraction maps, and a biexponential model was used to estimate regrowth (g) and regression (d) rates, time to tumor regrowth (TTG), and the depth of response (DpR). Response characteristics were compared to diffusion MR phenotypes previously shown to predict survival.ResultsOptimized thresholds occurred at g = 0.07 months-1 (phase II: HR = 0.2579, P = 5 × 10-20; phase III: HR = 0.2197, P = 5 × 10-5); d = 0.11 months-1 (HR = 0.3365, P < 0.0001; HR = 0.3675, P = 0.0113); TTG = 3.8 months (HR = 0.2702, P = 6 × 10-17; HR = 0.2061, P = 2 × 10-5); and DpR = 11.3% (HR = 0.6326, P = 0.0028; HR = 0.4785, P = 0.0206). Multivariable Cox regression controlling for age and baseline tumor volume confirmed these factors as significant predictors of survival. Patients with a favorable pretreatment diffusion MRI phenotype had a significantly longer TTG and slower regrowth.ConclusionsRecurrent glioblastoma patients with a large, durable radiographic response to antiangiogenic agents have significantly longer survival. This information is useful for interpreting activity of antiangiogenic agents in recurrent glioblastoma.

Published
2023

139. PKM2 rewires glucose metabolism during radiation therapy to promote an antioxidant response and glioblastoma radioresistance.

Author

Bailleul, Justine, Bailleul, Justine, Ruan, Yangjingyi, Abdulrahman, Lobna, Scott, Andrew J, Yazal, Taha, Sung, David, Park, Keunseok, Hoang, Hanna, Nathaniel, Juan, Chu, Fang-I, Palomera, Daisy, Sehgal, Anahita, Tsang, Jonathan E, Nathanson, David A, Xu, Shili, Park, Junyoung O, Ten Hoeve, Johanna, Bhat, Kruttika, Qi, Nathan, Kornblum, Harley I, Schaue, Dorthe, McBride, William H, Lyssiotis, Costas A, Wahl, Daniel R, Vlashi, Erina, Bailleul, Justine, Bailleul, Justine, Ruan, Yangjingyi, Abdulrahman, Lobna, Scott, Andrew J, Yazal, Taha, Sung, David, Park, Keunseok, Hoang, Hanna, Nathaniel, Juan, Chu, Fang-I, Palomera, Daisy, Sehgal, Anahita, Tsang, Jonathan E, Nathanson, David A, Xu, Shili, Park, Junyoung O, Ten Hoeve, Johanna, Bhat, Kruttika, Qi, Nathan, Kornblum, Harley I, Schaue, Dorthe, McBride, William H, Lyssiotis, Costas A, Wahl, Daniel R, and Vlashi, Erina

Abstract

BackgroundResistance to existing therapies is a significant challenge in improving outcomes for glioblastoma (GBM) patients. Metabolic plasticity has emerged as an important contributor to therapy resistance, including radiation therapy (RT). Here, we investigated how GBM cells reprogram their glucose metabolism in response to RT to promote radiation resistance.MethodsEffects of radiation on glucose metabolism of human GBM specimens were examined in vitro and in vivo with the use of metabolic and enzymatic assays, targeted metabolomics, and FDG-PET. Radiosensitization potential of interfering with PKM2 activity was tested via gliomasphere formation assays and in vivo human GBM models.ResultsHere, we show that RT induces increased glucose utilization by GBM cells, and this is accompanied with translocation of GLUT3 transporters to the cell membrane. Irradiated GBM cells route glucose carbons through the pentose phosphate pathway (PPP) to harness the antioxidant power of the PPP and support survival after radiation. This response is regulated in part by the M2 isoform of pyruvate kinase (PKM2). Activators of PKM2 can antagonize the radiation-induced rewiring of glucose metabolism and radiosensitize GBM cells in vitro and in vivo.ConclusionsThese findings open the possibility that interventions designed to target cancer-specific regulators of metabolic plasticity, such as PKM2, rather than specific metabolic pathways, have the potential to improve the radiotherapeutic outcomes in GBM patients.

Published
2023

140. Immune checkpoint blockade induces distinct alterations in the microenvironments of primary and metastatic brain tumors.

Author

Sun, Lu, Sun, Lu, Kienzler, Jenny, Reynoso, Jeremy, Lee, Alexander, Li, Shanpeng, Kim, Jiyoon, Ding, Lizhong, Monteleone, Amber, Nathanson, David, Cloughesy, Timothy, Li, Gang, Prins, Robert, Phillips, Joanna, Liau, Linda, Everson, Richard, Kim, Won, Shiuan, Eileen, Hugo, Willy, Owens, Geoffrey, Sun, Lu, Sun, Lu, Kienzler, Jenny, Reynoso, Jeremy, Lee, Alexander, Li, Shanpeng, Kim, Jiyoon, Ding, Lizhong, Monteleone, Amber, Nathanson, David, Cloughesy, Timothy, Li, Gang, Prins, Robert, Phillips, Joanna, Liau, Linda, Everson, Richard, Kim, Won, Shiuan, Eileen, Hugo, Willy, and Owens, Geoffrey

Abstract

In comparison with responses in recurrent glioblastoma (rGBM), the intracranial response of brain metastases (BrM) to immune checkpoint blockade (ICB) is less well studied. Here, we present an integrated single-cell RNA-Seq (scRNA-Seq) study of 19 ICB-naive and 9 ICB-treated BrM samples from our own and published data sets. We compared them with our previously published scRNA-Seq data from rGBM and found that ICB led to more prominent T cell infiltration into BrM than rGBM. These BrM-infiltrating T cells exhibited a tumor-specific phenotype and displayed greater activated/exhausted features. We also used multiplex immunofluorescence and spatial transcriptomics to reveal that ICB reduced a distinct CD206+ macrophage population in the perivascular space, which may modulate T cell entry into BrM. Furthermore, we identified a subset of progenitor exhausted T cells that correlated with longer overall survival in BrM patients. Our study provides a comprehensive immune cellular landscape of ICBs effect on metastatic brain tumors and offers insights into potential strategies for improving ICB efficacy for brain tumor patients.

Published
2023

141. Multi-nuclear sodium, diffusion, and perfusion MRI in human gliomas.

Author

Cho, Nicholas S, Cho, Nicholas S, Sanvito, Francesco, Thakuria, Shruti, Wang, Chencai, Hagiwara, Akifumi, Nagaraj, Raksha, Oshima, Sonoko, Lopez Kolkovsky, Alfredo L, Lu, Jianwen, Raymond, Catalina, Liau, Linda M, Everson, Richard G, Patel, Kunal S, Kim, Won, Yang, Isaac, Bergsneider, Marvin, Nghiemphu, Phioanh L, Lai, Albert, Nathanson, David A, Cloughesy, Timothy F, Ellingson, Benjamin M, Cho, Nicholas S, Cho, Nicholas S, Sanvito, Francesco, Thakuria, Shruti, Wang, Chencai, Hagiwara, Akifumi, Nagaraj, Raksha, Oshima, Sonoko, Lopez Kolkovsky, Alfredo L, Lu, Jianwen, Raymond, Catalina, Liau, Linda M, Everson, Richard G, Patel, Kunal S, Kim, Won, Yang, Isaac, Bergsneider, Marvin, Nghiemphu, Phioanh L, Lai, Albert, Nathanson, David A, Cloughesy, Timothy F, and Ellingson, Benjamin M

Abstract

PurposeThere is limited knowledge about the associations between sodium and proton MRI measurements in brain tumors. The purpose of this study was to quantify intra- and intertumoral correlations between sodium, diffusion, and perfusion MRI in human gliomas.MethodsTwenty glioma patients were prospectively studied on a 3T MRI system with multinuclear capabilities. Three mutually exclusive tumor volumes of interest (VOIs) were segmented: contrast-enhancing tumor (CET), T2/FLAIR hyperintense non-enhancing tumor (NET), and necrosis. Median and voxel-wise associations between apparent diffusion coefficient (ADC), normalized relative cerebral blood volume (nrCBV), and normalized sodium measurements were quantified for each VOI.ResultsBoth relative sodium concentration and ADC were significantly higher in areas of necrosis compared to NET (P = 0.003 and P = 0.008, respectively) and CET (P = 0.02 and P = 0.02). Sodium concentration was higher in CET compared to NET (P = 0.04). Sodium and ADC were higher in treated compared to treatment-naïve gliomas within NET (P = 0.006 and P = 0.01, respectively), and ADC was elevated in CET (P = 0.03). Median ADC and sodium concentration were positively correlated across patients in NET (r = 0.77, P < 0.0001) and CET (r = 0.84, P < 0.0001), but not in areas of necrosis (r = 0.45, P = 0.12). Median nrCBV and sodium concentration were negatively correlated across patients in areas of NET (r=-0.63, P = 0.003). Similar associations were observed when examining voxel-wise correlations within VOIs.ConclusionSodium MRI is positively correlated with proton diffusion MRI measurements in gliomas, likely reflecting extracellular water. Unique areas of multinuclear MRI contrast may be useful in future studies to understand the chemistry of the tumor microenvironment.

Published
2023

142. Calculation of ATP production rates using the Seahorse XF Analyzer.

Author

Desousa, Brandon, Desousa, Brandon, Kim, Kristen, Jones, Anthony, Ball, Andréa, Hsieh, Wei, Swain, Pamela, Morrow, Danielle, Brownstein, Alexandra, Ferrick, David, Shirihai, Orian, Neilson, Andrew, Nathanson, David, Rogers, George, Dranka, Brian, Murphy, Anne, Affourtit, Charles, Stiles, Linsey, Romero, Natalia, Bensinger, Steven, Divakaruni, Ajit, Desousa, Brandon, Desousa, Brandon, Kim, Kristen, Jones, Anthony, Ball, Andréa, Hsieh, Wei, Swain, Pamela, Morrow, Danielle, Brownstein, Alexandra, Ferrick, David, Shirihai, Orian, Neilson, Andrew, Nathanson, David, Rogers, George, Dranka, Brian, Murphy, Anne, Affourtit, Charles, Stiles, Linsey, Romero, Natalia, Bensinger, Steven, and Divakaruni, Ajit

Abstract

Oxidative phosphorylation and glycolysis are the dominant ATP-generating pathways in mammalian metabolism. The balance between these two pathways is often shifted to execute cell-specific functions in response to stimuli that promote activation, proliferation, or differentiation. However, measurement of these metabolic switches has remained mostly qualitative, making it difficult to discriminate between healthy, physiological changes in energy transduction or compensatory responses due to metabolic dysfunction. We therefore present a broadly applicable method to calculate ATP production rates from oxidative phosphorylation and glycolysis using Seahorse XF Analyzer data and empirical conversion factors. We quantify the bioenergetic changes observed during macrophage polarization as well as cancer cell adaptation to in vitro culture conditions. Additionally, we detect substantive changes in ATP utilization upon neuronal depolarization and T cell receptor activation that are not evident from steady-state ATP measurements. This method generates a single readout that allows the direct comparison of ATP produced from oxidative phosphorylation and glycolysis in live cells. Additionally, the manuscript provides a framework for tailoring the calculations to specific cell systems or experimental conditions.

Published
2023

143. Differential Susceptibility of Ex Vivo Primary Glioblastoma Tumors to Oncolytic Effect of Modified Zika Virus

Author

Garcia, Gustavo, Garcia, Gustavo, Chakravarty, Nikhil, Paiola, Sophia, Urena, Estrella, Gyani, Priya, Tse, Christopher, French, Samuel W, Danielpour, Moise, Breunig, Joshua J, Nathanson, David A, Arumugaswami, Vaithilingaraja, Garcia, Gustavo, Garcia, Gustavo, Chakravarty, Nikhil, Paiola, Sophia, Urena, Estrella, Gyani, Priya, Tse, Christopher, French, Samuel W, Danielpour, Moise, Breunig, Joshua J, Nathanson, David A, and Arumugaswami, Vaithilingaraja

Abstract

Glioblastoma (GBM), the most common primary malignant brain tumor, is a highly lethal form of cancer with a very limited set of treatment options. High heterogeneity in the tumor cell population and the invasive nature of these cells decrease the likely efficacy of traditional cancer treatments, thus requiring research into novel treatment options. The use of oncolytic viruses as potential therapeutics has been researched for some time. Zika virus (ZIKV) has demonstrated oncotropism and oncolytic effects on GBM stem cells (GSCs). To address the need for safe and effective GBM treatments, we designed an attenuated ZIKV strain (ZOL-1) that does not cause paralytic or neurological diseases in mouse models compared with unmodified ZIKV. Importantly, we found that patient-derived GBM tumors exhibited susceptibility (responders) and non-susceptibility (non-responders) to ZOL-1-mediated tumor cell killing, as evidenced by differential apoptotic cell death and cell viability upon ZOL-1 treatment. The oncolytic effect observed in responder cells was seen both in vitro in neurosphere models and in vivo upon xenograft. Finally, we observed that the use of ZOL-1 as combination therapy with multiple PI3K-AKT inhibitors in non-responder GBM resulted in enhanced chemotherapeutic efficacy. Altogether, this study establishes ZOL-1 as a safe and effective treatment against GBM and provides a foundation to conduct further studies evaluating its potential as an effective adjuvant with other chemotherapies and kinase inhibitors.

Published
2023

144. Standardising personalised diabetes care across European health settings: a person-centred outcome set agreed in a multinational Delphi study

Author

Porth, Ann-Kristin, Huberts, Anouk S., Rogge, Alizé, Bénard, Angèle H.M., Forbes, Angus, Strootker, Anja, Hurtado Del Pozo, Carmen, Kownatka, Dagmar, Hopkins, David, Nathanson, David, Aanstoot, Henk-Jan, Soderberg, Jeanette, Eeg-Olofsson, Katarina, Hamilton, Kathryn, Delbecque, Laure, Ninov, Lyudmil, Due-Christensen, Mette, Leutner, Michael, Vikstrom-Greve, Sara, Rössner, Sophia, Seidler, Yuki, Hasler, Yvonne, Stamm, Tanja, and Kautzky-Willer, Alexandra

Subjects
Health Outcomes Observatory, Health outcomes, Diabetes mellitus, Person-centered care, Patient-reported outcomes, Value-based healthcare
Abstract

This is an updated preprint of our Delphi study to develop a person-centered outcome set for routine diabetes care in Europe: Objective: Standardised patient-reported outcomes (PRO) data can contextualise clinical outcomes enabling precision diabetes monitoring and care. Comprehensive outcome sets can guide this process, but their implementation in routine diabetes care has remained challenging and has not been successful at the international level. We aimed to address this with a person-centred outcome set for Type 1 and 2 diabetes that can be feasibly implemented and sustained in international healthcare settings. Methods: A questionnaire-based Delphi study consisting of three consecutive survey rounds and based on previously identified outcomes was undertaken to reach consensus on the outcome set. Participants included patients (N=94), health professionals (N=65), representatives of industry (N=22) and health authorities (N=3). Subsequent consensus meetings were held to finalise the outcome set. Results: The list of preliminary person-centred outcomes presented in the Delphi study included 64outcomes and was shortlisted via the consensus process to 46 outcomes (27 clinical outcomes and 19 PROs). Two main collection times were recommended: 1) linked to a medical visit (e.g., diabetes-specific well-being, symptoms, and psychological health) and 2) annually (e.g., clinical data, general well-being, and diabetes self-management-related outcomes). Conclusions: PROs are often considered in a non-standardised way in routine diabetes care. We propose a person-centred outcome set for diabetes, specifically considering psychosocial and behavioural aspects, which was agreed by four international key stakeholder groups. It guides standardised patient-important outcome collection at scale to support individual and population level healthcare decision-making. It will be implemented and tested in Europe as part of the H2O project. &nbsp

Published
2023
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145. Biosafety and Biohazards: Understanding Biosafety Levels and Meeting Safety Requirements of a Biobank

Author

Ta, Lisa, Gosa, Laura, and Nathanson, David A

Subjects
Biochemistry and Cell Biology, Biological Sciences, Good Health and Well Being, Biological Specimen Banks, Containment of Biohazards, Hazardous Substances, Humans, Safety, Biosafety, Safety requirements, Biohazard, Biosafety levels, Personal protective equipment, Other Chemical Sciences, Developmental Biology, Biochemistry and cell biology, Medicinal and biomolecular chemistry
Abstract

When it comes to biobanking and working with different types of laboratory specimens, it is important to understand potential biohazards to ensure safety of the operator and laboratory personnel. Biological safety levels (BSL) are a series of designations used to inform laboratory personnel about the level of biohazardous risks in a laboratory setting. There are a total of four levels ranked in order of increasing risk as stipulated by the Center of Disease Control and Prevention (CDC) (Biosafety in microbiological and biomedical laboratories, 5th edn. HHS publication no. (CDC) 21-1112. https://www.cdc.gov/biosafety/publications/bmbl5/bmbl.pdf . Accessed 2 Jan 2016, 2009). We will address the main distinctions between these levels including briefly introducing hazards characteristics that classify biohazardous agents, as well as define the essentials in meeting safety requirements.

Published
2019

147. M2 isoform of pyruvate kinase rewires glucose metabolism during radiation therapy to promote an antioxidant response and glioblastoma radioresistance.

Author

Bailleul, Justine, Ruan, Yangjingyi, Abdulrahman, Lobna, Scott, Andrew J, Yazal, Taha, Sung, David, Park, Keunseok, Hoang, Hanna, Nathaniel, Juan, Chu, Fang-I, Palomera, Daisy, Sehgal, Anahita, Tsang, Jonathan E, Nathanson, David A, Xu, Shili, Park, Junyoung O, Hoeve, Johanna ten, Bhat, Kruttika, Qi, Nathan, and Kornblum, Harley I

Published
2023
Full Text
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148. Calculation of ATP production rates using the Seahorse XF Analyzer.

Author

Desousa, Brandon R, Kim, Kristen KO, Jones, Anthony E, Ball, Andréa B, Hsieh, Wei Y, Swain, Pamela, Morrow, Danielle H, Brownstein, Alexandra J, Ferrick, David A, Shirihai, Orian S, Neilson, Andrew, Nathanson, David A, Rogers, George W, Dranka, Brian P, Murphy, Anne N, Affourtit, Charles, Bensinger, Steven J, Stiles, Linsey, Romero, Natalia, and Divakaruni, Ajit S

Abstract

Oxidative phosphorylation and glycolysis are the dominant ATP‐generating pathways in mammalian metabolism. The balance between these two pathways is often shifted to execute cell‐specific functions in response to stimuli that promote activation, proliferation, or differentiation. However, measurement of these metabolic switches has remained mostly qualitative, making it difficult to discriminate between healthy, physiological changes in energy transduction or compensatory responses due to metabolic dysfunction. We therefore present a broadly applicable method to calculate ATP production rates from oxidative phosphorylation and glycolysis using Seahorse XF Analyzer data and empirical conversion factors. We quantify the bioenergetic changes observed during macrophage polarization as well as cancer cell adaptation to in vitro culture conditions. Additionally, we detect substantive changes in ATP utilization upon neuronal depolarization and T cell receptor activation that are not evident from steady‐state ATP measurements. This method generates a single readout that allows the direct comparison of ATP produced from oxidative phosphorylation and glycolysis in live cells. Additionally, the manuscript provides a framework for tailoring the calculations to specific cell systems or experimental conditions. Synopsis: This manuscript details a method to calculate ATP production rates using OCR and ECAR data obtained from the Seahorse XF Analyzer. This generates a single readout measuring real‐time rates of ATP produced from oxidative phosphorylation and glycolysis in live cells. ECAR can quantitatively reflect lactate efflux after adjusting for buffering power of the experimental medium, respiratory acidification, and sensor coverage of the measurement well.The approach quantifies changes in ATP produced from oxidative phosphorylation and glycolysis in response to physiologically relevant stimuli.Real‐time ATP production rates capture changes in ATP utilization that steady‐state ATP levels do not.Examples are given for acute activation of neurons, adipocytes, macrophages, and T cells. [ABSTRACT FROM AUTHOR]

Published
2023
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149. Differential Susceptibility of Ex Vivo Primary Glioblastoma Tumors to Oncolytic Effect of Modified Zika Virus.

Author

Garcia Jr., Gustavo, Chakravarty, Nikhil, Paiola, Sophia, Urena, Estrella, Gyani, Priya, Tse, Christopher, French, Samuel W., Danielpour, Moise, Breunig, Joshua J., Nathanson, David A., and Arumugaswami, Vaithilingaraja

Subjects
ZIKA virus, GLIOBLASTOMA multiforme, BRAIN tumors, NEUROLOGICAL disorders, CELL populations, VIRAL tropism
Abstract

Glioblastoma (GBM), the most common primary malignant brain tumor, is a highly lethal form of cancer with a very limited set of treatment options. High heterogeneity in the tumor cell population and the invasive nature of these cells decrease the likely efficacy of traditional cancer treatments, thus requiring research into novel treatment options. The use of oncolytic viruses as potential therapeutics has been researched for some time. Zika virus (ZIKV) has demonstrated oncotropism and oncolytic effects on GBM stem cells (GSCs). To address the need for safe and effective GBM treatments, we designed an attenuated ZIKV strain (ZOL-1) that does not cause paralytic or neurological diseases in mouse models compared with unmodified ZIKV. Importantly, we found that patient-derived GBM tumors exhibited susceptibility (responders) and non-susceptibility (non-responders) to ZOL-1-mediated tumor cell killing, as evidenced by differential apoptotic cell death and cell viability upon ZOL-1 treatment. The oncolytic effect observed in responder cells was seen both in vitro in neurosphere models and in vivo upon xenograft. Finally, we observed that the use of ZOL-1 as combination therapy with multiple PI3K-AKT inhibitors in non-responder GBM resulted in enhanced chemotherapeutic efficacy. Altogether, this study establishes ZOL-1 as a safe and effective treatment against GBM and provides a foundation to conduct further studies evaluating its potential as an effective adjuvant with other chemotherapies and kinase inhibitors. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
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