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3. Supplementary Figure S4 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression

Author

Kohlmeyer, Jordan L., primary, Lingo, Joshua J., primary, Kaemmer, Courtney A., primary, Scherer, Amanda, primary, Warrier, Akshaya, primary, Voigt, Ellen, primary, Raygoza Garay, Juan A., primary, McGivney, Gavin R., primary, Brockman, Qierra R., primary, Tang, Amy, primary, Calizo, Ana, primary, Pollard, Kai, primary, Zhang, Xiaochun, primary, Hirbe, Angela C., primary, Pratilas, Christine A., primary, Leidinger, Mariah, primary, Breheny, Patrick, primary, Chimenti, Michael S., primary, Sieren, Jessica C., primary, Monga, Varun, primary, Tanas, Munir R., primary, Meyerholz, David K., primary, Darbro, Benjamin W., primary, Dodd, Rebecca D., primary, and Quelle, Dawn E., primary

Published
2023
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4. Supplementary Table S1 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression

Author

Kohlmeyer, Jordan L., primary, Lingo, Joshua J., primary, Kaemmer, Courtney A., primary, Scherer, Amanda, primary, Warrier, Akshaya, primary, Voigt, Ellen, primary, Raygoza Garay, Juan A., primary, McGivney, Gavin R., primary, Brockman, Qierra R., primary, Tang, Amy, primary, Calizo, Ana, primary, Pollard, Kai, primary, Zhang, Xiaochun, primary, Hirbe, Angela C., primary, Pratilas, Christine A., primary, Leidinger, Mariah, primary, Breheny, Patrick, primary, Chimenti, Michael S., primary, Sieren, Jessica C., primary, Monga, Varun, primary, Tanas, Munir R., primary, Meyerholz, David K., primary, Darbro, Benjamin W., primary, Dodd, Rebecca D., primary, and Quelle, Dawn E., primary

Published
2023
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5. Data from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression

Author

Kohlmeyer, Jordan L., primary, Lingo, Joshua J., primary, Kaemmer, Courtney A., primary, Scherer, Amanda, primary, Warrier, Akshaya, primary, Voigt, Ellen, primary, Raygoza Garay, Juan A., primary, McGivney, Gavin R., primary, Brockman, Qierra R., primary, Tang, Amy, primary, Calizo, Ana, primary, Pollard, Kai, primary, Zhang, Xiaochun, primary, Hirbe, Angela C., primary, Pratilas, Christine A., primary, Leidinger, Mariah, primary, Breheny, Patrick, primary, Chimenti, Michael S., primary, Sieren, Jessica C., primary, Monga, Varun, primary, Tanas, Munir R., primary, Meyerholz, David K., primary, Darbro, Benjamin W., primary, Dodd, Rebecca D., primary, and Quelle, Dawn E., primary

Published
2023
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6. RABL6A inhibits tumor-suppressive PP2A/AKT signaling to drive pancreatic neuroendocrine tumor growth

Author

Umesalma, Shaikamjad, Kaemmer, Courtney A., Kohlmeyer, Jordan L., Letney, Blake, Schab, Angela M., Reilly, Jacqueline A., Sheehy, Ryan M., Hagen, Jussara, Tiwari, Nitija, Zhan, Fenghuang, Leidinger, Mariah R., O'Dorisio, Thomas M., Dillon, Joseph, Merrill, Ronald A., Meyerholz, David K., Perl, Abbey L., Brown, Bart J., Braun, Terry A., Scott, Aaron T., Ginader, Timothy, Taghiyev, Agshin F., Zamba, Gideon K., Howe, James R., Strack, Stefan, Bellizzi, Andrew M., Narla, Goutham, Darbro, Benjamin W., Quelle, Frederick W., and Quelle, Dawn E.

Subjects
Everolimus -- Usage, Neuroendocrine tumors -- Care and treatment -- Development and progression -- Patient outcomes, Cancer treatment, Sunitinib, Phosphatases, Tumors, Novels, Health care industry
Abstract

Hyperactivated AKT/mTOR signaling is a hallmark of pancreatic neuroendocrine tumors (PNETs). Drugs targeting this pathway are used clinically, but tumor resistance invariably develops. A better understanding of factors regulating AKT/mTOR signaling and PNET pathogenesis is needed to improve current therapies. We discovered that RABL6A, a new oncogenic driver of PNET proliferation, is required for AKT activity. Silencing RABL6A caused PNET cell-cycle arrest that coincided with selective loss of AKT-S473 (not T308) phosphorylation and AKT/mTOR inactivation. Restoration of AKT phosphorylation rescued the G1 phase block triggered by RABL6A silencing. Mechanistically, loss of AKT-S473 phosphorylation in RABL6A-depleted cells was the result of increased protein phosphatase 2A (PP2A) activity. Inhibition of PP2A restored phosphorylation of AKT-S473 in RABL6A-depleted cells, whereas PP2A reactivation using a specific small-molecule activator of PP2A (SMAP) abolished that phosphorylation. Moreover, SMAP treatment effectively killed PNET cells in a RABL6A-dependent manner and suppressed PNET growth in vivo. The present work identifies RABL6A as a new inhibitor of the PP2A tumor suppressor and an essential activator of AKT in PNET cells. Our findings offer what we believe is a novel strategy of PP2A reactivation for treatment of PNETs as well as other human cancers driven by RABL6A overexpression and PP2A inactivation., Introduction Neuroendocrine tumors (NETs) are malignancies that are clinically challenging to manage and treat whose incidence is steadily increasing (1, 2). They are slow growing, biologically diverse tumors that arise [...]

Published
2019
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7. CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression

Author

Kohlmeyer, Jordan L., primary, Lingo, Joshua J., additional, Kaemmer, Courtney A., additional, Scherer, Amanda, additional, Warrier, Akshaya, additional, Voigt, Ellen, additional, Raygoza Garay, Juan A., additional, McGivney, Gavin R., additional, Brockman, Qierra R., additional, Tang, Amy, additional, Calizo, Ana, additional, Pollard, Kai, additional, Zhang, Xiaochun, additional, Hirbe, Angela C., additional, Pratilas, Christine A., additional, Leidinger, Mariah, additional, Breheny, Patrick, additional, Chimenti, Michael S., additional, Sieren, Jessica C., additional, Monga, Varun, additional, Tanas, Munir R., additional, Meyerholz, David K., additional, Darbro, Benjamin W., additional, Dodd, Rebecca D., additional, and Quelle, Dawn E., additional

Published
2023
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8. Inhibition of serotonin biosynthesis in neuroendocrine neoplasm suppresses tumor growth in vivo

Author

Tow, Dane H, primary, Tran, Catherine G, additional, Borbon, Luis C, additional, Ridder, Maclain, additional, Li, Guiying, additional, Kaemmer, Courtney A., additional, Abusada, Ellen, additional, Mahalingam, Aswanth H, additional, Sadanandam, Anguraj, additional, Chandrasekharan, Chandrikha, additional, Dillon, Joseph, additional, Spitz, Douglas R, additional, Quelle, Dawn E, additional, Chan, Carlos H.F., additional, Bellizzi, Andrew M, additional, Howe, James R, additional, and Ear, Po Hien, additional

Published
2023
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9. Supplementary table 2 from Gene Expression Signatures Identify Novel Therapeutics for Metastatic Pancreatic Neuroendocrine Tumors

Author

Scott, Aaron T., primary, Weitz, Michelle, primary, Breheny, Patrick J., primary, Ear, Po Hien, primary, Darbro, Benjamin, primary, Brown, Bart J., primary, Braun, Terry A., primary, Li, Guiying, primary, Umesalma, Shaikamjad, primary, Kaemmer, Courtney A., primary, Maharjan, Chandra K., primary, Quelle, Dawn E., primary, Bellizzi, Andrew M., primary, Chandrasekharan, Chandrikha, primary, Dillon, Joseph S., primary, O'Dorisio, Thomas M., primary, and Howe, James R., primary

Published
2023
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10. Supplementary table 5 from Gene Expression Signatures Identify Novel Therapeutics for Metastatic Pancreatic Neuroendocrine Tumors

Author

Scott, Aaron T., primary, Weitz, Michelle, primary, Breheny, Patrick J., primary, Ear, Po Hien, primary, Darbro, Benjamin, primary, Brown, Bart J., primary, Braun, Terry A., primary, Li, Guiying, primary, Umesalma, Shaikamjad, primary, Kaemmer, Courtney A., primary, Maharjan, Chandra K., primary, Quelle, Dawn E., primary, Bellizzi, Andrew M., primary, Chandrasekharan, Chandrikha, primary, Dillon, Joseph S., primary, O'Dorisio, Thomas M., primary, and Howe, James R., primary

Published
2023
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11. Supplementary Data Figures from RABL6A Is an Essential Driver of MPNSTs that Negatively Regulates the RB1 Pathway and Sensitizes Tumor Cells to CDK4/6 Inhibitors

Author

Kohlmeyer, Jordan L., primary, Kaemmer, Courtney A., primary, Pulliam, Casey, primary, Maharjan, Chandra K., primary, Samayoa, Allison Moreno, primary, Major, Heather J., primary, Cornick, Kendall E., primary, Knepper-Adrian, Vickie, primary, Khanna, Rajesh, primary, Sieren, Jessica C., primary, Leidinger, Mariah R., primary, Meyerholz, David K., primary, Zamba, K.D., primary, Weimer, Jill M., primary, Dodd, Rebecca D., primary, Darbro, Benjamin W., primary, Tanas, Munir R., primary, and Quelle, Dawn E., primary

Published
2023
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12. Supplementary table 6 from Gene Expression Signatures Identify Novel Therapeutics for Metastatic Pancreatic Neuroendocrine Tumors

Author

Scott, Aaron T., primary, Weitz, Michelle, primary, Breheny, Patrick J., primary, Ear, Po Hien, primary, Darbro, Benjamin, primary, Brown, Bart J., primary, Braun, Terry A., primary, Li, Guiying, primary, Umesalma, Shaikamjad, primary, Kaemmer, Courtney A., primary, Maharjan, Chandra K., primary, Quelle, Dawn E., primary, Bellizzi, Andrew M., primary, Chandrasekharan, Chandrikha, primary, Dillon, Joseph S., primary, O'Dorisio, Thomas M., primary, and Howe, James R., primary

Published
2023
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13. Supplementary table 1 from Gene Expression Signatures Identify Novel Therapeutics for Metastatic Pancreatic Neuroendocrine Tumors

Author

Scott, Aaron T., primary, Weitz, Michelle, primary, Breheny, Patrick J., primary, Ear, Po Hien, primary, Darbro, Benjamin, primary, Brown, Bart J., primary, Braun, Terry A., primary, Li, Guiying, primary, Umesalma, Shaikamjad, primary, Kaemmer, Courtney A., primary, Maharjan, Chandra K., primary, Quelle, Dawn E., primary, Bellizzi, Andrew M., primary, Chandrasekharan, Chandrikha, primary, Dillon, Joseph S., primary, O'Dorisio, Thomas M., primary, and Howe, James R., primary

Published
2023
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14. Supplementary table 4 from Gene Expression Signatures Identify Novel Therapeutics for Metastatic Pancreatic Neuroendocrine Tumors

Author

Scott, Aaron T., primary, Weitz, Michelle, primary, Breheny, Patrick J., primary, Ear, Po Hien, primary, Darbro, Benjamin, primary, Brown, Bart J., primary, Braun, Terry A., primary, Li, Guiying, primary, Umesalma, Shaikamjad, primary, Kaemmer, Courtney A., primary, Maharjan, Chandra K., primary, Quelle, Dawn E., primary, Bellizzi, Andrew M., primary, Chandrasekharan, Chandrikha, primary, Dillon, Joseph S., primary, O'Dorisio, Thomas M., primary, and Howe, James R., primary

Published
2023
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15. Supplementary table 3 from Gene Expression Signatures Identify Novel Therapeutics for Metastatic Pancreatic Neuroendocrine Tumors

Author

Scott, Aaron T., primary, Weitz, Michelle, primary, Breheny, Patrick J., primary, Ear, Po Hien, primary, Darbro, Benjamin, primary, Brown, Bart J., primary, Braun, Terry A., primary, Li, Guiying, primary, Umesalma, Shaikamjad, primary, Kaemmer, Courtney A., primary, Maharjan, Chandra K., primary, Quelle, Dawn E., primary, Bellizzi, Andrew M., primary, Chandrasekharan, Chandrikha, primary, Dillon, Joseph S., primary, O'Dorisio, Thomas M., primary, and Howe, James R., primary

Published
2023
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16. CDK4/6-MEK Targeted Therapy Causes Regression and Reduced Metastatic Colonization of Pancreatic Neuroendocrine Tumors

Author

Kaemmer, Courtney, primary, Umesalma, Shaikamjad, additional, Maharjan, Chandra, additional, Kohlmeyer, Jordan, additional, Wilkerson, Emily, additional, Sheehy, Ryan, additional, Leidinger, Mariah, additional, Meyerholz, David, additional, Bell, Sarah, additional, Zamba, Gideon, additional, Breheny, Patrick, additional, Lattime, Edmund, additional, Chandrasekharan, Chandrikha, additional, Bellizzi, Andrew, additional, Herring, Laura, additional, Graves, Lee, additional, Darbro, Benjamin, additional, Yuan, Ziqiang, additional, Libutti, Steven, additional, and Quelle, Dawn, additional

Published
2023
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17. Inhibition of serotonin biosynthesis in neuroendocrine neoplasm suppresses tumor growthin vivo

Author

Tow, Dane H., Tran, Catherine G., Borbon, Luis C., Ridder, Maclain, Li, Guiying, Kaemmer, Courtney A., Abusada, Ellen, Mahalingam, Aswanth Harish, Sadanandam, Anguraj, Chandrasekaran, Chandrikha, Dillon, Joseph, Spitz, Douglas R., Quelle, Dawn E., Chan, Carlos H.F., Bellizzi, Andrew, Howe, James R., and Ear, Po Hien

Subjects
Article
Abstract

Small bowel neuroendocrine tumors (SBNETs) originate from enterochromaffin cells in the intestine which synthesize and secrete serotonin. SBNETs express high levels of tryptophan hydroxylase 1 (Tph1), a key enzyme in serotonin biosynthesis. Patients with high serotonin level may develop carcinoid syndrome, which can be treated with somatostatin analogues and the Tph1 inhibitor telotristat ethyl in severe cases. Although the active drug telotristat can efficiently reduce serotonin levels, its effect on tumor growth is unclear. This study determined the effect of serotonin inhibition on tumor cell growthin vitroandin vivo. The levels of Tph1 in various neuroendocrine neoplasms (NENs) were determined and the biological effects of Tph1 inhibitionin vitroandin vivousing genetic and pharmacologic approaches was tested. Gene and protein expression analyses were performed on patient tumors and cancer cell lines. shRNAs targetingTPH1were used to create stable knockdown in BON cells. Control and knockdown lines were assessed for their growth ratesin vitroandin vivo, angiogenesis potential, serotonin levels, endothelial cell tube formation, tumor weight, and tumor vascularity.TPH1is highly expressed in SBNETs and many cancer types.TPH1knockdown cells and telotristat treated cells showed similar growth rates as control cellsin vitro. However,TPH1knockdown cells formed smaller tumorsin vivoand tumors were less vascularized. Although Tph1 inhibition with telotristat showed no effect on tumor cell growthin vitro, Tph1 inhibition reduced tumor formationin vivo. Serotonin inhibition in combination with other therapies is a promising new avenue for targeting metabolic vulnerabilities in NENs.

Published
2023

18. Abstract A02: MEK-CDK4/6 inhibition induces plasma cell tumor infiltration and sensitizes de novo MPNSTs to immune checkpoint blockade

Author

Lingo, Joshua, primary, Kohlmeyer, Jordan, additional, Kaemmer, Courtney, additional, Scherer, Amanda, additional, Voigt, Ellen, additional, Chimenti, Michael, additional, Tanas, Munir, additional, Monga, Varun, additional, Darbro, Ben, additional, Meyerholz, David, additional, Dodd, Rebecca, additional, and Quelle, Dawn, additional

Published
2022
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19. Oncogenic RABL6A promotes NF1-associated MPNST progression in vivo

Author

Kohlmeyer, Jordan L, primary, Kaemmer, Courtney A, additional, Lingo, Joshua J, additional, Voigt, Ellen, additional, Leidinger, Mariah R, additional, McGivney, Gavin R, additional, Scherer, Amanda, additional, Koppenhafer, Stacia L, additional, Gordon, David J, additional, Breheny, Patrick, additional, Meyerholz, David K, additional, Tanas, Munir R, additional, Dodd, Rebecca D, additional, and Quelle, Dawn E, additional

Published
2022
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21. RABL6A Promotes Pancreatic Neuroendocrine Tumor Angiogenesis and Progression In Vivo

Author

Maharjan, Chandra K., primary, Umesalma, Shaikamjad, additional, Kaemmer, Courtney A., additional, Muniz, Viviane P., additional, Bauchle, Casey, additional, Mott, Sarah L., additional, Zamba, K. D., additional, Breheny, Patrick, additional, Leidinger, Mariah R., additional, Darbro, Benjamin W., additional, Stephens, Samuel B., additional, Meyerholz, David K., additional, and Quelle, Dawn E., additional

Published
2021
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23. RABL6A Is an Essential Driver of MPNSTs that Negatively Regulates the RB1 Pathway and Sensitizes Tumor Cells to CDK4/6 Inhibitors

Author

Kohlmeyer, Jordan L., primary, Kaemmer, Courtney A., additional, Pulliam, Casey, additional, Maharjan, Chandra K., additional, Samayoa, Allison Moreno, additional, Major, Heather J., additional, Cornick, Kendall E., additional, Knepper-Adrian, Vickie, additional, Khanna, Rajesh, additional, Sieren, Jessica C., additional, Leidinger, Mariah R., additional, Meyerholz, David K., additional, Zamba, K.D., additional, Weimer, Jill M., additional, Dodd, Rebecca D., additional, Darbro, Benjamin W., additional, Tanas, Munir R., additional, and Quelle, Dawn E., additional

Published
2020
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24. Gene Expression Signatures Identify Novel Therapeutics for Metastatic Pancreatic Neuroendocrine Tumors

Author

Scott, Aaron T., primary, Weitz, Michelle, additional, Breheny, Patrick J., additional, Ear, Po Hien, additional, Darbro, Benjamin, additional, Brown, Bart J., additional, Braun, Terry A., additional, Li, Guiying, additional, Umesalma, Shaikamjad, additional, Kaemmer, Courtney A., additional, Maharjan, Chandra K., additional, Quelle, Dawn E., additional, Bellizzi, Andrew M., additional, Chandrasekharan, Chandrikha, additional, Dillon, Joseph S., additional, O'Dorisio, Thomas M., additional, and Howe, James R., additional

Published
2020
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25. Inhibition of serotonin biosynthesis in neuroendocrine neoplasm suppresses tumor growth in vivo .

Author

Tow DH, Tran CG, Borbon LC, Ridder M, Li G, Kaemmer CA, Abusada E, Mahalingam AH, Sadanandam A, Chandrasekaran C, Dillon J, Spitz DR, Quelle DE, Chan CHF, Bellizzi A, Howe JR, and Ear PH

Abstract

Small bowel neuroendocrine tumors (SBNETs) originate from enterochromaffin cells in the intestine which synthesize and secrete serotonin. SBNETs express high levels of tryptophan hydroxylase 1 (Tph1), a key enzyme in serotonin biosynthesis. Patients with high serotonin level may develop carcinoid syndrome, which can be treated with somatostatin analogues and the Tph1 inhibitor telotristat ethyl in severe cases. Although the active drug telotristat can efficiently reduce serotonin levels, its effect on tumor growth is unclear. This study determined the effect of serotonin inhibition on tumor cell growth in vitro and in vivo . The levels of Tph1 in various neuroendocrine neoplasms (NENs) were determined and the biological effects of Tph1 inhibition in vitro and in vivo using genetic and pharmacologic approaches was tested. Gene and protein expression analyses were performed on patient tumors and cancer cell lines. shRNAs targeting TPH1 were used to create stable knockdown in BON cells. Control and knockdown lines were assessed for their growth rates in vitro and in vivo , angiogenesis potential, serotonin levels, endothelial cell tube formation, tumor weight, and tumor vascularity. TPH1 is highly expressed in SBNETs and many cancer types. TPH1 knockdown cells and telotristat treated cells showed similar growth rates as control cells in vitro . However, TPH1 knockdown cells formed smaller tumors in vivo and tumors were less vascularized. Although Tph1 inhibition with telotristat showed no effect on tumor cell growth in vitro , Tph1 inhibition reduced tumor formation in vivo . Serotonin inhibition in combination with other therapies is a promising new avenue for targeting metabolic vulnerabilities in NENs.

Published
2023
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