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3. Functional Copy-Number Alterations as Diagnostic and Prognostic Biomarkers in Neuroendocrine Tumors.

Author

Vaughn, Hayley, Major, Heather, Kadera, Evangeline, Keck, Kendall, Dunham, Timothy, Qian, Qining, Brown, Bartley, Scott, Aaron, Bellizzi, Andrew M., Braun, Terry, Breheny, Patrick, Quelle, Dawn E., Howe, James R., and Darbro, Benjamin

Subjects
NEUROENDOCRINE tumors, TUMOR markers, PROGNOSIS, FLUORESCENCE in situ hybridization, LOGISTIC regression analysis
Abstract

Functional copy-number alterations (fCNAs) are DNA copy-number changes with concordant differential gene expression. These are less likely to be bystander genetic lesions and could serve as robust and reproducible tumor biomarkers. To identify candidate fCNAs in neuroendocrine tumors (NETs), we integrated chromosomal microarray (CMA) and RNA-seq differential gene-expression data from 31 pancreatic (pNETs) and 33 small-bowel neuroendocrine tumors (sbNETs). Tumors were resected from 47 early-disease-progression (<24 months) and 17 late-disease-progression (>24 months) patients. Candidate fCNAs that accurately differentiated these groups in this discovery cohort were then replicated using fluorescence in situ hybridization (FISH) on formalin-fixed, paraffin-embedded (FFPE) tissues in a larger validation cohort of 60 pNETs and 82 sbNETs (52 early- and 65 late-disease-progression samples). Logistic regression analysis revealed the predictive ability of these biomarkers, as well as the assay-performance metrics of sensitivity, specificity, and area under the curve. Our results indicate that copy-number changes at chromosomal loci 4p16.3, 7q31.2, 9p21.3, 17q12, 18q21.2, and 19q12 may be used as diagnostic and prognostic NET biomarkers. This involves a rapid, cost-effective approach to determine the primary tumor site for patients with metastatic liver NETs and to guide risk-stratified therapeutic decisions. [ABSTRACT FROM AUTHOR]

Published
2024
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4. NF1+/ex42del miniswine model the cellular disruptions and behavioral presentations of NF1‐associated cognitive and motor impairment.

Author

Swier, Vicki J., White, Katherine A., Negrão de Assis, Pedro L., Johnson, Tyler B., Leppert, Hannah G., Rechtzigel, Mitchell J., Meyerholz, David K., Dodd, Rebecca D., Quelle, Dawn E., Khanna, Rajesh, Rogers, Christopher S., and Weimer, Jill M.

Subjects
COGNITION disorders, HUMAN anatomy, NEURAL circuitry, CINGULATE cortex, MEMORY disorders, EXECUTIVE function, MOTOR cortex, NEURAL transmission
Abstract

Cognitive or motor impairment is common among individuals with neurofibromatosis type 1 (NF1), an autosomal dominant tumor‐predisposition disorder. As many as 70% of children with NF1 report difficulties with spatial/working memory, attention, executive function, and fine motor movements. In contrast to the utilization of various Nf1 mouse models, here we employ an NF1+/ex42del miniswine model to evaluate the mechanisms and characteristics of these presentations, taking advantage of a large animal species more like human anatomy and physiology. The prefrontal lobe, anterior cingulate, and hippocampus from NF1+/ex42del and wild‐type miniswine were examined longitudinally, revealing abnormalities in mature oligodendrocytes and astrocytes, and microglial activation over time. Imbalances in GABA: Glutamate ratios and GAD67 expression were observed in the hippocampus and motor cortex, supporting the role of disruption in inhibitory neurotransmission in NF1 cognitive impairment and motor dysfunction. Moreover, NF1+/ex42del miniswine demonstrated slower and shorter steps, indicative of a balance‐preserving response commonly observed in NF1 patients, and progressive memory and learning impairments. Collectively, our findings affirm the effectiveness of NF1+/ex42del miniswine as a valuable resource for assessing cognitive and motor impairments associated with NF1, investigating the involvement of specific neural circuits and glia in these processes, and evaluating potential therapeutic interventions. [ABSTRACT FROM AUTHOR]

Published
2024
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7. 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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8. 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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9. 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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11. 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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12. 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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15. 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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16. Data from The ARF Tumor Suppressor Inhibits Tumor Cell Colonization Independent of p53 in a Novel Mouse Model of Pancreatic Ductal Adenocarcinoma Metastasis

Author

Muniz, Viviane Palhares, primary, Barnes, J. Matthew, primary, Paliwal, Seema, primary, Zhang, Xuefeng, primary, Tang, Xiaoyun, primary, Chen, Songhai, primary, Zamba, Kokou D., primary, Cullen, Joseph J., primary, Meyerholz, David K., primary, Meyers, Shari, primary, Davis, J. Nathan, primary, Grossman, Steven R., primary, Henry, Michael D., primary, and Quelle, Dawn E., primary

Published
2023
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17. Supplementary Figure 1 from The ARF Tumor Suppressor Inhibits Tumor Cell Colonization Independent of p53 in a Novel Mouse Model of Pancreatic Ductal Adenocarcinoma Metastasis

Author

Muniz, Viviane Palhares, primary, Barnes, J. Matthew, primary, Paliwal, Seema, primary, Zhang, Xuefeng, primary, Tang, Xiaoyun, primary, Chen, Songhai, primary, Zamba, Kokou D., primary, Cullen, Joseph J., primary, Meyerholz, David K., primary, Meyers, Shari, primary, Davis, J. Nathan, primary, Grossman, Steven R., primary, Henry, Michael D., primary, and Quelle, Dawn E., primary

Published
2023
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18. 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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19. 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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20. 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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21. 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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22. 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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23. 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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24. 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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25. Data from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner

Author

Hagen, Jussara, primary, Muniz, Viviane P., primary, Falls, Kelly C., primary, Reed, Sara M., primary, Taghiyev, Agshin F., primary, Quelle, Frederick W., primary, Gourronc, Francoise A., primary, Klingelhutz, Aloysius J., primary, Major, Heather J., primary, Askeland, Ryan W., primary, Sherman, Scott K., primary, O'Dorisio, Thomas M., primary, Bellizzi, Andrew M., primary, Howe, James R., primary, Darbro, Benjamin W., primary, and Quelle, Dawn E., primary

Published
2023
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26. Figure S4 from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner

Author

Hagen, Jussara, primary, Muniz, Viviane P., primary, Falls, Kelly C., primary, Reed, Sara M., primary, Taghiyev, Agshin F., primary, Quelle, Frederick W., primary, Gourronc, Francoise A., primary, Klingelhutz, Aloysius J., primary, Major, Heather J., primary, Askeland, Ryan W., primary, Sherman, Scott K., primary, O'Dorisio, Thomas M., primary, Bellizzi, Andrew M., primary, Howe, James R., primary, Darbro, Benjamin W., primary, and Quelle, Dawn E., primary

Published
2023
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27. Table S1 from RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner

Author

Hagen, Jussara, primary, Muniz, Viviane P., primary, Falls, Kelly C., primary, Reed, Sara M., primary, Taghiyev, Agshin F., primary, Quelle, Frederick W., primary, Gourronc, Francoise A., primary, Klingelhutz, Aloysius J., primary, Major, Heather J., primary, Askeland, Ryan W., primary, Sherman, Scott K., primary, O'Dorisio, Thomas M., primary, Bellizzi, Andrew M., primary, Howe, James R., primary, Darbro, Benjamin W., primary, and Quelle, Dawn E., primary

Published
2023
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28. Supplementary Tables S1 & S2 from Large-Scale Molecular Comparison of Human Schwann Cells to Malignant Peripheral Nerve Sheath Tumor Cell Lines and Tissues

Author

Miller, Shyra J., primary, Rangwala, Fatima, primary, Williams, Jon, primary, Ackerman, Peter, primary, Kong, Sue, primary, Jegga, Anil G., primary, Kaiser, Sergio, primary, Aronow, Bruce J., primary, Frahm, Silke, primary, Kluwe, Lan, primary, Mautner, Victor, primary, Upadhyaya, Meena, primary, Muir, David, primary, Wallace, Margaret, primary, Hagen, Jussara, primary, Quelle, Dawn E., primary, Watson, Mark A., primary, Perry, Arie, primary, Gutmann, David H., primary, and Ratner, Nancy, primary

Published
2023
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30. 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

31. Augmenting chemotherapy with low-dose decitabine through an immune-independent mechanism

Author

Gutierrez, Wade R., primary, Scherer, Amanda, additional, Rytlewski, Jeffrey D., additional, Laverty, Emily A., additional, Sheehan, Alexa P., additional, McGivney, Gavin R., additional, Brockman, Qierra R., additional, Knepper-Adrian, Vickie, additional, Roughton, Grace A., additional, Quelle, Dawn E., additional, Gordon, David J., additional, Monga, Varun, additional, and Dodd, Rebecca D., additional

Published
2022
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32. Preclinical Models of Neuroendocrine Neoplasia

Author

Sedlack, Andrew J. H., primary, Saleh-Anaraki, Kimia, additional, Kumar, Suresh, additional, Ear, Po Hien, additional, Lines, Kate E., additional, Roper, Nitin, additional, Pacak, Karel, additional, Bergsland, Emily, additional, Quelle, Dawn E., additional, Howe, James R., additional, Pommier, Yves, additional, and del Rivero, Jaydira, additional

Published
2022
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33. 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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35. Development and translational imaging of a TP53 porcine tumorigenesis model

Author

Sieren, Jessica C., Meyerholz, David K., Wang, Xiao-Jun, Davis, Bryan T., Newell, John D., Jr., Hammond, Emily, Rohret, Judy A., Rohret, Frank A., Struzynski, Jason T., Goeken, J. Adam, Naumann, Paul W., Leidinger, Mariah R., Taghiyev, Agshin, Van Rheeden, Richard, Hagen, Jussara, Darbro, Benjamin W., Quelle, Dawn E., and Rogers, Christopher S.

Subjects
Gene mutations -- Health aspects -- Research, Tumor proteins -- Research, Carcinogenesis -- Research -- Genetic aspects, Lymphomas -- Research -- Risk factors -- Patient outcomes -- Diagnosis -- Development and progression, Swine -- Research -- Genetic aspects, Genetically modified organisms -- Research, Health care industry
Abstract

Cancer is the second deadliest disease in the United States, necessitating improvements in tumor diagnosis and treatment. Current model systems of cancer are informative, but translating promising imaging approaches and therapies to clinical practice has been challenging. In particular, the lack of a large-animal model that accurately mimics human cancer has been a major barrier to the development of effective diagnostic tools along with surgical and therapeutic interventions. Here, we developed a genetically modified porcine model of cancer in which animals express a mutation in TP53 (which encodes p53) that is orthologous to one commonly found in humans (R175H in people, R167H in pigs). [TP53.sup.R167H/R167H] mutant pigs primarily developed lymphomas and osteogenic tumors, recapitulating the tumor types observed in mice and humans expressing orthologous TP53 mutant alleles. CT and MRI imaging data effectively detected developing tumors, which were validated by histopathological evaluation after necropsy. Molecular genetic analyses confirmed that these animals expressed the R167H mutant p53, and evaluation of tumors revealed characteristic chromosomal instability. Together, these results demonstrated that [TP53.sup.R167H/R167H] pigs represent a large-animal tumor model that replicates the human condition. Our data further suggest that this model will be uniquely suited for developing clinically relevant, noninvasive imaging approaches to facilitate earlier detection, diagnosis, and treatment of human cancers., Introduction The need for immediate and rapid progress in cancer detection, diagnosis, and treatment is apparent, with 1 of every 4 deaths in the United States resulting from cancer (1). [...]

Published
2014
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39. 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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41. Prognostic and therapeutic value of the Hippo pathway, RABL6A, and p53-MDM2 axes in sarcomas

Author

Desai, Chandni, primary, Thomason, Jon, additional, Kohlmeyer, Jordan L., additional, Reisetter, Anna C., additional, Ahirwar, Parmanand, additional, Jahanseir, Khadijeh, additional, Leidinger, Mariah, additional, Ofori-Amanfo, Georgina, additional, Fritchie, Karen, additional, Velu, Sadanandan E., additional, Breheny, Patrick, additional, Quelle, Dawn E., additional, and Tanas, Munir R., additional

Published
2021
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43. Pdgfrα-Cre mediated knockout of the aryl hydrocarbon receptor protects mice from high-fat diet induced obesity and hepatic steatosis

Author

Gourronc, Francoise A., primary, Markan, Kathleen R., additional, Kulhankova, Katarina, additional, Zhu, Zhiyong, additional, Sheehy, Ryan, additional, Quelle, Dawn E., additional, Zingman, Leonid V., additional, Kurago, Zoya B., additional, Ankrum, James A., additional, and Klingelhutz, Aloysius J., additional

Published
2020
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44. 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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46. 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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50. Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF

Author

Kamijo, Takehiko, Zindy, Frederique, Roussel, Martine F., Quelle, Dawn E., Downing, James R., Ashmun, Richard A., Grosveld, Gerard, and Sherr, Charles J.

Subjects
Tumor suppressor genes -- Research, Biological sciences
Abstract

A frequently inactivated tumor suppressor gene in human cancer is INK4a, which encodes p16INK4a, which is a specific inhibitor of CDK4 and CDK6, cyclin D-dependent kinases. The ARF function in mice was selectively disrupted through the deletion of exon 1Beta and leaving all p16INK4a coding sequences. The results indicate that ARF and p53 regulate senescence of mouse embryo fibroblasts.

Published
1997

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