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1. Virology under the Microscope-a Call for Rational Discourse.

Author

Goodrum, Felicia, Lowen, Anice C, Lakdawala, Seema, Alwine, James, Casadevall, Arturo, Imperiale, Michael J, Atwood, Walter, Avgousti, Daphne, Baines, Joel, Banfield, Bruce, Banks, Lawrence, Bhaduri-McIntosh, Sumita, Bhattacharya, Deepta, Blanco-Melo, Daniel, Bloom, David, Boon, Adrianus, Boulant, Steeve, Brandt, Curtis, Broadbent, Andrew, Brooke, Christopher, Cameron, Craig, Campos, Samuel, Caposio, Patrizia, Chan, Gary, Cliffe, Anna, Coffin, John, Collins, Kathleen, Damania, Blossom, Daugherty, Matthew, Debbink, Kari, DeCaprio, James, Dermody, Terence, Dikeakos, Jimmy, DiMaio, Daniel, Dinglasan, Rhoel, Duprex, W Paul, Dutch, Rebecca, Elde, Nels, Emerman, Michael, Enquist, Lynn, Fane, Bentley, Fernandez-Sesma, Ana, Flenniken, Michelle, Frappier, Lori, Frieman, Matthew, Frueh, Klaus, Gack, Michaela, Gaglia, Marta, Gallagher, Tom, Galloway, Denise, García-Sastre, Adolfo, Geballe, Adam, Glaunsinger, Britt, Goff, Stephen, Greninger, Alexander, Hancock, Meaghan, Harris, Eva, Heaton, Nicholas, Heise, Mark, Heldwein, Ekaterina, Hogue, Brenda, Horner, Stacy, Hutchinson, Edward, Hyser, Joseph, Jackson, William, Kalejta, Robert, Kamil, Jeremy, Karst, Stephanie, Kirchhoff, Frank, Knipe, David, Kowalik, Timothy, Lagunoff, Michael, Laimins, Laimonis, Langlois, Ryan, Lauring, Adam, Lee, Benhur, Leib, David, Liu, Shan-Lu, Longnecker, Richard, Lopez, Carolina, Luftig, Micah, Lund, Jennifer, Manicassamy, Balaji, McFadden, Grant, McIntosh, Michael, Mehle, Andrew, Miller, W Allen, Mohr, Ian, Moody, Cary, Moorman, Nathaniel, Moscona, Anne, Mounce, Bryan, Munger, Joshua, Münger, Karl, Murphy, Eain, Naghavi, Mojgan, Nelson, Jay, Neufeldt, Christopher, Nikolich, Janko, and O'Connor, Christine

Subjects
COVID-19, Coronavirus, DURC, Gain of function, SARS-CoV-2, biosafety, influenza, pandemic, vaccines, zoonosis, Infectious Diseases, Prevention, Vaccine Related, Immunization, Infection, Good Health and Well Being, Biological Sciences, Medical and Health Sciences, Microbiology
Abstract

Viruses have brought humanity many challenges: respiratory infection, cancer, neurological impairment and immunosuppression to name a few. Virology research over the last 60+ years has responded to reduce this disease burden with vaccines and antivirals. Despite this long history, the COVID-19 pandemic has brought unprecedented attention to the field of virology. Some of this attention is focused on concern about the safe conduct of research with human pathogens. A small but vocal group of individuals has seized upon these concerns - conflating legitimate questions about safely conducting virus-related research with uncertainties over the origins of SARS-CoV-2. The result has fueled public confusion and, in many instances, ill-informed condemnation of virology. With this article, we seek to promote a return to rational discourse. We explain the use of gain-of-function approaches in science, discuss the possible origins of SARS-CoV-2 and outline current regulatory structures that provide oversight for virological research in the United States. By offering our expertise, we - a broad group of working virologists - seek to aid policy makers in navigating these controversial issues. Balanced, evidence-based discourse is essential to addressing public concern while maintaining and expanding much-needed research in virology.

Published
2023

2. An international report on bacterial communities in esophageal squamous cell carcinoma

Author

Nomburg, Jason, Bullman, Susan, Nasrollahzadeh, Dariush, Collisson, Eric A, Abedi‐Ardekani, Behnoush, Akoko, Larry O, Atkins, Joshua R, Buckle, Geoffrey C, Gopal, Satish, Hu, Nan, Kaimila, Bongani, Khoshnia, Masoud, Malekzadeh, Reza, Menya, Diana, Mmbaga, Blandina T, Moody, Sarah, Mulima, Gift, Mushi, Beatrice P, Mwaiselage, Julius, Mwanga, Ally, Newton, Yulia, Ng, Dianna L, Radenbaugh, Amie, Rwakatema, Deogratias S, Selekwa, Msiba, Schüz, Joachim, Taylor, Philip R, Vaske, Charles, Goldstein, Alisa, Stratton, Michael R, McCormack, Valerie, Brennan, Paul, DeCaprio, James A, Meyerson, Matthew, Mmbaga, Elia J, and Van Loon, Katherine

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Human Genome, Esophageal Cancer, Microbiome, Rare Diseases, Cancer Genomics, Clinical Research, Dental/Oral and Craniofacial Disease, Genetics, Prevention, Digestive Diseases, Infectious Diseases, Cancer, Infection, Bacteria, Esophageal Neoplasms, Esophageal Squamous Cell Carcinoma, Humans, Kenya, Microbiota, Africa, esophageal cancer, esophageal squamous cell carcinoma, Fusobacterium, microbiome, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

The incidence of esophageal squamous cell carcinoma (ESCC) is disproportionately high in the eastern corridor of Africa and parts of Asia. Emerging research has identified a potential association between poor oral health and ESCC. One possible link between poor oral health and ESCC involves the alteration of the microbiome. We performed an integrated analysis of four independent sequencing efforts of ESCC tumors from patients from high- and low-incidence regions of the world. Using whole genome sequencing (WGS) and RNA sequencing (RNAseq) of ESCC tumors from 61 patients in Tanzania, we identified a community of bacteria, including members of the genera Fusobacterium, Selenomonas, Prevotella, Streptococcus, Porphyromonas, Veillonella and Campylobacter, present at high abundance in ESCC tumors. We then characterized the microbiome of 238 ESCC tumor specimens collected in two additional independent sequencing efforts consisting of patients from other high-ESCC incidence regions (Tanzania, Malawi, Kenya, Iran, China). This analysis revealed similar ESCC-associated bacterial communities in these cancers. Because these genera are traditionally considered members of the oral microbiota, we next explored whether there was a relationship between the synchronous saliva and tumor microbiomes of ESCC patients in Tanzania. Comparative analyses revealed that paired saliva and tumor microbiomes were significantly similar with a specific enrichment of Fusobacterium and Prevotella in the tumor microbiome. Together, these data indicate that cancer-associated oral bacteria are associated with ESCC tumors at the time of diagnosis and support a model in which oral bacteria are present in high abundance in both saliva and tumors of some ESCC patients.

Published
2022

3. Liquid biopsy epigenomic profiling for cancer subtyping

Author

Baca, Sylvan C., Seo, Ji-Heui, Davidsohn, Matthew P., Fortunato, Brad, Semaan, Karl, Sotudian, Shahabbedin, Lakshminarayanan, Gitanjali, Diossy, Miklos, Qiu, Xintao, El Zarif, Talal, Savignano, Hunter, Canniff, John, Madueke, Ikenna, Saliby, Renee Maria, Zhang, Ziwei, Li, Rong, Jiang, Yijia, Taing, Len, Awad, Mark, Chau, Cindy H., DeCaprio, James A., Figg, William D., Greten, Tim F., Hata, Aaron N., Hodi, F. Stephen, Hughes, Melissa E., Ligon, Keith L., Lin, Nancy, Ng, Kimmie, Oser, Matthew G., Meador, Catherine, Parsons, Heather A., Pomerantz, Mark M., Rajan, Arun, Ritz, Jerome, Thakuria, Manisha, Tolaney, Sara M., Wen, Patrick Y., Long, Henry, Berchuck, Jacob E., Szallasi, Zoltan, Choueiri, Toni K., and Freedman, Matthew L.

Published
2023
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4. Author Correction: Liquid biopsy epigenomic profiling for cancer subtyping

Author

Baca, Sylvan C., Seo, Ji-Heui, Davidsohn, Matthew P., Fortunato, Brad, Semaan, Karl, Sotudian, Shahabbedin, Lakshminarayanan, Gitanjali, Diossy, Miklos, Qiu, Xintao, El Zarif, Talal, Savignano, Hunter, Canniff, John, Madueke, Ikenna, Saliby, Renee Maria, Zhang, Ziwei, Li, Rong, Jiang, Yijia, Taing, Len, Awad, Mark, Chau, Cindy H., DeCaprio, James A., Figg, William D., Greten, Tim F., Hata, Aaron N., Hodi, F. Stephen, Hughes, Melissa E., Ligon, Keith L., Lin, Nancy, Ng, Kimmie, Oser, Matthew G., Meador, Catherine, Parsons, Heather A., Pomerantz, Mark M., Rajan, Arun, Ritz, Jerome, Thakuria, Manisha, Tolaney, Sara M., Wen, Patrick Y., Long, Henry, Berchuck, Jacob E., Szallasi, Zoltan, Choueiri, Toni K., and Freedman, Matthew L.

Published
2024
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5. A Murine Model of Chronic Lymphocytic Leukemia Based on B Cell-Restricted Expression of Sf3b1 Mutation and Atm Deletion

Author

Yin, Shanye, Gambe, Rutendo G, Sun, Jing, Martinez, Aina Zurita, Cartun, Zachary J, Regis, Fara Faye D, Wan, Youzhong, Fan, Jean, Brooks, Angela N, Herman, Sarah EM, Hacken, Elisa ten, Taylor-Weiner, Amaro, Rassenti, Laura Z, Ghia, Emanuela M, Kipps, Thomas J, Obeng, Esther A, Cibulskis, Carrie L, Neuberg, Donna, Campagna, Dean R, Fleming, Mark D, Ebert, Benjamin L, Wiestner, Adrian, Leshchiner, Ignaty, DeCaprio, James A, Getz, Gad, Reed, Robin, Carrasco, Ruben D, Wu, Catherine J, and Wang, Lili

Subjects
Rare Diseases, Lymphoma, Cancer, Genetics, Hematology, 2.1 Biological and endogenous factors, Aetiology, Adenine, Agammaglobulinaemia Tyrosine Kinase, Alternative Splicing, Animals, Antineoplastic Agents, Ataxia Telangiectasia Mutated Proteins, B-Lymphocytes, Cellular Senescence, DNA Damage, Gene Deletion, Genetic Predisposition to Disease, Genomic Instability, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Mice, 129 Strain, Mice, Inbred C57BL, Mice, Knockout, Mice, Mutant Strains, Mutation, Neoplasms, Experimental, Phenotype, Phosphoproteins, Piperidines, Protein Kinase Inhibitors, Pyrazoles, Pyrimidines, RNA Splicing Factors, Receptors, Antigen, B-Cell, Signal Transduction, Tumor Cells, Cultured, ATM, BCR signaling, CLL, SF3B1, murine model, Neurosciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

SF3B1 is recurrently mutated in chronic lymphocytic leukemia (CLL), but its role in the pathogenesis of CLL remains elusive. Here, we show that conditional expression of Sf3b1-K700E mutation in mouse B cells disrupts pre-mRNA splicing, alters cell development, and induces a state of cellular senescence. Combination with Atm deletion leads to the overcoming of cellular senescence and the development of CLL-like disease in elderly mice. These CLL-like cells show genome instability and dysregulation of multiple CLL-associated cellular processes, including deregulated B cell receptor signaling, which we also identified in human CLL cases. Notably, human CLLs harboring SF3B1 mutations exhibit altered response to BTK inhibition. Our murine model of CLL thus provides insights into human CLL disease mechanisms and treatment.

Published
2019

7. CDC7-independent G1/S transition revealed by targeted protein degradation

Author

Suski, Jan M., Ratnayeke, Nalin, Braun, Marcin, Zhang, Tian, Strmiska, Vladislav, Michowski, Wojciech, Can, Geylani, Simoneau, Antoine, Snioch, Konrad, Cup, Mikolaj, Sullivan, Caitlin M., Wu, Xiaoji, Nowacka, Joanna, Branigan, Timothy B., Pack, Lindsey R., DeCaprio, James A., Geng, Yan, Zou, Lee, Gygi, Steven P., Walter, Johannes C., Meyer, Tobias, and Sicinski, Piotr

Published
2022
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8. YAP1 and WWTR1 expression inversely correlates with neuroendocrine markers in Merkel cell carcinoma

Author

Fros, Thomas C., Gartin, Ashley K., Liu, Mofei, Cheng, Jingwei, Dharaneeswaran, Harita, Keskin, Derin B., Wu, Catherine J., Giobbie-Hurder, Anita, Thakuria, Manisha, and DeCaprio, James A.

Subjects
Merkel cell carcinoma -- Genetic aspects -- Development and progression, Transcription factors -- Physiological aspects -- Health aspects, Health care industry
Abstract

BACKGROUND. Merkel cell carcinoma (MCC) is an aggressive neuroendocrine (NE) skin cancer caused by severe UV-induced mutations or expression of Merkel cell polyomavirus (MCPyV) large and small T antigens (LT and ST). Despite deep genetic differences between MCPyV-positive and -negative subtypes, current clinical diagnostic markers are indistinguishable, and the expression profile of MCC tumors is, to our knowledge, unexplored. METHODS. Here, we leveraged bulk and single-cell RNA-Seq of patient-derived tumor biopsies and cell lines to explore the underlying transcriptional environment of MCC. RESULTS. Strikingly, MCC samples could be separated into transcriptional subtypes that were independent of MCPyV status. Instead, we observed an inverse correlation between a NE gene signature and the Hippo pathway transcription factors Yes1-associated transcriptional regulator (YAP1) and WW domain-containing transcriptional regulator 1 (WWTR1). This inverse correlation was broadly present at the transcript and protein levels in the tumor biopsies as well as in established and patient-derived cell lines. Mechanistically, expression of YAP1 or WWTR1 in a MCPyV-positive MCC cell line induced cellcycle arrest at least in part through TEA domain-dependent (TEAD-dependent) transcriptional repression of MCPyV LT. CONCLUSION. These findings identify what we believe to be a previously unrecognized heterogeneity in NE gene expression within MCC and support a model of YAP1/WWTR1 silencing as essential for the development of MCPyV-positive MCC. FUNDING. US Public Health Service grants R35CA232128, P01CA203655, and P30CA06516., Introduction MCC can be defined by viral status and NE marker expression. Merkel cell carcinoma (MCC) is a neuroendocrine (NE) carcinoma of the skin with 2 etiological subtypes distinguished by [...]

Published
2023
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9. Tumor cell–intrinsic PD-1 promotes Merkel cell carcinoma growth by activating downstream mTOR-mitochondrial ROS signaling

Author

Martins, Christina, primary, Rasbach, Erik, additional, Heppt, Markus V., additional, Singh, Praveen, additional, Kulcsar, Zsofi, additional, Holzgruber, Julia, additional, Chakraborty, Asmi, additional, Mucciarone, Kyla, additional, Kleffel, Sonja, additional, Brandenburg, Anne, additional, Hoetzenecker, Wolfram, additional, Rahbari, Nuh N., additional, DeCaprio, James A., additional, Thakuria, Manisha, additional, Murphy, George F., additional, Ramsey, Matthew R., additional, Posch, Christian, additional, Barthel, Steven R., additional, and Schatton, Tobias, additional

Published
2024
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10. Author Correction: Liquid biopsy epigenomic profiling for cancer subtyping

Author

Baca, Sylvan C., primary, Seo, Ji-Heui, additional, Davidsohn, Matthew P., additional, Fortunato, Brad, additional, Semaan, Karl, additional, Sotudian, Shahabbedin, additional, Lakshminarayanan, Gitanjali, additional, Diossy, Miklos, additional, Qiu, Xintao, additional, El Zarif, Talal, additional, Savignano, Hunter, additional, Canniff, John, additional, Madueke, Ikenna, additional, Saliby, Renee Maria, additional, Zhang, Ziwei, additional, Li, Rong, additional, Jiang, Yijia, additional, Taing, Len, additional, Awad, Mark, additional, Chau, Cindy H., additional, DeCaprio, James A., additional, Figg, William D., additional, Greten, Tim F., additional, Hata, Aaron N., additional, Hodi, F. Stephen, additional, Hughes, Melissa E., additional, Ligon, Keith L., additional, Lin, Nancy, additional, Ng, Kimmie, additional, Oser, Matthew G., additional, Meador, Catherine, additional, Parsons, Heather A., additional, Pomerantz, Mark M., additional, Rajan, Arun, additional, Ritz, Jerome, additional, Thakuria, Manisha, additional, Tolaney, Sara M., additional, Wen, Patrick Y., additional, Long, Henry, additional, Berchuck, Jacob E., additional, Szallasi, Zoltan, additional, Choueiri, Toni K., additional, and Freedman, Matthew L., additional

Published
2023
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13. Subtype heterogeneity and epigenetic convergence in neuroendocrine prostate cancer

Author

Cejas, Paloma, Xie, Yingtian, Font-Tello, Alba, Lim, Klothilda, Syamala, Sudeepa, Qiu, Xintao, Tewari, Alok K., Shah, Neel, Nguyen, Holly M., Patel, Radhika A., Brown, Lisha, Coleman, Ilsa, Hackeng, Wenzel M., Brosens, Lodewijk, Dreijerink, Koen M. A., Ellis, Leigh, Alaiwi, Sarah Abou, Seo, Ji-Heui, Baca, Sylvan, Beltran, Himisha, Khani, Francesca, Pomerantz, Mark, Dall’Agnese, Alessandra, Crowdis, Jett, Van Allen, Eliezer M., Bellmunt, Joaquim, Morrisey, Colm, Nelson, Peter S., DeCaprio, James, Farago, Anna, Dyson, Nicholas, Drapkin, Benjamin, Liu, X. Shirley, Freedman, Matthew, Haffner, Michael C., Corey, Eva, Brown, Myles, and Long, Henry W.

Published
2021
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15. Disrupting the DREAM complex enables proliferation of adult human pancreatic [beta] cells

Author

Wang, Peng, Karakose, Esra, Argmann, Carmen, Wang, Huan, Balev, Metodi, Brody, Rachel I., Rivas, Hembly G., Liu, Xinyue, Wood, Olivia, Liu, Hongtao, Choleva, Lauryn, Hasson, Dan, Bernstein, Emily, Paulo, Joao A., Scott, Donald K., Lambertini, Luca, DeCaprio, James A., and Stewart, Andrew F.

Subjects
Binding proteins -- Physiological aspects -- Health aspects, Diabetes -- Development and progression, Pancreatic beta cells -- Physiological aspects -- Health aspects, Protein kinases -- Physiological aspects -- Health aspects, Health care industry
Abstract

Resistance to regeneration of insulin-producing pancreatic [beta] cells is a fundamental challenge for type 1 and type 2 diabetes. Recently, small molecule inhibitors of the kinase DYRK1A have proven effective in inducing adult human [beta] cells to proliferate, but their detailed mechanism of action is incompletely understood. We interrogated our human insulinoma and [beta] cell transcriptomic databases seeking to understand why [beta] cells in insulinomas proliferate, while normal [beta] cells do not. This search reveals the DREAM complex as a central regulator of quiescence in human [beta] cells. The DREAM complex consists of a module of transcriptionally repressive proteins that assemble in response to DYRK1A kinase activity, thereby inducing and maintaining cellular quiescence. In the absence of DYRK1A, DREAM subunits reassemble into the pro-proliferative MMB complex. Here, we demonstrate that small molecule DYRK1A inhibitors induce human [beta] cells to replicate by converting the repressive DREAM complex to its pro-proliferative MMB conformation., Introduction Type 1 (T1D) and type 2 (T2D) diabetes together afflict 463 million people globally (1). While T1D results from autoimmune destruction of pancreatic insulin-producing [beta] cells, and T2D is [...]

Published
2022
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20. Transcriptional landscape of the human cell cycle

Author

Liu, Yin, Chen, Sujun, Wang, Su, Soares, Fraser, Fischer, Martin, Meng, Feilong, Du, Zhou, Lin, Charles, Meyer, Clifford, DeCaprio, James A., Brown, Myles, Liu, X. Shirley, and He, Housheng Hansen

Published
2017

28. Abstract 6130: Cancer sensitivity to therapy is constrained by apoptosis regulation in cells of origin

Author

Fraser, Cameron, primary, Qin, Xingping, additional, Shimada, Kenichi, additional, Spetz, Johan, additional, Florido, Mary Heather, additional, Singh, Rumani, additional, Yu, Stacey, additional, Presser, Adam, additional, Inde, Zintis, additional, Joshi, Gaurav, additional, Guerriero, Jennifer, additional, Sanchez-Rivera, Francisco, additional, Karst, Alison, additional, Lopez, Omar, additional, Li, Chendi, additional, Winter, Peter, additional, Yue, Ying, additional, Sorger, Peter, additional, Cheng, Jingwei, additional, Lossos, Izidore, additional, Hata, Aaron, additional, Drapkin, Ronny, additional, Palmer, Adam, additional, Decaprio, James, additional, Thakuria, Manisha, additional, Yoon, Charles, additional, Matulonis, Ursula, additional, Meyerson, Matthew, additional, Stover, Elizabeth, additional, Cardona, Diana, additional, Wood, Kris, additional, Sarosiek, Shayna, additional, Kirsch, David, additional, Mancias, Joseph, additional, Cherniack, Andrew, additional, Letai, Anthony, additional, and Sarosiek, Kristopher, additional

Published
2023
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32. Virology under the Microscope—a Call for Rational Discourse

Author

Goodrum, Felicia, primary, Lowen, Anice C., additional, Lakdawala, Seema, additional, Alwine, James, additional, Casadevall, Arturo, additional, Imperiale, Michael J., additional, Atwood, Walter, additional, Avgousti, Daphne, additional, Baines, Joel, additional, Banfield, Bruce, additional, Banks, Lawrence, additional, Bhaduri-McIntosh, Sumita, additional, Bhattacharya, Deepta, additional, Blanco-Melo, Daniel, additional, Bloom, David, additional, Boon, Adrianus, additional, Boulant, Steeve, additional, Brandt, Curtis, additional, Broadbent, Andrew, additional, Brooke, Christopher, additional, Cameron, Craig, additional, Campos, Samuel, additional, Caposio, Patrizia, additional, Chan, Gary, additional, Cliffe, Anna, additional, Coffin, John, additional, Collins, Kathleen, additional, Damania, Blossom, additional, Daugherty, Matthew, additional, Debbink, Kari, additional, DeCaprio, James, additional, Dermody, Terence, additional, Dikeakos, Jimmy, additional, DiMaio, Daniel, additional, Dinglasan, Rhoel, additional, Duprex, W. Paul, additional, Dutch, Rebecca, additional, Elde, Nels, additional, Emerman, Michael, additional, Enquist, Lynn, additional, Fane, Bentley, additional, Fernandez-Sesma, Ana, additional, Flenniken, Michelle, additional, Frappier, Lori, additional, Frieman, Matthew, additional, Frueh, Klaus, additional, Gack, Michaela, additional, Gaglia, Marta, additional, Gallagher, Tom, additional, Galloway, Denise, additional, García-Sastre, Adolfo, additional, Geballe, Adam, additional, Glaunsinger, Britt, additional, Goff, Stephen, additional, Greninger, Alexander, additional, Hancock, Meaghan, additional, Harris, Eva, additional, Heaton, Nicholas, additional, Heise, Mark, additional, Heldwein, Ekaterina, additional, Hogue, Brenda, additional, Horner, Stacy, additional, Hutchinson, Edward, additional, Hyser, Joseph, additional, Jackson, William, additional, Kalejta, Robert, additional, Kamil, Jeremy, additional, Karst, Stephanie, additional, Kirchhoff, Frank, additional, Knipe, David, additional, Kowalik, Timothy, additional, Lagunoff, Michael, additional, Laimins, Laimonis, additional, Langlois, Ryan, additional, Lauring, Adam, additional, Lee, Benhur, additional, Leib, David, additional, Liu, Shan-Lu, additional, Longnecker, Richard, additional, Lopez, Carolina, additional, Luftig, Micah, additional, Lund, Jennifer, additional, Manicassamy, Balaji, additional, McFadden, Grant, additional, McIntosh, Michael, additional, Mehle, Andrew, additional, Miller, W. Allen, additional, Mohr, Ian, additional, Moody, Cary, additional, Moorman, Nathaniel, additional, Moscona, Anne, additional, Mounce, Bryan, additional, Munger, Joshua, additional, Münger, Karl, additional, Murphy, Eain, additional, Naghavi, Mojgan, additional, Nelson, Jay, additional, Neufeldt, Christopher, additional, Nikolich, Janko, additional, O'Connor, Christine, additional, Ono, Akira, additional, Orenstein, Walter, additional, Ornelles, David, additional, Ou, Jing-hsiung, additional, Parker, John, additional, Parrish, Colin, additional, Pekosz, Andrew, additional, Pellett, Philip, additional, Pfeiffer, Julie, additional, Plemper, Richard, additional, Polyak, Stephen, additional, Purdy, John, additional, Pyeon, Dohun, additional, Quinones-Mateu, Miguel, additional, Renne, Rolf, additional, Rice, Charles, additional, Schoggins, John, additional, Roller, Richard, additional, Russell, Charles, additional, Sandri-Goldin, Rozanne, additional, Sapp, Martin, additional, Schang, Luis, additional, Schmid, Scott, additional, Schultz-Cherry, Stacey, additional, Semler, Bert, additional, Shenk, Thomas, additional, Silvestri, Guido, additional, Simon, Viviana, additional, Smith, Gregory, additional, Smith, Jason, additional, Spindler, Katherine, additional, Stanifer, Megan, additional, Subbarao, Kanta, additional, Sundquist, Wesley, additional, Suthar, Mehul, additional, Sutton, Troy, additional, Tai, Andrew, additional, Tarakanova, Vera, additional, tenOever, Benjamin, additional, Tibbetts, Scott, additional, Tompkins, Stephen, additional, Toth, Zsolt, additional, van Doorslaer, Koenraad, additional, Vignuzzi, Marco, additional, Wallace, Nicholas, additional, Walsh, Derek, additional, Weekes, Michael, additional, Weinberg, Jason, additional, Weitzman, Matthew, additional, Weller, Sandra, additional, Whelan, Sean, additional, White, Elizabeth, additional, Williams, Bryan, additional, Wobus, Christiane, additional, Wong, Scott, additional, and Yurochko, Andrew, additional

Published
2023
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34. Abstract A057: Therapeutic efficacy of selective CDK7 inhibition in pancreatic cancer mediated by induction of R-loop formation, DNA replication stress and genomic instability

Author

Yang, Annan, primary, Jiang, Jie, additional, Li, Ziyue, additional, Kapner, Kevin S., additional, Feng, Hanrong, additional, Lowder, Kristen E., additional, Kuljanin, Miljan, additional, Johnson, Whiteny, additional, Uribe, Giselle, additional, Neggers, Jasper E., additional, Liu, Shengwu, additional, Zhang, Tinghu, additional, Decaprio, James, additional, Sicinska, Ewa, additional, Wolpin, Brian M., additional, Kwiatkowski, Nicholas P., additional, Dougan, Stephanie K., additional, Mancias, Joseph D., additional, Gray, Nathanael S., additional, and Aguirre, Andrew J., additional

Published
2022
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35. Virally mediated mechanisms of HLA class I loss in Merkel cell carcinoma and implications for viral epitope presentation

Author

Keskin, Derin B., primary, Lee, Patrick C., additional, Klaeger, Susan, additional, Le, Phuong M., additional, Korthauer, Keegan, additional, Cheng, Jingwei, additional, Ananthapadmanabhan, Varsha, additional, Frost, Thomas C., additional, Iorgulescu, J. Bryan, additional, Lemvigh, Camilla K., additional, Pedersen, Christina B., additional, Sarkizova, Siranush, additional, Li, Shuqiang, additional, Liu, Xiaoxi, additional, Doherty, Laura M., additional, Neuberg, Donna, additional, Zhang, Guanglan, additional, Olsen, Lars R., additional, Thakuria, Manisha, additional, Rodig, Scott J., additional, Clauser, Karl R., additional, Starrett, Gabriel J., additional, Doench, John G., additional, Buhrlage, Sara J., additional, Carr, Steven A., additional, DeCaprio, James A., additional, and Wu, Catherine J., additional

Published
2022
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37. Disrupting the DREAM complex enables proliferation of adult human pancreatic β cells

Author

Wang, Peng, primary, Karakose, Esra, additional, Argmann, Carmen, additional, Wang, Huan, additional, Balev, Metodi, additional, Brody, Rachel I., additional, Rivas, Hembly G., additional, Liu, Xinyue, additional, Wood, Olivia, additional, Liu, Hongtao, additional, Choleva, Lauryn, additional, Hasson, Dan, additional, Bernstein, Emily, additional, Paulo, Joao A., additional, Scott, Donald K., additional, Lambertini, Luca, additional, DeCaprio, James A., additional, and Stewart, Andrew F., additional

Published
2022
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39. Reversal of viral and epigenetic HLA class I repression in Merkel cell carcinoma

Author

Lee, Patrick C., primary, Klaeger, Susan, additional, Le, Phuong M., additional, Korthauer, Keegan, additional, Cheng, Jingwei, additional, Ananthapadmanabhan, Varsha, additional, Frost, Thomas C., additional, Stevens, Jonathan D., additional, Wong, Alan Y.L., additional, Iorgulescu, J. Bryan, additional, Tarren, Anna Y., additional, Chea, Vipheaviny A., additional, Carulli, Isabel P., additional, Lemvigh, Camilla K., additional, Pedersen, Christina B., additional, Gartin, Ashley K., additional, Sarkizova, Siranush, additional, Wright, Kyle T., additional, Li, Letitia W., additional, Nomburg, Jason, additional, Li, Shuqiang, additional, Huang, Teddy, additional, Liu, Xiaoxi, additional, Pomerance, Lucas, additional, Doherty, Laura M., additional, Apffel, Annie M., additional, Wallace, Luke J., additional, Rachimi, Suzanna, additional, Felt, Kristen D., additional, Wolff, Jacquelyn O., additional, Witten, Elizabeth, additional, Zhang, Wandi, additional, Neuberg, Donna, additional, Lane, William J., additional, Zhang, Guanglan, additional, Olsen, Lars R., additional, Thakuria, Manisha, additional, Rodig, Scott J., additional, Clauser, Karl R., additional, Starrett, Gabriel J., additional, Doench, John G., additional, Buhrlage, Sara J., additional, Carr, Steven A., additional, DeCaprio, James A., additional, Wu, Catherine J., additional, and Keskin, Derin B., additional

Published
2022
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42. Reversal of viral and epigenetic HLA class I repression in Merkel cell carcinoma

Author

Lee, Patrick C., Klaeger, Susan, Le, Phuong M., Korthauer, Keegan, Cheng, Jingwei, Ananthapadmanabhan, Varsha, Frost, Thomas C., Stevens, Jonathan D., Wong, Alan Y.L., Iorgulescu, J. Bryan, Tarren, Anna Y., Chea, Vipheaviny A., Carulli, Isabel P., Lemvigh, Camilla K., Pedersen, Christina B., Gartin, Ashley K., Sarkizova, Siranush, Wright, Kyle T., Li, Letitia W., Nomburg, Jason, Li, Shuqiang, Huang, Teddy, Liu, Xiaoxi, Pomerance, Lucas, Doherty, Laura M., Apffel, Annie M., Wallace, Luke J., Rachimi, Suzanna, Felt, Kristen D., Wolff, Jacquelyn O., Witten, Elizabeth, Zhang, Wandi, Neuberg, Donna, Lane, William J., Zhang, Guanglan, Olsen, Lars R., Thakuria, Manisha, Rodig, Scott J., Clauser, Karl R., Starrett, Gabriel J., Doench, John G., Buhrlage, Sara J., Carr, Steven A., DeCaprio, James A., Wu, Catherine J., Keskin, Derin B., Lee, Patrick C., Klaeger, Susan, Le, Phuong M., Korthauer, Keegan, Cheng, Jingwei, Ananthapadmanabhan, Varsha, Frost, Thomas C., Stevens, Jonathan D., Wong, Alan Y.L., Iorgulescu, J. Bryan, Tarren, Anna Y., Chea, Vipheaviny A., Carulli, Isabel P., Lemvigh, Camilla K., Pedersen, Christina B., Gartin, Ashley K., Sarkizova, Siranush, Wright, Kyle T., Li, Letitia W., Nomburg, Jason, Li, Shuqiang, Huang, Teddy, Liu, Xiaoxi, Pomerance, Lucas, Doherty, Laura M., Apffel, Annie M., Wallace, Luke J., Rachimi, Suzanna, Felt, Kristen D., Wolff, Jacquelyn O., Witten, Elizabeth, Zhang, Wandi, Neuberg, Donna, Lane, William J., Zhang, Guanglan, Olsen, Lars R., Thakuria, Manisha, Rodig, Scott J., Clauser, Karl R., Starrett, Gabriel J., Doench, John G., Buhrlage, Sara J., Carr, Steven A., DeCaprio, James A., Wu, Catherine J., and Keskin, Derin B.

Abstract

Cancers avoid immune surveillance through an array of mechanisms, including perturbation of HLA class I antigen presentation. Merkel cell carcinoma (MCC) is an aggressive, HLA-I–low, neuroendocrine carcinoma of the skin often caused by the Merkel cell polyomavirus (MCPyV). Through the characterization of 11 newly generated MCC patient-derived cell lines, we identified transcriptional suppression of several class I antigen presentation genes. To systematically identify regulators of HLA-I loss in MCC, we performed parallel, genome-scale, gain- and loss-of-function screens in a patient-derived MCPyV-positive cell line and identified MYCL and the non-canonical Polycomb repressive complex 1.1 (PRC1.1) as HLA-I repressors. We observed physical interaction of MYCL with the MCPyV small T viral antigen, supporting a mechanism of virally mediated HLA-I suppression. We further identify the PRC1.1 component USP7 as a pharmacologic target to restore HLA-I expression in MCC.

Published
2022

50. Improved detection suggests all Merkel cell carcinomas harbor Merkel polyomavirus

Author

Rodig, Scott J., Cheng, Jingwei, Wardzala, Jacek, DoRosario, Andrew, Scanlon, Jessica J., Laga, Alvaro C., Martinez-Fernandez, Alejandro, Barletta, Justine A., Bellizzi, Andrew M., Sadasivam, Subhashini, Holloway, Dustin T., Cooper, Dylan J., Kupper, Thomas S., Wang, Linda C., and DeCaprio, James A.

Subjects
Gene mutations -- Identification and classification, Merkel cell carcinoma -- Diagnosis -- Care and treatment, Antigens -- Properties, Polyoma virus -- Genetic aspects, Health care industry
Abstract

A human polyomavirus was recently discovered in Merkel cell carcinoma (MCC) specimens. The Merkel cell polyomavirus (MCPyV) genome undergoes clonal integration into the host cell chromosomes of MCC tumors and expresses small T antigen and truncated large T antigen. Previous studies have consistently reported that MCPyV can be detected in approximately 80% of all MCC tumors. We sought to increase the sensitivity of detection of MCPyV in MCC by developing antibodies capable of detecting large T antigen by immunohistochemistry. In addition, we expanded the repertoire of quantitative PCR primers specific for MCPyV to improve the detection of viral DNA in MCC. Here we report that a novel monoclonal antibody detected MCPyV large T antigen expression in 56 of 58 (97%) unique MCC tumors. PCR analysis specifically detected viral DNA in all 60 unique MCC tumors tested. We also detected inactivating point substitution mutations of TP53 in the two MCC specimens that lacked large T antigen expression and in only 1 of 56 tumors positive for large T antigen. These results indicate that MCPyV is present in MCC tumors more frequently than previously reported and that mutations in TP53 tend to occur in MCC tumors that fail to express MCPyV large T antigen., Introduction Merkel cell carcinoma (MCC) is a rare skin cancer with high risk for metastasis and death (1). MCC has features of a neuroendocrine tumor, with expression of synaptophysin (SYP) [...]

Published
2012
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