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1. Sox7‐positive endothelial progenitors establish coronary arteries and govern ventricular compaction

Author

Chiang, Ivy KN, primary, Humphrey, David, additional, Mills, Richard J, additional, Kaltzis, Peter, additional, Pachauri, Shikha, additional, Graus, Matthew, additional, Saha, Diptarka, additional, Wu, Zhijian, additional, Young, Paul, additional, Sim, Choon Boon, additional, Davidson, Tara, additional, Hernandez‐Garcia, Andres, additional, Shaw, Chad A, additional, Renwick, Alexander, additional, Scott, Daryl A, additional, Porrello, Enzo R, additional, Wong, Emily S, additional, Hudson, James E, additional, Red‐Horse, Kristy, additional, del Monte‐Nieto, Gonzalo, additional, and Francois, Mathias, additional

Published
2023
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2. Combinatorial inhibition of PTPN12-regulated receptors leads to a broadly effective therapeutic strategy in triple-negative breast cancer

Author

Nair, Amritha, Chung, Hsiang-Ching, Sun, Tingting, Tyagi, Siddhartha, Dobrolecki, Lacey E, Dominguez-Vidana, Rocio, Kurley, Sarah J, Orellana, Mayra, Renwick, Alexander, Henke, David M, Katsonis, Panagiotis, Schmitt, Earlene, Chan, Doug W, Li, Hui, Mao, Sufeng, Petrovic, Ivana, Creighton, Chad J, Gutierrez, Carolina, Dubrulle, Julien, Stossi, Fabio, Tyner, Jeffrey W, Lichtarge, Olivier, Lin, Charles Y, Zhang, Bing, Scott, Kenneth L, Hilsenbeck, Susan G, Sun, Jinpeng, Yu, Xiao, Osborne, C Kent, Schiff, Rachel, Christensen, James G, Shields, David J, Rimawi, Mothaffar F, Ellis, Matthew J, Shaw, Chad A, Lewis, Michael T, and Westbrook, Thomas F

Subjects
Cell receptors -- Health aspects, Esterases -- Health aspects, Gene mutation -- Health aspects, Breast cancer -- Genetic aspects -- Development and progression -- Care and treatment, Gene expression -- Health aspects, Biological sciences, Health
Abstract

Author(s): Amritha Nair [1, 2]; Hsiang-Ching Chung [1, 2, 3]; Tingting Sun [1, 2]; Siddhartha Tyagi [1, 2]; Lacey E Dobrolecki [4]; Rocio Dominguez-Vidana [1, 2, 3]; Sarah J Kurley [...]

Published
2018
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3. Supplementary Tables from HER2 Reactivation through Acquisition of the HER2 L755S Mutation as a Mechanism of Acquired Resistance to HER2-targeted Therapy in HER2+ Breast Cancer

Author

Xu, Xiaowei, primary, De Angelis, Carmine, primary, Burke, Kathleen A., primary, Nardone, Agostina, primary, Hu, Huizhong, primary, Qin, Lanfang, primary, Veeraraghavan, Jamunarani, primary, Sethunath, Vidyalakshmi, primary, Heiser, Laura M., primary, Wang, Nicholas, primary, Ng, Charlotte K.Y., primary, Chen, Edward S., primary, Renwick, Alexander, primary, Wang, Tao, primary, Nanda, Sarmistha, primary, Shea, Martin, primary, Mitchell, Tamika, primary, Rajendran, Mahitha, primary, Waters, Ian, primary, Zabransky, Daniel J., primary, Scott, Kenneth L., primary, Gutierrez, Carolina, primary, Nagi, Chandandeep, primary, Geyer, Felipe C., primary, Chamness, Gary C., primary, Park, Ben H., primary, Shaw, Chad A., primary, Hilsenbeck, Susan G., primary, Rimawi, Mothaffar F., primary, Gray, Joe W., primary, Weigelt, Britta, primary, Reis-Filho, Jorge S., primary, Osborne, C. Kent, primary, and Schiff, Rachel, primary

Published
2023
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4. Supplementary information from HER2 Reactivation through Acquisition of the HER2 L755S Mutation as a Mechanism of Acquired Resistance to HER2-targeted Therapy in HER2+ Breast Cancer

Author

Xu, Xiaowei, primary, De Angelis, Carmine, primary, Burke, Kathleen A., primary, Nardone, Agostina, primary, Hu, Huizhong, primary, Qin, Lanfang, primary, Veeraraghavan, Jamunarani, primary, Sethunath, Vidyalakshmi, primary, Heiser, Laura M., primary, Wang, Nicholas, primary, Ng, Charlotte K.Y., primary, Chen, Edward S., primary, Renwick, Alexander, primary, Wang, Tao, primary, Nanda, Sarmistha, primary, Shea, Martin, primary, Mitchell, Tamika, primary, Rajendran, Mahitha, primary, Waters, Ian, primary, Zabransky, Daniel J., primary, Scott, Kenneth L., primary, Gutierrez, Carolina, primary, Nagi, Chandandeep, primary, Geyer, Felipe C., primary, Chamness, Gary C., primary, Park, Ben H., primary, Shaw, Chad A., primary, Hilsenbeck, Susan G., primary, Rimawi, Mothaffar F., primary, Gray, Joe W., primary, Weigelt, Britta, primary, Reis-Filho, Jorge S., primary, Osborne, C. Kent, primary, and Schiff, Rachel, primary

Published
2023
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5. Supplementary Figures from HER2 Reactivation through Acquisition of the HER2 L755S Mutation as a Mechanism of Acquired Resistance to HER2-targeted Therapy in HER2+ Breast Cancer

Author

Xu, Xiaowei, primary, De Angelis, Carmine, primary, Burke, Kathleen A., primary, Nardone, Agostina, primary, Hu, Huizhong, primary, Qin, Lanfang, primary, Veeraraghavan, Jamunarani, primary, Sethunath, Vidyalakshmi, primary, Heiser, Laura M., primary, Wang, Nicholas, primary, Ng, Charlotte K.Y., primary, Chen, Edward S., primary, Renwick, Alexander, primary, Wang, Tao, primary, Nanda, Sarmistha, primary, Shea, Martin, primary, Mitchell, Tamika, primary, Rajendran, Mahitha, primary, Waters, Ian, primary, Zabransky, Daniel J., primary, Scott, Kenneth L., primary, Gutierrez, Carolina, primary, Nagi, Chandandeep, primary, Geyer, Felipe C., primary, Chamness, Gary C., primary, Park, Ben H., primary, Shaw, Chad A., primary, Hilsenbeck, Susan G., primary, Rimawi, Mothaffar F., primary, Gray, Joe W., primary, Weigelt, Britta, primary, Reis-Filho, Jorge S., primary, Osborne, C. Kent, primary, and Schiff, Rachel, primary

Published
2023
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6. The Oncogenic STP Axis Promotes Triple-Negative Breast Cancer via Degradation of the REST Tumor Suppressor

Author

Karlin, Kristen L., Mondal, Gourish, Hartman, Jessica K., Tyagi, Siddhartha, Kurley, Sarah J., Bland, Chris S., Hsu, Tiffany Y.T., Renwick, Alexander, Fang, Justin E., Migliaccio, Ilenia, Callaway, Celetta, Nair, Amritha, Dominguez-Vidana, Rocio, Nguyen, Don X., Osborne, C. Kent, Schiff, Rachel, Yu-Lee, Li-Yuan, Jung, Sung Y., Edwards, Dean P., Hilsenbeck, Susan G., Rosen, Jeffrey M., Zhang, Xiang H.-F., Shaw, Chad A., Couch, Fergus J., and Westbrook, Thomas F.

Published
2014
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7. The spliceosome is a therapeutic vulnerability in MYC-driven cancer

Author

Hsu, Tiffany Y.-T., Simon, Lukas M., Neill, Nicholas J., Marcotte, Richard, Sayad, Azin, Bland, Christopher S., Echeverria, Gloria V., Sun, Tingting, Kurley, Sarah J., Tyagi, Siddhartha, Karlin, Kristen L., Dominguez-Vidaha, Rocio, Hartman, Jessica D., Renwick, Alexander, Scorsone, Kathleen, Bernardi, Ronald J., Skinner, Samuel O., Jain, Antrix, Orellana, Mayra, Lagisetti, Chandraiah, Golding, Ido, Jung, Sung Y., Neilson, Joel R., Zhang, Xiang H.-F., Cooper, Thomas A., Webb, Thomas R., Neel, Benjamin G., Shaw, Chad A., and Westbrook, Thomas F.

Subjects
Gene therapy -- Methods, Cancer -- Care and treatment, Transcription factors, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

MYC (also known as c-MYC) overexpression or hyperactivation is one of the most common drivers of human cancer. Despite intensive study, the MYC oncogene remains recalcitrant to therapeutic inhibition. MYC is a transcription factor, and many of its protumorigenic functions have been attributed to its ability to regulate gene expression programs (1-3). Notably, oncogenic MYC activation has also been shown to increase total RNA and protein production in many tissue and disease contexts (4-7). While such increases in RNA and protein production may endow cancer cells with pro-tumour hallmarks, this increase in synthesis may also generate new or heightened burden on MYC-driven cancer cells to process these macromolecules properly (8). Here we discover that the spliceosome is a new target of oncogenic stress in MYC-driven cancers. We identify BUD31 as a MYC-synthetic lethal gene in human mammary epithelial cells, and demonstrate that BUD31 is a component of the core spliceosome required for its assembly and catalytic activity. Core spliceosomal factors (such as SF3B1 and U2AF1) associated with BUD31 are also required to tolerate oncogenic MYC. Notably, MYC hyperactivation induces an increase in total precursor messenger RNA synthesis, suggesting an increased burden on the core spliceosome to process pre-mRNA. In contrast to normal cells, partial inhibition of the spliceosome in MYC-hyperactivated cells leads to global intron retention, widespread defects in pre-mRNA maturation, and deregulation of many essential cell processes. Notably, genetic or pharmacological inhibition of the spliceosome in vivo impairs survival, tumorigenicity and metastatic proclivity of MYC-dependent breast cancers. Collectively, these data suggest that oncogenic MYC confers a collateral stress on splicing, and that components of the spliceosome may be therapeutic entry points for aggressive MYC-driven cancers., To discover genes and cellular processes required to tolerate oncogenic MYC expression, we previously performed a genome-wide MYC-synthetic lethal screen in human mammary epithelial cells (HMECs) engineered with an inducible [...]

Published
2015

11. DNA dinucleotide evolution in humans: fitting theory to facts

Author

Renwick, Alexander, Davison, Leslea, Spratt, Heidi, King, J. Patrick, and Kimmel, Marek

Subjects
Nucleotides -- Research, Biological sciences
Abstract

We examine length distributions of ~6000 human dinucleotide microsatellite loci, representing chromosomes 1-22, from the GDB database. Under the stepwise mutation model, results from theory and simulation are compared with the empirical data. In both constant and expanding population scenarios, a simple single-step model with parameters chosen to account for the observed variance of microsatellite lengths produces results inconsistent with the observed heterozygosity and the dispersion of length skewness. Complicating the model by allowing a variable mutation rate accounts for the homozygosity, and introducing a small probability of a large mutation step accounts for the dispersion in skewnesses. We discuss these results in light of the long-term evolution of microsatellites.

Published
2001

12. HER2 Reactivation through Acquisition of the HER2 L755S Mutation as a Mechanism of Acquired Resistance to HER2-targeted Therapy in HER2+ Breast Cancer

Author

Xu, Xiaowei, primary, De Angelis, Carmine, additional, Burke, Kathleen A., additional, Nardone, Agostina, additional, Hu, Huizhong, additional, Qin, Lanfang, additional, Veeraraghavan, Jamunarani, additional, Sethunath, Vidyalakshmi, additional, Heiser, Laura M., additional, Wang, Nicholas, additional, Ng, Charlotte K.Y., additional, Chen, Edward S., additional, Renwick, Alexander, additional, Wang, Tao, additional, Nanda, Sarmistha, additional, Shea, Martin, additional, Mitchell, Tamika, additional, Rajendran, Mahitha, additional, Waters, Ian, additional, Zabransky, Daniel J., additional, Scott, Kenneth L., additional, Gutierrez, Carolina, additional, Nagi, Chandandeep, additional, Geyer, Felipe C., additional, Chamness, Gary C., additional, Park, Ben H., additional, Shaw, Chad A., additional, Hilsenbeck, Susan G., additional, Rimawi, Mothaffar F., additional, Gray, Joe W., additional, Weigelt, Britta, additional, Reis-Filho, Jorge S., additional, Osborne, C. Kent, additional, and Schiff, Rachel, additional

Published
2017
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13. Correction: Integrative genomic analysis of the human immune response to influenza vaccination

Author

Franco, Luis M, primary, Bucasas, Kristine L, additional, Wells, Janet M, additional, Niño, Diane, additional, Wang, Xueqing, additional, Zapata, Gladys E, additional, Arden, Nancy, additional, Renwick, Alexander, additional, Yu, Peng, additional, Quarles, John M, additional, Bray, Molly S, additional, Couch, Robert B, additional, Belmont, John W, additional, and Shaw, Chad A, additional

Published
2016
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14. Clonal Evolution of the HER2 L755S Mutation Leads to Acquired HER‐targeted Therapy Resistance That Can Be Reversed by the Irreversible HER1/2 Inhibitor Afatinib

Author

Xu, Xiaowei, primary, Nardone, Agostina, additional, Hu, Huizhong, additional, Qin, Lanfang, additional, Nanda, Sarmistha, additional, Mitchell, Tamika, additional, Shea, Marty, additional, Heiser, Laura, additional, Wang, Nicholas, additional, Covington, Kyle, additional, Chen, Edward, additional, Renwick, Alexander, additional, Wang, Tao, additional, De Angelis, Carmine, additional, Contreras, Alejandro, additional, Gutierrez, Carolina, additional, Fuqua, Suzanne, additional, Chamness, Gary, additional, Shaw, Chad, additional, Wheeler, David, additional, Gray, Joe, additional, Hilsenbeck, Susan, additional, Rimawi, Mothaffar, additional, Osborne, Kent, additional, and Schiff, Rachel, additional

Published
2016
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15. Erratum: Corrigendum: Mutations in the transcriptional repressor REST predispose to Wilms tumor

Author

Mahamdallie, Shazia S, primary, Hanks, Sandra, additional, Karlin, Kristen L, additional, Zachariou, Anna, additional, Perdeaux, Elizabeth R, additional, Ruark, Elise, additional, Shaw, Chad A, additional, Renwick, Alexander, additional, Ramsay, Emma, additional, Yost, Shawn, additional, Elliott, Anna, additional, Birch, Jillian, additional, Capra, Michael, additional, Gray, Juliet, additional, Hale, Juliet, additional, Kingston, Judith, additional, Levitt, Gill, additional, McLean, Thomas, additional, Sheridan, Eamonn, additional, Renwick, Anthony, additional, Seal, Sheila, additional, Stiller, Charles, additional, Sebire, Neil, additional, Westbrook, Thomas F, additional, and Rahman, Nazneen, additional

Published
2016
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16. Mutations in the transcriptional repressor REST predispose to Wilms tumor

Author

Mahamdallie, Shazia S, primary, Hanks, Sandra, additional, Karlin, Kristen L, additional, Zachariou, Anna, additional, R Perdeaux, Elizabeth, additional, Ruark, Elise, additional, Shaw, Chad A, additional, Renwick, Alexander, additional, Ramsay, Emma, additional, Yost, Shawn, additional, Elliott, Anna, additional, Birch, Jillian, additional, Capra, Michael, additional, Gray, Juliet, additional, Hale, Juliet, additional, Kingston, Judith, additional, Levitt, Gill, additional, McLean, Thomas, additional, Sheridan, Eamonn, additional, Renwick, Anthony, additional, Seal, Sheila, additional, Stiller, Charles, additional, Sebire, Neil, additional, Westbrook, Thomas F, additional, and Rahman, Nazneen, additional

Published
2015
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17. Abstract 737: Clonal evolution of the HER2 L755S mutation as a mechanism of acquired HER-targeted therapy resistance

Author

Xu, Xiaowei, primary, Nardone, Agostina, additional, Hu, Huizhong, additional, Qin, Lanfang, additional, Nanda, Sarmistha, additional, Heiser, Laura, additional, Wang, Nicholas, additional, Covington, Kyle, additional, Chen, Edward, additional, Renwick, Alexander, additional, Mitchell, Tamika, additional, Shea, Marty, additional, Wang, Tao, additional, De Angelis, Carmine, additional, Contreras, Alejandro, additional, Gutierrez, Carolina, additional, Fuqua, Suzanne, additional, Chamness, Gary, additional, Shaw, Chad, additional, Li, Marilyn, additional, Wheeler, David, additional, Hilsenbeck, Susan, additional, Rimawi, Mothaffar Fahed, additional, Gray, Joe, additional, Osborne, C.Kent, additional, and Schiff, Rachel, additional

Published
2015
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18. Abstract P5-05-03: Clonal evolution of the HER2 L755S mutation leads to acquired HER-targeted therapy resistance that can be reversed by the irreversible HER1/2 inhibitor afatinib

Author

Xu, Xiaowei, primary, Nardone, Agostina, additional, Hu, Huizhong, additional, Qin, Lanfang, additional, Nanda, Sarmistha, additional, Heiser, Laura M, additional, Wang, Nicholas, additional, Covington, Kyle R, additional, Chen, Edward S, additional, Renwick, Alexander, additional, Wang, Tao, additional, De Angelis, Carmine, additional, Contreras, Alejandro, additional, Gutierrez, Carolina, additional, Fuqua, Suzanne AW, additional, Chamness, Gary C, additional, Shaw, Chad, additional, Wheeler, David A, additional, Gray, Joe W, additional, Hilsenbeck, Susan G, additional, Rimawi, Mothaffar F, additional, Osborne, C Kent, additional, and Schiff, Rachel, additional

Published
2015
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19. Integrative genomic analysis of the human immune response to influenza vaccination

Author

Franco, Luis M, primary, Bucasas, Kristine L, additional, Wells, Janet M, additional, Niño, Diane, additional, Wang, Xueqing, additional, Zapata, Gladys E, additional, Arden, Nancy, additional, Renwick, Alexander, additional, Yu, Peng, additional, Quarles, John M, additional, Bray, Molly S, additional, Couch, Robert B, additional, Belmont, John W, additional, and Shaw, Chad A, additional

Published
2013
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21. Author response: Integrative genomic analysis of the human immune response to influenza vaccination

Author

Franco, Luis M, primary, Bucasas, Kristine L, additional, Wells, Janet M, additional, Niño, Diane, additional, Wang, Xueqing, additional, Zapata, Gladys E, additional, Arden, Nancy, additional, Renwick, Alexander, additional, Yu, Peng, additional, Quarles, John M, additional, Bray, Molly S, additional, Couch, Robert B, additional, Belmont, John W, additional, and Shaw, Chad A, additional

Published
2012
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22. Around the yards.

Author

Renwick, Alexander

Abstract

The article offers news briefs related to boatbuilding. Chief Designer Bob Stephens and his associate Paul Waring of Brooklin Boat Yard Design Associates will design the appointed 90'9" cruising yawl. D. N. Hylan and Associates enters a process of careful restoration for the Aida, a 1926 N. G. Herreshoff keel-centerboard yawl. The North East Maritime Trust has ventured a restoration of Henry Frederick Swan of 1918, a historically significant lifeboat.

Published
2008

23. Corrigendum: Mutations in the transcriptional repressor REST predispose to Wilms tumor

Author

Mahamdallie, Shazia S, Hanks, Sandra, Karlin, Kristen L, Zachariou, Anna, Perdeaux, Elizabeth R, Ruark, Elise, Shaw, Chad A, Renwick, Alexander, Ramsay, Emma, Yost, Shawn, Elliott, Anna, Birch, Jillian, Capra, Michael, Gray, Juliet, Hale, Juliet, Kingston, Judith, Levitt, Gill, McLean, Thomas, Sheridan, Eamonn, Renwick, Anthony, Seal, Sheila, Stiller, Charles, Sebire, Neil, Westbrook, Thomas F, and Rahman, Nazneen

Published
2016
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24. HER2 Reactivation through Acquisition of the HER2 L755S Mutation as a Mechanism of Acquired Resistance to HER2-targeted Therapy in HER2 + Breast Cancer.

Author

Xu X, De Angelis C, Burke KA, Nardone A, Hu H, Qin L, Veeraraghavan J, Sethunath V, Heiser LM, Wang N, Ng CKY, Chen ES, Renwick A, Wang T, Nanda S, Shea M, Mitchell T, Rajendran M, Waters I, Zabransky DJ, Scott KL, Gutierrez C, Nagi C, Geyer FC, Chamness GC, Park BH, Shaw CA, Hilsenbeck SG, Rimawi MF, Gray JW, Weigelt B, Reis-Filho JS, Osborne CK, and Schiff R

Subjects
Afatinib, Animals, Antibodies, Monoclonal, Humanized administration & dosage, Breast Neoplasms genetics, Breast Neoplasms pathology, Cell Line, Tumor, Cell Proliferation drug effects, Female, Humans, Lapatinib, Mice, Mutation, Quinazolines administration & dosage, Quinazolines adverse effects, Receptor, ErbB-2 antagonists & inhibitors, Receptors, Estrogen genetics, Signal Transduction drug effects, Trastuzumab administration & dosage, Trastuzumab adverse effects, Xenograft Model Antitumor Assays, Breast Neoplasms drug therapy, Drug Resistance, Neoplasm genetics, Molecular Targeted Therapy, Receptor, ErbB-2 genetics
Abstract

Purpose: Resistance to anti-HER2 therapies in HER2 + breast cancer can occur through activation of alternative survival pathways or reactivation of the HER signaling network. Here we employed BT474 parental and treatment-resistant cell line models to investigate a mechanism by which HER2 + breast cancer can reactivate the HER network under potent HER2-targeted therapies. Experimental Design: Resistant derivatives to lapatinib (L), trastuzumab (T), or the combination (LR/TR/LTR) were developed independently from two independent estrogen receptor ER + /HER2 + BT474 cell lines (AZ/ATCC). Two derivatives resistant to the lapatinib-containing regimens (BT474/AZ-LR and BT474/ATCC-LTR lines) that showed HER2 reactivation at the time of resistance were subjected to massive parallel sequencing and compared with parental lines. Ectopic expression and mutant-specific siRNA interference were applied to analyze the mutation functionally. In vitro and in vivo experiments were performed to test alternative therapies for mutant HER2 inhibition. Results: Genomic analyses revealed that the HER2 L755S mutation was the only common somatic mutation gained in the BT474/AZ-LR and BT474/ATCC-LTR lines. Ectopic expression of HER2 L755S induced acquired lapatinib resistance in the BT474/AZ, SK-BR-3, and AU565 parental cell lines. HER2 L755S-specific siRNA knockdown reversed the resistance in BT474/AZ-LR and BT474/ATCC-LTR lines. The HER1/2-irreversible inhibitors afatinib and neratinib substantially inhibited both resistant cell growth and the HER2 and downstream AKT/MAPK signaling driven by HER2 L755S in vitro and in vivo Conclusions: HER2 reactivation through acquisition of the HER2 L755S mutation was identified as a mechanism of acquired resistance to lapatinib-containing HER2-targeted therapy in preclinical HER2-amplified breast cancer models, which can be overcome by irreversible HER1/2 inhibitors. Clin Cancer Res; 23(17); 5123-34. ©2017 AACR ., (©2017 American Association for Cancer Research.)

Published
2017
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