Search

Your search keyword '"Mawson, A"' showing total 37 results
Start Over Author "Mawson, A" Journal nature
37 results on '"Mawson, A"'

1. Whole genomes redefine the mutational landscape of pancreatic cancer

Author

Biankin, Andrew V, Johns, Amber L, Mawson, Amanda, Chang, David K, Scarlett, Christopher J, Brancato, Mary-Anne L, Rowe, Sarah J, Simpson, Skye H, Martyn-Smith, Mona, Thomas, Michelle T, Chantrill, Lorraine A, Chin, Venessa T, Chou, Angela, Cowley, Mark J, Humphris, Jeremy L, Jones, Marc D, Scott Mead, R, Nagrial, Adnan M, Pajic, Marina, Pettit, Jessica, Pinese, Mark, Rooman, Ilse, Wu, Jianmin, Tao, Jiang, DiPietro, Renee, Watson, Clare, Steinmann, Angela, Ching Lee, Hong, Wong, Rachel, Pinho, Andreia V, Giry-Laterriere, Marc, Daly, Roger J, Musgrove, Elizabeth A, Sutherland, Robert L, Grimmond, Sean M, Waddell, Nicola, Kassahn, Karin S, Miller, David K, Wilson, Peter J, Patch, Ann-Marie, Song, Sarah, Harliwong, Ivon, Idrisoglu, Senel, Nourse, Craig, Nourbakhsh, Ehsan, Manning, Suzanne, Wani, Shivangi, Gongora, Milena, Anderson, Matthew, Holmes, Oliver, Leonard, Conrad, Taylor, Darrin, Wood, Scott, Xu, Christina, Nones, Katia, Lynn Fink, J, Christ, Angelika, Bruxner, Tim, Cloonan, Nicole, Newell, Felicity, Pearson, John V, Bailey, Peter, Quinn, Michael, Nagaraj, Shivashankar, Kazakoff, Stephen, Waddell, Nick, Krisnan, Keerthana, Quek, Kelly, Wood, David, Fadlullah, Muhammad ZH, Samra, Jaswinder S, Gill, Anthony J, Pavlakis, Nick, Guminski, Alex, Toon, Christopher, Asghari, Ray, Merrett, Neil D, Pavey, Darren, Das, Amitabha, Cosman, Peter H, Ismail, Kasim, O’Connnor, Chelsie, Lam Duncan McLeod, Vincent W, Pleass, Henry C, Richardson, Arthur, James, Virginia, Kench, James G, Cooper, Caroline L, Joseph, David, Sandroussi, Charbel, Crawford, Michael, Gallagher, James, Texler, Michael, Forest, Cindy, Laycock, Andrew, Epari, Krishna P, Ballal, Mo, Fletcher, David R, Mukhedkar, Sanjay, and Spry, Nigel A

Subjects
Cancer, Human Genome, Pancreatic Cancer, Digestive Diseases, Genetics, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Adenocarcinoma, Animals, Carcinoma, Pancreatic Ductal, DNA Mutational Analysis, DNA Repair, Female, Genes, BRCA1, Genes, BRCA2, Genetic Markers, Genome, Human, Genomic Instability, Genomics, Genotype, Humans, Mice, Mutation, Pancreatic Neoplasms, Platinum, Point Mutation, Poly(ADP-ribose) Polymerase Inhibitors, Xenograft Model Antitumor Assays, Australian Pancreatic Cancer Genome Initiative, General Science & Technology
Abstract

Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded.

Published
2015

2. Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes.

Author

Biankin, Andrew, Waddell, Nicola, Kassahn, Karin, Gingras, Marie-Claude, Muthuswamy, Lakshmi, Johns, Amber, Miller, David, Wilson, Peter, Patch, Ann-Marie, Wu, Jianmin, Chang, David, Cowley, Mark, Gardiner, Brooke, Song, Sarah, Harliwong, Ivon, Idrisoglu, Senel, Nourse, Craig, Nourbakhsh, Ehsan, Manning, Suzanne, Wani, Shivangi, Gongora, Milena, Pajic, Marina, Scarlett, Christopher, Gill, Anthony, Pinho, Andreia, Rooman, Ilse, Anderson, Matthew, Holmes, Oliver, Leonard, Conrad, Taylor, Darrin, Wood, Scott, Xu, Qinying, Nones, Katia, Fink, J, Christ, Angelika, Bruxner, Tim, Cloonan, Nicole, Kolle, Gabriel, Newell, Felicity, Pinese, Mark, Mead, R, Humphris, Jeremy, Kaplan, Warren, Jones, Marc, Colvin, Emily, Nagrial, Adnan, Humphrey, Emily, Chou, Angela, Chin, Venessa, Chantrill, Lorraine, Mawson, Amanda, Samra, Jaswinder, Kench, James, Lovell, Jessica, Daly, Roger, Merrett, Neil, Toon, Christopher, Epari, Krishna, Nguyen, Nam, Barbour, Andrew, Zeps, Nikolajs, Kakkar, Nipun, Zhao, Fengmei, Wu, Yuan, Wang, Min, Muzny, Donna, Fisher, William, Brunicardi, F, Hodges, Sally, Reid, Jeffrey, Drummond, Jennifer, Chang, Kyle, Han, Yi, Lewis, Lora, Dinh, Huyen, Buhay, Christian, Beck, Timothy, Timms, Lee, Sam, Michelle, Begley, Kimberly, Brown, Andrew, Pai, Deepa, Panchal, Ami, Buchner, Nicholas, De Borja, Richard, Denroche, Robert, Yung, Christina, Serra, Stefano, Onetto, Nicole, Mukhopadhyay, Debabrata, Tsao, Ming-Sound, Shaw, Patricia, Petersen, Gloria, Gallinger, Steven, Hruban, Ralph, Maitra, Anirban, Iacobuzio-Donahue, Christine, Schulick, Richard, Wolfgang, Christopher, and Morgan, Richard

Subjects
Animals, Axons, Carcinoma, Pancreatic Ductal, Gene Dosage, Gene Expression Regulation, Neoplastic, Genome, Humans, Kaplan-Meier Estimate, Mice, Mutation, Pancreatic Neoplasms, Proteins, Signal Transduction
Abstract

Pancreatic cancer is a highly lethal malignancy with few effective therapies. We performed exome sequencing and copy number analysis to define genomic aberrations in a prospectively accrued clinical cohort (n = 142) of early (stage I and II) sporadic pancreatic ductal adenocarcinoma. Detailed analysis of 99 informative tumours identified substantial heterogeneity with 2,016 non-silent mutations and 1,628 copy-number variations. We define 16 significantly mutated genes, reaffirming known mutations (KRAS, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1), and uncover novel mutated genes including additional genes involved in chromatin modification (EPC1 and ARID2), DNA damage repair (ATM) and other mechanisms (ZIM2, MAP2K4, NALCN, SLC16A4 and MAGEA6). Integrative analysis with in vitro functional data and animal models provided supportive evidence for potential roles for these genetic aberrations in carcinogenesis. Pathway-based analysis of recurrently mutated genes recapitulated clustering in core signalling pathways in pancreatic ductal adenocarcinoma, and identified new mutated genes in each pathway. We also identified frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, which was also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement of axon guidance genes in pancreatic carcinogenesis.

Published
2012

3. Corrigendum: Whole-genome landscape of pancreatic neuroendocrine tumours

Author

Scarpa, Aldo, Chang, David K., Nones, Katia, Corbo, Vincenzo, Patch, Ann-Marie, Bailey, Peter, Lawlor, Rita T., Johns, Amber L., Miller, David K., Mafficini, Andrea, Rusev, Borislav, Scardoni, Maria, Antonello, Davide, Barbi, Stefano, Sikora, Katarzyna O., Cingarlini, Sara, Vicentini, Caterina, McKay, Skye, Quinn, Michael C. J., Bruxner, Timothy J. C., Christ, Angelika N., Harliwong, Ivon, Idrisoglu, Senel, McLean, Suzanne, Nourse, Craig, Nourbakhsh, Ehsan, Wilson, Peter J., Anderson, Matthew J., Fink, Lynn J., Newell, Felicity, Waddell, Nick, Holmes, Oliver, Kazakoff, Stephen H., Leonard, Conrad, Wood, Scott, Xu, Qinying, Nagaraj, Shivashankar Hiriyur, Amato, Eliana, Dalai, Irene, Bersani, Samantha, Cataldo, Ivana, Dei Tos, Angelo P., Capelli, Paola, Davì, Maria Vittoria, Landoni, Luca, Malpaga, Anna, Miotto, Marco, Whitehall, Vicki L. J., Leggett, Barbara A., Harris, Janelle L., Harris, Jonathan, Jones, Marc D., Humphris, Jeremy, Chantrill, Lorraine A., Chin, Venessa, Nagrial, Adnan M., Pajic, Marina, Scarlett, Christopher J., Pinho, Andreia, Rooman, Ilse, Toon, Christopher, Wu, Jianmin, Pinese, Mark, Cowley, Mark, Barbour, Andrew, Mawson, Amanda, Humphrey, Emily S., Colvin, Emily K., Chou, Angela, Lovell, Jessica A., Jamieson, Nigel B., Duthie, Fraser, Gingras, Marie-Claude, Fisher, William E., Dagg, Rebecca A., Lau, Loretta M. S., Lee, Michael, Pickett, Hilda A., Reddel, Roger R., Samra, Jaswinder S., Kench, James G., Merrett, Neil D., Epari, Krishna, Nguyen, Nam Q., Zeps, Nikolajs, Falconi, Massimo, Simbolo, Michele, Butturini, Giovanni, Van Buren, George, Partelli, Stefano, Fassan, Matteo, Khanna, Kum Kum, Gill, Anthony J., Wheeler, David A., Gibbs, Richard A., Musgrove, Elizabeth A., Bassi, Claudio, Tortora, Giampaolo, Pederzoli, Paolo, Pearson, John V., Waddell, Nicola, Biankin, Andrew V., and Grimmond, Sean M.

Published
2017
Full Text
View/download PDF

4. Whole-genome landscape of pancreatic neuroendocrine tumours

Author

Scarpa, Aldo, Chang, David K., Nones, Katia, Corbo, Vincenzo, Patch, Ann-Marie, Bailey, Peter, Lawlor, Rita T., Johns, Amber L., Miller, David K., Mafficini, Andrea, Rusev, Borislav, Scardoni, Maria, Antonello, Davide, Barbi, Stefano, Sikora, Katarzyna O., Cingarlini, Sara, Vicentini, Caterina, McKay, Skye, Quinn, Michael C. J., Bruxner, Timothy J. C., Christ, Angelika N., Harliwong, Ivon, Idrisoglu, Senel, McLean, Suzanne, Nourse, Craig, Nourbakhsh, Ehsan, Wilson, Peter J., Anderson, Matthew J., Fink, Lynn J., Newell, Felicity, Waddell, Nick, Holmes, Oliver, Kazakoff, Stephen H., Leonard, Conrad, Wood, Scott, Xu, Qinying, Nagaraj, Shivashankar Hiriyur, Amato, Eliana, Dalai, Irene, Bersani, Samantha, Cataldo, Ivana, Dei Tos, Angelo P., Capelli, Paola, Davì, Maria Vittoria, Landoni, Luca, Malpaga, Anna, Miotto, Marco, Whitehall, Vicki L. J., Leggett, Barbara A., Harris, Janelle L., Harris, Jonathan, Jones, Marc D., Humphris, Jeremy, Chantrill, Lorraine A., Chin, Venessa, Nagrial, Adnan M., Pajic, Marina, Scarlett, Christopher J., Pinho, Andreia, Rooman, Ilse, Toon, Christopher, Wu, Jianmin, Pinese, Mark, Cowley, Mark, Barbour, Andrew, Mawson, Amanda, Humphrey, Emily S., Colvin, Emily K., Chou, Angela, Lovell, Jessica A., Jamieson, Nigel B., Duthie, Fraser, Gingras, Marie-Claude, Fisher, William E., Dagg, Rebecca A., Lau, Loretta M. S., Lee, Michael, Pickett, Hilda A., Reddel, Roger R., Samra, Jaswinder S., Kench, James G., Merrett, Neil D., Epari, Krishna, Nguyen, Nam Q., Zeps, Nikolajs, Falconi, Massimo, Simbolo, Michele, Butturini, Giovanni, Van Buren, George, Partelli, Stefano, Fassan, Matteo, Khanna, Kum Kum, Gill, Anthony J., Wheeler, David A., Gibbs, Richard A., Musgrove, Elizabeth A., Bassi, Claudio, Tortora, Giampaolo, Pederzoli, Paolo, Pearson, John V., Waddell, Nicola, Biankin, Andrew V., and Grimmond, Sean M.

Published
2017
Full Text
View/download PDF

5. Genomic analyses identify molecular subtypes of pancreatic cancer

Author

Bailey, Peter, Chang, David K., Nones, Katia, Johns, Amber L., Patch, Ann-Marie, Gingras, Marie-Claude, Miller, David K., Christ, Angelika N., Bruxner, Tim J. C., Quinn, Michael C., Nourse, Craig, Murtaugh, Charles L., Harliwong, Ivon, Idrisoglu, Senel, Manning, Suzanne, Nourbakhsh, Ehsan, Wani, Shivangi, Fink, Lynn, Holmes, Oliver, Chin, Venessa, Anderson, Matthew J., Kazakoff, Stephen, Leonard, Conrad, Newell, Felicity, Waddell, Nick, Wood, Scott, Xu, Qinying, Wilson, Peter J., Cloonan, Nicole, Kassahn, Karin S., Taylor, Darrin, Quek, Kelly, Robertson, Alan, Pantano, Lorena, Mincarelli, Laura, Sanchez, Luis N., Evers, Lisa, Wu, Jianmin, Pinese, Mark, Cowley, Mark J., Jones, Marc D., Colvin, Emily K., Nagrial, Adnan M., Humphrey, Emily S., Chantrill, Lorraine A., Mawson, Amanda, Humphris, Jeremy, Chou, Angela, Pajic, Marina, Scarlett, Christopher J., Pinho, Andreia V., Giry-Laterriere, Marc, Rooman, Ilse, Samra, Jaswinder S., Kench, James G., Lovell, Jessica A., Merrett, Neil D., Toon, Christopher W., Epari, Krishna, Nguyen, Nam Q., Barbour, Andrew, Zeps, Nikolajs, Moran-Jones, Kim, Jamieson, Nigel B., Graham, Janet S., Duthie, Fraser, Oien, Karin, Hair, Jane, Grützmann, Robert, Maitra, Anirban, Iacobuzio-Donahue, Christine A., Wolfgang, Christopher L., Morgan, Richard A., Lawlor, Rita T., Corbo, Vincenzo, Bassi, Claudio, Rusev, Borislav, Capelli, Paola, Salvia, Roberto, Tortora, Giampaolo, Mukhopadhyay, Debabrata, Petersen, Gloria M., Munzy, Donna M., Fisher, William E., Karim, Saadia A., Eshleman, James R., Hruban, Ralph H., Pilarsky, Christian, Morton, Jennifer P., Sansom, Owen J., Scarpa, Aldo, Musgrove, Elizabeth A., Bailey, Ulla-Maja Hagbo, Hofmann, Oliver, Sutherland, Robert L., Wheeler, David A., Gill, Anthony J., Gibbs, Richard A., Pearson, John V., Waddell, Nicola, Biankin, Andrew V., and Grimmond, Sean M.

Published
2016
Full Text
View/download PDF

6. Whole genomes redefine the mutational landscape of pancreatic cancer

Author

Waddell, Nicola, Pajic, Marina, Patch, Ann-Marie, Chang, David K., Kassahn, Karin S., Bailey, Peter, Johns, Amber L., Miller, David, Nones, Katia, Quek, Kelly, Quinn, Michael C. J., Robertson, Alan J., Fadlullah, Muhammad Z. H., Bruxner, Tim J. C., Christ, Angelika N., Harliwong, Ivon, Idrisoglu, Senel, Manning, Suzanne, Nourse, Craig, Nourbakhsh, Ehsan, Wani, Shivangi, Wilson, Peter J., Markham, Emma, Cloonan, Nicole, Anderson, Matthew J., Fink, Lynn J., Holmes, Oliver, Kazakoff, Stephen H., Leonard, Conrad, Newell, Felicity, Poudel, Barsha, Song, Sarah, Taylor, Darrin, Waddell, Nick, Wood, Scott, Xu, Qinying, Wu, Jianmin, Pinese, Mark, Cowley, Mark J., Lee, Hong C., Jones, Marc D., Nagrial, Adnan M., Humphris, Jeremy, Chantrill, Lorraine A., Chin, Venessa, Steinmann, Angela M., Mawson, Amanda, Humphrey, Emily S., Colvin, Emily K., Chou, Angela, Scarlett, Christopher J., Pinho, Andreia V., Giry-Laterriere, Marc, Rooman, Ilse, Samra, Jaswinder S., Kench, James G., Pettitt, Jessica A., Merrett, Neil D., Toon, Christopher, Epari, Krishna, Nguyen, Nam Q., Barbour, Andrew, Zeps, Nikolajs, Jamieson, Nigel B., Graham, Janet S., Niclou, Simone P., Bjerkvig, Rolf, Grützmann, Robert, Aust, Daniela, Hruban, Ralph H., Maitra, Anirban, Iacobuzio-Donahue, Christine A., Wolfgang, Christopher L., Morgan, Richard A., Lawlor, Rita T., Corbo, Vincenzo, Bassi, Claudio, Falconi, Massimo, Zamboni, Giuseppe, Tortora, Giampaolo, Tempero, Margaret A., Gill, Anthony J., Eshleman, James R., Pilarsky, Christian, Scarpa, Aldo, Musgrove, Elizabeth A., Pearson, John V., Biankin, Andrew V., Grimmond, Sean M., Brancato, Mary-Anne L., Rowe, Sarah J., Simpson, Skye H., Martyn-Smith, Mona, Thomas, Michelle T., Chin, Venessa T., Humphris, Jeremy L., Mead, Scott R., Pettit, Jessica, Tao, Jiang, DiPietro, Renee, Watson, Clare, Steinmann, Angela, Lee, Hong Ching, Wong, Rachel, Daly, Roger J., Sutherland, Robert L., Miller, David K., Gongora, Milena, Anderson, Matthew, Xu, Christina, Christ, Angelika, Bruxner, Tim, Quinn, Michael, Nagaraj, Shivashankar, Kazakoff, Stephen, Krisnan, Keerthana, Wood, David, Pavlakis, Nick, Guminski, Alex, Asghari, Ray, Pavey, Darren, Das, Amitabha, Cosman, Peter H., Ismail, Kasim, OʼConnnor, Chelsie, Lam Duncan McLeod, Vincent W., Pleass, Henry C., Richardson, Arthur, James, Virginia, Cooper, Caroline L., Joseph, David, Sandroussi, Charbel, Crawford, Michael, Gallagher, James, Texler, Michael, Forest, Cindy, Laycock, Andrew, Epari, Krishna P., Ballal, Mo, Fletcher, David R., Mukhedkar, Sanjay, Spry, Nigel A., DeBoer, Bastiaan, Chai, Ming, Beilin, Maria, Feeney, Kynan, Nguyen, Nan Q., Ruszkiewicz, Andrew R., Worthley, Chris, Tan, Chuan P., Debrencini, Tamara, Chen, John, Brooke-Smith, Mark E., Papangelis, Virginia, Tang, Henry, Barbour, Andrew P., Clouston, Andrew D., Martin, Patrick, OʼRourke, Thomas J., Chiang, Amy, Fawcett, Jonathan W., Slater, Kellee, Yeung, Shinn, Hatzifotis, Michael, Hodgkinson, Peter, Christophi, Christopher, Nikfarjam, Mehrdad, Mountain, Angela, Schulick, Richard D., Hodgin, Mary, Beghelli, Stefania, Scardoni, Maria, Oien, Karen, and Hair, Jane

Published
2015
Full Text
View/download PDF

7. The deubiquitinase USP9X suppresses pancreatic ductal adenocarcinoma

Author

Pérez-Mancera, Pedro A., Rust, Alistair G., van der Weyden, Louise, Kristiansen, Glen, Li, Allen, Sarver, Aaron L., Silverstein, Kevin A. T., Grützmann, Robert, Aust, Daniela, Rümmele, Petra, Knösel, Thomas, Herd, Colin, Stemple, Derek L., Kettleborough, Ross, Brosnan, Jacqueline A., Li, Ang, Morgan, Richard, Knight, Spencer, Yu, Jun, Stegeman, Shane, Collier, Lara S., ten Hoeve, Jelle J., de Ridder, Jeroen, Klein, Alison P., Goggins, Michael, Hruban, Ralph H., Chang, David K., Biankin, Andrew V., Grimmond, Sean M., Johns, Amber L., Mawson, Amanda, Brancato, Mary-Anne L., Rowe, Sarah J., Simpson, Skye L., Martyn-Smith, Mona, Chantrill, Lorraine A., Chin, Venessa T., Chou, Angela, Cowley, Mark J., Humphris, Jeremy L., Jones, Marc D., Mead, Scott R., Nagrial, Adnan M., Pajic, Marina, Pettit, Jessica, Pinese, Mark, Rooman, Ilse, Wu, Jianmin, Daly, Roger J., Musgrove, Elizabeth A., Sutherland, Robert L., Waddell, Nicola, Kassahn, Karin S., Miller, David K., Wilson, Peter J., Patch, Ann-Marie, Song, Sarah, Harliwong, Ivon, Idrisoglu, Senel, Nourse, Craig, Nourbakhsh, Ehsan, Manning, Suzanne, Wani, Shivangi, Gongora, Milena, Anderson, Matthew, Holmes, Oliver, Leonard, Conrad, Taylor, Darrin, Wood, Scott, Xu, Christina, Nones, Katia, Fink, Lynn J., Christ, Angelika, Bruxner, Tim, Cloonan, Nicole, Newell, Felicity, Pearson, John V., Samra, Jaswinder S., Gill, Anthony J., Pavlakis, Nick, Guminski, Alex, Toon, Christopher, Blankin, Andrew V., Asghari, Ray, Merrett, Neil D., Pavey, Darren A., Das, Amithabad, Cosman, Peter H., Ismail, Kasim, O’Connor, Chelsie, Lam, Vincent W., McLeod, Duncan, Pleass, Henry C., James, Virginia, Kench, James G., Cooper, Caroline L., Joseph, David, Sandroussi, Charbel, Crawford, Michael, Texler, Michael, Forrest, Cindy, Laycock, Andrew, Epari, Krishna P., Ballal, Mo, Fletcher, David R., Mukhedkar, Sanjay, Spry, Nigel A., DeBoer, Bastiaan, Chai, Ming, Feeney, Kynan, Zeps, Nikolajs, Beilin, Maria, Nguyen, Nam Q., Ruszkiewicz, Andrew R., Worthley, Chris, Tan, Chuan P., Debrencini, Tamara, Chen, John, Brooke-Smith, Mark E., Papangelis, Virginia, Tang, Henry, Barbour, Andrew P., Clouston, Andrew D., Martin, Patrick, O’Rourke, Thomas J., Chiang, Amy, Fawcett, Jonathan W., Slater, Kellee, Yeung, Shinn, Hatzifotis, Michael, Hodgkinson, Peter, Christophi, Christopher, Nikfarjam, Mehrdad, Biobank, Victorian Cancer, Eshleman, James R., Maitra, Anirban, Iacobuzio-Donahue, Christine A., Schulick, Richard D., Wolfgang, Christopher L., Morgan, Richard A., Lawlor, Rita T., Beghelli, Stefania, Corbo, Vincenzo, Scardoni, Maria, Bassi, Claudio, Tempero, Margaret A., Wessels, Lodewyk F. A., Wood, Stephen A., Pilarsky, Christian, Largaespada, David A., Adams, David J., and Tuveson, David A.

Published
2012
Full Text
View/download PDF

8. The dispersion-brightness relation for fast radio bursts from a wide-field survey

Author

Ron Ekers, Jordan D. Collier, Ryan Shannon, Maxim Voronkov, A. Brown, Aaron Chippendale, E. R. Troup, Hao Qiu, C. J. Riseley, Elaine M. Sadler, G. Gürkan, Matthew Whiting, C. Haskins, Mawson W. Sammons, C. S. Anderson, John D. Bunton, Keith W. Bannister, Aidan Hotan, J. Tuthill, David McConnell, George Heald, Jean-Pierre Macquart, M. Marquarding, Martin Bell, M. Leach, Ron Beresford, C. W. James, Stefan Oslowski, James R. Allison, and M. A. Pilawa

Subjects
Physics, Brightness, education.field_of_study, Multidisciplinary, 010308 nuclear & particles physics, Fast radio burst, High-energy astronomy, Canadian Hydrogen Intensity Mapping Experiment, Astrophysics::High Energy Astrophysical Phenomena, Population, Astrophysics, Astrophysics::Cosmology and Extragalactic Astrophysics, 01 natural sciences, 0103 physical sciences, Radio frequency, education, 010303 astronomy & astrophysics, Time domain astronomy, Dwarf galaxy
Abstract

Despite considerable efforts over the past decade, only 34 fast radio bursts—intense bursts of radio emission from beyond our Galaxy—have been reported1,2. Attempts to understand the population as a whole have been hindered by the highly heterogeneous nature of the searches, which have been conducted with telescopes of different sensitivities, at a range of radio frequencies, and in environments corrupted by different levels of radio-frequency interference from human activity. Searches have been further complicated by uncertain burst positions and brightnesses—a consequence of the transient nature of the sources and the poor angular resolution of the detecting instruments. The discovery of repeating bursts from one source3, and its subsequent localization4 to a dwarf galaxy at a distance of 3.7 billion light years, confirmed that the population of fast radio bursts is located at cosmological distances. However, the nature of the emission remains elusive. Here we report a well controlled, wide-field radio survey for these bursts. We found 20, none of which repeated during follow-up observations between 185–1,097 hours after the initial detections. The sample includes both the nearest and the most energetic bursts detected so far. The survey demonstrates that there is a relationship between burst dispersion and brightness and that the high-fluence bursts are the nearby analogues of the more distant events found in higher-sensitivity, narrower-field surveys5.

Published
2018

9. Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes

Author

Conrad Leonard, Stefano Serra, Jeremy L. Humphris, J. Lynn Fink, Vincenzo Corbo, Deepa Pai, Ami Panchal, Jennifer Drummond, Anirban Maitra, Katia Nones, Mark J. Cowley, Nam Q. Nguyen, Marc D. Jones, David A. Largaespada, Karen M. Mann, Ralph H. Hruban, Nicole Cloonan, Timothy Beck, Marie-Claude Gingras, Sally E. Hodges, Darrin Taylor, Andrew V. Biankin, Angela Chou, Craig Nourse, Marina Pajic, Gloria M. Petersen, Kimberly Begley, Richard A. Morgan, Rita T. Lawlor, Senel Idrisoglu, Jessica A. Lovell, Lincoln Stein, Christina K. Yung, Lee Timms, Adnan Nagrial, Giampaolo Tortora, Shivangi Wani, Mark Pinese, Angelika N. Christ, Amanda Mawson, Neil D. Merrett, Maria Scardoni, Min Wang, Ann-Marie Patch, Steven Gallinger, Huyen Dinh, Richard A. Gibbs, John Douglas Mcpherson, Amber L. Johns, Nipun Kakkar, David A. Wheeler, Andrew Barbour, Patricia Shaw, Milena Gongora, Emily S. Humphrey, Christopher J. Scarlett, Matthew J. Anderson, Lodewyk F. A. Wessels, Andrew M.K. Brown, Christopher W. Toon, Felicity Newell, Margaret A. Tempero, Fengmei Zhao, Richard D. Schulick, Paola Capelli, Timothy J. C. Bruxner, Christine A. Iacobuzio-Donahue, Ivon Harliwong, Richard de Borja, Pedro A. Perez-Mancera, Jianmin Wu, Emily K. Colvin, Michelle Sam, Warren Kaplan, Debabrata Mukhopadhyay, John V. Pearson, Gabriel Kolle, Oliver Holmes, Lorraine A. Chantrill, Lora Lewis, Jaswinder S. Samra, Scott Wood, Lakshmi Muthuswamy, James R. Eshleman, Neal G. Copeland, Peter Wilson, David Miller, Anthony J. Gill, Qinying Xu, Nicola Waddell, Ming-Sound Tsao, Karin S. Kassahn, Venessa T. Chin, James G. Kench, David K. Chang, William E. Fisher, Kyle Chang, Aldo Scarpa, Christopher L. Wolfgang, Roger J. Daly, Alistair G. Rust, Ehsan Nourbakhsh, Jeffrey G. Reid, Nikolajs Zeps, Nicole Onetto, Donna M. Muzny, Brooke Gardiner, Robert E. Denroche, Yuan Qing Wu, Nancy A. Jenkins, Sean M. Grimmond, R. Scott Mead, David A. Tuveson, David J. Adams, Yi Han, F. Charles Brunicardi, Andreia V. Pinho, Elizabeth A. Musgrove, Sarah Song, Ilse Rooman, Thomas J. Hudson, Christian J. Buhay, Robert L. Sutherland, Suzanne Manning, Nicholas Buchner, Krishna Epari, Basic (bio-) Medical Sciences, and Laboratory for Medical and Molecular Oncology

Subjects
Exome sequencing, Gene Dosage, Copy number analysis, PDAC, KRAS, Kaplan-Meier Estimate, Biology, medicine.disease_cause, Mice, CDKN2A, Pancreatic cancer, medicine, Animals, Humans, Genetics, Mutation, Genome, Multidisciplinary, Proteins, Cancer, medicine.disease, Axons, Gene Expression Regulation, Neoplastic, Pancreatic Neoplasms, Cancer research, Carcinogenesis, Carcinoma, Pancreatic Ductal, Signal Transduction
Abstract

Pancreatic cancer is a highly lethal malignancy with few effective therapies. We performed exome sequencing and copy number analysis to define genomic aberrations in a prospectively accrued clinical cohort (n = 142) of early (stage I and II) sporadic pancreatic ductal adenocarcinoma. Detailed analysis of 99 informative tumours identified substantial heterogeneity with 2,016 non-silent mutations and 1,628 copy-number variations. We define 16 significantly mutated genes, reaffirming known mutations (KRAS, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1), and uncover novel mutated genes including additional genes involved in chromatin modification (EPC1 and ARID2), DNA damage repair (ATM) and other mechanisms (ZIM2, MAP2K4, NALCN, SLC16A4 and MAGEA6). Integrative analysis with in vitro functional data and animal models provided supportive evidence for potential roles for these genetic aberrations in carcinogenesis. Pathway-based analysis of recurrently mutated genes recapitulated clustering in core signalling pathways in pancreatic ductal adenocarcinoma, and identified new mutated genes in each pathway. We also identified frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, which was also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement of axon guidance genes in pancreatic carcinogenesis.

Published
2012

10. Genomic analyses identify molecular subtypes of pancreatic cancer

Author

J. Lynn Fink, Jeremy L. Humphris, Katia Nones, Robert Grützmann, Anirban Maitra, Paola Capelli, Peter J. Wilson, William E. Fisher, Aldo Scarpa, Christopher J. Scarlett, Richard A. Morgan, Ann-Marie Patch, Debabrata Mukhopadhyay, Murtaugh Lc, Oliver Hofmann, Marc Giry-Laterriere, Borislav Rusev, Jennifer P. Morton, Nicole Cloonan, David A. Wheeler, Anthony J. Gill, Krishna Epari, Nam Q. Nguyen, Amber L. Johns, James G. Kench, Saadia A. Karim, Lorena Pantano, Craig Nourse, Nigel B. Jamieson, Ivon Harliwong, Stephen H. Kazakoff, Darrin Taylor, Felicity Newell, Christian Pilarsky, Giampaolo Tortora, Shivangi Wani, Nicola Waddell, Mark J. Cowley, Jaswinder S. Samra, Scott Wood, Munzy Dm, Conrad Leonard, Laura Mincarelli, Suzanne Manning, Timothy J. C. Bruxner, Mark Pinese, Michael C.J. Quinn, Hair J, Andreia V. Pinho, R. L. Sutherland, Amanda Mawson, Neil D. Merrett, Andrew Barbour, Rita T. Lawlor, Jones, Corbo, Ilse Rooman, Lorraine A. Chantrill, Marie-Claude Gingras, Christopher W. Toon, Senel Idrisoglu, Emily S. Humphrey, Kelly Quek, Sean M. Grimmond, Christopher L. Wolfgang, Oliver Holmes, Andrew V. Biankin, Fraser Duthie, Qinying Xu, Kim Moran-Jones, Gloria M. Petersen, Lisa Evers, Peter Bailey, Elizabeth A. Musgrove, Alan J. Robertson, Marina Pajic, Emily K. Colvin, John V. Pearson, Nikolajs Zeps, David K. Chang, Karin S. Kassahn, David Miller, Janet Graham, Ehsan Nourbakhsh, Ralph H. Hruban, Luis Navarro Sanchez, Ulla-Maja Bailey, Chin, Jessica A. Lovell, Angelika N. Christ, Richard A. Gibbs, Eshleman, Karin A. Oien, Christine A. Iacobuzio-Donahue, Claudio Bassi, Adnan Nagrial, Matthew J. Anderson, Owen J. Sansom, Angela Chou, Roberto Salvia, Jianmin Wu, Cell Differentiation, Basic (bio-) Medical Sciences, and Laboratory for Medical and Molecular Oncology

Subjects
0301 basic medicine, Transcription, Genetic, Receptors, Cytoplasmic and Nuclear, medicine.disease_cause, Transcriptome, Mice, 0302 clinical medicine, RNA-SEQ DATA, DUCTAL ADENOCARCINOMA, NETWORK ANALYSIS, EXPRESSION DATA, CELL FORMATION, BREAST-CANCER, MUTATIONS, PACKAGE, TUMOR, DIFFERENTIATION, Basic Helix-Loop-Helix Transcription Factors, Gene Regulatory Networks, Regulation of gene expression, Histone Demethylases, Multidisciplinary, Wnt signaling pathway, Nuclear Proteins, Genomics, Prognosis, DNA-Binding Proteins, Gene Expression Regulation, Neoplastic, Homeobox Protein Nkx-2.2, 030220 oncology & carcinogenesis, DNA methylation, Hepatocyte Nuclear Factor 3-beta, PDX1, KRAS, Carcinoma, Pancreatic Ductal, Biology, 03 medical and health sciences, Downregulation and upregulation, Pancreatic cancer, Cell Line, Tumor, medicine, Animals, Humans, Homeodomain Proteins, Settore MED/06 - ONCOLOGIA MEDICA, Genome, Human, Tumor Suppressor Proteins, DNA Methylation, Zebrafish Proteins, medicine.disease, Molecular biology, Survival Analysis, Pancreatic Neoplasms, 030104 developmental biology, Mutation, Trans-Activators, Tumor Suppressor Protein p53, Hepatocyte Nuclear Factor 3-gamma, Genes, Neoplasm, Transcription Factors
Abstract

Integrated genomic analysis of 456 pancreatic ductal adenocarcinomas identified 32 recurrently mutated genes that aggregate into 10 pathways: KRAS, TGF-β, WNT, NOTCH, ROBO/SLIT signalling, G1/S transition, SWI-SNF, chromatin modification, DNA repair and RNA processing. Expression analysis defined 4 subtypes: (1) squamous; (2) pancreatic progenitor; (3) immunogenic; and (4) aberrantly differentiated endocrine exocrine (ADEX) that correlate with histopathological characteristics. Squamous tumours are enriched for TP53 and KDM6A mutations, upregulation of the TP63∆N transcriptional network, hypermethylation of pancreatic endodermal cell-fate determining genes and have a poor prognosis. Pancreatic progenitor tumours preferentially express genes involved in early pancreatic development (FOXA2/3, PDX1 and MNX1). ADEX tumours displayed upregulation of genes that regulate networks involved in KRAS activation, exocrine (NR5A2 and RBPJL), and endocrine differentiation (NEUROD1 and NKX2-2). Immunogenic tumours contained upregulated immune networks including pathways involved in acquired immune suppression. These data infer differences in the molecular evolution of pancreatic cancer subtypes and identify opportunities for therapeutic development.

Published
2015

11. Erratum: Corrigendum: Whole-genome landscape of pancreatic neuroendocrine tumours

Author

Irene Dalai, Conrad Leonard, Eliana Amato, Andrew B. Barbour, Marc D. Jones, Rita T. Lawlor, Andreia V. Pinho, Amanda Mawson, Neil D. Merrett, Caterina Vicentini, Matteo Fassan, Ivon Harliwong, J. Lynn Fink, Giovanni Butturini, Anthony J. Gill, David Miller, Senel Idrisoglu, James G. Kench, Andrew V. Biankin, Ilse Rooman, Angela Chou, Marie-Claude Gingras, Katia Nones, Venessa T. Chin, Marco Miotto, Davide Antonello, Borislav Rusev, Paola Capelli, Rebecca A. Dagg, Christopher W. Toon, Jeremy L. Humphris, Samantha Bersani, David K. Chang, Nigel B. Jamieson, George Van Buren, Vincenzo Corbo, Jaswinder S. Samra, Stephen H. Kazakoff, Scott Wood, Claudio Bassi, Emily K. Colvin, Stefano Barbi, Amber L. Johns, Christopher J. Scarlett, Nicola Waddell, Jianmin Wu, Michael Lee, Michele Simbolo, Luca Landoni, Katarzyna O. Sikora, Michael C.J. Quinn, John V. Pearson, Nam Q. Nguyen, Angelo Paolo Dei Tos, Mark J. Cowley, Adnan Nagrial, Peter Bailey, Roger R. Reddel, Sean M. Grimmond, Peter Wilson, Skye McKay, Richard A. Gibbs, Jessica A. Lovell, Nikolajs Zeps, Kum Kum Khanna, Stefano Partelli, Timothy J. C. Bruxner, Janelle L. Harris, Andrea Mafficini, Barbara A. Leggett, Angelika N. Christ, Oliver Holmes, Craig Nourse, Krishna Epari, Felicity Newell, Ivana Cataldo, Paolo Pederzoli, Vicki L. J. Whitehall, Matthew J. Anderson, William E. Fisher, Maria Scardoni, Loretta Lau, Massimo Falconi, Ann-Marie Patch, Aldo Scarpa, Lorraine A. Chantrill, Shivashankar H. Nagaraj, Giampaolo Tortora, Sara Cingarlini, Elizabeth A. Musgrove, Ehsan Nourbakhsh, Maria Vittoria Davì, David A. Wheeler, Suzanne McLean, Fraser Duthie, Qinying Xu, Mark Pinese, Anna Malpaga, Nick Waddell, Emily S. Humphrey, Jonathan M. Harris, Marina Pajic, and Hilda A. Pickett

Subjects
0301 basic medicine, 03 medical and health sciences, 030104 developmental biology, Multidisciplinary, Breakpoint, RNA splicing, Computational biology, Biology, Genome
Abstract

Nature 543, 65–71 (2017); doi:10.1038/nature21063 It has been brought to our attention that in Fig. 2d of this Article, an incorrect Sanger trace was used to represent the breakpoint of the EWSR1 and FLI1 type 2 fusion. This was due to an error during manuscript preparation, when we inadvertently inserted the electrophoretic trace referring to EWSR1 splicing variants.

Published
2017

23. Stability of Ascorbic Acid in Metaphosphoric Acid Extracts

Author

C. A. Mawson and L. W. Mapson

Subjects
Multidisciplinary, Chromatography, Biochemistry, Metaphosphoric acid, Chemistry, Titration, Ascorbic acid
Abstract

IT is frequently impossible to perform an analysis of ascorbic acid in foods immediately after sampling. In some cases a delay of as long as 24 hours is unavoidable, and doubts have arisen as to the reliability of the results then obtained. Most analysts now employ metaphosphoric acid or a mixture of metaphosphoric and trichloroacetic acids as the extractant, when determining ascorbic acid by titration against 2,6-dichlorophenolindophenol. We have accordingly investigated the rate of oxidation of ascorbic acid in 5 per cent metaphosphoric acid solution and in a mixture containing 2 per cent metaphosphoric acid and 5 per cent trichloroacetic acids. The solutions were pure ascorbic acid and extracts of cabbage, potato and swede.

Published
1943

24. Sulphonamides and Potato Starch Refection in the Rat

Author

Kathleen M. Henry, E. H. Mawson, J. E. Stanier, S. Y. Thompson, M. E. Coates, P. M. Kon, and S. K. Kon

Subjects
Sulfonamides, Multidisciplinary, biology, Chemistry, Microorganism, Retinol, Starch, Riboflavin, Vitamins, Cod liver oil, biology.organism_classification, Rats, Excretion, Caecum, chemistry.chemical_compound, Sulfanilamide, Biochemistry, Casein, Sulfanilamides, Vitamin B Complex, Animals, Food science, Feces, Solanum tuberosum
Abstract

IN the last few years much work has been done, mostly in the United States, on the effect of sulphonamide drugs on the synthetic activities of intestinal bacteria. These studies have yielded valuable information about the synthesis of vitamins and other substances in the gut and their availability to the host. As experimental animals, rats receiving purified diets supplemented with various vitamins have been largely used. It has occurred to us that rats displaying the phenomenon of refection1,2,3, that is, the ability to grow and thrive in the absence of the vitamin B complex from the diet, would be particularly suitable for such work. Refected rats are entirely dependent on their symbiotic microflora for the supply of certain essential factors ; any interference, therefore, with the activities of these microorganisms can be easily detected. In the absence of an exogenous supply, metabolic balances of vitamin synthesis and utilization become possible with refected animals. Finally, refection renders rats in some respects akin to ruminants4, and a study of digestive phenomena in the refected rat may help to throw some light on these processes in the bovine.

Published
1946

27. Nature of the Causative Agent of the Rous Fowl Sarcoma

Author

E. M. Fraenkel and C. A. Mawson

Subjects
Rous sarcoma virus, Multidisciplinary, biology, viruses, Cancer, Virus diseases, Causative, Working hypothesis, biology.organism_classification, medicine.disease, Virology, Virus, chemistry.chemical_compound, chemistry, medicine, Sarcoma, Vaccinia
Abstract

THE opinions of workers in the field of Rous sarcoma are divided into two schools, one of which uses as a working hypothesis the suggestion of Fraenkel1 that the agent is a pure chemical substance or a virus-enzyme, while the other considers it to be a particle resembling a virus. These opinions are represented by two quotations from recent publications. Murphy2 states that ” Without proof that normal tissues harbour the cancer virus, a fantastic conception and one difficult of experimental test, the virus theory for the etiology of cancer appears untenable. The only proved relationship is that a virus may act as a carcinogenic agent in initiating changes leading to malignancy, but has no part in the formal genesis of neoplasms.” Against this may be set the contention of Amies3 that ” The total evidence seems, therefore, sufficiently strong to justify the conclusion that the tumour agents exist in the form of elementary bodies similar to but somewhat smaller than those which represent the causal agents of such typical virus diseases as Vaccinia and Fowl-Pox”.

Published
1937

28. Carbonic Anhydrase, Sulphonamides and Shell Formation in the Domestic Fowl

Author

C. A. Mawson, R. Benesch, and N. S. Barron

Subjects
Multidisciplinary, biology, Fowl, Carbonic anhydrase activity, biology.organism_classification, Uterine epithelium, chemistry.chemical_compound, chemistry, Biochemistry, Carbonic anhydrase, Pyridine, biology.protein, Oviduct, Secretion, Ultraviolet radiation
Abstract

Meldrum and Roughton1 were the first to advance the hypothesis that carbonic anhydrase might play a part in egg-shell formation by influencing the rate of formation of the anion of calcium carbonate by catalysis of the reaction CO2 + H2O = H2CO3. Following up this suggestion, Common2 examined the tissues of the hen's oviduct for their carbonic anhydrase activity, and concluded "that the carbonic anhydrase activity of the uterine epithelium is higher than that of the remaining oviducal tissues, and that this activity may play a part in shell secretion". On the other hand, it has been demonstrated by Keilin and Mann3 that compounds of the RSO2NH2type (where R is a benzene, naphthalene or pyridine ring) specifically inhibit carbonic anhydrase in very small concentrations. This property, however, is absent in all such compounds in which the sulphonamide group is substituted, as it is, for example, in sulphapyridine or sulphathiazole.

Published
1944

29. Influence of Ethylenediamine-tetra-acetic Acid on the Excretion of Zinc by the Rat

Author

P. V. Elcoate, C. A. Mawson, M. J. Millar, and M. I. Fischer

Subjects
Multidisciplinary, Inorganic chemistry, chemistry.chemical_element, Biological Transport, Ethylenediamine, Zinc, Metabolism, Acetates, Calcium, Body Fluids, Rats, Metal, Excretion, Leadership, Acetic acid, chemistry.chemical_compound, chemistry, visual_art, visual_art.visual_art_medium, Animals, Chelation, Edetic Acid, Nuclear chemistry
Abstract

THE administration of ethylenediamine-tetra-acetic acid (versene, sequestrene) causes increased urinary excretion of calcium, iron, lead and other metallic ions1. We became interested in this chelating agent as a possible means for reducing zinc stores and thus hastening the onset of deficiency in rats maintained on a diet low in zinc. Information on the effect of ethylenediamine-tetra-acetic acid on zinc metabolism was also required in planning an investigation of the excretion of recently absorbed zinc-65. Stability constants indicate2 that zinc forms one of the most stable complexes with ethylenediamine-tetra-acetic acid, but we are not aware of any previous experiments to test its action on body stores of zinc, apart from a brief reference to unpublished work by Mager3.

Published
1954

31. Zinc Content of the Genital Organs of the Rat

Author

C. A. Mawson and M. I. Fischer

Subjects
medicine.medical_specialty, Multidisciplinary, Horse, chemistry.chemical_element, Anatomy, Zinc, Biology, Epididymis, Rats, medicine.anatomical_structure, Seminal vesicle, Endocrinology, chemistry, Prostate, Internal medicine, medicine, Human testis, Animals, Sex organ, Genitalia, Male genital organs
Abstract

IN a recent review, Vallee and Altschule1 have suggested that though many workers have estimated zinc in living tissues, the methods used have often been inaccurate. We have estimated the zinc content of certain tissues of the Collip hooded rat by the dithizone method of Vallee and Gibson2. Mature animals were used which were fed on a diet of fox chow containing about 75 µgm. zinc per gm., supplemented with carrot and cabbage. Most tissues contained about 15–30 µgm. zinc per gm.; but certain male genital organs showed wide deviations from this range. The literature contains few references to the zinc content of the genital system, though Bertrand and Vladesco3 reported high results in herring's and horse's testis, pig's seminal vesicle, rat's epididymis and in the prostate of the bull and of man. Kadota4 mentioned briefly that zinc could be detected by a relatively insensitive histochemical method in the rabbit prostate. The figures given by Leiner and Leiner5 for rat's testis and by Eggleton6 for human testis were within the usual range for soft mammalian tissues.

Published
1951

32. Meaning of ‘Turnover’ in Biochemistry

Author

C. A. Mawson

Subjects
Multidisciplinary, Biochemical Phenomena, Terminology as Topic, Names, Meaning (existential), Psychology, Biochemistry, Reciprocal, Epistemology, Term (time)
Abstract

IN a recent communication, Kleiber1 has discussed two different definitions of the term ‘turnover-rate’. Some workers, particularly those associated with Chaikoff, regard the turnover-rate as the rate at which a substance is replaced in the tissue cells (definition 1). This is essentially the concentration of the substance in the tissue divided by the turnover-time. Others, including Kleiber, consider it to be the rate at which the whole ‘pool’ of the substance, however large or small, is replaced in the tissue, given by the reciprocal of the turnover-time (definition 2). Both groups agree that the turnover-time is the biological ‘average life’, given by 1.44 × biological half-life.

Published
1955

33. Honeydew on Lime Trees

Author

C. A. Mawson

Subjects
Aphis, Horticulture, Honeydew, Multidisciplinary, biology, Coating, Chemistry, engineering, engineering.material, biology.organism_classification, Lime
Abstract

THE dry summer of 1947 led to the accumulation of large amounts of honeydew secreted by the aphis Therioaphis tilice (L.) on the leaves of European lime trees. Sufficient often dripped to the earth to give a hard coating to the surface.

Published
1948

34. Zinc in Aspermic Human Semen

Author

C. A. Mawson and M. Isabel Fischer

Subjects
High concentration, Multidisciplinary, Chromatography, chemistry, Relative Volume, chemistry.chemical_element, Semen, Centrifugation, Zinc, Contamination, Sperm
Abstract

NORMAL human seminal plasma has been shown to contain a higher concentration of zinc than any tissue except sperm1. The sperm contain a very high concentration of zinc, but their removal from semen by centrifugation causes no significant reduction in the zinc concentration of the fluid because of their small relative volume. No previous opportunity had occurred for analysis of naturally aspermic semen, but recently a specimen of this nature was received. It had not been collected in specially cleaned glassware, but any contamination due to this fact could not have added more than a few µgm./ml. to the zinc content.

Published
1956

Catalog

Books, media, physical & digital resources
See catalog results