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27 results on '"Harvey, Amanda J"'

10. Biodegradation of Bacillus anthracis endospores in compost

Author

Selinger, L. Brent, McAllister, Tim A., Harvey, Amanda J. D., University of Lethbridge. Faculty of Arts and Science, Selinger, L. Brent, McAllister, Tim A., Harvey, Amanda J. D., and University of Lethbridge. Faculty of Arts and Science

Abstract

Anthrax, a lethal infectious disease affecting primarily herbivores, is caused by an endospore-forming bacterium, Bacillus anthracis (BA). Endospores from BA are extremely stable in the environment and pose a communicable risk as a natural zoonosis and as a potential bioweapon. Composting results in microbial biodegradation of organic matter, reaching temperatures up to 70°C. I investigated the ability of compost to inactivate BA. Surrogate strains were sporulated over a range of temperatures to mimic natural sporulation environmental variations and tested in two separate experiments. The first, exposed four surrogate strains to temperatures mimicking a previous long-term (150 days) field-scale compost temperature profile. The second, composted BA endospores from two surrogate strains in laboratory scale composters for 33 days. Composting resulted in a 2 and 4 log10 reduction in endospore viability in oven and lab scale experiments, respectively. Results suggest composting has potential as a disposal method for anthrax related mortalities.

Published
2019

11. MTOR function and therapeutic targeting in breast cancer

Author

Hare, Stephen H and Harvey, Amanda J

Subjects
breast cancer, mTOR, cell signaling, Review Article, everolimus, PI3K, rapalogues
Abstract

The mTOR pathway was discovered in the late 1970s after the compound and natural inhibitor of mTOR, rapamycin was isolated from the bacterium Streptomyces hygroscopicus. mTOR is serine/threonine kinase belonging to the phosphoinositide 3-kinase related kinase (PIKK) family. It forms two distinct complexes; mTORC1 and mTORC2. mTORC1 has a key role in regulating protein synthesis and autophagy whilst mTORC2 is involved in regulating kinases of the AGC family. mTOR signaling is often over active in multiple cancer types including breast cancer. This can involve mutations in mTOR itself but more commonly, in breast cancer, this is related to an increase in activity of ErbB family receptors or alterations and mutations of PI3K signaling. Rapamycin and its analogues (rapalogues) bind to the intercellular receptor FKBP12, and then predominantly inhibit mTORC1 signaling via an allosteric mechanism. Research has shown that inhibition of mTOR is a useful strategy in tackling cancers, with it acting to slow tumor growth and limit the spread of a cancer. Rapalogues have now made their way into the clinic with the rapalogue everolimus (RAD-001/Afinitor) approved for use in conjunction with exemestane, in post-menopausal breast cancer patients with advanced disease who are HER-2 negative (normal expression), hormone receptor positive and whose prior treatment with non-steroidal aromatase inhibitors has failed. Testing across multiple trials has proven that everolimus and other rapalogues are a viable way of treating certain types of cancer. However, rapalogues have shown some drawbacks both in research and clinically, with their use often activating feedback pathways that counter their usefulness. As such, new types of inhibitors are being explored that work via different mechanisms, including inhibitors that are ATP competitive with mTOR and which act to perturb signaling from both mTOR complexes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5385631/

Published
2016

13. Critical research gaps and translational priorities for the successful prevention and treatment of breast cancer

Author

Eccles, Suzanne A, primary, Aboagye, Eric O, additional, Ali, Simak, additional, Anderson, Annie S, additional, Armes, Jo, additional, Berditchevski, Fedor, additional, Blaydes, Jeremy P, additional, Brennan, Keith, additional, Brown, Nicola J, additional, Bryant, Helen E, additional, Bundred, Nigel J, additional, Burchell, Joy M, additional, Campbell, Anna M, additional, Carroll, Jason S, additional, Clarke, Robert B, additional, Coles, Charlotte E, additional, Cook, Gary JR, additional, Cox, Angela, additional, Curtin, Nicola J, additional, Dekker, Lodewijk V, additional, dos Santos Silva, Isabel, additional, Duffy, Stephen W, additional, Easton, Douglas F, additional, Eccles, Diana M, additional, Edwards, Dylan R, additional, Edwards, Joanne, additional, Evans, D Gareth, additional, Fenlon, Deborah F, additional, Flanagan, James M, additional, Foster, Claire, additional, Gallagher, William M, additional, Garcia-Closas, Montserrat, additional, Gee, Julia M W, additional, Gescher, Andy J, additional, Goh, Vicky, additional, Groves, Ashley M, additional, Harvey, Amanda J, additional, Harvie, Michelle, additional, Hennessy, Bryan T, additional, Hiscox, Stephen, additional, Holen, Ingunn, additional, Howell, Sacha J, additional, Howell, Anthony, additional, Hubbard, Gill, additional, Hulbert-Williams, Nick, additional, Hunter, Myra S, additional, Jasani, Bharat, additional, Jones, Louise J, additional, Key, Timothy J, additional, Kirwan, Cliona C, additional, Kong, Anthony, additional, Kunkler, Ian H, additional, Langdon, Simon P, additional, Leach, Martin O, additional, Mann, David J, additional, Marshall, John F, additional, Martin, Lesley Ann, additional, Martin, Stewart G, additional, Macdougall, Jennifer E, additional, Miles, David W, additional, Miller, William R, additional, Morris, Joanna R, additional, Moss, Sue M, additional, Mullan, Paul, additional, Natrajan, Rachel, additional, O’Connor, James PB, additional, O’Connor, Rosemary, additional, Palmieri, Carlo, additional, Pharoah, Paul D P, additional, Rakha, Emad A, additional, Reed, Elizabeth, additional, Robinson, Simon P, additional, Sahai, Erik, additional, Saxton, John M, additional, Schmid, Peter, additional, Smalley, Matthew J, additional, Speirs, Valerie, additional, Stein, Robert, additional, Stingl, John, additional, Streuli, Charles H, additional, Tutt, Andrew N J, additional, Velikova, Galina, additional, Walker, Rosemary A, additional, Watson, Christine J, additional, Williams, Kaye J, additional, Young, Leonie S, additional, and Thompson, Alastair M, additional

Published
2013
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26. mTOR function and therapeutic targeting in breast cancer.

Author

Hare SH and Harvey AJ

Abstract

The mTOR pathway was discovered in the late 1970s after the compound and natural inhibitor of mTOR, rapamycin was isolated from the bacterium Streptomyces hygroscopicus. mTOR is serine/threonine kinase belonging to the phosphoinositide 3-kinase related kinase (PIKK) family. It forms two distinct complexes; mTORC1 and mTORC2. mTORC1 has a key role in regulating protein synthesis and autophagy whilst mTORC2 is involved in regulating kinases of the AGC family. mTOR signaling is often over active in multiple cancer types including breast cancer. This can involve mutations in mTOR itself but more commonly, in breast cancer, this is related to an increase in activity of ErbB family receptors or alterations and mutations of PI3K signaling. Rapamycin and its analogues (rapalogues) bind to the intercellular receptor FKBP12, and then predominantly inhibit mTORC1 signaling via an allosteric mechanism. Research has shown that inhibition of mTOR is a useful strategy in tackling cancers, with it acting to slow tumor growth and limit the spread of a cancer. Rapalogues have now made their way into the clinic with the rapalogue everolimus (RAD-001/Afinitor) approved for use in conjunction with exemestane, in post-menopausal breast cancer patients with advanced disease who are HER-2 negative (normal expression), hormone receptor positive and whose prior treatment with non-steroidal aromatase inhibitors has failed. Testing across multiple trials has proven that everolimus and other rapalogues are a viable way of treating certain types of cancer. However, rapalogues have shown some drawbacks both in research and clinically, with their use often activating feedback pathways that counter their usefulness. As such, new types of inhibitors are being explored that work via different mechanisms, including inhibitors that are ATP competitive with mTOR and which act to perturb signaling from both mTOR complexes.

Published
2017

27. Evolution of breast cancer therapeutics: Breast tumour kinase's role in breast cancer and hope for breast tumour kinase targeted therapy.

Author

Hussain HA and Harvey AJ

Abstract

There have been significant improvements in the detection and treatment of breast cancer in recent decades. However, there is still a need to develop more effective therapeutic techniques that are patient specific with reduced toxicity leading to further increases in patients' overall survival; the ongoing progress in understanding recurrence, resistant and spread also needs to be maintained. Better understanding of breast cancer pathology, molecular biology and progression as well as identification of some of the underlying factors involved in breast cancer tumourgenesis and metastasis has led to the identification of novel therapeutic targets. Over a number of years interest has risen in breast tumour kinase (Brk) also known as protein tyrosine kinase 6; the research field has grown and Brk has been described as a desirable therapeutic target in relation to tyrosine kinase inhibition as well as disruption of its kinase independent activity. This review will outline the current "state of play" with respect to targeted therapy for breast cancer, as well as discussing Brk's role in the processes underlying tumour development and metastasis and its potential as a therapeutic target in breast cancer.

Published
2014
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