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101. Tumour-infiltrating regulatory T cell density before neoadjuvant chemoradiotherapy for rectal cancer does not predict treatment response

Author

McCoy, Melanie J., primary, Hemmings, Chris, additional, Anyaegbu, Chidozie C., additional, Austin, Stephanie J., additional, Lee-Pullen, Tracey F., additional, Miller, Timothy J., additional, Bulsara, Max K., additional, Zeps, Nikolajs, additional, Nowak, Anna K., additional, Lake, Richard A., additional, and Platell, Cameron F., additional

Published
2017
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103. Additional file 2: Table S2. of Consistent gene expression profiles in MexTAg transgenic mouse and wild type mouse asbestos-induced mesothelioma

Author

Robinson, Cleo, Dick, Ian, Wise, Michael, Holloway, Andrew, Dileepa Diyagama, Robinson, Bruce, Jenette Creaney, and Lake, Richard

Subjects
body regions, nervous system, fungi
Abstract

List of differentially expressed genes in ascending order of fold difference in hiTAgtu compared to WTtu. (PDF 135Â kb)

Published
2015
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104. Additional file 4: Table S4. of Consistent gene expression profiles in MexTAg transgenic mouse and wild type mouse asbestos-induced mesothelioma

Author

Robinson, Cleo, Dick, Ian, Wise, Michael, Holloway, Andrew, Dileepa Diyagama, Robinson, Bruce, Jenette Creaney, and Lake, Richard

Subjects
body regions, nervous system, fungi, neoplasms, respiratory tract diseases
Abstract

List of differentially expressed genes in human mesothelioma compared with normal human mesothelial cells. (PDF 307Â kb)

Published
2015
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109. Transient Treg depletion enhances therapeutic anti‐cancer vaccination

Author

Fisher, Scott A., primary, Aston, Wayne J., additional, Chee, Jonathan, additional, Khong, Andrea, additional, Cleaver, Amanda L., additional, Solin, Jessica N., additional, Ma, Shaokang, additional, Lesterhuis, W. Joost, additional, Dick, Ian, additional, Holt, Robert A., additional, Creaney, Jenette, additional, Boon, Louis, additional, Robinson, Bruce, additional, and Lake, Richard A., additional

Published
2016
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116. Programmed Death Ligand 2 in Cancer-Induced Immune Suppression

Author

Rozali, Esdy N., Hato, Stanleyson V., Robinson, Bruce W., Lake, Richard A., and Lesterhuis, W. Joost

Subjects
Article Subject
Abstract

Inhibitory molecules of the B7/CD28 family play a key role in the induction of immune tolerance in the tumor microenvironment. The programmed death-1 receptor (PD-1), with its ligands PD-L1 and PD-L2, constitutes an important member of these inhibitory pathways. The relevance of the PD-1/PD-L1 pathway in cancer has been extensively studied and therapeutic approaches targeting PD-1 and PD-L1 have been developed and are undergoing human clinical testing. However, PD-L2 has not received as much attention and its role in modulating tumor immunity is less clear. Here, we review the literature on the immunobiology of PD-L2, particularly on its possible roles in cancer-induced immune suppression and we discuss the results of recent studies targeting PD-L2 in cancer.

Published
2012
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121. Strong spontaneous tumor neoantigen responses induced by a natural human carcinogen

Author

Creaney, Jenette, primary, Ma, Shaokang, additional, Sneddon, Sophie A, additional, Tourigny, Michelle R, additional, Dick, Ian M, additional, Leon, Justine S, additional, Khong, Andrea, additional, Fisher, Scott A, additional, Lake, Richard A, additional, Lesterhuis, W Joost, additional, Nowak, Anna K, additional, Leary, Shay, additional, Watson, Mark W, additional, and Robinson, Bruce W, additional

Published
2015
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123. A better way for a cancer cell to die

Author

van der Most, Robbert G. and Lake, Richard A.

Subjects
Cancer cells -- Research, Antimitotic agents -- Health aspects, Antineoplastic agents -- Health aspects
Abstract

A study of the lethal effects of chemotherapy on cancer cells shows that, after the fatal blow, cancer cells take different routes to destruction, depending on the chemotherapeutic agent used. The experiments indicate that if a chemotherapeutic agent kills cancer cells in a way that renders them immunogenic, it has a therapeutic benefit over and above the cytotoxic action of the drug.

Published
2006

124. Prescription drugs: uses and effects

Author

Lake, Richard and Jordan, Sue

Subjects
Drugs -- Prescribing, Anticoagulants (Medicine) -- Dosage and administration, Nursing -- Practice, Health, Health care industry, Practice, Dosage and administration
Abstract

Anticoagulants disease control Anticoagulants reduce the formation of new blood clots and the extension of existing clots, particularly in veins. They do not dissolve existing clots. Normal blood flow depends [...]

Published
2005

125. Transient Treg depletion enhances therapeutic anti-cancer vaccination.

Author

Fisher, Scott A., Aston, Wayne J., Chee, Jonathan, Khong, Andrea, Cleaver, Amanda L., Solin, Jessica N., Ma, Shaokang, Lesterhuis, W. Joost, Dick, Ian, Holt, Robert A., Creaney, Jenette, Boon, Louis, Robinson, Bruce, and Lake, Richard A.

Subjects
CANCER immunotherapy, T cells, LABORATORY mice, HOMEOSTASIS, DIPHTHERIA toxin
Abstract

Introduction Regulatory T cells (Treg) play an important role in suppressing anti- immunity and their depletion has been linked to improved outcomes. To better understand the role of Treg in limiting the efficacy of anti-cancer immunity, we used a Diphtheria toxin (DTX) transgenic mouse model to specifically target and deplete Treg. Methods Tumor bearing BALB/c FoxP3.dtr transgenic mice were subjected to different treatment protocols, with or without Treg depletion and tumor growth and survival monitored. Results DTX specifically depleted Treg in a transient, dose-dependent manner. Treg depletion correlated with delayed tumor growth, increased effector T cell (Teff) activation, and enhanced survival in a range of solid tumors. Tumor regression was dependent on Teffs as depletion of both CD4 and CD8 T cells completely abrogated any survival benefit. Severe morbidity following Treg depletion was only observed, when consecutive doses of DTX were given during peak CD8 T cell activation, demonstrating that Treg can be depleted on multiple occasions, but only when CD8 T cell activation has returned to base line levels. Finally, we show that even minimal Treg depletion is sufficient to significantly improve the efficacy of tumor-peptide vaccination. Conclusions BALB/c.FoxP3.dtr mice are an ideal model to investigate the full therapeutic potential of Treg depletion to boost anti-tumor immunity. DTX-mediated Treg depletion is transient, dose-dependent, and leads to strong anti-tumor immunity and complete tumor regression at high doses, while enhancing the efficacy of tumor-specific vaccination at low doses. Together this data highlight the importance of Treg manipulation as a useful strategy for enhancing current and future cancer immunotherapies. [ABSTRACT FROM AUTHOR]

Published
2017
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136. TRANSP modelling of experimentally measured fast particle redistribution and losses on MAST

Author

Wodniak, Iwona, Cecconello, Marco, Lake, Richard, Jones, Owen, Turnyanskiy, Mikhail, Sangaroon, Siriyaporn, Ericsson, Goran, Wodniak, Iwona, Cecconello, Marco, Lake, Richard, Jones, Owen, Turnyanskiy, Mikhail, Sangaroon, Siriyaporn, and Ericsson, Goran

Abstract

MAST is a mid-size spherical tokamak with BT = 0.3-0.6 T and two NBI systems delivering up to 3.5 MW of super-Alfvénic deuterons and therefore suitable for understanding the dynamics of fast particles in ITER-relevant scenarios. It is well known that MHD instabilities can cause redistribution and/or losses of fast ions as observed in many tokamaks (such as NSTX, TFTR, DIII-D, JET, ASDEX, NSTX and MAST). In particular, on MAST, the effect of fast particle driven instabilities, such as fishbones and long-lived modes upon the total neutron yield measured by fission chamber (FC) and the neutron count rates measured by Neutron Camera (NC) has been observed [1]. Fishbones are characterized by burst-like behaviour observed in magnetic and SXR diagnostics and by the sweeping of the mode frequency during a burst. The resonant interaction between the toroidal and poloidal motion of the fast ions in the plasma with the n = 1, m = 1 internal kink mode is the mechanism responsible for driving the fishbone instability [2].

Published
2013

138. The identification of the fouling mechanism during the crossflow filtration of a model fermentation broth

Author

Lake, Richard Charles.

Abstract

Experiments have been conducted to identify the fouling mechanism during the crossflow filtration of a model yeast fermentation broth of Vinyl Acetate particles suspended in a Bovine Serum Albumin (BSA) solution. These have been conducted with filter modules, to obtain quantitative data for the rate and the extent of flux decline due to membrane fouling, and with filter coupons, to obtain quantitative data for the build up of the fouling layer with each individual system and the mixed system. The data from the individual systems have been analysed and then used to determine their fouling mechanisms; this information has been used to predict the fouling mechanism for the mixed system. Finally, this prediction has been compared to the actual fouling mechanism determined by analysis of the mixed system data. For the model particulate suspension, the fouling was due to the build up of a cake layer, as with dead end filtration; however, fouling was limited by membrane scouring. For the model macromolecular solution, a four part fouling mechanism was identified: initially aggregates formed within the pores; the concentration at the membrane surface increased until protein came out of solution as strands; the strands disappeared causing increased aggregation in the pores; finally, a mesh formed on the membrane surface. For the mixed system, fouling was due to the formation of a particle cake on the membrane surface with protein aggregates forming in the pores. The fouling kinetics could be predicted by considering the results from the individual systems; however, the fouling mechanism could not be predicted without using visualisation experiments due to the interactions between the particles and the macromolecules.

Published
1996

145. The nuclear deubiquitinase BAP1 is commonly inactivated by somatic mutations and 3p21.1 losses in malignant pleural mesothelioma

Author

Bott, Matthew, primary, Brevet, Marie, additional, Taylor, Barry S, additional, Shimizu, Shigeki, additional, Ito, Tatsuo, additional, Wang, Lu, additional, Creaney, Jenette, additional, Lake, Richard A, additional, Zakowski, Maureen F, additional, Reva, Boris, additional, Sander, Chris, additional, Delsite, Robert, additional, Powell, Simon, additional, Zhou, Qin, additional, Shen, Ronglai, additional, Olshen, Adam, additional, Rusch, Valerie, additional, and Ladanyi, Marc, additional

Published
2011
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