tbuckley/cabot-search huggingface dataset:
Abstract P3-04-10: Utility of the orally bioavailable selective estrogen receptor degrader AZD9496 in ESR1 mutant preclinical models of estrogen receptor positive breast cancer
Authors: CJ Morrow, M Lawson, B Ladd, C de Almeida, N James, JO Curwen, L Hanson, K Bell, A Goeppert, D Fisher, E Gangl, C De Savi, JS Scott, C D'Cruz, T Klinowska, HM Weir
Journal: Cancer Research (2017)

Abstract Approximately 70% of breast cancers express estrogen receptor alpha (ERα) and anti-hormonal therapies which either block the production of estrogen (e.g. anastrozole) or directly block ERα function (e.g. tamoxifen) remain the mainstay of treatment for these patients. While these therapies are highly effective resistance can occur. A common resistance mechanism to anti-hormonal agents is the mutation of ESR1, the gene that encodes ERα, which leads to ligand independent activity. Evidence is emerging that the selective estrogen receptor degrader (SERD) fulvestrant is effective in patients with ESR1 mutations. However, given the low bioavailability of fulvestrant and the still detectable levels of ER in clinical samples after treatment with fulvestrant it is hypothesised that SERDs with improved pharmacokinetic properties which are able to drive greater degradation of ERα may provide additional clinical benefit. We have previously described the discovery and characterisation of the orally bioavailable SERD AZD9496, which is currently in phase I clinical trials in ER+ breast cancer patients. Here we report the preclinical activity of AZD9496 in cell line and patient derived xenograft models expressing clinically relevant ESR1 mutations. We have engineered MCF-7 cells to express Y537S ESR1 which confers the ability to proliferate in the absence of estradiol, consistent with ligand independent activation of ER signalling. AZD9496 is able to inhibit proliferation of these cells and downregulate progesterone receptor protein expression at low nanomolar concentrations. Furthermore, when MCF-7 Y537S ESR1 cells are implanted as xenografts they grow in the absence of exogenous estradiol, are as sensitive to AZD9496 as parental MCF7 xenografts and demonstrate downregulation of ER dependent biomarkers. AZD9496 also has anti-tumour and pharmacodynamic efficacy in patient derived xenograft models expressing D538G ESR1. Taken together, these data strengthen the body of data suggesting that SERDs may be active in patients with tumours containing ESR1 mutations and supports the inclusion of this patient population in AZD9496 clinical trials. Citation Format: Morrow CJ, Lawson M, Ladd B, de Almeida C, James N, Curwen JO, Hanson L, Bell K, Goeppert A, Fisher D, Gangl E, De Savi C, Scott JS, D'Cruz C, Klinowska T, Weir HM. Utility of the orally bioavailable selective estrogen receptor degrader AZD9496 in ESR1 mutant preclinical models of estrogen receptor positive breast cancer [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P3-04-10.
Allogeneic Transplanst for ACUTE Myeloid Leukemia: Cut Off Levels of WT1 Expression in 207 Patients and Pre-Emptive Therapy of Relapse
Authors: Carmen Di Grazia, Simona Geroldi, Raffaella Grasso, Maurizio Miglino, Nicoletta Colombo, Elisabetta Tedone, Silvia Luchetti, Teresa Lamparelli, Francesca Gualandi, Adalberto Ibatici, Stefania Bregante, Maria Teresa van Lint, Anna Maria Raiola, Alida Dominietto, Riccardo Varaldo, Federica Galaverna, Anna Ghiso, Andrea Bacigalupo
Journal: Blood (2015)
The Extraordinary Book
Authors: Harold L. Levitan, Astrid Heiberg, A.K. Tebecis, Y. Ohno, H. Matsubara, H. Sugano, T. Takeya, Y. Ikemi, M. Takasaki, J.W. Paulley, Kazimierz Wrześniewski, Richard L. Steele, Jean Hamilton Holcomb
Journal: Psychotherapy and Psychosomatics (1976)
Survival and Efficacy of Decitabine in Myelodysplastic Syndromes (MDS), Analysis of the 5-Day IV Dosing Regimen.
Authors: Hagop Kantarjian, Guillermo Garcia-Manero, Susan O’Brien, Zeev Estrov, Farhad Ravandi, Jorge Cortes, Jianqin Shan, Jan Davisson, Jean-Pierre Issa
Journal: Blood (2007)
Molecular Signature of CD8+ T Cell Exhaustion during Chronic Viral Infection
Authors: E. John Wherry, Sang-Jun Ha, Susan M. Kaech, W. Nicholas Haining, Surojit Sarkar, Vandana Kalia, Shruti Subramaniam, Joseph N. Blattman, Daniel L. Barber, Rafi Ahmed
Journal: Immunity (2007)
Comparison of Results from a Phase 1/2 Study of Lumiliximab (Anti-CD23) in Combination with FCR for Patients with Relapsed CLL with Published FCR Results.
Authors: John C. Byrd, Januario Castro, Susan O’Brien, Ian W. Flinn, Andres Forero-Torres, Thomas J. Kipps, Nyla A. Heerema, Thomas Lin, Thian Kheoh, Dee Wynnem, Arturo Molina
Journal: Blood (2006)
Bortezomib with HIG-Dose Dexamethasone as First Line Therapy in Patients with Multiple Myeloma Candidates to High-Dose Therapy.
Authors: Alessandro Corso, Luciana Barbarano, Silvia Mangiacavalli, Luigi Montalbetti, Paola Brasca, Patrizia Zappasodi, Angelo Carella, Mauro Spriano, Emilio Paolo Alessandrino, Roberto Cairoli, Daniela Petrò, Marzia Varettoni, Paolo Bernasconi, Mario Lazzarino, Enrica Morra
Journal: Blood (2007)
Destabilizing the autoinhibitory conformation of Zap70 induces up-regulation of inhibitory receptors and T cell unresponsiveness
Authors: Lih-Yun Hsu, Debra A. Cheng, Yiling Chen, Hong-Erh Liang, Arthur Weiss
Journal: The Journal of Experimental Medicine (2017)

Zap70 plays a critical role in normal T cell development and T cell function. However, little is known about how perturbation of allosteric autoinhibitory mechanisms in Zap70 impacts T cell biology. Here, we analyze mice with a hypermorphic Zap70 mutation, W131A, which destabilizes the autoinhibitory conformation of Zap70, rendering the kinase in a semiactive state. W131A mutant mice with wild-type T cell receptor (TCR) repertoires exhibited relatively normal T cell development. However, crossing the W131A mutant mice to OTII TCR transgenic mice resulted in increased negative selection of OTII+ thymocytes and in increased thymic and peripheral T regulatory cells. Strikingly, increased basal TCR signaling was associated with a marked increase in inhibitory receptor expression and with T cells that were relatively refractory to TCR stimulation. PD-1 inhibitory receptor blockade partially reversed T cell unresponsiveness. Collectively, disruption of normal Zap70 autoinhibition engaged negative feedback mechanisms by which negative selection and inhibitory receptors restrain TCR signaling to enforce both central and peripheral tolerance.
SOX2 Drives Bronchial Dysplasia in a Novel Organotypic Model of Early Human Squamous Lung Cancer
Authors: Lúcia L. Correia, Jo-Anne Johnson, Peter McErlean, Julien Bauer, Hassan Farah, Doris M. Rassl, Robert C. Rintoul, Tariq Sethi, Paul Lavender, Emma L. Rawlins, Trevor D. Littlewood, Gerard I. Evan, Frank M. McCaughan
Journal: American Journal of Respiratory and Critical Care Medicine (2017)

Improving the early detection and chemoprevention of lung cancer are key to improving outcomes. The pathobiology of early squamous lung cancer is poorly understood. We have shown that amplification of sex-determining region Y-box 2 (SOX2) is an early and consistent event in the pathogenesis of this disease, but its functional oncogenic potential remains uncertain. We tested the impact of deregulated SOX2 expression in a novel organotypic system that recreates the molecular and microenvironmental context in which squamous carcinogenesis occurs.
Phase I, Dose-Escalation, Two-Part Trial of the PARP Inhibitor Talazoparib in Patients with Advanced Germline <i>BRCA1/2</i> Mutations and Selected Sporadic Cancers
Authors: Johann de Bono, Ramesh K. Ramanathan, Lida Mina, Rashmi Chugh, John Glaspy, Saeed Rafii, Stan Kaye, Jasgit Sachdev, John Heymach, David C. Smith, Joshua W. Henshaw, Ashleigh Herriott, Miranda Patterson, Nicola J. Curtin, Lauren Averett Byers, Zev A. Wainberg
Journal: Cancer Discovery (2017)

Talazoparib inhibits PARP catalytic activity, trapping PARP1 on damaged DNA and causing cell death in BRCA1/2-mutated cells. We evaluated talazoparib therapy in this two-part, phase I, first-in-human trial. Antitumor activity, MTD, pharmacokinetics, and pharmacodynamics of once-daily talazoparib were determined in an open-label, multicenter, dose-escalation study (NCT01286987). The MTD was 1.0 mg/day, with an elimination half-life of 50 hours. Treatment-related adverse events included fatigue (26/71 patients; 37%) and anemia (25/71 patients; 35%). Grade 3 to 4 adverse events included anemia (17/71 patients; 24%) and thrombocytopenia (13/71 patients; 18%). Sustained PARP inhibition was observed at doses ≥0.60 mg/day. At 1.0 mg/day, confirmed responses were observed in 7 of 14 (50%) and 5 of 12 (42%) patients with BRCA mutation-associated breast and ovarian cancers, respectively, and in patients with pancreatic and small cell lung cancer. Talazoparib demonstrated single-agent antitumor activity and was well tolerated in patients at the recommended dose of 1.0 mg/day.Significance: In this clinical trial, we show that talazoparib has single-agent antitumor activity and a tolerable safety profile. At its recommended phase II dose of 1.0 mg/day, confirmed responses were observed in patients with BRCA mutation-associated breast and ovarian cancers and in patients with pancreatic and small cell lung cancer. Cancer Discov; 7(6); 620-9. ©2017 AACR.This article is highlighted in the In This Issue feature, p. 539.
Molecular and Transcriptional Characterization of the Novel 17p11.2-p12 Chromosome Amplification in Multiple Myeloma.
Authors: Sonia Fabris, Katia Todoerti, Laura Mosca, Luca Agnelli, Domenica Ronchetti, Daniela Intini, Marta Lionetti, Gabriella Ciceri, Giorgio Lambertenghi Deliliers, Francesco Bertoni, Antonino Neri
Journal: Blood (2007)
Prioritizing Shared Decision Making—Reply
Authors: Paul C. Tang, Mark D. Smith
Journal: JAMA (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Procedure-specific Risks of Thrombosis and Bleeding in Urological Non-cancer Surgery: Systematic Review and Meta-analysis
Authors: Kari A.O. Tikkinen, Samantha Craigie, Arnav Agarwal, Reed A.C. Siemieniuk, Rufus Cartwright, Philippe D. Violette, Giacomo Novara, Richard Naspro, Chika Agbassi, Bassel Ali, Maha Imam, Nofisat Ismaila, Denise Kam, Michael K. Gould, Per Morten Sandset, Gordon H. Guyatt
Journal: European Urology (2017)

Pharmacological thromboprophylaxis involves a trade-off between a reduction in venous thromboembolism (VTE) and increased bleeding. No guidance specific for procedure and patient factors exists in urology.To inform estimates of absolute risk of symptomatic VTE and bleeding requiring reoperation in urological non-cancer surgery.We searched for contemporary observational studies and estimated the risk of symptomatic VTE or bleeding requiring reoperation in the 4 wk after urological surgery. We used the GRADE approach to assess the quality of the evidence.The 37 eligible studies reported on 11 urological non-cancer procedures. The duration of prophylaxis varied widely both within and between procedures; for example, the median was 12.3 d (interquartile range [IQR] 3.1-55) for open recipient nephrectomy (kidney transplantation) studies and 1 d (IQR 0-1.3) for percutaneous nephrolithotomy, open prolapse surgery, and reconstructive pelvic surgery studies. Studies of open recipient nephrectomy reported the highest risks of VTE and bleeding (1.8-7.4% depending on patient characteristics and 2.4% for bleeding). The risk of VTE was low for 8/11 procedures (0.2-0.7% for patients with low/medium risk; 0.8-1.4% for high risk) and the risk of bleeding was low for 6/7 procedures (≤0.5%; no bleeding estimates for 4 procedures). The quality of the evidence supporting these estimates was low or very low.Although inferences are limited owing to low-quality evidence, our results suggest that extended prophylaxis is warranted for some procedures (eg, kidney transplantation procedures in high-risk patients) but not others (transurethral resection of the prostate and reconstructive female pelvic surgery in low-risk patients).The best evidence suggests that the benefits of blood-thinning drugs to prevent clots after surgery outweigh the risks of bleeding in some procedures (such as kidney transplantation procedures in patients at high risk of clots) but not others (such as prostate surgery in patients at low risk of clots).
Primary respiratory and food allergy to mealworm
Authors: Henrike C.H.P. Broekman, André C. Knulst, Constance F. den Hartog Jager, Jolanda H.M. van Bilsen, Florine M.L. Raymakers, Astrid G. Kruizinga, Marco Gaspari, Caterine Gabriele, Carla A.F.M. Bruijnzeel-Koomen, Geert F. Houben, Kitty C.M. Verhoeckx
Journal: Journal of Allergy and Clinical Immunology (2017)
Islet encapsulation with polyphenol coatings decreases pro-inflammatory chemokine synthesis and T cell trafficking
Authors: Dana Pham-Hua, Lindsey E. Padgett, Bing Xue, Brian Anderson, Michael Zeiger, Jessie M. Barra, Maigen Bethea, Chad S. Hunter, Veronika Kozlovskaya, Eugenia Kharlampieva, Hubert M. Tse
Journal: Biomaterials (2017)
Insulin Signaling Regulates the FoxM1/PLK1/CENP-A Pathway to Promote Adaptive Pancreatic β Cell Proliferation
Authors: Jun Shirakawa, Megan Fernandez, Tomozumi Takatani, Abdelfattah El Ouaamari, Prapaporn Jungtrakoon, Erin R. Okawa, Wei Zhang, Peng Yi, Alessandro Doria, Rohit N. Kulkarni
Journal: Cell Metabolism (2017)
Cell-Free DNA and Active Rejection in Kidney Allografts
Authors: Roy D. Bloom, Jonathan S. Bromberg, Emilio D. Poggio, Suphamai Bunnapradist, Anthony J. Langone, Puneet Sood, Arthur J. Matas, Shikha Mehta, Roslyn B. Mannon, Asif Sharfuddin, Bernard Fischbach, Mohanram Narayanan, Stanley C. Jordan, David Cohen, Matthew R. Weir, David Hiller, Preethi Prasad, Robert N. Woodward, Marica Grskovic, John J. Sninsky, James P. Yee, Daniel C. Brennan
Journal: Journal of the American Society of Nephrology (2017)

Histologic analysis of the allograft biopsy specimen is the standard method used to differentiate rejection from other injury in kidney transplants. Donor-derived cell-free DNA (dd-cfDNA) is a noninvasive test of allograft injury that may enable more frequent, quantitative, and safer assessment of allograft rejection and injury status. To investigate this possibility, we prospectively collected blood specimens at scheduled intervals and at the time of clinically indicated biopsies. In 102 kidney recipients, we measured plasma levels of dd-cfDNA and correlated the levels with allograft rejection status ascertained by histology in 107 biopsy specimens. The dd-cfDNA level discriminated between biopsy specimens showing any rejection (T cell–mediated rejection or antibody-mediated rejection [ABMR]) and controls (no rejection histologically), P &lt;0.001 (receiver operating characteristic area under the curve [AUC], 0.74; 95% confidence interval [95% CI], 0.61 to 0.86). Positive and negative predictive values for active rejection at a cutoff of 1.0% dd-cfDNA were 61% and 84%, respectively. The AUC for discriminating ABMR from samples without ABMR was 0.87 (95% CI, 0.75 to 0.97). Positive and negative predictive values for ABMR at a cutoff of 1.0% dd-cfDNA were 44% and 96%, respectively. Median dd-cfDNA was 2.9% (ABMR), 1.2% (T cell–mediated types ≥IB), 0.2% (T cell–mediated type IA), and 0.3% in controls ( P =0.05 for T cell–mediated rejection types ≥IB versus controls). Thus, dd-cfDNA may be used to assess allograft rejection and injury; dd-cfDNA levels &lt;1% reflect the absence of active rejection (T cell–mediated type ≥IB or ABMR) and levels &gt;1% indicate a probability of active rejection.
Blood flow reprograms lymphatic vessels to blood vessels
Authors: Chiu-Yu Chen, Cara Bertozzi, Zhiying Zou, Lijun Yuan, John S. Lee, MinMin Lu, Stan J. Stachelek, Sathish Srinivasan, Lili Guo, Andres Vicente, Patricia Mericko, Robert J. Levy, Taija Makinen, Guillermo Oliver, Mark L. Kahn
Journal: Journal of Clinical Investigation (2012)

shown that inhibition of Chk1 in a p53-deficient background results in apoptosis in response to DNA damage.
OTT-MAL Activates the Notch Signaling Transcription Factor RBPJ and Cooperates with Mutant MPL to Induce Acute Megakaryoblastic Leukemia
Authors: Thomas Mercher, Glen D. Raffel, Sandra A Moore, Melanie G Cornejo, Dominique Baudry-Bluteau, Nicolas Cagnard, Jonathan Jesneck, Yana Pikman, Dana E. Cullen, Ifor Williams, Koichi Akashi, Hirokazu Shigematsu, Jean-Pierre Bourquin, Marco Giovannini, William Vainchenker, Ross L Levine, Benjamin H. Lee, Olivier Bernard, D. Gary Gilliland
Journal: Blood (2008)
Impact of Charlson Comorbidity Index (CCI) and Refining the MIPI Index in Mantle Cell Lymphoma (MCL)
Authors: Andre Goy, Tommy Wu, Eric Hansen, Srikesh Arunajadai, Ewelina Protomastro, Marisa Valentinetti, Maureen Murphy, Judith E Smith, Ruth Pe Benito, Ali Hasan, Kiran Suryadevara, Tatyana Feldman, Alan P Skarbnik, Lori A. Leslie, Scott D. Rowley, Michele L. Donato, Andrew L. Pecora, Stuart L. Goldberg
Journal: Blood (2016)
HDAC6-mediated acetylation of lipid droplet–binding protein CIDEC regulates fat-induced lipid storage
Authors: Hui Qian, Yuanying Chen, Zongqian Nian, Lu Su, Haoyong Yu, Feng-Jung Chen, Xiuqin Zhang, Wenyi Xu, Linkang Zhou, Jiaming Liu, Jinhai Yu, Luxin Yu, Yan Gao, Hongchao Zhang, Haihong Zhang, Shimin Zhao, Li Yu, Rui-Ping Xiao, Yuqian Bao, Shaocong Hou, Pingping Li, Jiada Li, Haiteng Deng, Weiping Jia, Peng Li
Journal: Journal of Clinical Investigation (2017)

Obesity is characterized by aberrant fat accumulation. However, the intracellular signaling pathway that senses dietary fat and leads to fat storage remains elusive. Here, we have observed that the levels of histone deacetylase 6 (HDAC6) and the related family member HDAC10 are markedly reduced in adipose tissues of obese animals and humans. Mice with adipocyte-specific depletion of Hdac6 exhibited increased fat accumulation and reduced insulin sensitivity. In normal adipocytes, we found that reversal of P300/CBP-associated factor-induced (PCAF-induced) acetylation at K56 on cell death-inducing DFFA-like effector C (CIDEC, also known as FSP27) critically regulated lipid droplet fusion and lipid storage. Importantly, HDAC6 deacetylates CIDEC, leading to destabilization and reduced lipid droplet fusion. Accordingly, we observed elevated levels of CIDEC and its acetylated form in HDAC-deficient adipocytes as well as the adipose tissue of obese animals and humans. Fatty acids (FAs) prevented CIDEC deacetylation by promoting the dissociation of CIDEC from HDAC6, which resulted in increased association of CIDEC with PCAF on the endoplasmic reticulum. Control of CIDEC acetylation required the conversion of FAs to triacylglycerols. Thus, we have revealed a signaling axis that is involved in the coordination of nutrient availability, protein acetylation, and cellular lipid metabolic responses.
BTG1, a Gene Frequently Deleted in Pre-B ALL, Controls Glucocorticoid Receptor-Mediated Gene Expression.
Authors: Frank N. van Leeuwen, Joost Casper van Galen, Roland P. Kuiper, Liesbeth van Emst, Marloes R Levers, Esther Tijchon, Blanca Scheijen, Esmee Waanders, Simon V van Reijmersdal, Christian Gillissen, Ad Geurts van Kessel, Peter M. Hoogerbrugge
Journal: Blood (2009)
Diagnosing and Managing Carcinoid Heart Disease in Patients With Neuroendocrine Tumors
Authors: Joseph Davar, Heidi M. Connolly, Martyn E. Caplin, Marianne Pavel, Jerome Zacks, Sanjeev Bhattacharyya, Daniel J. Cuthbertson, Rebecca Dobson, Simona Grozinsky-Glasberg, Richard P. Steeds, Giles Dreyfus, Patricia A. Pellikka, Christos Toumpanakis
Journal: Journal of the American College of Cardiology (2017)
PP63. PROGRESSIVE T2/FLAIR SIGNAL CHANGE AFTER LOW-GRADE GLIOMA RESECTION – WHAT DOES IT SIGNIFY?
Authors: Mr John Goodden, Mrs Suzanne Spink, Dr Stuart Currie, Dr Tufail Patankar, Dr Jeremy Macmullen-price, Dr Daniel O’hara, Dr Melissa Maguire, Dr Azzam Ismail, Dr Arundhati Chakrabarty, Dr Carmel Loughrey, Mr Paul Chumas
Journal: Neuro-Oncology (2017)

BACKGROUND: Several international series’ have demonstrated the importance of extensive resection in controlling Low Grade Glioma (LGG). After surgery, regular MRI monitoring is undertaken for evidence of recurrence. Since LGG are typically demonstrated as hyperintense signal on T2 and FLAIR MRI scans, an increase in T2/FLAIR signal around the resection cavity would be expected to signify tumour progression. We describe our experience and unusual cases. METHOD: Prospective analysis of LGG patients treated at Leeds General Infirmary from 2010–2015 (5.5 years). Inclusion criteria: patients with evidence of increasing T2/FLAIR signal change around the tumour cavity following LGG surgery. RESULTS: 130 resections of LGG were undertaken in Leeds (77 awake, 53 asleep). Following surgery, patients were monitored with a standardised protocol of MRI scans. During this period 38 repeat operations were performed for suspected tumour regrowth, indicated by progressive T2/FLAIR signal change. Two patterns of regrowth were observed – a thin marginal increase at the previous resection margin (Type 1 – 13 patients) or a thicker more globular regrowth into the resection cavity (Type 2 – 22 patients). Histopathology confirmed tumour of the same grade for all patients with Type 1 regrowth. In the Type 2 group however, 60% patients (13/22) had histopathological evidence of progression of grade. In the group with Type 2 regrowth, the resected en-bloc specimen contained only gliotic tissue in 2 patients, and in 1 it contained 80% gliotic tissue and 20% tumour. Post-operative scans confirmed the correct area was resected. Finally, a further cohort of patients have had a delayed progression in T2/FLAIR imaging which then stabilised. They remain on active monitoring without further surgery. CONCLUSION: Progressive T2 change that is limited to the resection margin appears to be most likely be of the same grade of tumour but can also represent gliotic tissue. Globular regrowth into the resection cavity represents a high risk of transformation of grade. Uncertainty remains over the significance of delayed progression of T2/FLAIR change that then stabilises. This presents challenges – when should we re-operate and when should we just monitor? Furthermore, what is the optimal management decision when initial surgery was supra-marginal and a temporary progression in signal change occurs outside the original tumour boundary?