Inhibition and flare patterns of metabolic response to the heat shock protein 90 (Hsp90) inhibitor IPI-504 visualized by FDG-PET in patients (pts) with advanced gastrointestinal stromal tumors (GIST) resistant to tyrosine kinase inhibitor (TKI) therapy

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 3530-3530 ◽  
Author(s):  
A. D. Van den Abbeele ◽  
J. T. Yap ◽  
D. S. Grayzel ◽  
J. Walker ◽  
G. D. Demetri
Keyword(s):  
Fdg Pet ◽  
Kinase Inhibitor ◽  
Metabolic Response ◽  
Clinical Investigation ◽  
Heat Shock Protein 90 ◽  
Hsp90 Inhibitor ◽  
Resistance Mutations ◽  
Hsp90 Inhibition ◽  
Standardized Uptake Values ◽  
Time Point

3530 Background: We have previously demonstrated the inhibition and rebound of GIST glycolytic metabolism with FDG-PET while pts were on or off TKI in prior trials of imatinib and sunitinib. We tested the same principle in a phase I trial of IPI-504, a novel potent inhibitor of Hsp90 (a chaperone for protein homeostasis) that results in selective destruction of the mutated KIT kinase in human GIST cell lines regardless of TKI-resistance mutations. Methods: Twenty-one patients with metatastic and/or unresectable GIST following failure of prior therapy with TKI were treated with IPI-504. Serial FDG-PET imaging was performed at baseline, during the 1st cycle after at least 2 doses (C1, days 4–11, “ON”, n = 18), and at the end of the 10-day off-treatment period prior to the start of the 2nd cycle (C1, “OFF”, n = 20). A subset of 5 pts also had FDG-PET at the end of the 3rd cycle (C3, day 11, “ON”). Maximum standardized uptake values (SUVmax) were measured in up to 3 lesions/pt with the greatest FDG uptake, and the SUVmax of all lesions was summed at each time point. Percent change in the summed mean SUVmax was calculated at each time point relative to the previous scan. Temporal changes were evaluated in those pts showing more than a 10% decrease in SUVmax during C1 “ON” compared to baseline. Results: We observed a >10% reduction in SUVmax (mean = - 28%) during the 1st cycle (C1, “ON”) in 8/18 pts. All these pts showed an increase in SUVmax (mean = +29%) when off therapy (C1, “OFF”). Three of these 8 pts had a scan during cycle 3. All demonstrated a decrease in SUVmax (mean = -30%) while on the drug (C3, “ON”). Conclusion: These preliminary findings suggest that: (1) tumor metabolic response as measured with FDG-PET parallels the intermittent pattern of IPI-504 administration in this study as early as after the 2nd dose administration; and, (2) IPI-504 has a rapid downstream effect on glucose metabolism similar to that observed with TKIs despite the very different mechanism of action of IPI-504. The pattern of response to Hsp90 inhibition seen in this heavily pretreated population strongly supports further clinical investigation. No significant financial relationships to disclose.

Activity of AT13387, a novel, non-ansamycin inhibitor of heat shock protein 90, against gastrointestinal stromal tumors (GIST).

2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 105-105 ◽  
Author(s):  
Daruka Mahadevan ◽  
Geoffrey Shapiro ◽  
Sandra E. Kurtin ◽  
James M. Cleary ◽  
John F. Lyons ◽  
...  
Keyword(s):  
Phase I ◽  
Kinase Inhibitor ◽  
Heat Shock Protein 90 ◽  
Tumor Growth Inhibition ◽  
Resistance Mutations ◽  
Hsp90 Inhibition ◽  
Secondary Resistance ◽  
Imatinib Resistant

105 Background: AT13387 is a second-generation potent, novel non-ansamycin HSP90 inhibitor (Kd 0.71nM). The majority of GIST tumors are characterized by activating mutations of c-KIT, an HSP90 client protein. Secondary resistance mutations within c-KIT limit clinical responses to TKIs. The dependence of c-KIT and its mutated forms on HSP90 suggests that HSP90 inhibition may be a valuable treatment option for imatinib-sensitive and resistant clones. In vitro, AT13387 inhibited the proliferation of imatinib-sensitive (GIST882, GIST-T1) and imatinib-resistant (GIST430, GIST48) cell lines. In vivo, AT13387 demonstrated anti-tumor activity in the imatinib-sensitive (GIST-PSW) and imatinib-resistant (GIST430) xenograft models. Induction of HSP70, depletion of phospho-c-KIT and inhibition of c-KIT signaling were observed in both models. Combination treatment of imatinib and AT13387 in the GIST430 model was well tolerated and significantly enhanced tumor growth inhibition over either monotherapies. Methods: In a completed phase I study, AT13387 was administered IV over 1 hour twice weekly or weekly of a 28-day cycle in a standard 3+3 dose-escalation design. The primary endpoint was to determine the MTD; secondary endpoints included PK, PD, safety and tolerability. Results: The PK exposures were dose-dependent and linear. AT13387 was well tolerated on both schedules. DLTs included primarily G2 AEs of GI toxicities, fatigue and infusion site reactions. The once weekly RP2D was determined to be 260 mg/m2. HSP70 induction was 2–7 fold at higher doses. A total of 7 GIST subjects were enrolled. An objective and durable PR was observed in one subject and 2 SDs at 8, 7 and 11 months, respectively. The PR subject demonstrated molecular resistance to kinase inhibitor treatment in the c-KIT gene prior to initiation of AT13387 therapy in two resected lesions by harboring the same activating c-KIT deletion in exon 11 and two separate TKI resistance mutations in exon 17. Conclusions: Overall, these results suggest AT13387 is a promising agent in GIST, including TKI-resistant c-Kit positive GIST. AT13387 is currently being evaluated in combination with imatinib in an ongoing phase I/II study. Clinical trial information: NCT01294202.

Assessment of response using FDG-PET and CT in a phase I study of AMN107 alone or in combination with imatinib (IM) in patients with imatinib-resistant (IM-R) gastrointestinal stromal tumors (GIST)

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 3087-3087 ◽  
Author(s):  
A. D. Van Den Abbeele ◽  
A. S. Barnes ◽  
D. J. De Vries ◽  
J. T. Yap ◽  
P. Reichardt ◽  
...  
Keyword(s):  
Fdg Pet ◽  
Metabolic Response ◽  
Rapid Assessment ◽  
Single Agent ◽  
Metastatic Gist ◽  
Standardized Uptake Values ◽  
Imatinib Resistant ◽  
Imaging Results ◽  
Time Point

3087 Background: Although IM induces durable clinical benefit in pts with metastatic GIST, resistance to this single agent may emerge over time and new approaches are needed. AMN107 is a new agent rationally designed to inhibit in a structurally different manner the tyrosine kinase activities of KIT, PDGFR, and Bcr-Abl. Since AMN107 has demonstrated the ability to inhibit the proliferation of both IM-sensitive and IM-R GIST cells in vitro, a clinical trial was begun to test this agent with rapid assessment of impact using FDG-PET. Methods: Pts with IM-R GIST were treated with AMN107 alone (400 mg p.o. bid), or a combination of IM (400 mg p.o. bid) and inter-cohort dose escalations of AMN107 (200 mg qd, 400 mg qd, and 400 mg p.o. bid). FDG-PET and CT were performed at baseline and after 1 and 4 wks on therapy. Maximum standardized uptake values (SUVmax) were measured in 11 pts in up to 5 lesions with the greatest FDG uptake/pt (n=46 lesions). For each patient, the summation SUVmax (sSUVmax) of all lesions was calculated at each time point. Percentage change in SUVmax and sSUVmax was calculated at wks 1 and 4 compared to baseline. Metabolic response was assessed using EORTC thresholds for % SUVmax change (PR≤ -25% <SD< +25%≤ PD). The longest diameters of all lesions analyzed by PET were measured on corresponding CT images, summed at each time point, and the % change was calculated at wks 1 and 4 compared to baseline. CT response was assessed using conventional RECIST thresholds. Results: At 1 wk, PET imaging of 11 evaluable pts documented metabolic PR in 3/11, SD in 7/11, and PD in 1/11. After 4 wks on therapy, 2 pts whose PET was stable after 1 wk had converted to metabolic PR, and all other imaging results were unchanged. The CT response for all 11 pts was SD after 1 and 4 wks on therapy. Conclusions: These findings suggest that a metabolic response to AMN107, or the combination of AMN107 plus IM, is seen with FDG-PET while CT anatomic response remains SD at 1 and 4 wks. [Table: see text] [Table: see text]

scholarly journals HSP90 is a chaperone for DLK and is required for axon injury signaling

2018 ◽  
Vol 115 (42) ◽  
pp. E9899-E9908 ◽  
Author(s):  
Scott Karney-Grobe ◽  
Alexandra Russo ◽  
Erin Frey ◽  
Jeffrey Milbrandt ◽  
Aaron DiAntonio
Keyword(s):  
Leucine Zipper ◽  
Axon Regeneration ◽  
Heat Shock Protein 90 ◽  
Hsp90 Inhibitor ◽  
Loss Of Function ◽  
Hsp90 Inhibition ◽  
Axon Injury ◽  
Evolutionarily Conserved ◽  
The Stability

Peripheral nerve injury induces a robust proregenerative program that drives axon regeneration. While many regeneration-associated genes are known, the mechanisms by which injury activates them are less well-understood. To identify such mechanisms, we performed a loss-of-function pharmacological screen in cultured adult mouse sensory neurons for proteins required to activate this program. Well-characterized inhibitors were present as injury signaling was induced but were removed before axon outgrowth to identify molecules that block induction of the program. Of 480 compounds, 35 prevented injury-induced neurite regrowth. The top hits were inhibitors to heat shock protein 90 (HSP90), a chaperone with no known role in axon injury. HSP90 inhibition blocks injury-induced activation of the proregenerative transcription factor cJun and several regeneration-associated genes. These phenotypes mimic loss of the proregenerative kinase, dual leucine zipper kinase (DLK), a critical neuronal stress sensor that drives axon degeneration, axon regeneration, and cell death. HSP90 is an atypical chaperone that promotes the stability of signaling molecules. HSP90 and DLK show two hallmarks of HSP90–client relationships: (i) HSP90 binds DLK, and (ii) HSP90 inhibition leads to rapid degradation of existing DLK protein. Moreover, HSP90 is required for DLK stability in vivo, where HSP90 inhibitor reduces DLK protein in the sciatic nerve. This phenomenon is evolutionarily conserved in Drosophila. Genetic knockdown of Drosophila HSP90, Hsp83, decreases levels of Drosophila DLK, Wallenda, and blocks Wallenda-dependent synaptic terminal overgrowth and injury signaling. Our findings support the hypothesis that HSP90 chaperones DLK and is required for DLK functions, including proregenerative axon injury signaling.

Early prediction of response in patients with advanced/metastatic non-small cell lung cancer during chemotherapy with FDG-PET-CT

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 13154-13154
Author(s):  
D. Lee ◽  
S. Kim ◽  
H. Kim ◽  
J. Choo ◽  
J. Song ◽  
...  
Keyword(s):  
Predictive Value ◽  
Fdg Pet ◽  
Standard Treatment ◽  
Metabolic Response ◽  
Response To Therapy ◽  
Prediction Of Response ◽  
Fdg Uptake ◽  
Standardized Uptake Values ◽  
Best Response ◽  
Pet Ct

13154 Background: To evaluate the use of 18-fluorodeoxyglucose positron emission tomography-computed tomography (PET-CT) for prediction of response and survival early during the course of treatment in patients with advanced/metastatic NSCLC. Methods: Between May 2004 and November 2005, 31 patients (gender, 23M, 8F; stage, 2IIIB/29IV, histology, 6 squamous cell ca, 22 adenoca, 3 NOS; age median 57 (30–73 y)) with histopathologically proven NSCLC stage IIIB/IV were enrolled into this study. PET-CT was performed prior to and after one cycle of treatment. Early changes of primary tumor FDG-uptake measured by standardized uptake values (SUV) were correlated with best response to therapy as assessed by CT scan according to WHO response criteria. Results: Patients underwent standard treatment with gemcitabine/vinorelbine (15), gemcitabine/cisplatin (1) gemcitabine/vinorelbine/cisplatin (1), irinotecan/cisplatin (9) or gefitinib (5). In the 25 patients evaluable for response, other 6 patients ongoing, 9 patients achieved a partial response (36%), 5 showed stable diseases and 11 were progressive. Using a cut-off value of 20% reduction of FDG-uptake as a criterion for a response in PET-CT, subsequent best response was predicted with a sensitivity of 88.9% and a specificity of 87.5%. The positive predictive value of a metabolic response was 80.0% and the negative predictive value 93.3%, respectively. There was a significant correlation between the decrease of tumor metabolic activity and subsequent best response (p< 0.001). The median time to progression for PET-CT responder was 10.1 months when compared with that of non-responders with 2.6 months (log-rank p=0.009). Conclusions: Using FDG-PET best response to standard treatment and patient outcome can be predicted very early and therefore, the use of PET-CT may allow to reduce side effects and costs of ineffective therapy in non-responding patients No significant financial relationships to disclose.

Assessment of the heat shock protein 90 (HSP90) inhibitor IPI504 alone or in combination with the tyrosine kinase inhibitor (TKI) imatinib in mice carrying xenografts of human gastrointestinal stromal tumors (GIST)

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 10534-10534 ◽  
Author(s):  
P. Schoffski ◽  
G. Floris ◽  
R. Sciot ◽  
C. Stefan ◽  
A. Wozniak ◽  
...  
Keyword(s):  
Kinase Inhibitor ◽  
Single Agent ◽  
Substantial Reduction ◽  
Heat Shock Protein 90 ◽  
Dose Schedule ◽  
Hsp90 Inhibitor ◽  
Antitumor Effects ◽  
New Strategy ◽  
Grade 3 ◽  
Anti Tumor Activity

10534 Background: Inhibition of HSP90 is a new strategy for treatment of GIST. IPI-504 is a potent i.v. HSP90 inhibitor. We assessed the activity of IPI-504 in imatinib-sensitive GIST xenografts, alone/combined with the TKI. Methods: Human GIST882 cells (KIT exon 13 mut.) were grafted in 43 nude mice, who were randomized to 4 groups: A (n=13; control); B (n=18; IPI-504 100 mg/kg 3x/wk p.o.); C (n=8; imatinib 50 mg/kg 2x/d p.o.); D (n=4; IPI-504+imatinib, dose/schedule as above) for 2 weeks. Histopathological assessment was done by H&E and KIT immunostaining, histological response (HR) was defined by magnitude of necrosis and myxoid degeneration [grade 1 (0–10%), 2 (>10% - ≤ 50%), 3 (> 50% - ≤90%), 4 (>90%)]. Expression/activation of KIT and its signaling (AKT, S6, MAPK) was assessed by Western blot. Results: IPI-504 alone significantly reduced tumor volume (41%) at day 14, further enhanced by adding imatinib (58%). Imatinib alone led to only a 5% reduction. IPI-504 induced grade 2 HR in 17/36 tumors, while the majority of tumors (13/15) treated with imatinib showed grade 1 HR. Grade 3/4 HRs were only seen with the combination. Mitosis decreased 3.3-fold, apoptosis increased 1.3-fold with IPI-504. Despite substantial reduction in mitotic activity in C and D (8.2- and 82-fold), apoptosis was virtually unaffected. In the IPI-504 arm, KIT levels were partially downregulated. Imatinib alone had no effect on KIT expression, while the combination produced a marked suppression of total KIT, accompanied by complete downregulation of the signaling. Loss of KIT in the combination arm was confirmed by immunostaining. Although KIT was not completely degraded with IPI-504, measurable effects on activation of AKT, S6 and MAPK were observed. Conclusions: IPI-504 has consistent antitumor effects in GIST xenografts, both histologically and on the molecular level. Combining IPI-504 with imatinib substantially enhances anti-tumor activity, providing a strong rationale for clinical trials of IPI-504 in GIST as single agent and in combination. [Table: see text]

scholarly journals Indoxyl Sulfate Induces Renal Fibroblast Activation through a Targetable Heat Shock Protein 90-Dependent Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Samantha Milanesi ◽  
Silvano Garibaldi ◽  
Michela Saio ◽  
Giorgio Ghigliotti ◽  
Daniela Picciotto ◽  
...  
Keyword(s):  
Heat Shock Protein 90 ◽  
Hsp90 Inhibitor ◽  
Indoxyl Sulfate ◽  
Collagen I ◽  
Hsp90 Inhibition ◽  
Fibroblast Activation ◽  
Tubular Necrosis ◽  
Pathway Activation ◽  
Potential Strategy ◽  
Dependent Pathway

Indoxyl sulfate (IS) accumulation occurs early during chronic kidney disease (CKD) progression and contributes to renal dysfunction by inducing fibrosis, inflammation, oxidative stress, and tissue remodeling. Renal toxicity of high IS concentrations (250 μM) has been widely explored, particularly in resident tubular and glomerular cells, while the effect of a moderate IS increase on kidneys is still mostly unknown. To define the effects of IS accumulation on renal fibroblasts, we first analyzed kidneys of C57BL/6 mice receiving IS (0.1%) in drinking water for 12 weeks. As a next step, we treated renal fibroblasts (NRK-49F) with IS (20 μM) with or without the HSP90 inhibitor 17-AAG (1 μM). In mouse kidneys, IS increased the collagen deposition and HSP90 and α-SMA expression (immunohistochemistry) in interstitial fibroblasts and caused tubular necrosis (histological H&E and picrosirius red staining). In NRK-49F cells, IS induced MCP1, TGF-β, collagen I, α-SMA, and HSP90 gene/protein expression and Smad2/3 pathway activation. IS had no effects on fibroblast proliferation and ROS production. 17-AAG counteracted IS-induced MCP1, TGF-β, collagen I, and α-SMA expression and Smad2/3 phosphorylation. Our study demonstrates that the IS increase promotes renal fibroblast activation by a HSP90-dependent pathway and indicates HSP90 inhibition as a potential strategy to restrain IS-induced kidney inflammation and fibrosis in CKD.

scholarly journals SNX-2112, a selective Hsp90 inhibitor, potently inhibits tumor cell growth, angiogenesis, and osteoclastogenesis in multiple myeloma and other hematologic tumors by abrogating signaling via Akt and ERK

Blood ◽  
2009 ◽  
Vol 113 (4) ◽  
pp. 846-855 ◽  
Author(s):  
Yutaka Okawa ◽  
Teru Hideshima ◽  
Paul Steed ◽  
Sonia Vallet ◽  
Steven Hall ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Cell Growth ◽  
Umbilical Vein ◽  
Conformational Stability ◽  
Heat Shock Protein 90 ◽  
Hsp90 Inhibitor ◽  
Tube Formation ◽  
Osteoclast Formation ◽  
Hsp90 Inhibition

AbstractHeat-shock protein 90 (Hsp90) acts as a molecular chaperone required for maintaining the conformational stability of client proteins regulating cell proliferation, survival, and apoptosis. Here we investigate the biologic significance of Hsp90 inhibition in multiple myeloma (MM) and other hematologic tumors using an orally available novel small molecule inhibitor SNX-2112, which exhibits unique activities relative to 17-allyamino-17-demethoxy-geldanamycin (17-AAG). SNX-2112 triggers growth inhibition and is more potent than 17-AAG against MM and other malignancies. It induces apoptosis via caspase-8, -9, -3, and poly (ADP-ribose) polymerase cleavage. SNX-2112 inhibits cytokine-induced Akt and extracellular signal-related kinase (ERK) activation and also overcomes the growth advantages conferred by interleukin-6, insulin-like growth factor-1, and bone marrow stromal cells. Importantly, SNX-2112 inhibits tube formation by human umbilical vein endothelial cells via abrogation of eNOS/Akt pathway and markedly inhibits osteoclast formation via down-regulation of ERK/c-fos and PU.1. Finally, SNX-2112, delivered by its prodrug SNX-5422, inhibits MM cell growth and prolongs survival in a xenograft murine model. Our results indicate that blockade of Hsp90 by SNX-2112 not only inhibits MM cell growth but also acts in the bone marrow microenvironment to block angiogenesis and osteoclastogenesis. Taken together, our data provide the framework for clinical studies of SNX-2112 to improve patient outcome in MM and other hematologic malignancies.

Early Prediction of Response to Sunitinib After Imatinib Failure by 18F-Fluorodeoxyglucose Positron Emission Tomography in Patients With Gastrointestinal Stromal Tumor

2009 ◽  
Vol 27 (3) ◽  
pp. 439-445 ◽  
Author(s):  
John O. Prior ◽  
Michael Montemurro ◽  
Maria-Victoria Orcurto ◽  
Olivier Michielin ◽  
François Luthi ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Treatment Response ◽  
Fdg Pet ◽  
Progressive Disease ◽  
Kinase Inhibitor ◽  
Emission Tomography ◽  
Early Assessment ◽  
Standardized Uptake Values ◽  
Mutational Status ◽  
Positron Emission

Purpose Positron emission tomography with 18F-fluorodeoxyglucose (FDG-PET) was used to evaluate treatment response in patients with gastrointestinal stromal tumors (GIST) after administration of sunitinib, a multitargeted tyrosine kinase inhibitor, after imatinib failure. Patients and Methods Tumor metabolism was assessed with FDG-PET before and after the first 4 weeks of sunitinib therapy in 23 patients who received one to 12 cycles of sunitinib therapy (4 weeks of 50 mg/d, 2 weeks off). Treatment response was expressed as the percent change in maximal standardized uptake values (SUV). The primary end point of time to tumor progression was compared with early PET results on the basis of traditional Response Evaluation Criteria in Solid Tumors (RECIST) criteria. Results Progression-free survival (PFS) was correlated with early FDG-PET metabolic response (P < .0001). Using −25% and +25% thresholds for SUV variations from baseline, early FDG-PET response was stratified in metabolic partial response, metabolically stable disease, or metabolically progressive disease; median PFS rates were 29, 16, and 4 weeks, respectively. Similarly, when a single FDG-PET positive/negative was considered after 4 weeks of sunitinib, the median PFS was 29 weeks for SUVs less than 8 g/mL versus 4 weeks for SUVs of 8 g/mL or greater (P < .0001). None of the patients with metabolically progressive disease subsequently responded according to RECIST criteria. Multivariate analysis showed shorter PFS in patients who had higher residual SUVs (P < .0001), primary resistance to imatinib (P = .024), or nongastric GIST (P = .002), regardless of the mutational status of the KIT and PDGFRA genes. Conclusion Week 4 FDG-PET is useful for early assessment of treatment response and for the prediction of clinical outcome. Thus, it offers opportunities to individualize and optimize patient therapy.

scholarly journals Delayed FDG PET Provides Superior Glioblastoma Conspicuity Compared to Conventional Image Timing

2021 ◽  
Vol 12 ◽  
Author(s):  
Jason Michael Johnson ◽  
Melissa M. Chen ◽  
Eric M. Rohren ◽  
Sujit Prabhu ◽  
Beth Chasen ◽  
...  
Keyword(s):  
Fdg Pet ◽  
Conventional Imaging ◽  
Delayed Imaging ◽  
Time Points ◽  
Non Invasive ◽  
Imaging Time ◽  
Standardized Uptake Values ◽  
Pre Treatment ◽  
True Progression ◽  
Time Point

Background: Glioblastomas are malignant, often incurable brain tumors. Reliable discrimination between recurrent disease and treatment changes is a significant challenge. Prior work has suggested glioblastoma FDG PET conspicuity is improved at delayed time points vs. conventional imaging times. This study aimed to determine the ideal FDG imaging time point in a population of untreated glioblastomas in preparation for future trials involving the non-invasive assessment of true progression vs. pseudoprogression in glioblastoma.Methods: Sixteen pre-treatment adults with suspected glioblastoma received FDG PET at 1, 5, and 8 h post-FDG injection within the 3 days prior to surgery. Maximum standard uptake values were measured at each timepoint for the central enhancing component of the lesion and the contralateral normal-appearing brain.Results: Sixteen patients (nine male) had pathology confirmed IDH-wildtype, glioblastoma. Our results revealed statistically significant improvements in the maximum standardized uptake values and subjective conspicuity of glioblastomas at later time points compared to the conventional (1 h time point). The tumor to background ratio at 1, 5, and 8 h was 1.4 ± 0.4, 1.8 ± 0.5, and 2.1 ± 0.6, respectively. This was statistically significant for the 5 h time point over the 1 h time point (p &gt; 0.001), the 8 h time point over the 1 h time point (p = 0.026), and the 8 h time point over the 5 h time point (p = 0.036).Conclusions: Our findings demonstrate that delayed imaging time point provides superior conspicuity of glioblastoma compared to conventional imaging. Further research based on these results may translate into improvements in the determination of true progression from pseudoprogression.

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