***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: UNLABELLED Gastrointestinal stromal tumors ( GISTs ) are gaining the interest of research ers because of impressive metabolic response to the targeted molecular therapeutic drug imatinib mesylate . Initial reports suggest an impressive role for (18)F-FDG PET in follow-up of therapy for these tumors . However , the role of (18)F-FDG PET versus that of CT has not been established . Therefore , we compared the roles of (18)F-FDG PET and CT in staging and evaluation of early response to imatinib mesylate  therapy in recurrent or metastatic GIST . METHODS The study included 54 patients who underwent (18)F-FDG PET and CT scans within 3 wk before initiation of imatinib mesylate therapy . Forty-nine of these patients underwent repeat scans 2 mo after therapy . The numbers of sites or organs containing lesions on (18)F-FDG PET and CT scans were compared . Corresponding lesions on (18)F-FDG PET and CT scans or those confirmed to be malignant in appearance by other imaging modalities or on follow-up were considered true positives . Lesions seen on (18)F-FDG PET or CT scans but not seen or confirmed to be of benign appearance with other imaging modalities or on follow-up were considered false positives . Measurements of the maximum st and ard uptake value ( SUV ) on (18)F-FDG PET scans and tumor size on CT scans were used for quantitative evaluation of early tumor response to therapy . RESULTS A total of 122 and 114 sites and /or organs were involved on pretherapy (18)F-FDG PET and CT scans , respectively . The sensitivity and positive predictive values ( PPVs ) for CT were 93 % and 100 % ; whereas these values for (18)F-FDG PET were 86 % and 98 % . However , the differences between these values for CT and (18)F-FDG PET were not statistically significant ( P = 0.27 for sensitivity and 0.25 for PPV ) . This suggests comparable performance of (18)F-FDG PET and CT in staging GISTs . Repeat scans at 2 mo after therapy showed agreement between (18)F-FDG PET and CT scans in 71.4 % of patients ( 57.1 % having a good response to therapy and 14.3 % lacking a response ) . Discrepant results between (18)F-FDG PET and CT were recorded for 28.6 % of the patients . (18)F-FDG PET predicted response to therapy earlier than did CT in 22.5 % of patients during a longer follow-up interval ( 4 - 16 mo ) , whereas CT predicted lack of response to therapy earlier than (18)F-FDG PET in 4.1 % . One patient did not undergo long-term follow-up . These findings suggest that (18)F-FDG PET is superior to CT in predicting early response to therapy in recurrent or metastatic GIST patients . CONCLUSION The performances of (18)F-FDG PET and CT are comparable in staging GISTs before initiation of imatinib mesylate therapy . However , (18)F-FDG PET is superior to CT in predicting early response to therapy . Thus , (18)F-FDG PET is a better guide for imatinib mesylate therapy AIM The aim of this study was to evaluate the utility of positron emission tomography with 18F-fluorodeoxyglucose ( FDG-PET ) in monitoring response in refractory GIST . METHODS This multicenter study prospect ively evaluated 21 patients with locally advanced and /or metastatic GIST refractory to with high-dose imatinib ( 800 mg/day ) treated with doxorubicin 15 - 20 mg/m2/weekly for 4 cycles , followed by imatinib maintenance ( 400 mg/day ) .  CT and FDG-PET were performed at baseline and after completion of therapy . RESULTS Mean baseline tumor size on CT was 5.9 cm . Median progression-free survival ( PFS ) was 219 days ( range 62 - 1108 ) . Three out of 21 patients ( 14 % ) had partial responses ( PR ) under RECIST criteria , 12 patients ( 57 % ) remained stable ( SD ) and 6 showed progression ( PD ) of the disease during treatment ( 29 % ) . Six patients had PR by FDG-PET , 15 showed SD ( n=9 ) or PD ( n=6 ) based on EORTC criteria . Patients with a PFS < 6 mo showed a significantly higher ∑SUVmax at baseline ( 26.04±13.4 ) than those with PFS≥6 mo ( 9.82±5.0 ) ( P<0.05 ) . A correlation was found between PET response and PFS : PR 14±6.1 mo , SD 5.5±0.8 mo and PD 3.5±4.1 mo ( P<0.05 ) . A residual SUVmax < 5 after treatment correlated with improved PFS ( 314±315 days vs 131±91 days ) ( P<0.01 ) . Survival curves showed a significant association between PET response and PFS ( P<0.05 ) . Patients with wild-type genotype KIT ( KIT-WT ) showed a significantly lower baseline SUVmax ( 5.36±1.4 ) than non-WT KIT ( 8.40±3.6 ) ( P<0.05 ) . CONCLUSION FDG-PET is useful in assessing response of GIST refractory to imatinib and correlates with the presence of KIT-WT . Baseline ∑SUVmax can predict response to treatment in this series BACKGROUND Although most patients with gastrointestinal stromal tumor ( GIST ) treated with imatinib mesylate  achieve remission or disease stabilization , a significant proportion show progressive disease ( PD ) with or without initial favorable responses . We evaluated and categorized the patterns of progression of metastatic or unresectable GIST treated with imatinib to identify the prognostic significance and contribution to further treatment decision-making . METHODS We prospect ively gathered clinical data from 62 GIST patients treated with imatinib mesylate ( 400 mg/day ) over a median period of 26 months . Twenty-one of these patients showed evidence of PD based on Response Evaluation Criteria in Solid Tumor criteria . RESULTS Four patterns of PD were defined : focal progression ( FP , N = 4 ) , general progression ( GP , N = 6 ) , new cystic lesion ( NCL , N = 6 ) and new solid lesion ( NSL , N = 5 ) . The groups were found to differ in terms of time to progression and prior response to imatinib .  The proportion of patients who responded to escalated doses of imatinib  ( 600 - 800 mg/day ) was significantly higher in NCL patients ( P = 0.04 ) . Overall survival and survival from the confirmation of PD were significantly better in NCL or FP patients compared with NSL or GP patients ( P = 0.0157 , P = 0.0013 ) . CONCLUSIONS We identified four patterns of disease progression based on radiographic criteria with different clinical characteristics and impact on survival . Knowledge of these patterns was relevant for early detection and may be helpful in further treatment decision-making BACKGROUND Assessment of the change in tumour burden is an important feature of the clinical evaluation of cancer therapeutics : both tumour shrinkage ( objective response ) and disease progression are useful endpoints in clinical trials . Since RECIST was published in 2000 , many investigators , cooperative groups , industry and government authorities have adopted these criteria in the assessment of treatment outcomes . However , a number of questions and issues have arisen which have led to the development of a revised RECIST guideline ( version 1.1 ) . Evidence for changes , summarised in separate papers in this special issue , has come from assessment of a large data warehouse ( > 6500 patients ) , simulation studies and literature review s. HIGHLIGHTS OF REVISED RECIST 1.1 : Major changes include : Number of lesions to be assessed : based on evidence from numerous trial data bases merged into a data warehouse for analysis purpose s , the number of lesions required to assess tumour burden for response determination has been reduced from a maximum of 10 to a maximum of five total ( and from five to two per organ , maximum ) . Assessment of pathological lymph nodes is now incorporated : nodes with a short axis of 15 mm are considered measurable and assessable as target lesions . The short axis measurement should be included in the sum of lesions in calculation of tumour response . Nodes that shrink to < 10 mm short axis are considered normal . Confirmation of response is required for trials with response primary endpoint but is no longer required in r and omised studies since the control arm serves as appropriate means of interpretation of data . Disease progression is clarified in several aspects : in addition to the previous definition of progression in target disease of 20 % increase in sum , a 5 mm absolute increase is now required as well to guard against over calling PD when the total sum is very small . Furthermore , there is guidance offered on what constitutes ' unequivocal progression ' of non-measurable/non-target disease , a source of confusion in the original RECIST guideline . Finally , a section on detection of new lesions , including the interpretation of FDG-PET scan assessment is included . Imaging guidance : the revised RECIST includes a new imaging appendix with up date d recommendations on the optimal anatomical assessment of lesions . FUTURE WORK A key question considered by the RECIST Working Group in developing RECIST 1.1 was whether it was appropriate to move from anatomic unidimensional assessment of tumour burden to either volumetric anatomical assessment or to functional assessment with PET or MRI . It was concluded that , at present , there is not sufficient st and ardisation or evidence to ab and on anatomical assessment of tumour burden . The only exception to this is in the use of FDG-PET imaging as an adjunct to determination of progression . As is detailed in the final paper in this special issue , the use of these promising newer approaches requires appropriate clinical validation studies BACKGROUND HSP90 inhibition leads to proteosomal degradation of activated KIT and has in vitro activity against gastrointestinal stromal tumors ( GIST ) .  BIIB021 is an oral non-ansamycin HSP90 inhibitor . We carried out a phase II study of BIIB021 in patients with GIST refractory to imatinib and sunitinib .  PATIENTS AND METHODS The primary end-point was metabolic partial response ( mPR ) as assessed by  fluorodeoxyglucose positron emission tomography ( FDG-PET ) .  The secondary end-points were pharmacokinetic assessment s of BIIB021 and pharmacodynamic assessment s of HSP70 .  Twenty-three patients were treated on two schedules : 12 pts received 600 mg twice a week ( BIW ) and 11 patients received 400 mg three times a week ( TIW ) . All had prior imatinib and sunitinib but stopped>14 days before starting BIIB021 . RESULTS The median age was 59 years ( 33 - 88 years ) , 61 % male , 44 % Eastern Cooperative Oncology Group 1 ( ECOG1 ) . The best response was PR by FDG-PET for five patients ( 3/12 at 600 mg BIW and 2/9 at 400 TIW ) for an overall response rate of 22 % . The response duration was 25 - 138 days . Adverse events ( AEs ) were mild to moderate . The mean Cmax was 1.5 µmol and the mean AUC was 2.9 µmol h. Cmax>1.5 µmol was associated with a decrease in st and ardized uptake value ( SUVmax ) . HSP70 increased substantially following treatment . CONCLUSIONS This study met its primary end-point . BIIB021 leads to objective responses in refractory GIST patients . Pharmacodynamic studies confirmed HSP90 inhibition . Further evaluation of BIIB021 in GIST is warranted Typical MRI findings for gastro-intestinal stromal tumours ( GIST ) under treatment with imatinib were evaluated . MRI was performed in 45 patients ( 25 responders , 20 non-responders ) with metastatic or locally advanced , unresectable GIST . Target lesions were selected and re-evaluated after 2 , 4 , and 6 months of therapy with imatinib . The target tumour response ( TTR ) was classified according to RECIST criteria . TTR , signal intensity in the centre and border of the lesion and the presence and the extension of a hypervascular rim were analysed . The mean diameter of the marker lesions decreased significantly ( P<0.001 ) from 7.1±2.6 cm to 5.9±2.3 cm after 6 months . Accuracy of RECIST criteria was 51 % , 69 % and 73 % on MRI 2 , 4 and 6 months for response assessment . In addition , responders had higher signal-to-noise ratios on T2-w images after 2 months ( P<0.05 ) and a decrease of vascularised areas in the lesion 4 and 6 months after treatment ( each P<0.01 ) , when compared with non-responders . Beyond the size measurement for response assessment , MRI provides additional information of tumour response using SI of T2-w images and quantification 
    Output:
    
CT is still the st and ard method for the evaluation of therapy response despite its several limitations .