183 Background: Radionuclide therapy targeting the prostate specific membrane antigen (177Lu-PSMA therapy) has proven to be an effective treatment in men with metastatic castration resistant prostate cancer (mCRPCs). Despite representing a significant therapeutic breakthrough, a critical unmet need in 177Lu-PSMA therapy, is a prognostic biomarker for treatment optimization. Imaging and standard biomarkers have limited value. The PROSTest is a new 27-gene algorithmic signature originally developed for prostate adenocarcinoma diagnosis (0 to 100, positive score ≥20). We hypothesized that PROSTest would be elevated in mCRPCs and could have utility as a biomarker for mCRPC management. Methods: Prospective enrollment of 113 mCRPC for 177Lu-PSMA therapy (KlbB-5338-0302021 study). Pathology, clinical and biomarker data were available as was PSMA-PET/CT. Blood samples were collected for PROSTest prior to therapy. Target genes were isolated and amplified using qPCR. PROSTest scores (0-100) were obtained following algorithmic analysis. Scores were correlated with mCRPC diagnosis and baseline information. Scores and standard clinical measures were evaluated as prognostic factors with survival as endpoint. Mann-Whitney U-test, Kaplan-Meier survival and Cox proportional hazards regression analysis were utilized. All data: median (IQ range). Results: 89 (79%) patients were evaluable. Age was 75 (68-80). Disease characteristics at time of diagnosis included Gleason scores 8-10 (70%) and TMM: T3-T4 tumors (67%), N1 (53%), M1 (45%). At the time of therapy all patients were metastatic and all exhibited PSMA-positive disease. The highest tumor SUVmax was 51 (28-78). PSA levels were 69ng/mL (18-305). The PROSTest score was 89 (81-92). PROSTest scores were weakly correlated with age (r=0.33, p=0.0015) but not with baseline histopathological parameters (e.g., Gleason score, TNM) or pretreatment imaging results (e.g., SUVmax). Twenty-four (27%) patients have perished. Treatment and follow-up (5 months, 3-18) are ongoing. The mOS was 15 months. No factors were associated with death as an outcome except for the PROSTest score. PROSTest scores ≥79 (based on ROC analysis) were associated with significantly increased risk for mortality (HR: 2.9, 95% CI: 1.5-7.4). The mOS was 14 months in patients with pre-therapy PROSTest scores >79 compared to mOS not reached for PROSTest scores <79 ( p=0.02). In the COX model, baseline PROSTest was confirmed to be significantly predictive of death despite therapy (β = 1.51, p=0.01). Conclusions: The PROSTest blood gene expression score is elevated in mCRPCs. Levels are not associated with baseline clinical, histopathological, pretreatment PSA or imaging parameters. Elevated expression (≥79) of this biomarker prior to treatment was associated with a lower survival and could be used to predict survival in patients undergoing 177Lu-PSMA.

Purpose To assess early tumor response with quantitated SPECT/CT and to correlate it with clinical outcome in metastatic castration–resistant prostate cancer (mCRPC) patients treated with 177 Lutetium-PSMA I&T therapy. Methods Single-center, observational study, part of the prospective Swiss national cancer registry study investigating the safety and efficacy of [ 177 Lu]Lu-PSMA I&T (EKNZ: 2021–01271) in mCRPC patients treated with at least two cycles of [ 177 Lu]Lu-PSMA I&T 6-weekly. After the first and second cycle quantitated SPECT/CT (Symbia Intevo, Siemens) was acquired 48 h after injection (three fields of view from head to thigh, 5 s/frame) and reconstructed using xQuant® (48i, 1 s, 10-mm Gauss). Image analysis: The PSMA-positive total tumor volumes (TTV) were semi-automatically delineated using a SUV threshold of 3 with MIMencore® (version 7.1.3, Medical Image Merge Software Inc.). Changes in TTV, highest tumor SUVmax, and total tumor SUVmean between cycles 1 and 2 were calculated and grouped into a) stable or decrease and b) increase. Serum PSA levels were assessed at each therapy cycle and at follow-up until progression or death. Changes in TTV, PSA, SUVmax, and SUVmean were correlated with PSA-progression-free survival (PSA-PFS) and the overall survival (OS) using the Kaplan–Meier methodology (log-rank test). Results Between 07/2020 and 04/2022, 111 patients were screened and 73 finally included in the data analysis. The median follow-up was 8.9 months (range 1.4–26.6 months). Stable or decreased TTV at cycle 2 was associated with longer OS (hazard ratio (HR) 0.28, 95% confidence interval (CI) 0.09–0.86, p < 0.01). Similar, stable, or decreased PSA was associated with longer OS (HR 0.21; CI 0.07–0.62, p < 0.01) and PSA-PFS (HR 0.34; 95% CI 0.16–0.72, p < 0.01). Combining TTV and PSA will result in an augmented prognostic value for OS (HR 0.09; CI 0.01–0.63; p < 0.01) and for PSA-PFS (HR 0.11; CI 0.02–0.68; p < 0.01). A reduction of SUVmax or SUVmean was not prognostically relevant, neither for OS ( p 0.88 and 0.7) nor for PSA-PFS ( p 0.73 and 0.62, respectively). Conclusion Six weeks after initiating [ 177 Lu]Lu-PSMA I&T, TTV and serum PSA appear to be good prognosticators for OS. Combined together, TTV + PSA change demonstrates augmented prognostic value and can better predict PSA-PFS. Larger studies using TTV change prospectively as an early-response biomarker are warranted for implementing management change towards a more personalized clinical practice.

PURPOSE:11-C-methionine (MET)-positron emission tomography (PET) as an adjunct to magnetic resonance imaging (MRI) has been proposed as a suitable molecular imaging modality for localizing pituitary adenomas in Cushing's disease. 18-F-Fluoroethyl-L-tyrosine (FET)-PET, which is more widely available has not yet been reported in this context.METHODS:Retrospective double-center cohort study on 15 patients who underwent transsphenoidal surgery for biochemically proven Cushing's disease between 2011 and 2019. Preoperative MET-PET/MRI and/or FET-PET/MRI were compared with intraoperative and histopathological examinations using the Mann Whitney U test and the Fisher's Exact test, along with positive predictive value calculations.RESULTS:Fifteen patients were included, with a mean age of 47.2 (18-69) years. Six patients received either a MET-PET/MRI or a FET-PET/MRI and 3 patients both exams, respectively. 67% of the tumors were detected by MRI (MET-PET-group [56%]; FET-PET-group [78%]). All tumors were microadenomas with a mean adenoma volume of 0.19 cm3 (0.02-0.78), all of which displayed a circumscribed pathological FET- and/or MET-uptake. FET-PET/MRI results positively correlated with the localization of the tumor confirmed intraoperatively and histopathologically in all cases, resulting in a sensitivity and specificity of FET-PET/MRI for tumor localization of 100% (95% CI 66.37-100%). One MET-PET/MRI suggested a localization contralateral to the expected spot. The sensitivity and specificity of MET-PET for tumor localization hence was 89% (95% CI 51.75-99.72%).CONCLUSIONS:Preoperative hybrid FET-PET/MRI and MET-PET/MRI have a high predictive value in localizing corticotroph adenoma for selective adenomectomy in Cushing's disease.

Behandlung des fortgeschrittenen Prostatakarzinoms – eine interdisziplinäre EmpfehlungAurelius Omlin*, Martin Spahn*, Jörg Beyer, Daniel Eberli, Silke Gillessen, Wolfram Jochum, Marc Kueng, Egbert Nitzsche, Cyrill A. Rentsch, Enrico Roggero, Hans-Peter Schmid, Frank Stenner, Arnoud J. Templeton, Damian Wild, Stephen Wyler, Daniel Zwahlen*, and Richard Cathomas*Aurelius Omlin* Abteilung für Onkologie und Hämatologie, Kantonsspital St. Gallen Universitätsklinik für Medizinische Onkologie, Inselspital, Universität BernSearch for more papers by this author, Martin Spahn* Zentrum für Urologie Zürich und Prostatakarzinomzentrum Hirslanden Zürich, Klinik Hirslanden Zürich Kinderurologie Universität Duisburg/EssenSearch for more papers by this author, Jörg Beyer Universitätsklinik für Medizinische Onkologie, Inselspital, Universität BernSearch for more papers by this author, Daniel Eberli Klinik für Urologie, Universitätsspital ZürichSearch for more papers by this author, Silke Gillessen Abteilung für Onkologie und Hämatologie, Kantonsspital St. Gallen Universitätsklinik für Medizinische Onkologie, Inselspital, Universität Bern Division of Cancer Sciences, University of Manchester and The Christie, Manchester, UKSearch for more papers by this author, Wolfram Jochum Klinik für Pathologie, Kantonsspital St. GallenSearch for more papers by this author, Marc Kueng Klinik für Onkologie, HFR Kantonsspital FreiburgSearch for more papers by this author, Egbert Nitzsche Klinik für Nuklearmedizin, Kantonsspital AarauSearch for more papers by this author, Cyrill A. Rentsch Klinik für Urologie, Universitätsspital BaselSearch for more papers by this author, Enrico Roggero IOSI, Oncology Institute of Southern Switzerland, BellinzonaSearch for more papers by this author, Hans-Peter Schmid Klinik für Urologie, Kantonsspital St. GallenSearch for more papers by this author, Frank Stenner Klinik für Onkologie, Universitätsspital BaselSearch for more papers by this author, Arnoud J. Templeton Klinik für Onkologie, Claraspital BaselSearch for more papers by this author, Damian Wild Abteilung für Nuklearmedizin, Universitätsspital BaselSearch for more papers by this author, Stephen Wyler Klinik für Urologie, Kantonsspital AarauSearch for more papers by this author, Daniel Zwahlen* Institut Radio-Onkologie, Kantonsspital ChurSearch for more papers by this author, and Richard Cathomas* Abteilung für Onkologie, Kantonsspital ChurSearch for more papers by this authorPublished Online:September 19, 2018https://doi.org/10.1024/1661-8157/a003054PDFView Full Text ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinkedInReddit SectionsMoreBibliografie Gillessen S, Attard G, Beer TM, et al.: Management of patients with advanced prostate cancer: the report of the Advanced Prostate Cancer Consensus Conference APCCC 2017. Eur Urol 2018; 73: 178–211. First citation in articleCrossref Medline, Google Scholar Stephenson AJ, Bolla M, Briganti A, et al.: Postoperative radiation therapy for pathologically advanced prostate cancer after radical prostatectomy. Eur Urol 2012; 61: 443–451. First citation in articleCrossref Medline, Google Scholar Ghadjar P, Zwahlen D, Aebersold DM, Zimmermann F: Postoperative radiotherapy after radical prostatectomy: indications and open questions. Prostate Cancer 2012; 2012: 963417. First citation in articleCrossref Medline, Google Scholar Bolla M, van Poppel H, Tombal B, et al.: Postoperative radiotherapy after radical prostatectomy for high-risk prostate cancer: long-term results of a randomised controlled trial (EORTC trial 22911). Lancet 2012; 380: 2018–2027. First citation in articleCrossref Medline, Google Scholar Thompson IM, Tangen CM, Paradelo J, et al.: Adjuvant radiotherapy for pathological T3N0M0 prostate cancer significantly reduces risk of metastases and improves survival: long-term followup of a randomized clinical trial. The Journal of urology 2009; 181: 956–962. First citation in articleCrossref Medline, Google Scholar Wiegel T, Bartkowiak D, Bottke D, et al.: Adjuvant radiotherapy versus wait-and-see after radical prostatectomy: 10-year follow-up of the ARO 96–02/AUO AP 09/95 trial. Eur Urol 2014; 66: 243–250. First citation in articleCrossref Medline, Google Scholar Abugharib A, Jackson WC Tumati V , et al.: Very early salvage radiotherapy improves distant metastasis-free survival. J Urol 2017; 197: 662–668. First citation in articleCrossref Medline, Google Scholar Tendulkar RD, Agrawal S, Gao T , et al.: Contemporary update of a multi-institutional predictive nomogram for salvage radiotherapy after radical prostatectomy. J Clin Oncol 2016; pii: JCO679647 . [Epub ahead of print] First citation in articleGoogle Scholar Cornford P, Bellmunt J, Bolla M, et al.: EAU-ESTRO-SIOG guidelines on prostate cancer. Part II: Treatment of relapsing, metastatic, and castration-resistant prostate cancer. Eur Urol 2017; 71: 630–642. First citation in articleCrossref Medline, Google Scholar Network NCC: Prostate Cancer 2017. Verfügbar unter https://www.nccn.org/professionals/physician_gls/f_guidelines.asp; letzter Zugriff am 16.07.2018. First citation in articleGoogle Scholar Ghadjar P, Hayoz S, Bernhard J, et al.: Acute toxicity and quality of life after dose-intensified salvage radiation therapy for biochemically recurrent prostate cancer after prostatectomy: first results of the randomized trial SAKK 09/10. J Clin Oncol 2015; 33: 4158–4166. First citation in articleGoogle Scholar Carrie C, Hasbini A, de Laroche G, et al.: Salvage radiotherapy with or without short-term hormone therapy for rising prostate-specific antigen concentration after radical prostatectomy (GETUG-AFU 16): a randomised, multicentre, open-label phase 3 trial. Lancet Oncol 2016; 17: 747–756. First citation in articleCrossref Medline, Google Scholar Shipley WU, Seiferheld W, Lukka HR, et al.: Radiation with or without antiandrogen therapy in recurrent prostate cancer. N Engl J Med 2017; 376: 417–428. First citation in articleCrossref Medline, Google Scholar Hellman S, Weichselbaum RR: Oligometastases. J Clin Oncol 1995; 13: 8–10. First citation in articleCrossref Medline, Google Scholar Sweeney CJ, Chen YH, Carducci M, et al.: Chemohormonal therapy in metastatic hormone-sensitive prostate cancer. N Engl J Med 2015; 373: 737–746. First citation in articleCrossref Medline, Google Scholar James ND, Sydes MR, Clarke NW, et al.: Addition of docetaxel, zoledronic acid, or both to first-line long-term hormone therapy in prostate cancer (STAMPEDE): survival results from an adaptive, multiarm, multistage, platform randomised controlled trial. Lancet 2016; 387: 1163–11677. First citation in articleCrossref Medline, Google Scholar James N, de Bono JS, Spears MR, et al.: Abiraterone for prostate cancer not previously treated with hormone therapy. N Engl J Med 2017; 377: 338–351. First citation in articleCrossref Medline, Google Scholar Fizazi N, Tran N, Fein L, et al.: Abiraterone plus prednisone in metastatic, castration-sensitive prostate cancer. N Engl J Med 2017; 377: 352–360. First citation in articleCrossref Medline, Google Scholar Tannock IF, de Wit R, Berry WR, et al.: Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer. N Engl J Med 2004; 351: 1502–1512. First citation in articleCrossref Medline, Google Scholar Parker C, Nilsson S, Heinrich D, et al.: Alpha emitter radium-223 and survival in metastatic prostate cancer. N Engl J Med 2013; 369: 213–223. First citation in articleCrossref Medline, Google Scholar de Bono JS, Oudard S, Ozguroglu M, et al.: Prednisone plus cabazitaxel or mitoxantrone for metastatic castration-resistant prostate cancer progressing after docetaxel treatment: a randomised open-label trial. Lancet 2010; 376: 1147–1154. First citation in articleCrossref Medline, Google Scholar de Bono JS, Logothetis CJ, Molina A, et al.: Abiraterone and increased survival in metastatic prostate cancer. N Engl J Med 2011; 364: 1995–2005. First citation in articleCrossref Medline, Google Scholar Ryan CJ, Smith MR, de Bono JS, et al.: Abiraterone in metastatic prostate cancer without previous chemotherapy. N Engl J Med 2013; 368: 138–148. First citation in articleCrossref Medline, Google Scholar Beer TM, Armstrong AJ, Rathkopf DE, et al.: Enzalutamide in metastatic prostate cancer before chemotherapy. N Engl J Med 2014; 371: 424–433. First citation in articleCrossref Medline, Google Scholar Scher HI, Fizazi K, Saad F, et al.: Increased survival with enzalutamide in prostate cancer after chemotherapy. N Engl J Med 2012; 367: 1187–1197. First citation in articleCrossref Medline, Google Scholar Mateo J, Carreira S, Sandhu S, et al.: DNA-repair cefects and olaparib in metastatic prostate cancer. N Engl J Med 2015; 373: 1697–1708. First citation in articleCrossref Medline, Google Scholar Schweizer MT, Cheng HH, Tretiakova MS, et al.: Mismatch repair deficiency may be common in ductal adenocarcinoma of the prostate. Oncotarget 2016; 7: 82504–82510. First citation in articleCrossref Medline, Google Scholar Padhani AR, Lecouvet FE, Tunariu N, et al.: METastasis reporting and cata system for prostate cancer: practical guidelines for acquisition, interpretation, and reporting of whole-body magnetic resonance imaging-based evaluations of multiorgan involvement in advanced prostate cancer. Eur Urol 2017; 71: 81–92. First citation in articleCrossref Medline, Google Scholar Saad F, Gleason DM, Murray R, et al.: Long-term efficacy of zoledronic acid for the prevention of skeletal complications in patients with metastatic hormone-refractory prostate cancer. J Natl Cancer Inst 2004; 96: 879–882. First citation in articleCrossref Medline, Google Scholar Fizazi K, Carducci M, Smith M , et al.: Denosumab versus zoledronic acid for treatment of bone metastases in men with castration-resistant prostate cancer: a randomised, double-blind study. Lancet 2011; 377: 813–822. First citation in articleCrossref Medline, Google Scholar Gillessen S, Omlin A, Attard G, et al.: Management of patients with advanced prostate cancer: recommendations of the St Gallen Advanced Prostate Cancer Consensus Conference (APCCC) 2015. Ann Oncol 2015; 26: 1589–1604. First citation in articleCrossref Medline, Google ScholarFiguresReferencesRelatedDetails Volume 107Issue 19September 2018ISSN: 1661-8157eISSN: 1661-8165 Received9. Dezember 2017Accepted7. Juni 2018 InformationPraxis (2018), 107, pp. 1043-1051 https://doi.org/10.1024/1661-8157/a003054.© 2018Hogrefe AGAcknowledgments:* Diese Autoren haben zu gleichen Teilen zu dieser Publikation beigetragen.PDF download

Development of clinical treatment protocols for radiation therapy is dependent on the availability of information on the biological efficacy of radiation doses.In order to gain robust data, multiple cell irradiation experiments must be performed at different dose points, using a range of cell lines.Therefore, it is important to be able to verify the biological effects of complex dose distributions in homeomorphic phantoms, alongside measurements of physical dose.One of the ENTERVISION projects focuses on the development of a biological dosimetric phantom.Firstly, the phantom and desired set-ups were evaluated then its suitability for radiobiology studies were accessed during a set of cell irradiations.Status: The phantom was irradiated mimicking the patients′ pathway starting with the CT scan, followed by treatment planning and being irradiated.For the irradiation, an uniform dose distribution was delivered with a proton beam and the process was repeated using a carbon ion beam.The dose was measured from pinpoint ionisation chambers readings and the uniformity was assessed with radiochromic films.The experimental results were compared with the TPS and Monte Carlo calculations.Using MC simulations it was also investigated how the simulation of a more detailed geometry would affect the obtained results.From the radiobiology studies the cell survival by analyzing its proliferation was studied.Results: The calculated mean deviation was below 2% for both beams used.This brings the result within the acceptance threshold as desired by CNAO QA procedures.Conclusion: The experimental results obtained showed good agreement with both TPS and Monte Carlo simulations.And the radiobiological results showed the possibility of multivariable analysis (LET and Dose) that is available to be done with the ENTERVISION Phantom.

UNLABELLED:Low-grade gliomas (LGGs) may harbor malignant foci, which are characterized by increased tumor cellularity and angiogenesis. We used diffusion-weighted MR imaging (apparent diffusion coefficient [ADC]) and PET with the amino acid O-(2-(18)F-fluorethyl)-L-tyrosine ((18)F-FET) to search for focal changes of diffusion (ADC) and amino acid uptake and to investigate whether focal changes in these parameters colocalize within LGGs. METHODS:We retrospectively selected 18 patients with nonenhancing LGG. All patients had undergone (18)F-FET PET and MR imaging for preoperative evaluation or for therapy monitoring in recurrent or progressive LGG. Region-of-interest analysis was performed to compare (18)F-FET uptake and ADC values in areas with focal intratumoral maximum metabolic activity and diffusion restriction and between tumor and normal brain. (18)F-FET uptake was normalized to the mean cerebellar uptake (ratio). ADC values were also compared with the (18)F-FET uptake on a voxel-by-voxel basis across the whole tumor. RESULTS:The mean focal maximum (mean ± SD, 1.69 ± 0.85) and global (18)F-FET uptake in tumors (1.14 ± 0.41) exceeded that of normal cortex (0.85 ± 0.09) and cerebrospinal fluid (0.82 ± 0.20). ADC values in the area with most restricted diffusion (1.07 ± 0.22 × 10(-3) mm(2)/s) and in the whole tumor (1.38 ± 0.27 × 10(-3) mm(2)/s) were in the range between normal cortex (0.73 ± 0.06 × 10(-3) mm(2)/s) and cerebrospinal fluid (2.84 ± 0.09 × 10(-3) mm(2)/s). (18)F-FET uptake did not correlate with corresponding (colocalizing) ADC values, either in the area with focal maximum metabolic activity or in the area with most restricted diffusion or in the whole tumor. CONCLUSION:There is no congruency between (18)F-FET uptake and diffusivity in nonenhancing LGG. Diffusion restriction in these tumors most likely represents changes in brain and tumor cell densities as well as alteration of water distribution and is probably not directly correlated with the density of tumor cells.

Purpose: Positron emission tomography (PET) with radiolabeled amino acids provides information on biopsy target and chemotherapy response in patients with low-grade gliomas (LGG). In this article, we addressed whether PET with F-18 choline (CHO) detects increased metabolism in F-18 fluoroethyltyrosine (FET)-negative LGG patients. Methods: Six LGG patients with nongadolinium-enhancing (magnetic resonance) FET-negative LGG were imaged with CHO PET. Regions of interest were positioned over tumor and contralateral brain. Uptake of FET and CHO was quantified as count ratio of tumor to contralateral brain. Results: The mean FET uptake ratio for FET-negative LGG was 0.95 ± 0.03 (mean ± standard deviation). Five tumors did not show increased uptake ratios for CHO (0.96 ± 0.12). Slightly increased CHO uptake was found in 1 patient (1.24), which, however, was not associated with tumor visualization. Conclusions: Amino acid and choline uptake appear to behave similar in nongadolinium-enhancing LGG. For clinical purposes, CHO PET is not superior to FET PET.

Die SPECT/CT-Untersuchung des Skelettes bereichert die nuklearmedizinische Knochendiag­nostik. Hierzu tragen die CT-basierte Photonenschwächungskorrektur der SPECT-Bilder, hohe Spezifität der Diagnose sowie CT-basierte akkurate Befundlokalisation am Knochen bzw. am Knochen umgebenden Weichteilgewebe bei. Durch diese Vorteile wird aus einem hochsensitiven, aber unspezifischen skelettszintigrafischen Befund ein hoch sensitiver und hoch spezifischer 2-in-1-SPECT/CT-Befund eines Knochenabschnittes, eines Skelettteilkörperabschnittes bzw. eines Skelett-Ganzkörper-SPECT/CT in analoger Weise wie bei der PET/CT und PET/MRT. Keine Frage, dass auch SPECT/MRT des Skelettes in absehbarer Zeit Eingang in die klinische Diag­nostik finden wird. Die SPECT/CT ergänzt die bildgebende Diagnostik angefangen bei häufigen Erkrankungen wie Rückenschmerzen über komplexe Krankheitsbilder wie das diabetische Fußsyndrom bis hin zu SPECT/CT-navigierten interventionellen Eingriffen am Skelett und Operations- bzw. Therapieplanungen. Die Bandbreite der SPECT/CT und die intensivierte kooperative Befundung seitens Nuklearmedizin und Radiologie erfreuen sich wachsender klinischer Wertschätzung z. B. in der Rheumatologie, Orthopädie, (Sport)Traumatologie und Onkologie und stellt eine willkommene Ergänzung bewährter Verfahren wie konventioneller Röntgenuntersuchung und MRT des Skelettes dar.

A three-phase bone scan, before conventional radiography shows morphological changes in CRPS 1, represents a valuable diagnostic tool thanks to the depiction of pathognomonic findings and the localisation ability in all 3 phases. It must be interpreted within the clinical context. In late or subsequent stages the lack of scintigraphic uptake seems to represent the end of the active disease process. The role of three-phase bone scintigraphy in CRPS I is to support or even confirm the diagnosis, given its various presentations. Furthermore, it enables exclusion of other diagnoses such as arthritis, benign or malignant bony lesions, or even metabolic bone diseases such as Paget's disease, particularly if an integrated SPECT/CT is added. Moreover, the earlier the diagnosis is finally established and treatment of CRPS I is initiated, the better the prognosis. Therefore, bone scintigraphy potentially has a major impact on patient management of this disorder.

. Abstract ▼ A three-phase bone scan, before conventional radiography shows morphological changes in CRPS 1, represents a valuable diagnostic tool thanks to the depiction of pathognomonic fi ndings and the localisation ability in all 3 phases. It must be interpreted within the clinical context. In late or subsequent stages the lack of scintigraphic uptake seems to represent the end of the active disease process. The role of three-phase bone scintigraphy in CRPS I is to support or even con-fi rm the diagnosis, given its various presentations. Furthermore, it enables exclusion of other diagnoses such as arthritis, benign or malignant bony lesions, or even metabolic bone diseases such as Paget ’ s disease, particularly if an integrated SPECT / CT is added. Moreover, the earlier the diagnosis is fi nally established and treatment of CRPS I is initiated, the better the prognosis. Therefore, bone scintigraphy potentially has a major impact on patient management of this disorder.

1-2 18 Multizentrische Phase-II-Studie mit pegyliertem liposomalen Doxorubicin in Kombination mit Vinorelbin als Erstlinientherapie des fortgeschrittenen Mammakarzinoms bei älteren Patientinnen Mlineritsch, B. (Salzburg); Schabel-Moser, R. (Graz); Andel, J. (Steyr); Fridrik, M. (Linz); Moik, M.; Mayer, P.; Russ, G.; Rass, C.; Greil, R. (Salzburg) on behalf of the Arbeitsgemeinschaft medikamentöse Tumortherapie Study Group (AGMT)

BACKGROUND:Only responding patients benefit from preoperative therapy for locally advanced esophageal carcinoma. Early detection of non-responders may avoid futile treatment and delayed surgery.PATIENTS AND METHODS:In a multi-center phase ll trial, patients with resectable, locally advanced esophageal carcinoma were treated with 2 cycles of induction chemotherapy followed by chemoradiotherapy (CRT) and surgery. Positron emission tomography with 2[fluorine-18]fluoro-2-deoxy-d-glucose (FDG-PET) was performed at baseline and after induction chemotherapy. The metabolic response was correlated with tumor regression grade (TRG). A decrease in FDG tumor uptake of less than 40% was prospectively hypothesized as a predictor for histopathological non-response (TRG > 2) after CRT.RESULTS:45 patients were included. The median decrease in FDG tumor uptake after chemotherapy correlated well with TRG after completion of CRT (p = 0.021). For an individual patient, less than 40% decrease in FDG tumor uptake after induction chemotherapy predicted histopathological non-response after completion of CRT, with a sensitivity of 68% and a specificity of 52% (positive predictive value 58%, negative predictive value 63%).CONCLUSIONS:Metabolic response correlated with histopathology after preoperative therapy. However, FDG-PET did not predict non-response after induction chemotherapy with sufficient clinical accuracy to justify withdrawal of subsequent CRT and selection of patients to proceed directly to surgery.