ZUSAMMENFASSUNG Hintergrund Der extrakorporale hochintensive fokussierte Ultraschall (HIFU) ist ein vielversprechendes Verfahren zur nichtinvasiven Thermoablation gutartigen und bösartigen Gewebes. Derzeitige HIFU-Therapien nutzen Ultraschall (US-HIFU) oder MRT (MR-HIFU) zur Bildsteuerung mit der Möglichkeit zur integrierten Therapieplanung, Echtzeit-Therapiekontrolle (räumliche Orientierung und Temperatursteuerung) und Therapieevaluation. Methode Dieser Übersichtsartikel basiert auf Publikationen aus Fachzeitschriften, die die thermale Ablation mittels HIFU thematisieren, und beinhaltet zudem eigene klinische Ergebnisse. Es wird ein kurzer Überblick über die häufigsten CEzertifizierten klinischen Applikationen für MR-HIFU gegeben. Ergebnisse Im Laufe des letzten Jahrzehnts erhielten zahlreiche HIFU-basierte Applikationen die Zulassung in diversen Ländern. Im Speziellen ist MR-HIFU nun zugelassen für die Therapie von Uterusmyomen, Linderung von Knochenschmerzen, der Ablation der Prostata und die Therapie des essenziellen Tremors als erste neurologische Applikationsform. Schlussfolgerung MR-HIFU ist eine patientenfreundliche, nichtinvasive Methode zur Thermoablation, welche mittlerweile für mehrere klinische Applikationen zugelassen wurde. Insgesamt bestätigen die bisherigen klinischen Daten die Wirksamkeit und Sicherheit der Therapie sowie die Kosteneffizienz der Methode.Kernaussagen: ▪ HIFU stellt eine vielversprechende Technik zur nichtinvasiven Thermoablation von Gewebe dar. ▪ HIFU wird üblicherweise unter Bildkontrolle mittels Ultraschall (US-HIFU) oder MRT (MR-HIFU) durchgeführt. ▪ Die bevorzugte Bildkontrolle (US-HIFU vs. MR-HIFU) hängt von der geplanten Applikation ab. ▪ MRT bietet einen höheren Weichteilkontrast zur Therapieplanung, eine nahezu in Echtzeit und nichtinvasiv erfolgende Temperaturkontrolle und eine postinterventionelle Therapieevaluation. ▪ MR-HIFU ist CE-zertifiziert für die Therapie von Uterusmyomen, Linderung von Knochenschmerzen, Ablation der Prostata und Therapie des essenziellen Tremors. ABSTR AC TBackground Extracorporeal high-intensity focused ultrasound (HIFU) is a promising method for the noninvasive thermal ablation of benign and malignant tissue. Current HIFU treatments are performed under ultrasound (US-HIFU) or magnetic resonance (MR-HIFU) image guidance offering integrated therapy planning, real-time control (spatial and temperature guidance) and evaluation.Methods This review is based on publications in peer-reviewed journals addressing thermal ablation using HIFU and includes our own clinical results as well. The technical background of HIFU is explained with an emphasis on MR-HIFU applications. A brief overview of the most commonly performed CE-approved clinical applications for MR-HIFU is given.Results Over the last decade, several HIFU-based applications have received clinical approval in various countries. In particular, MR-HIFU is now approved for the clinical treatment of uterine fibroids, palliation of bone pain, ablation of the prostate and treatment of essential tre...

Semiautomatic short-axis diameter, particularly volume measurements, of lymph nodes are, irrespective of location, precise in terms of reproducibility and appear to be considerably more reliable than manual lymph node assessment.

The aim of this study was to determine whether individually tailored protocols for the injection of contrast medium (CM) result in higher and more homogeneous vascular attenuation throughout the coronary arteries at coronary CT angiography compared with conventional injection protocols using fixed injection parameters. Of 120 patients included in the study, 80 patients were randomized into two groups. Group 1 received 80 mL of CM at 6 mL/s. For group 2 injection parameters were individually adjusted to patient weight, the duration of CT data acquisition, and attenuation parameters following a test bolus. In the control group (group 3) the volume of CM was adjusted to the duration of CT data acquisition and injected at 5 mL/s. Attenuation was measured in the proximal, middle, and distal right coronary artery (RCA), in the proximal and middle left anterior descending artery (LAD), and in cranial and caudal sections of both ventricles. Patient parameters, scan delay, and scan duration did not differ significantly between the groups. Mean CM volume was 82.5 mL (flow rate 5.1 mL/s) in group 2 and 73.5 mL in group 3. Attenuation in both RCA and LAD was significantly higher for group 2 vs. group 3 (RCA: 414.9 + or - 49.9)-396.1(+ or - 52.1) HU vs. 366.0(+ or - 64.3)-341.6(+ or - 72.5) HU; LAD: 398.9(+ or - 48.6)-364.6(+ or - 44.6) HU vs. 356.3(+ or - 69.5)-323.0(+ or - 67.2) HU). For group 1 vs. group 2 only attenuation in the distal RCA differed significantly: 396.1(+ or - 52.1) vs. 370.7(+ or - 70.5) HU. Individually tailored CM injection protocols yield higher attenuation, especially in the distal segments of the coronary vessels, compared with injection protocols using fixed injection parameters.

Double-syringe injectors used with disposable or prefilled contrast agent syringes, as well as roller pump injectors, ensure hygienic conditions in clinical routine. However, time efficiency and handling are aspects that favor prefilled and roller pump systems.

Use of prefilled contrast syringes with single-use saline syringes is associated with time-efficient assembly of injection systems and prevents microbiologic contamination in clinical routine, especially in the care of immunocompromised patients.

PURPOSE Third-generation epidermal growth factor receptor ( EGFR) tyrosine kinase inhibitors (TKIs) are effective in acquired resistance (AR) to early-generation EGFR TKIs in EGFR-mutant lung cancer. However, efficacy is marked by interindividual heterogeneity. We present the molecular profiles of pretreatment and post-treatment samples from patients treated with third-generation EGFR TKIs and their impact on treatment outcomes. METHODS Using the databases of two lung cancer networks and two lung cancer centers, we molecularly characterized 124 patients with EGFR p.T790M-positive AR to early-generation EGFR TKIs. In 56 patients, correlative analyses of third-generation EGFR TKI treatment outcomes and molecular characteristics were feasible. In addition, matched post-treatment biopsy samples were collected for 29 patients with progression to third-generation EGFR TKIs. RESULTS Co-occurring genetic aberrations were found in 74.4% of EGFR p.T790-positive samples (n = 124). Mutations in TP53 were the most frequent aberrations detected (44.5%; n = 53) and had no significant impact on third-generation EGFR TKI treatment. Mesenchymal-epithelial transition factor ( MET) amplifications were found in 5% of samples (n = 6) and reduced efficacy of third-generation EGFR TKIs significantly (eg, median progression-free survival, 1.0 months; 95% CI, 0.37 to 1.72 v 8.2 months; 95% CI, 1.69 to 14.77 months; P ≤ .001). Genetic changes in the 29 samples with AR to third-generation EGFR TKIs were found in EGFR (eg, p.T790M loss, acquisition of p.C797S or p.G724S) or in other genes (eg, MET amplification, KRAS mutations). CONCLUSION Additional genetic aberrations are frequent in EGFR-mutant lung cancer and may mediate innate and AR to third-generation EGFR TKIs. MET amplification was strongly associated with primary treatment failure and was a common mechanism of AR to third-generation EGFR TKIs. Thus, combining EGFR inhibitors with TKIs targeting common mechanisms of resistance may delay AR.

Inflammatory myofibroblastic tumors are rare mesenchymal neoplasms frequently harboring oncogenic chromosomal rearrangements, most commonly, involving the ALK (anaplastic lymphoma kinase) gene. Treatment of this molecularly defined subgroup with the anaplastic lymphoma kinase inhibitor crizotinib has shown to be effective. However, comparable to lung adenocarcinoma, resistance inevitably develops. Second generation anaplastic lymphoma kinase inhibitors such as ceritinib are able to overcome acquired resistance to crizotinib. Here, we report the case of a patient with an inflammatory myofibroblastic tumors harboring a DCTN1-ALK fusion who developed resistance to crizotinib treatment. Next-generation sequencing of a rebiopsy sample revealed the acquisition of the ALK G1269A mutation as a mechanism of resistance. Therapy with ceritinib resulted in a short but profound clinical, metabolic and morphologic response. This case illustrates that (i) different tumor entities may share similar oncogenic driver mechanisms, rendering them vulnerable for the same therapeutic substances and (ii) likewise, the same mode of resistance may occur under targeted therapy among different tumor entities.

No abstract