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Purpose: Due to limited imaging options, the visualization of a local relapse of prostate cancer used to pose a considerable challenge. However, since the integration of 18F-PSMA-1007-PET/CT into the clinic, a relapsed tumor can now easily be detected by hybrid imaging. The present study aimed to evaluate and map the allocate relapse in a large cohort of prostate cancer patients focusing on individual patient management conclusions for radiation therapy. Procedures: The current study included 135 men with prostate cancer after primary treatment who underwent 18F-PSMA-1007-PET/CT due to biochemical relapse detecting a local relapse. Imaging data were reassessed and analyzed with regard to relapse locations. For the correlation of tumor foci with clinical data, we used binary logistic regression models as well as the Kruskal–Wallis test and Mann–Whitney test. Results: In total, 69.6% of all patients (mean age: 65 years) underwent prostatectomy while 30.4% underwent radiation therapy. PET imaging detected most frequently a unifocal relapse (72.6%). There was a statistically significantly higher rate of ipsilateral cases among the relapsed tumors. Comparing both treatment approaches, tumors relapsed most commonly within the posterior region after surgery and transition/peripheral zone after radiation therapy, respectively. Conclusions: The present study confirms that 18F-PSMA-1007-PET/CT is highly suitable for the localization and allocation of a local relapse in patients with prostate cancer. The data enable further optimizing dose prescriptions and target volume delineations of radiation therapy in the future. [ABSTRACT FROM AUTHOR]

Tyrosine kinase inhibitors (TKI) have improved prognosis in metastatic anaplastic lymphoma kinase (ALK)‐driven lung adenocarcinoma, but patient outcomes vary widely. We retrospectively analyzed the clinical course of all cases with assessable baseline TP53 status and/or ALK fusion variant treated at our institutions (n = 102). TP53 mutations were present in 17/87 (20%) and the echinoderm microtubule‐associated protein‐like 4 (EML4)‐ALK variant 3 (V3) in 41/92 (45%) patients. The number of metastatic sites at diagnosis was affected more by the presence of V3 than by TP53 mutations, and highest with both factors (mean 5.3, p < 0.001). Under treatment with ALK TKI, progression‐free survival (PFS) was shorter with either TP53 mutations or V3, while double positive cases appeared to have an even higher risk (hazard ratio [HR] = 2.9, p = 0.015). The negative effect of V3 on PFS of TKI‐treated patients was strong already in the first line (HR = 2.5, p = 0.037) and decreased subsequently, whereas a trend for PFS impairment under first‐line TKI by TP53 mutations became stronger and statistically significant only when considering all treatment lines together. Overall survival was impaired more by TP53 mutations (HR = 4.9, p = 0.003) than by V3 (HR = 2.4, p = 0.018), while patients with TP53 mutated V3‐driven tumors carried the highest risk of death (HR = 9.1, p = 0.02). Thus, TP53 mutations and V3 are independently associated with enhanced metastatic spread, shorter TKI responses and inferior overall survival in ALK+ lung adenocarcinoma. Both markers could assist selection of cases for more aggressive management and guide development of novel therapeutic strategies. In combination, they define a patient subset with very poor outcome. What's new? This is the first study on the clinical impact of TP53 mutations in ALK‐driven lung adenocarcinoma that simultaneously considers the adverse effects of EML4‐ALK fusion variant 3. Both molecular features are independently associated with more aggressive disease course, including metastases to more organs, shorter responses to tyrosine kinase inhibitors, and worse overall survival. Their effects appear to be synergistic, and double‐positive cases have a very poor outcome. Both markers could assist patient selection for more aggressive management and help develop novel therapeutic strategies. [ABSTRACT FROM AUTHOR]

The Mw 7.8 Kaikōura earthquake ruptured at least 17 faults for a distance of approximately 165 km across the New Zealand plate boundary zone in the northeastern South Island. In the epicentral area, the earthquake produced displacement at the surface on The Humps, Leader, Conway-Charwell, and Stone Jug faults, which are the primary focus of this article. Analysis of the surface rupture, aftershocks, focal mechanisms, and Interferometric Synthetic Aperture Radar (InSAR)-derived uplift from the earthquake provides new information on the dimensions, geometries, and kinematics of these faults, which was not previously available from the active faults or bedrock structure. Relocation of the mainshock indicates that it initiated on The Humps fault with rupture mainly propagating to the northeast. The resulting ground ruptures comprise two intersecting sets that strike east-northeast with right-lateral and reverse displacements, and north-northwest to north-northeast faults with left-lateral reverse displacement. Reverse faulting was accompanied by folding associated with differential uplift and bedding-parallel slip. On a regional scale, faulting accommodated transpression consistent with the oblique relative plate motion vector and Quaternary bedrock deformation. Whereas the kinematics of faults that ruptured during the earthquake was predictable, the fault-rupture complexity could not have been anticipated or explicitly incorporated into seismic hazard models. [ABSTRACT FROM AUTHOR]

A moment magnitude (Mw) 6.2 earthquake struck beneath the outer suburbs of Christchurch, New Zealand's second largest city, on 22 February 2011 local time. The Christchurch earthquake was the deadliest in New Zealand since the 1931 Mw 7.8 Hawkes Bay earthquake and the most expensive in New Zealand's recorded history. The effects of the earthquake on the region's population and infrastructure were severe including 181 fatalities, widespread building damage, liquefaction and landslides. The Christchurch earthquake was an aftershock of the Mw 7.1 Darfield Earthquake of September 2010, occurring towards the eastern edge of the aftershock zone. This was a low recurrence earthquake for New Zealand and occurred on a fault unrecognised prior to the Darfield event. Geodetic and seismological source models show that oblique-reverse slip occurred along a northeast–southwest-striking fault dipping southeast at c. 69°, with maximum slip at 3–4 km depth. Ground motions during the earthquake were unusually large at near-source distances for an earthquake of its size, registering up to 2.2 g (vertical) and 1.7 g (horizontal) near the epicentre and up to 0.8 g (vertical) and 0.7 g (horizontal) in the city centre. Acceleration response spectra exceeded 2500 yr building design codes and estimates based on standard New Zealand models. The earthquake was associated with high apparent stress indicative of a strong fault. Furthermore, rupture in an updip direction towards Christchurch likely led to strong directivity effects in the city. Site effects including long period amplification and near-surface effects also contributed to the severity of ground motions. [ABSTRACT FROM AUTHOR]