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LIDAR (Light Detection and Ranging) is one of the most recent technologies in surveying and mapping. LIDAR is based on the combination of three different data collection tools: a laser scanner mounted on an aircraft, a Global Positioning System (GPS) used in phase differential kinematic modality to provide the sensor position and an Inertial Navigation System (INS) to provide the orientation. The laser sends towards the ground an infrared signal, which is reflected back to the sensor. The time employed by the signal, given the aircraft position and attitude, allows computation of the earth point elevation. In standard conditions, taking into account the flight (speed 200–250 km/hour, altitude 500–2,000 m) and sensor characteristics (scan angle ± 10–20 degrees, emission rate 2,000–50,000 pulses per second), earth elevations are collected within a density of one point every 0.5–3 m. The technology allows us therefore to obtain very accurate (5–20 cm) and high resolution Digital Surface Models (DSM). For many applications, the Digital Terrain Model (DTM) is needed: we have to automatically detect and discard from the previous DSM all the features (buildings, trees, etc.) present on the terrain. This paper describes a procedure that has been implemented within GRASS to construct DTMs from LIDAR source data. [ABSTRACT FROM AUTHOR]

Background & Aims: The highly heterogeneous cellular and molecular makeup of pancreatic ductal adenocarcinoma (PDAC) not only fosters exceptionally aggressive tumor biology, but contradicts the current concept of one-size-fits-all therapeutic strategies to combat PDAC. Therefore, we aimed to exploit the tumor biological implication and therapeutic vulnerabilities of a clinically relevant molecular PDAC subgroup characterized by SMAD4 deficiency and high expression of the nuclear factor of activated T cells (SMAD4 -/- /NFATc1 High )., Methods: Transcriptomic and clinical data were analyzed to determine the prognostic relevance of SMAD4 -/- /NFATc1 High cancers. In vitro and in vivo oncogenic transcription factor complex formation was studied by immunoprecipitation, proximity ligation assays, and validated cross model and species. The impact of SMAD4 status on therapeutically targeting canonical KRAS signaling was mechanistically deciphered and corroborated by genome-wide gene expression analysis and genetic perturbation experiments, respectively. Validation of a novel tailored therapeutic option was conducted in patient-derived organoids and cells and transgenic as well as orthotopic PDAC models., Results: Our findings determined the tumor biology of an aggressive and chemotherapy-resistant SMAD4 -/- /NFATc1 High subgroup. Mechanistically, we identify SMAD4 deficiency as a molecular prerequisite for the formation of an oncogenic NFATc1/SMAD3/cJUN transcription factor complex, which drives the expression of RRM1/2. RRM1/2 replenishes nucleoside pools that directly compete with metabolized gemcitabine for DNA strand incorporation. Disassembly of the NFATc1/SMAD3/cJUN complex by mitogen-activated protein kinase signaling inhibition normalizes RRM1/2 expression and synergizes with gemcitabine treatment in vivo to reduce the proliferative index., Conclusions: Our results suggest that PDAC characterized by SMAD4 deficiency and oncogenic NFATc1/SMAD3/cJUN complex formation exposes sensitivity to a mitogen-activated protein kinase signaling inhibition and gemcitabine combination therapy., (Copyright © 2024 AGA Institute. Published by Elsevier Inc. All rights reserved.)

Background: Pancreatic ductal adenocarcinoma (PDAC) remains a major challenge in cancer medicine and is characterized by a 5-year survival rate of <10%. Compelling evidence suggests that the devastating disease outcome of PDAC patients is linked to a high degree of intra- and interindividual tumor heterogeneity, which is predominantly installed at the level of gene transcription. The cellular and molecular complexities of the disease explain the poor efficacy of "one-size-fits-all" therapeutic approaches in PDAC treatment and strongly argue for pursuing tailored therapeutic strategies to tackle PDAC. In a highly dynamic manner, a network of transcription factors and epigenetic regulatory proteins temporally and spatially control the diverse transcriptomic states determining PDAC heterogeneity. Given the reversibility of epigenetic processes, pharmacological intervention with key epigenetic drivers of PDAC heterogeneity appeals as a promising concept to shift the transcriptomic phenotype of PDAC toward a less aggressive and more chemosensible state., Summary: In this review, we discuss the chances and pitfalls of epigenetic treatment strategies in overcoming and shifting molecular and cellular PDAC heterogeneities in order to combat PDAC. To this end, we utilized the keywords "pancreatic cancer," "heterogeneity," and "epigenetics" to search for relevant articles on the database PubMed and selected interventional studies enrolling PDAC patients as displayed in clinicaltrails.gov to generate a synopsis of clinical trials involving epigenetic targeting., Key Messages: Targeting epigenetic regulators in PDAC represents a promising concept to reprogram molecular and cellular tumor heterogeneities in the pancreas and hence to modulate the PDAC phenotype in favor of a less aggressive and more therapy susceptible disease course. However, we just start to understand the complex interactions of epigenetic regulators in controlling PDAC plasticity, and a clinical breakthrough utilizing epigenetic targeting in PDAC patients has not been achieved yet. Nevertheless, increasing translational efforts which consider the pleiotropic effects of targeting epigenetic regulation in different cellular compartments of the tumor and that focus on the utility and sequence of combinatory treatment approaches might pave the way toward novel epigenetic treatment strategies in PDAC therapy., Competing Interests: The authors have no conflict of interest to declare., (Copyright © 2021 by S. Karger AG, Basel.)