An unsupervised domain adaptation brain CT segmentation method across image modalities and diseases

International audienceComputed tomography (CT) is the primary diagnostic tool for brain diseases. To determine the appropriate treatment plan, it is necessary to ascertain the patient's bleeding volume. Automatic segmentation algorithms for hemorrhagic lesions can significantly improve efficiency and avoid treatment delays. However, for deep supervised learning algorithms, a large amount of labeled training data is usually required, making them difficult to apply clinically. In this study, we propose an unsupervised domain adaptation method that is an unsupervised domain adaptation segmentation model that can be trained across modalities and diseases. We call it AMD-DAS for brain CT hemorrhage segmentation tasks. This circumvents the heavy data labeling task by converting the source domain data (MRI with glioma) to our task's required data (CT with Intraparenchymal hemorrhage (IPH)). Our model implements a two-stage domain adaptation process to achieve this objective. In the first stage, we train a pseudo-CT image synthesis network using the CycleGAN architecture through a matching mechanism and domain adaptation approach. In the second stage, we use the model trained in the first stage to synthesize the pseudo-CT images. We use the pseudo-CT with source domain labels and real CT images to train a domain-adaptation segmentation model. Our method exhibits a better performance than the basic one-stage domain adaptation segmentation method (+11.55 Dice score) and achieves an 86.93 Dice score in the IPH unsupervised segmentation task. Our model can be trained without using a ground-truth label, therefore increasing its application potential. Our implementation is publicly available at https://github.com/GuanghuiFU/AMD-DAS-Brain-CT-Segmentation

PLOD3 contributes to HER-2 therapy resistance in gastric cancer through FoxO3/Survivin pathway

Abstract Human epidermal growth factor receptor 2 (HER-2), a famous therapeutic target for breast cancer, is also associated with an increased risk of recurrence and poor outcomes of other malignancies, including gastric cancer. Yet the mechanism of HER-2 therapy resistance remains controversial due to the heterogeneity of gastric adenocarcinoma. We know, Procollagen-Lysine,2-Oxoglutarate 5-Dioxygenase 3 (PLOD3), a key gene coding enzymes that catalyze the lysyl hydroxylation of extracellular matrix collagen, plays an important contributor to HER-2 targeting agent Trastuzumab resistance in gastric cancer. Herein, we analyzed clinical samples of gastric cancer patients and gastric cancer cell lines and identified PLOD3, unveiled that depletion of PLOD3 leads to decreased cell proliferation, tumor growth and Trastuzumab sensitivity in these Trastuzumab resistant GC cell lines. Clinically, increased PLOD3 expression correlates with decreased Trastuzumab therapy responsiveness in GC patients. Mechanistically, we show that PLOD3 represses tumor suppressor FoxO3 expression, therefore upregulating Survivin protein expression that contributes to Trastuzumab resistance in GC. Therefore, our study identifies a new signaling axis PLOD3-FoxO3- Survivin pathway that may be therapeutically targeted in HER-2 positive gastric cancer